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rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00835.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00830.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00841.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12090"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00850.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00853.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00884.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12058"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12040"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12093"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00940.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00944.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00956.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00965.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00964.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00959.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12104"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12095"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12094"/></rdf:Seq></items></channel><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12065" xmlns="http://purl.org/rss/1.0/"><title>A double-blind placebo-controlled clinical evaluation of MultiStem for the treatment of ischemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12065</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A double-blind placebo-controlled clinical evaluation of MultiStem for the treatment of ischemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">David C. Hess, Cathy A. Sila, Anthony J. Furlan, Larry R. Wechsler, Jeffrey A. Switzer, Robert W. Mays</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-22T04:39:23.613336-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12065</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12065</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12065</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12065-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>There is growing interest in neurorestorative and reparative therapies after acute stroke. MultiStem® is an allogeneic cell therapy treatment comprising a population of multipotent adherent bone marrow cells that has shown safety in clinical trials of myocardial infarction and graft vs. host disease, as well as preclinical evidence of activity in stroke and other neurological damage models. MultiStem is now being evaluated in a clinical trial in patients that have suffered an ischemic stroke, in which the product is administered intravenously 24–36 h after the ischemic event.</p></div></div>
<div class="section" id="ijs12065-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The Phase 2 randomized, double-blind, placebo-controlled, multicenter dose-escalation trial will consist of three treatment cohorts, including a placebo group, and two treatment groups involving dose tiers of either 400 million or 1200 million cells per patient. Patients will be treated at 24–36 h after stroke. The two primary objectives are to determine the highest well-tolerated and safe single dose of MultiStem up to a maximum of 1200 million total cells in subjects with ischemic stroke and to determine the efficacy of MultiStem on functional outcome in subjects with stroke as measured by the modified Rankin Scale at 90 days. Patients will also be evaluated using the National Institutes of Health Stroke Scale and Barthel Index. The study will explore other aspects including, uniquely, the measurement of spleen size after stroke by magnetic resonance imaging or computed tomography imaging.</p></div></div>
<div class="section" id="ijs12065-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions and future direction</h4><div class="para"><p>If MultiStem is safe and there is a signal of efficacy, a late stage phase IIb-III trial is planned.</p></div></div>
]]></content:encoded><description>

Background
There is growing interest in neurorestorative and reparative therapies after acute stroke. MultiStem® is an allogeneic cell therapy treatment comprising a population of multipotent adherent bone marrow cells that has shown safety in clinical trials of myocardial infarction and graft vs. host disease, as well as preclinical evidence of activity in stroke and other neurological damage models. MultiStem is now being evaluated in a clinical trial in patients that have suffered an ischemic stroke, in which the product is administered intravenously 24–36 h after the ischemic event.


Methods
The Phase 2 randomized, double-blind, placebo-controlled, multicenter dose-escalation trial will consist of three treatment cohorts, including a placebo group, and two treatment groups involving dose tiers of either 400 million or 1200 million cells per patient. Patients will be treated at 24–36 h after stroke. The two primary objectives are to determine the highest well-tolerated and safe single dose of MultiStem up to a maximum of 1200 million total cells in subjects with ischemic stroke and to determine the efficacy of MultiStem on functional outcome in subjects with stroke as measured by the modified Rankin Scale at 90 days. Patients will also be evaluated using the National Institutes of Health Stroke Scale and Barthel Index. The study will explore other aspects including, uniquely, the measurement of spleen size after stroke by magnetic resonance imaging or computed tomography imaging.


Conclusions and future direction
If MultiStem is safe and there is a signal of efficacy, a late stage phase IIb-III trial is planned.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12062" xmlns="http://purl.org/rss/1.0/"><title>Past, present, and future of stroke in middle-income countries: the Brazilian experience</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12062</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Past, present, and future of stroke in middle-income countries: the Brazilian experience</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sheila Cristina Ouriques Martins, Octávio Marques Pontes-Neto, Cloer Vescia Alves, Gabriel Rodriguez Freitas, Jamary Oliveira Filho, Elza Dias Tosta, Norberto Luiz Cabral, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-22T04:39:08.30403-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12062</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12062</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12062</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12062-sec-1001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Stroke is one of the major public health challenges in middle-income countries. Brazil is the world's sixth largest economy but was clearly behind the milestones in the fight against stroke, which is the leading cause of death and disability in the country. Nevertheless, many initiatives are now reshaping stroke prevention, care, and rehabilitation in the country.</p></div></div>
<div class="section" id="ijs12062-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The present article discusses the evolution of stroke care in Brazil over the last decade.</p></div></div>
<div class="section" id="ijs12062-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We describe the main characteristics of stroke care before 2008; a pilot study in a Southern Brazilian city between 2008 and 2010, the Brazilian Stroke Project initiative; and the 2012 National Stroke Policy Act.</p></div></div>
<div class="section" id="ijs12062-sec-1004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The National Stroke Project was followed by a major increased on the number of stroke center in the country. The key elements of the 2012 National Stroke Policy Act included: definition of the requirements and levels of stroke centers; improved reimbursement for stroke care; promotion of stroke telemedicine; definition of the Line of Stroke Care (to integrate available resources and other health programs); increased funding for stroke rehabilitation; funding for training of healthcare professionals and initiatives to increase awareness about stroke within the population.</p></div></div>
<div class="section" id="ijs12062-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The evolution of stroke care in Brazil over the last decade is a pathway that exemplifies the challenges that middle-income countries have to face in order to improve stroke prevention, treatment and rehabilitation. The reported Brazilian experience can be extrapolated to understand the past, present, and future of stroke care in middle-income countries.</p></div></div>
]]></content:encoded><description>

Background
Stroke is one of the major public health challenges in middle-income countries. Brazil is the world's sixth largest economy but was clearly behind the milestones in the fight against stroke, which is the leading cause of death and disability in the country. Nevertheless, many initiatives are now reshaping stroke prevention, care, and rehabilitation in the country.


Aims
The present article discusses the evolution of stroke care in Brazil over the last decade.

 Methods
We describe the main characteristics of stroke care before 2008; a pilot study in a Southern Brazilian city between 2008 and 2010, the Brazilian Stroke Project initiative; and the 2012 National Stroke Policy Act.

 Results
The National Stroke Project was followed by a major increased on the number of stroke center in the country. The key elements of the 2012 National Stroke Policy Act included: definition of the requirements and levels of stroke centers; improved reimbursement for stroke care; promotion of stroke telemedicine; definition of the Line of Stroke Care (to integrate available resources and other health programs); increased funding for stroke rehabilitation; funding for training of healthcare professionals and initiatives to increase awareness about stroke within the population.


Conclusions
The evolution of stroke care in Brazil over the last decade is a pathway that exemplifies the challenges that middle-income countries have to face in order to improve stroke prevention, treatment and rehabilitation. The reported Brazilian experience can be extrapolated to understand the past, present, and future of stroke care in middle-income countries.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12059" xmlns="http://purl.org/rss/1.0/"><title>Thrombolysis for acute ischemic stroke in South Africa</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12059</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Thrombolysis for acute ischemic stroke in South Africa</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Alan Bryer, Sean Wasserman</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-22T04:38:57.053932-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12059</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12059</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12059</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Short Report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12059-sec-1001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Stroke is an important cause of death and disability in sub-Saharan Africa. Thrombolysis with recombinant tissue plasminogen activator (tPA) is the only effective therapy for acute ischaemic stroke. Essential requirements for stroke thrombolysis include availability of CT scanning and arrival at hospital within 4.5 hours of symptom onset. However, in developing countries where the prerequisites are met at certain centres, the efficacy and safety of thrombolysis have not been firmly established.</p></div></div>
<div class="section" id="ijs12059-sec-1002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>We aimed to evaluate the early outcomes and safety of stroke thrombolysis in a South African setting.</p></div></div>
<div class="section" id="ijs12059-sec-1003" xmlns="http://www.w3.org/1999/xhtml"><h4>Method</h4><div class="para"><p>We conducted a prospective observational study of all stroke patients receiving tPA for thrombolysis over the period January 2000 to February 2011. The primary outcome measure was the proportion of patients achieving significant early neurological recovery defined as an improvement of four or more points on the NIHSS score at discharge. The safety endpoint was the rate of symptomatic intracranial haemorrhage (SICH) and death.</p></div></div>
<div class="section" id="ijs12059-sec-1004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Forty-two patients received thrombolysis over the study period. Sixty-seven percent achieved significant neurological improvement. The majority of patients (53.8%) were discharged home, and by the time of discharge 17 (40.5%) were functionally independent. SICH occurred in 2 (4.8%) patients with an overall mortality rate of 7.1%.</p></div></div>
<div class="section" id="ijs12059-sec-1005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Our findings indicate that the use of thrombolysis in routine clinical practice in a South African setting has similar safety and early efficacy outcomes to developed and other developing countries.</p></div></div>
]]></content:encoded><description>

Background
Stroke is an important cause of death and disability in sub-Saharan Africa. Thrombolysis with recombinant tissue plasminogen activator (tPA) is the only effective therapy for acute ischaemic stroke. Essential requirements for stroke thrombolysis include availability of CT scanning and arrival at hospital within 4.5 hours of symptom onset. However, in developing countries where the prerequisites are met at certain centres, the efficacy and safety of thrombolysis have not been firmly established.


Aims
We aimed to evaluate the early outcomes and safety of stroke thrombolysis in a South African setting.

 Method
We conducted a prospective observational study of all stroke patients receiving tPA for thrombolysis over the period January 2000 to February 2011. The primary outcome measure was the proportion of patients achieving significant early neurological recovery defined as an improvement of four or more points on the NIHSS score at discharge. The safety endpoint was the rate of symptomatic intracranial haemorrhage (SICH) and death.


Results
Forty-two patients received thrombolysis over the study period. Sixty-seven percent achieved significant neurological improvement. The majority of patients (53.8%) were discharged home, and by the time of discharge 17 (40.5%) were functionally independent. SICH occurred in 2 (4.8%) patients with an overall mortality rate of 7.1%.


Conclusions
Our findings indicate that the use of thrombolysis in routine clinical practice in a South African setting has similar safety and early efficacy outcomes to developed and other developing countries.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12056" xmlns="http://purl.org/rss/1.0/"><title>Functional cortical reorganization after low-frequency repetitive transcranial magnetic stimulation plus intensive occupational therapy for upper limb hemiparesis: evaluation by functional magnetic resonance imaging in poststroke patients</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12056</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Functional cortical reorganization after low-frequency repetitive transcranial magnetic stimulation plus intensive occupational therapy for upper limb hemiparesis: evaluation by functional magnetic resonance imaging in poststroke patients</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Naoki Yamada, Wataru Kakuda, Atsushi Senoo, Takahiro Kondo, Sugao Mitani, Masato Shimizu, Masahiro Abo</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-22T04:38:53.650605-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12056</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12056</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12056</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12056-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Low-frequency repetitive transcranial magnetic stimulation of the nonlesional hemisphere combined with occupational therapy significantly improves motor function of the affected upper limb in poststroke hemiparetic patients, but the recovery mechanism remains unclear.</p></div></div>
<div class="section" id="ijs12056-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>To investigate the recovery mechanism using functional magnetic resonance imaging.</p></div></div>
<div class="section" id="ijs12056-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Forty-seven poststroke hemiparetic patients were hospitalized to receive 12 sessions of 40-min low-frequency repetitive transcranial magnetic stimulation over the nonlesional hemisphere and daily occupational therapy for 15 days. Motor function was evaluated with the Fugl–Meyer Assessment and Wolf Motor Function Test. The functional magnetic resonance imaging with motor tasks was performed at admission and discharge. The laterality index of activated voxel number in Brodmann areas 4 and 6 on functional magnetic resonance imaging was calculated (laterality index range of −1 to +1). Patients were divided into two groups based on functional magnetic resonance imaging findings before the intervention: group 1: patients who showed bilateral activation (<em>n</em> = 27); group 2: patients with unilateral activation (<em>n</em> = 20).</p></div></div>
<div class="section" id="ijs12056-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Treatment resulted in improvement in Fugl–Meyer Assessment and Wolf Motor Function Test in the two groups (<em>P</em> &lt; 0·01). The treatment also resulted in a significant increase in laterality index in group 1 (<em>P</em> &lt; 0·05), suggesting a shift in activated voxels to the lesional hemisphere. Patients of group 2 showed a significant increase in lesional hemisphere activation (<em>P</em> &lt; 0·05).</p></div></div>
<div class="section" id="ijs12056-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The results of serial functional magnetic resonance imaging indicated that our proposed treatment can induce functional cortical reorganization, leading to motor functional recovery of the affected upper limb. Especially, it seems that neural activation in the lesional hemisphere plays an important role in such recovery in poststroke hemiparetic patients.</p></div></div>
]]></content:encoded><description>

Background
Low-frequency repetitive transcranial magnetic stimulation of the nonlesional hemisphere combined with occupational therapy significantly improves motor function of the affected upper limb in poststroke hemiparetic patients, but the recovery mechanism remains unclear.


Aims
To investigate the recovery mechanism using functional magnetic resonance imaging.


Methods
Forty-seven poststroke hemiparetic patients were hospitalized to receive 12 sessions of 40-min low-frequency repetitive transcranial magnetic stimulation over the nonlesional hemisphere and daily occupational therapy for 15 days. Motor function was evaluated with the Fugl–Meyer Assessment and Wolf Motor Function Test. The functional magnetic resonance imaging with motor tasks was performed at admission and discharge. The laterality index of activated voxel number in Brodmann areas 4 and 6 on functional magnetic resonance imaging was calculated (laterality index range of −1 to +1). Patients were divided into two groups based on functional magnetic resonance imaging findings before the intervention: group 1: patients who showed bilateral activation (n = 27); group 2: patients with unilateral activation (n = 20).


Results
Treatment resulted in improvement in Fugl–Meyer Assessment and Wolf Motor Function Test in the two groups (P &lt; 0·01). The treatment also resulted in a significant increase in laterality index in group 1 (P &lt; 0·05), suggesting a shift in activated voxels to the lesional hemisphere. Patients of group 2 showed a significant increase in lesional hemisphere activation (P &lt; 0·05).


Conclusions
The results of serial functional magnetic resonance imaging indicated that our proposed treatment can induce functional cortical reorganization, leading to motor functional recovery of the affected upper limb. Especially, it seems that neural activation in the lesional hemisphere plays an important role in such recovery in poststroke hemiparetic patients.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12055" xmlns="http://purl.org/rss/1.0/"><title>HIMALAIA (Hypertension Induction in the Management of AneurysmaL subArachnoid haemorrhage with secondary IschaemiA): a randomized single-blind controlled trial of induced hypertension vs. no induced hypertension in the treatment of delayed cerebral ischemia after subarachnoid hemorrhage</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12055</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">HIMALAIA (Hypertension Induction in the Management of AneurysmaL subArachnoid haemorrhage with secondary IschaemiA): a randomized single-blind controlled trial of induced hypertension vs. no induced hypertension in the treatment of delayed cerebral ischemia after subarachnoid hemorrhage</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">C. S. Gathier, W. M. Bergh, A. J. C. Slooter, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-22T04:38:42.787515-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12055</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12055</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12055</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12055-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Delayed cerebral ischemia (DCI) is a major complication after aneurysmal subarachnoid hemorrhage (SAH). One option to treat delayed cerebral ischemia is to use induced hypertension, but its efficacy on the eventual outcome has not been proven in a randomized clinical trial. This article describes the design of the HIMALAIA trial (Hypertension Induction in the Management of AneurysmaL subArachnoid haemorrhage with secondary IschaemiA), designed to assess the effectiveness of induced hypertension on neurological outcome in patients with DCI after SAH.</p></div></div>
<div class="section" id="ijs12055-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>To investigate whether induced hypertension improves the functional outcome in patients with delayed cerebral ischemia after SAH.</p></div></div>
<div class="section" id="ijs12055-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>The HIMALAIA trial is a multicenter, singe-blinded, randomized controlled trial in patients with DCI after a recent SAH. Eligible patients will be randomized to either induced hypertension (<em>n</em> = 120) or to no induced hypertension (<em>n</em> = 120). In selected centers, the efficacy of induced hypertension in augmenting cerebral blood flow will be measured by means of cerebral perfusion computerized tomography scanning. Follow-up assessments will be performed at 3 and 12 months after randomization by trial nurses who are blinded to the treatment allocation and management. We will include patients during five years.</p></div></div>
<div class="section" id="ijs12055-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study outcomes</h4><div class="para"><p>The primary outcome is the proportion of subarachnoid hemorrhage patients with delayed cerebral ischemia with poor outcome three-months after randomization, defined as a modified Rankin scale of more than 3. Secondary outcome measures are related to treatment failure, functional outcome, adverse events, and cerebral hemodynamics. The HIMALAIA trial is registered at clinicaltrials.gov under identifier NCT01613235.</p></div></div>
]]></content:encoded><description>

Rationale
Delayed cerebral ischemia (DCI) is a major complication after aneurysmal subarachnoid hemorrhage (SAH). One option to treat delayed cerebral ischemia is to use induced hypertension, but its efficacy on the eventual outcome has not been proven in a randomized clinical trial. This article describes the design of the HIMALAIA trial (Hypertension Induction in the Management of AneurysmaL subArachnoid haemorrhage with secondary IschaemiA), designed to assess the effectiveness of induced hypertension on neurological outcome in patients with DCI after SAH.


Aims
To investigate whether induced hypertension improves the functional outcome in patients with delayed cerebral ischemia after SAH.


Design
The HIMALAIA trial is a multicenter, singe-blinded, randomized controlled trial in patients with DCI after a recent SAH. Eligible patients will be randomized to either induced hypertension (n = 120) or to no induced hypertension (n = 120). In selected centers, the efficacy of induced hypertension in augmenting cerebral blood flow will be measured by means of cerebral perfusion computerized tomography scanning. Follow-up assessments will be performed at 3 and 12 months after randomization by trial nurses who are blinded to the treatment allocation and management. We will include patients during five years.


Study outcomes
The primary outcome is the proportion of subarachnoid hemorrhage patients with delayed cerebral ischemia with poor outcome three-months after randomization, defined as a modified Rankin scale of more than 3. Secondary outcome measures are related to treatment failure, functional outcome, adverse events, and cerebral hemodynamics. The HIMALAIA trial is registered at clinicaltrials.gov under identifier NCT01613235.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12054" xmlns="http://purl.org/rss/1.0/"><title>Enlarged perivascular spaces and cerebral small vessel disease</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12054</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Enlarged perivascular spaces and cerebral small vessel disease</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Gillian M. Potter, Fergus N. Doubal, Caroline A. Jackson, Francesca M. Chappell, Cathie L. Sudlow, Martin S. Dennis, Joanna M. Wardlaw</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-22T04:38:30.574583-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12054</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12054</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12054</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12054-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and aims</h4><div class="para"><p>Enlarged perivascular spaces (also known as Virchow–Robin spaces) on T2-weighted brain magnetic resonance imaging are common, but their etiology, and specificity to small vessel as opposed to general cerebrovascular disease or ageing, is unclear. We tested the association between enlarged perivascular spaces and ischemic stroke subtype, other markers of small vessel disease, and common vascular risk factors.</p></div></div>
<div class="section" id="ijs12054-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We prospectively recruited patients with acute stroke, diagnosed and subtyped by a stroke physician using clinical features and brain magnetic resonance imaging. A neuroradiologist rated basal ganglia and centrum semiovale enlarged perivascular spaces on a five-point scale, white matter lesions, recent and old infarcts, and cerebral atrophy. We assessed associations between basal ganglia-, centrum semiovale- and total (combined basal ganglia and centrum semiovale) enlarged perivascular spaces, stroke subtype, white matter lesions, atrophy, and vascular risk factors.</p></div></div>
<div class="section" id="ijs12054-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Among 298 patients (mean age 68 years), after adjusting for vascular risk factors and white matter lesions, basal ganglia–enlarged perivascular spaces were associated with increasing age (<em>P</em> = 0·001), centrum semiovale–enlarged perivascular spaces (<em>P</em> &lt; 0·001), cerebral atrophy (<em>P</em> = 0·03), and lacunar stroke subtype (<em>P</em> = 0·04). Centrum semiovale–enlarged perivascular spaces were associated mainly with basal ganglia–enlarged perivascular spaces. Total enlarged perivascular spaces were associated with increasing age (<em>P</em> = 0·01), deep white matter lesions (<em>P</em> = 0·005), and previous stroke (<em>P</em> = 0·006).</p></div></div>
<div class="section" id="ijs12054-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Enlarged perivascular spaces are associated with age, lacunar stroke subtype and white matter lesions and should be considered as another magnetic resonance imaging marker of cerebral small vessel disease. Further evaluation of enlarged perivascular spaces in studies of ageing, stroke, and dementia is needed to determine their pathophysiological importance.</p></div></div>
]]></content:encoded><description>

Background and aims
Enlarged perivascular spaces (also known as Virchow–Robin spaces) on T2-weighted brain magnetic resonance imaging are common, but their etiology, and specificity to small vessel as opposed to general cerebrovascular disease or ageing, is unclear. We tested the association between enlarged perivascular spaces and ischemic stroke subtype, other markers of small vessel disease, and common vascular risk factors.


Methods
We prospectively recruited patients with acute stroke, diagnosed and subtyped by a stroke physician using clinical features and brain magnetic resonance imaging. A neuroradiologist rated basal ganglia and centrum semiovale enlarged perivascular spaces on a five-point scale, white matter lesions, recent and old infarcts, and cerebral atrophy. We assessed associations between basal ganglia-, centrum semiovale- and total (combined basal ganglia and centrum semiovale) enlarged perivascular spaces, stroke subtype, white matter lesions, atrophy, and vascular risk factors.


Results
Among 298 patients (mean age 68 years), after adjusting for vascular risk factors and white matter lesions, basal ganglia–enlarged perivascular spaces were associated with increasing age (P = 0·001), centrum semiovale–enlarged perivascular spaces (P &lt; 0·001), cerebral atrophy (P = 0·03), and lacunar stroke subtype (P = 0·04). Centrum semiovale–enlarged perivascular spaces were associated mainly with basal ganglia–enlarged perivascular spaces. Total enlarged perivascular spaces were associated with increasing age (P = 0·01), deep white matter lesions (P = 0·005), and previous stroke (P = 0·006).


Conclusions
Enlarged perivascular spaces are associated with age, lacunar stroke subtype and white matter lesions and should be considered as another magnetic resonance imaging marker of cerebral small vessel disease. Further evaluation of enlarged perivascular spaces in studies of ageing, stroke, and dementia is needed to determine their pathophysiological importance.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12053" xmlns="http://purl.org/rss/1.0/"><title>Paracetamol (Acetaminophen) in stroke 2 (PAIS 2): Protocol for a randomized, placebo-controlled, double-blind clinical trial to assess the effect of high-dose paracetamol on functional outcome in patients with acute stroke and a body temperature of 36·5°C or above</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12053</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Paracetamol (Acetaminophen) in stroke 2 (PAIS 2): Protocol for a randomized, placebo-controlled, double-blind clinical trial to assess the effect of high-dose paracetamol on functional outcome in patients with acute stroke and a body temperature of 36·5°C or above</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Inger R. Ridder, Frank Jan Jong, Heleen M. Hertog, Hester F. Lingsma, H. Maarten A. Gemert, A. H. C. M. L. (Tobien) Schreuder, Annemieke Ruitenberg, E. (Lisette) Maasland, Ritu Saxena, Peter Oomes, Jordie Tuijl, Peter J. Koudstaal, L. Jaap Kappelle, Ale Algra, H. Bart Worp, Diederik W. J. Dippel</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-22T04:38:23.332357-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12053</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12053</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12053</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12053-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>In the first hours after stroke onset, subfebrile temperatures and fever have been associated with poor functional outcome. In the first Paracetamol (Acetaminophen) in Stroke trial, a randomized clinical trial of 1400 patients with acute stroke, patients who were treated with high-dose paracetamol showed more improvement on the modified Rankin Scale at three-months than patients treated with placebo, but this difference was not statistically significant. In the 661 patients with a baseline body temperature of 37·0°C or above, treatment with paracetamol increased the odds of functional improvement (odds ratio 1·43; 95% confidence interval: 1·02–1·97). This relation was also found in the patients with a body temperature of 36·5°C or higher (odds ratio 1·31; 95% confidence interval 1·01–1·68). These findings need confirmation.</p></div></div>
<div class="section" id="ijs12053-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>The study aims to assess the effect of high-dose paracetamol in patients with acute stroke and a body temperature of 36·5°C or above on functional outcome.</p></div></div>
<div class="section" id="ijs12053-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>The Paracetamol (Acetaminophen) In Stroke 2 trial is a multicenter, randomized, double-blind, placebo-controlled clinical trial. We use a power of 85% to detect a significant difference in the scores on the modified Rankin Scale of the paracetamol group compared with the placebo group at a level of significance of 0·05 and assume a treatment effect of 7%. Fifteen-hundred patients with acute ischemic stroke or intracerebral hemorrhage and a body temperature of 36·5°C or above will be included within 12 h of symptom onset. Patients will be treated with paracetamol in a daily dose of six-grams or matching placebo for three consecutive days. The Paracetamol (Acetaminophen) In Stroke 2 trial has been registered as NTR2365 in The Netherlands Trial Register.</p></div></div>
<div class="section" id="ijs12053-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study outcomes</h4><div class="para"><p>The primary outcome will be improvement on the modified Rankin Scale at three-months as analyzed by ordinal logistic regression.</p></div></div>
<div class="section" id="ijs12053-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Discussion</h4><div class="para"><p>If high-dose paracetamol will be proven effective, a simple, safe, and extremely cheap therapy will be available for many patients with acute stroke worldwide.</p></div></div>
]]></content:encoded><description>

Rationale
In the first hours after stroke onset, subfebrile temperatures and fever have been associated with poor functional outcome. In the first Paracetamol (Acetaminophen) in Stroke trial, a randomized clinical trial of 1400 patients with acute stroke, patients who were treated with high-dose paracetamol showed more improvement on the modified Rankin Scale at three-months than patients treated with placebo, but this difference was not statistically significant. In the 661 patients with a baseline body temperature of 37·0°C or above, treatment with paracetamol increased the odds of functional improvement (odds ratio 1·43; 95% confidence interval: 1·02–1·97). This relation was also found in the patients with a body temperature of 36·5°C or higher (odds ratio 1·31; 95% confidence interval 1·01–1·68). These findings need confirmation.


Aim
The study aims to assess the effect of high-dose paracetamol in patients with acute stroke and a body temperature of 36·5°C or above on functional outcome.


Design
The Paracetamol (Acetaminophen) In Stroke 2 trial is a multicenter, randomized, double-blind, placebo-controlled clinical trial. We use a power of 85% to detect a significant difference in the scores on the modified Rankin Scale of the paracetamol group compared with the placebo group at a level of significance of 0·05 and assume a treatment effect of 7%. Fifteen-hundred patients with acute ischemic stroke or intracerebral hemorrhage and a body temperature of 36·5°C or above will be included within 12 h of symptom onset. Patients will be treated with paracetamol in a daily dose of six-grams or matching placebo for three consecutive days. The Paracetamol (Acetaminophen) In Stroke 2 trial has been registered as NTR2365 in The Netherlands Trial Register.


Study outcomes
The primary outcome will be improvement on the modified Rankin Scale at three-months as analyzed by ordinal logistic regression.


Discussion
If high-dose paracetamol will be proven effective, a simple, safe, and extremely cheap therapy will be available for many patients with acute stroke worldwide.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12050" xmlns="http://purl.org/rss/1.0/"><title>Effect of addition of clopidogrel to aspirin on stroke incidence: Meta-analysis of randomized trials</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12050</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Effect of addition of clopidogrel to aspirin on stroke incidence: Meta-analysis of randomized trials</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Santiago Palacio, Robert G. Hart, Lesly A. Pearce, David C. Anderson, Mukul Sharma, Lee A. Birnbaum, Oscar R. Benavente</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-22T04:38:10.512423-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12050</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12050</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12050</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12050-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>It remains controversial whether dual antiplatelet therapy reduces stroke more than aspirin alone.</p></div></div>
<div class="section" id="ijs12050-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>We aimed to assess the effects of adding clopidogrel to aspirin on the occurrence of stroke and major haemorrhage in patients with vascular disease.</p></div></div>
<div class="section" id="ijs12050-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Meta-analysis of published randomized trials comparing the combination of clopidogrel and aspirin vs. aspirin alone that reported stroke and major bleeding.</p></div></div>
<div class="section" id="ijs12050-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Thirteen randomized trials were included with a total of 90 433 participants (mean age 63 years; 63% male) with a mean follow-up of 1·0 years and 2011 strokes. Stroke was reduced 19% by dual antiplatelet therapy (odds ratio = 0·81, 95% confidence interval 0·74–0·89) with no evidence of heterogeneity of effect across different trial populations (I<sup>2</sup> index = 5%, <em>P</em> = 0·4 for heterogeneity). Dual antiplatelet therapy reduced ischemic stroke by 23% (odds ratio = 0·77; 95% confidence interval 0·70–0·85); there was a nonsignificant 12% increase in intracerebral haemorrhage (odds ratio = 1·12, 95% confidence interval 0·86–1·46). Among 1930 participants with recent (&lt;30 days) brain ischemia from four trials, stroke was reduced by 33% (odds ratio = 0·67, 95% confidence interval 0·46–0·97) by dual antiplatelet therapy vs. aspirin alone. The risk of major bleeding was increased by 40% (odds ratio = 1·40, 95% confidence interval 1·26–1·55) by dual antiplatelet therapy.</p></div></div>
<div class="section" id="ijs12050-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>This meta-analysis demonstrates a substantial relative risk reduction in stroke by clopidogrel plus aspirin vs. aspirin alone that is consistent across different trial cohorts. Major haemorrhage is increased by dual antiplatelet therapy.</p></div></div>
]]></content:encoded><description>

Background
It remains controversial whether dual antiplatelet therapy reduces stroke more than aspirin alone.


Aim
We aimed to assess the effects of adding clopidogrel to aspirin on the occurrence of stroke and major haemorrhage in patients with vascular disease.


Methods
Meta-analysis of published randomized trials comparing the combination of clopidogrel and aspirin vs. aspirin alone that reported stroke and major bleeding.


Results
Thirteen randomized trials were included with a total of 90 433 participants (mean age 63 years; 63% male) with a mean follow-up of 1·0 years and 2011 strokes. Stroke was reduced 19% by dual antiplatelet therapy (odds ratio = 0·81, 95% confidence interval 0·74–0·89) with no evidence of heterogeneity of effect across different trial populations (I2 index = 5%, P = 0·4 for heterogeneity). Dual antiplatelet therapy reduced ischemic stroke by 23% (odds ratio = 0·77; 95% confidence interval 0·70–0·85); there was a nonsignificant 12% increase in intracerebral haemorrhage (odds ratio = 1·12, 95% confidence interval 0·86–1·46). Among 1930 participants with recent (&lt;30 days) brain ischemia from four trials, stroke was reduced by 33% (odds ratio = 0·67, 95% confidence interval 0·46–0·97) by dual antiplatelet therapy vs. aspirin alone. The risk of major bleeding was increased by 40% (odds ratio = 1·40, 95% confidence interval 1·26–1·55) by dual antiplatelet therapy.


Conclusions
This meta-analysis demonstrates a substantial relative risk reduction in stroke by clopidogrel plus aspirin vs. aspirin alone that is consistent across different trial cohorts. Major haemorrhage is increased by dual antiplatelet therapy.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12049" xmlns="http://purl.org/rss/1.0/"><title>Aortic stiffness and plasma brain natriuretic peptide predicts mortality in acute ischemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12049</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Aortic stiffness and plasma brain natriuretic peptide predicts mortality in acute ischemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Murat Biteker, Temel Özden, Akın Dayan, Ahmet İlker Tekkeşin, Cemile Handan Mısırlı</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-22T04:37:54.615986-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12049</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12049</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12049</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12049-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The study aimed to evaluate the prognostic role and discriminative power of aortic stiffness and plasma brain natriuretic peptide levels in a cohort of patients hospitalized for acute ischemic stroke.</p></div></div>
<div class="section" id="ijs12049-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods and Results</h4><div class="para"><p>Three hundred and ten consecutive patients aged 50 years and older with a first episode of acute ischemic stroke were prospectively evaluated. All patients were admitted to the hospital within 24 h of the onset of stroke symptoms. The type of acute ischemic stroke was classified according to the Trial of Org 10172 in Acute Stroke Treatment classification. Blood samples were taken for measurement of brain natriuretic peptide levels at admission. Aortic stiffness indices, aortic strain and distensibility, were calculated from the aortic diameters measured by transthoracic echocardiography. The patients were followed for one-year or until death, whichever came first. Death occurred in 51 (16·5%) patients. On multivariate logistic regression analysis, National Institutes of Health Stroke Scale score &gt;13, diabetes, brain natriuretic peptide &gt;235 pg/mL, aortic distensibility, and aortic strain were associated with all-cause mortality. The optimal cutoff level of brain natriuretic peptide to distinguish the deceased group from the survival group was 235 pg/mL (sensitivity 71·0% and specificity 63·0%) and to distinguish cardioembolic stroke from noncardioembolic stroke was 155 pg/mL (sensitivity 81% and specificity 63%).</p></div></div>
<div class="section" id="ijs12049-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Aortic stiffness and brain natriuretic peptide predict mortality in patients with first-ever acute ischemic stroke. Brain natriuretic peptide also differentiates cardioembolic stroke from noncardioembolic stroke.</p></div></div>
]]></content:encoded><description>

Background
The study aimed to evaluate the prognostic role and discriminative power of aortic stiffness and plasma brain natriuretic peptide levels in a cohort of patients hospitalized for acute ischemic stroke.


Methods and Results
Three hundred and ten consecutive patients aged 50 years and older with a first episode of acute ischemic stroke were prospectively evaluated. All patients were admitted to the hospital within 24 h of the onset of stroke symptoms. The type of acute ischemic stroke was classified according to the Trial of Org 10172 in Acute Stroke Treatment classification. Blood samples were taken for measurement of brain natriuretic peptide levels at admission. Aortic stiffness indices, aortic strain and distensibility, were calculated from the aortic diameters measured by transthoracic echocardiography. The patients were followed for one-year or until death, whichever came first. Death occurred in 51 (16·5%) patients. On multivariate logistic regression analysis, National Institutes of Health Stroke Scale score &gt;13, diabetes, brain natriuretic peptide &gt;235 pg/mL, aortic distensibility, and aortic strain were associated with all-cause mortality. The optimal cutoff level of brain natriuretic peptide to distinguish the deceased group from the survival group was 235 pg/mL (sensitivity 71·0% and specificity 63·0%) and to distinguish cardioembolic stroke from noncardioembolic stroke was 155 pg/mL (sensitivity 81% and specificity 63%).


Conclusions
Aortic stiffness and brain natriuretic peptide predict mortality in patients with first-ever acute ischemic stroke. Brain natriuretic peptide also differentiates cardioembolic stroke from noncardioembolic stroke.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00921.x" xmlns="http://purl.org/rss/1.0/"><title>Burden of stroke in Estonia</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00921.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Burden of stroke in Estonia</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Janika Kõrv, Riina Vibo</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-29T04:23:19.677723-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00921.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00921.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00921.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Panorama</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Estonia is the smallest of the three Baltic countries. The decline in incidence of first-ever stroke during the 1990s has left Tartu, Estonia with a relatively low stroke incidence. However, the incidence rates for younger age groups, and the 28-day case fatality rate are higher compared with several other studies. Developments in the national health care system in recent years have been positive: the decline of mortality rate of stroke in Estonia is greater than the European Union average. However, the mortality of cardiovascular diseases is higher compared with several European countries. The prevalence of most stroke risk factors is comparable with European Union countries, while atrial fibrillation is somewhat more frequent (30%) among the patients having suffered from ischemic stroke. The management of stroke in Estonia has been in accordance with European and national stroke guidelines. Stroke units are organized in regional and central hospitals in bigger cities. A well-developed and free ambulance service, and a high priority of stroke code, enable a quick transportation of patients to the nearest hospital providing thrombolytic therapy. The number of thrombolyzed stroke cases has increased since 2003. The Estonian Stroke Initiative was founded in 2008 to improve stroke care, promote regional networks, and increase stroke knowledge among the general population and medical professionals. Since then, several activities regarding stroke awareness have been organized.</p></div>
]]></content:encoded><description>
Estonia is the smallest of the three Baltic countries. The decline in incidence of first-ever stroke during the 1990s has left Tartu, Estonia with a relatively low stroke incidence. However, the incidence rates for younger age groups, and the 28-day case fatality rate are higher compared with several other studies. Developments in the national health care system in recent years have been positive: the decline of mortality rate of stroke in Estonia is greater than the European Union average. However, the mortality of cardiovascular diseases is higher compared with several European countries. The prevalence of most stroke risk factors is comparable with European Union countries, while atrial fibrillation is somewhat more frequent (30%) among the patients having suffered from ischemic stroke. The management of stroke in Estonia has been in accordance with European and national stroke guidelines. Stroke units are organized in regional and central hospitals in bigger cities. A well-developed and free ambulance service, and a high priority of stroke code, enable a quick transportation of patients to the nearest hospital providing thrombolytic therapy. The number of thrombolyzed stroke cases has increased since 2003. The Estonian Stroke Initiative was founded in 2008 to improve stroke care, promote regional networks, and increase stroke knowledge among the general population and medical professionals. Since then, several activities regarding stroke awareness have been organized.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12029" xmlns="http://purl.org/rss/1.0/"><title>Stroke rehabilitation in China: a systematic review and meta-analysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12029</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Stroke rehabilitation in China: a systematic review and meta-analysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Wen Wen Zhang, Sally Speare, Leonid Churilov, Matthew Thuy, Geoffrey Donnan, Julie Bernhardt</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-29T04:23:16.665386-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12029</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12029</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12029</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Systematic Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12029-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Stroke rehabilitation is regarded as an essential component of organized care, therefore withholding treatment is considered unethical in Western trials. Poststroke rehabilitation is not standard in China, and trials with no treatment controls have been possible. We believed aggregation of these data represented a unique opportunity to examine the ‘effect size’ of this intervention.</p></div></div>
<div class="section" id="ijs12029-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>The aim of this study was to systematically review randomized controlled trials that compare rehabilitation to standard care after stroke in China.</p></div></div>
<div class="section" id="ijs12029-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We searched 24 databases including Wanfangdata (China), MEDLINE, EMBASE, CENTRAL, Cochrane Stroke Group Register, and Cochrane Central Register of Controlled trials. The primary outcome of interest was activities of daily living (Barthel Index), and the secondary outcome was disability (Fugl-Meyer Score). Random-effect meta-analysis was performed.</p></div></div>
<div class="section" id="ijs12029-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Thirty-seven randomized controlled trials consisting of 5916 patients met inclusion criteria. Mean age reported in each study range from 47·2 to 72·5 years, 52·6% were male and 23·8% had a haemorrhagic stroke. Rehabilitation interventions varied between studies, but all included additional exercise therapy. Control patients had no formal rehabilitation. Patients who received rehabilitation showed marked improvements in Barthel Index (standardized mean difference: 1·04, 95% confidence interval: 0·88–1·21, <em>P</em> &lt; 0·001, <em>I</em><sup>2</sup> = 85·9%) and Fugl-Meyer Score (standardized mean difference: 1·10, 95% confidence interval: 0·82–1·38, <em>P</em> &lt; 0·001, <em>I</em><sup>2</sup> = 94·3%) compared with controls. However, reporting quality was low, and time to start of rehabilitation was often unclear.</p></div></div>
<div class="section" id="ijs12029-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>These data provide some evidence that rehabilitation poststroke is more effective than no rehabilitation, improving activities of daily living and reducing disability. Although results are limited by low reporting quality and study heterogeneity, conducting research in countries in which rehabilitation is not standard care provides an opportunity to advance our understanding and should be encouraged.</p></div></div>
]]></content:encoded><description>

Background
Stroke rehabilitation is regarded as an essential component of organized care, therefore withholding treatment is considered unethical in Western trials. Poststroke rehabilitation is not standard in China, and trials with no treatment controls have been possible. We believed aggregation of these data represented a unique opportunity to examine the ‘effect size’ of this intervention.


Aim
The aim of this study was to systematically review randomized controlled trials that compare rehabilitation to standard care after stroke in China.


Methods
We searched 24 databases including Wanfangdata (China), MEDLINE, EMBASE, CENTRAL, Cochrane Stroke Group Register, and Cochrane Central Register of Controlled trials. The primary outcome of interest was activities of daily living (Barthel Index), and the secondary outcome was disability (Fugl-Meyer Score). Random-effect meta-analysis was performed.


Results
Thirty-seven randomized controlled trials consisting of 5916 patients met inclusion criteria. Mean age reported in each study range from 47·2 to 72·5 years, 52·6% were male and 23·8% had a haemorrhagic stroke. Rehabilitation interventions varied between studies, but all included additional exercise therapy. Control patients had no formal rehabilitation. Patients who received rehabilitation showed marked improvements in Barthel Index (standardized mean difference: 1·04, 95% confidence interval: 0·88–1·21, P &lt; 0·001, I2 = 85·9%) and Fugl-Meyer Score (standardized mean difference: 1·10, 95% confidence interval: 0·82–1·38, P &lt; 0·001, I2 = 94·3%) compared with controls. However, reporting quality was low, and time to start of rehabilitation was often unclear.


Conclusion
These data provide some evidence that rehabilitation poststroke is more effective than no rehabilitation, improving activities of daily living and reducing disability. Although results are limited by low reporting quality and study heterogeneity, conducting research in countries in which rehabilitation is not standard care provides an opportunity to advance our understanding and should be encouraged.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12039" xmlns="http://purl.org/rss/1.0/"><title>Body temperature, blood infection parameters, and outcome of thrombolysis-treated ischemic stroke patients</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12039</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Body temperature, blood infection parameters, and outcome of thrombolysis-treated ischemic stroke patients</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Marjaana Tiainen, Atte Meretoja, Daniel Strbian, Joel Suvanto, Sami Curtze, Perttu J. Lindsberg, Lauri Soinne, Turgut Tatlisumak, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-17T05:21:37.857374-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12039</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12039</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12039</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12039-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and Aims</h4><div class="para"><p>Body temperature, inflammation, and infections may modify response to thrombolytic therapy. We studied their associations with clinical improvement after intravenous thrombolysis and three-month outcome.</p></div></div>
<div class="section" id="ijs12039-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We included 985 consecutive acute ischemic stroke patients treated with intravenous thrombolysis at the Helsinki University Central Hospital during 1995–2008. Body temperature, blood leukocyte count, and C-reactive protein levels were analyzed on arrival and at day one. Clinical improvement was defined as National Institutes of Health Stroke Scale score decrease of ≥4 points or a score of 0 at 24 h. Functional outcome was assessed at three-months with the modified Rankin Scale dichotomized at 0–2 (good) vs. 3–6 (poor). Associations were tested with multivariable logistic regression analysis.</p></div></div>
<div class="section" id="ijs12039-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Of the baseline variables, lower C-reactive protein independently predicted clinical improvement at 24 h (odds ratio 0·94 per 5 mg/L; 95% confidence interval 0·89–1·00; <em>P</em> = 0·03), whereas higher leukocyte count (odds ratio 1·10 per E9/L; 1·03–1·17; <em>P</em> &lt; 0·01) and C-reactive protein (odds ratio 1·07 per 5 mg/L; 1·01–1·14; <em>P</em> = 0·02) were associated with poor three-month outcome. When body temperature increased over the first 24 h, clinical improvement after thrombolysis was unlikely (odds ratio 0·66 per °C; 0·45–0·95; <em>P</em> = 0·03) and poor outcome more common (odds ratio 1·63 per °C; 1·24–2·14; <em>P</em> &lt; 0·001). Elevated leukocytes at baseline increased the risk of symptomatic intracerebral hemorrhage (odds ratio 1·07 per E9/L; 1·00–1·13; <em>P</em> = 0·04).</p></div></div>
<div class="section" id="ijs12039-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>A lower level of systemic inflammation at time of thrombolysis may be associated with clinical improvement and good outcome at three-months. Increase in body temperature during the first 24 h associates with lack of clinical improvement and worse patient outcome.</p></div></div>
]]></content:encoded><description>

Background and Aims
Body temperature, inflammation, and infections may modify response to thrombolytic therapy. We studied their associations with clinical improvement after intravenous thrombolysis and three-month outcome.


Methods
We included 985 consecutive acute ischemic stroke patients treated with intravenous thrombolysis at the Helsinki University Central Hospital during 1995–2008. Body temperature, blood leukocyte count, and C-reactive protein levels were analyzed on arrival and at day one. Clinical improvement was defined as National Institutes of Health Stroke Scale score decrease of ≥4 points or a score of 0 at 24 h. Functional outcome was assessed at three-months with the modified Rankin Scale dichotomized at 0–2 (good) vs. 3–6 (poor). Associations were tested with multivariable logistic regression analysis.


Results
Of the baseline variables, lower C-reactive protein independently predicted clinical improvement at 24 h (odds ratio 0·94 per 5 mg/L; 95% confidence interval 0·89–1·00; P = 0·03), whereas higher leukocyte count (odds ratio 1·10 per E9/L; 1·03–1·17; P &lt; 0·01) and C-reactive protein (odds ratio 1·07 per 5 mg/L; 1·01–1·14; P = 0·02) were associated with poor three-month outcome. When body temperature increased over the first 24 h, clinical improvement after thrombolysis was unlikely (odds ratio 0·66 per °C; 0·45–0·95; P = 0·03) and poor outcome more common (odds ratio 1·63 per °C; 1·24–2·14; P &lt; 0·001). Elevated leukocytes at baseline increased the risk of symptomatic intracerebral hemorrhage (odds ratio 1·07 per E9/L; 1·00–1·13; P = 0·04).


Conclusion
A lower level of systemic inflammation at time of thrombolysis may be associated with clinical improvement and good outcome at three-months. Increase in body temperature during the first 24 h associates with lack of clinical improvement and worse patient outcome.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00952.x" xmlns="http://purl.org/rss/1.0/"><title>Posterior circulation stroke is associated with prolonged door-to-needle time</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00952.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Posterior circulation stroke is associated with prolonged door-to-needle time</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Amrou Sarraj, Sarah Medrek, Karen Albright, Sheryl Martin-Schild, Wafi Bibars, Farhaan Vahidy, James C. Grotta, Sean I. Savitz</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-21T23:15:19.431793-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00952.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00952.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00952.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs952-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Lack of recognition of early symptoms of acute posterior circulation ischaemic stroke might delay timely diagnosis and treatment with tissue plasminogen activator.</p></div></div>
<div class="section" id="ijs952-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims and hypothesis</h4><div class="para"><p>We hypothesized that patients with posterior circulation stroke receive delayed thrombolytic treatment in comparison to anterior circulation stroke. We investigated the differences in times to evaluation or treatment between patients with anterior circulation ischaemic stroke and posterior circulation stroke in our aim to understand the barriers that might have caused these delays.</p></div></div>
<div class="section" id="ijs952-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>A cross-sectional study was conducted using consecutive patients presenting to our tertiary academic centre with acute ischaemic stroke who were treated with intravenous tissue plasminogen activator within 4·5 h from symptom onset. We compared demographics, stroke severity, symptoms and signs, and time intervals among onset, emergency department arrival, emergency department physician evaluation, neurologist evaluation, brain imaging, and tissue plasminogen activator treatment in patients with anterior circulation stroke and posterior circulation stroke.</p></div></div>
<div class="section" id="ijs952-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Among 252 patients treated with intravenous tissue plasminogen activator, 12% had posterior circulation stroke. Patients with posterior circulation stroke had significantly lower median baseline the National Institutes of Health and Stroke Scale (NIHSS) score (<em>P</em> = 0·01), higher frequency of nausea (<em>P</em> &lt; 0·01), vomiting (<em>P</em> &lt; 0·01), dizziness (<em>P</em> &lt; 0·01), and lower frequency of aphasia (<em>P</em> = 0·002) or neglect (<em>P</em> = 0·048). The emergency department physician evaluation-to-neurologist evaluation and door-to-needle intervals were significantly longer for posterior circulation stroke patients compared with anterior circulation stroke patients. The neurologist-to-needle time, however, was similar in the two groups. The presence of nausea and vomiting was associated with a longer time from emergency department evaluation to neurology evaluation and had a significant association with delayed treatment.</p></div></div>
<div class="section" id="ijs952-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Posterior circulation stroke patients had a delay in neurology evaluation after initial emergency department evaluation and a delay in intravenous tissue plasminogen activator administration compared with anterior circulation stroke patients. There may be difficulties in rapidly recognizing the symptoms of posterior circulation stroke, in contrast to anterior circulation stroke, in the emergency department.</p></div></div>
]]></content:encoded><description>

Background
Lack of recognition of early symptoms of acute posterior circulation ischaemic stroke might delay timely diagnosis and treatment with tissue plasminogen activator.


Aims and hypothesis
We hypothesized that patients with posterior circulation stroke receive delayed thrombolytic treatment in comparison to anterior circulation stroke. We investigated the differences in times to evaluation or treatment between patients with anterior circulation ischaemic stroke and posterior circulation stroke in our aim to understand the barriers that might have caused these delays.


Methods
A cross-sectional study was conducted using consecutive patients presenting to our tertiary academic centre with acute ischaemic stroke who were treated with intravenous tissue plasminogen activator within 4·5 h from symptom onset. We compared demographics, stroke severity, symptoms and signs, and time intervals among onset, emergency department arrival, emergency department physician evaluation, neurologist evaluation, brain imaging, and tissue plasminogen activator treatment in patients with anterior circulation stroke and posterior circulation stroke.


Results
Among 252 patients treated with intravenous tissue plasminogen activator, 12% had posterior circulation stroke. Patients with posterior circulation stroke had significantly lower median baseline the National Institutes of Health and Stroke Scale (NIHSS) score (P = 0·01), higher frequency of nausea (P &lt; 0·01), vomiting (P &lt; 0·01), dizziness (P &lt; 0·01), and lower frequency of aphasia (P = 0·002) or neglect (P = 0·048). The emergency department physician evaluation-to-neurologist evaluation and door-to-needle intervals were significantly longer for posterior circulation stroke patients compared with anterior circulation stroke patients. The neurologist-to-needle time, however, was similar in the two groups. The presence of nausea and vomiting was associated with a longer time from emergency department evaluation to neurology evaluation and had a significant association with delayed treatment.


Conclusions
Posterior circulation stroke patients had a delay in neurology evaluation after initial emergency department evaluation and a delay in intravenous tissue plasminogen activator administration compared with anterior circulation stroke patients. There may be difficulties in rapidly recognizing the symptoms of posterior circulation stroke, in contrast to anterior circulation stroke, in the emergency department.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12042" xmlns="http://purl.org/rss/1.0/"><title>White matter disease and an incomplete circle of Willis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12042</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">White matter disease and an incomplete circle of Willis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Daniel James Ryan, Susan Byrne, Ruth Dunne, Mark Harmon, Joseph Harbison</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-21T23:11:56.056822-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12042</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12042</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12042</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12042-sec-1001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Introduction</h4><div class="para"><p>White matter disease occurs as a consequence of small vessel disease; however, hypoperfusion may also play a role. We investigated whether patients with less cerebral vessel anastomosis may develop more white matter disease.</p></div></div>
<div class="section" id="ijs12042-sec-1002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Magnetic resonance imaging (1.5t) with intracranial magnetic resonance angiography data was collected on a convenience sample between July 2008 and January 2009. All patients were independently assessed for circle of Willis variants by two researchers and categorized into two groups: those with a complete circle of Willis and those with an incomplete circle of Willis (absent vessels). The complete group was sub-divided into a classical group (entirely normal circle of Willis) and a hypoplastic group (hypoplasia but no absent vessels). White matter disease assessment was conducted for these groups, by two researchers blind to magnetic resonance angiography findings, on all patients over 50 years old.</p></div></div>
<div class="section" id="ijs12042-sec-1003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The circle of Willis was characterized in 163 patients, while 90 (&gt;50 years) underwent white matter disease assessment. The kappa inter-rater reliability between both circle of Willis assessors and between both white matter disease assessors was 0·57 and 0·63, respectively. The prevalence of circle of Willis variants strongly correlated with the seminal paper by Riggs and Rupp. Independent of age and gender, those with an incomplete circle of Willis (<em>n</em> = 68) exhibited 58% more white matter disease than those with a complete circle of Willis (<em>n</em> = 22) (white matter disease score 6·52 vs. 4·11, respectively, <em>P</em> = 0·03). Patients with absent anterior vessels exhibited more frontal white matter disease than those with intact anterior vessels (3·7 vs. 1·72, <em>P</em> &lt; 0·001). Patients with absent posterior vessels exhibited more occipital white matter disease than those with intact posterior vessels (2·52 vs. 1·34, <em>P</em> = 0·014).</p></div></div>
<div class="section" id="ijs12042-sec-1004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>These data suggest that congenital absence of anastomotic capacity correlates with incident white matter disease, thus alluding to a hypoperfusion mechanism in the development of white matter disease.</p></div></div>
]]></content:encoded><description>

Introduction
White matter disease occurs as a consequence of small vessel disease; however, hypoperfusion may also play a role. We investigated whether patients with less cerebral vessel anastomosis may develop more white matter disease.


Methods
Magnetic resonance imaging (1.5t) with intracranial magnetic resonance angiography data was collected on a convenience sample between July 2008 and January 2009. All patients were independently assessed for circle of Willis variants by two researchers and categorized into two groups: those with a complete circle of Willis and those with an incomplete circle of Willis (absent vessels). The complete group was sub-divided into a classical group (entirely normal circle of Willis) and a hypoplastic group (hypoplasia but no absent vessels). White matter disease assessment was conducted for these groups, by two researchers blind to magnetic resonance angiography findings, on all patients over 50 years old.


Results
The circle of Willis was characterized in 163 patients, while 90 (&gt;50 years) underwent white matter disease assessment. The kappa inter-rater reliability between both circle of Willis assessors and between both white matter disease assessors was 0·57 and 0·63, respectively. The prevalence of circle of Willis variants strongly correlated with the seminal paper by Riggs and Rupp. Independent of age and gender, those with an incomplete circle of Willis (n = 68) exhibited 58% more white matter disease than those with a complete circle of Willis (n = 22) (white matter disease score 6·52 vs. 4·11, respectively, P = 0·03). Patients with absent anterior vessels exhibited more frontal white matter disease than those with intact anterior vessels (3·7 vs. 1·72, P &lt; 0·001). Patients with absent posterior vessels exhibited more occipital white matter disease than those with intact posterior vessels (2·52 vs. 1·34, P = 0·014).


Conclusion
These data suggest that congenital absence of anastomotic capacity correlates with incident white matter disease, thus alluding to a hypoperfusion mechanism in the development of white matter disease.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12041" xmlns="http://purl.org/rss/1.0/"><title>Approaches to economic evaluations of stroke rehabilitation</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12041</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Approaches to economic evaluations of stroke rehabilitation</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Louise E Craig, Olivia Wu, Julie Bernhardt, Peter Langhorne</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-21T23:10:00.933719-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12041</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12041</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12041</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Many stroke rehabilitation services and interventions are complex in that they involve a number of components, interactions, and outcomes. Much of the onus of stroke care lies with rehabilitation services and because stroke rehabilitation is highly resource intensive, it is important for policy makers to consider the potential trade-offs between all relevant costs and benefits. The primary aim of this systematic review was to assess the methods used to conduct economic evaluations of stroke rehabilitation. Studies that compared two or more alternative stroke rehabilitation interventions or services with the costs and outcomes being examined for each alternative were included. EMBASE, MEDLINE In-Process, and National Health Service's Economic Evaluation Database were searched using search strategies. The methodological quality of the included studies was appraised using a checklist for the conduct and reporting of economic evaluations. Twenty-one studies met the selection criteria. The economic evaluations in the majority of these studies were inadequate based on their ability to identify, measure, and value all resources and benefits pertinent to the complexity of stroke rehabilitation. This study highlights that complex interventions such as stroke rehabilitation have widespread effects, which may not be represented by the changes on a single outcome. This study recommends the adoption of a wider cost and benefit perspective in the economic evaluations of complex interventions. It supports a move away from conventional economic evaluation and decision making, based purely on cost-effectiveness, toward multicriteria decision analysis frameworks for complex interventions, where a broader range of criteria may be assessed by policy makers.</p></div>
]]></content:encoded><description>
Many stroke rehabilitation services and interventions are complex in that they involve a number of components, interactions, and outcomes. Much of the onus of stroke care lies with rehabilitation services and because stroke rehabilitation is highly resource intensive, it is important for policy makers to consider the potential trade-offs between all relevant costs and benefits. The primary aim of this systematic review was to assess the methods used to conduct economic evaluations of stroke rehabilitation. Studies that compared two or more alternative stroke rehabilitation interventions or services with the costs and outcomes being examined for each alternative were included. EMBASE, MEDLINE In-Process, and National Health Service's Economic Evaluation Database were searched using search strategies. The methodological quality of the included studies was appraised using a checklist for the conduct and reporting of economic evaluations. Twenty-one studies met the selection criteria. The economic evaluations in the majority of these studies were inadequate based on their ability to identify, measure, and value all resources and benefits pertinent to the complexity of stroke rehabilitation. This study highlights that complex interventions such as stroke rehabilitation have widespread effects, which may not be represented by the changes on a single outcome. This study recommends the adoption of a wider cost and benefit perspective in the economic evaluations of complex interventions. It supports a move away from conventional economic evaluation and decision making, based purely on cost-effectiveness, toward multicriteria decision analysis frameworks for complex interventions, where a broader range of criteria may be assessed by policy makers.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12021" xmlns="http://purl.org/rss/1.0/"><title>Cerebral CT perfusion in patients with perimesencephalic and those with aneurysmal subarachnoid hemorrhage</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12021</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Cerebral CT perfusion in patients with perimesencephalic and those with aneurysmal subarachnoid hemorrhage</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Charlotte H. P. Cremers, Irene C. Schaaf, Jan Willem Dankbaar, Birgitta K. Velthuis, Gabriel J. E. Rinkel</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-21T21:21:59.048329-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12021</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12021</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12021</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12021-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The cause of perimesencephalic hemorrhage is unknown, but a venous source is suggested. If perimesencephalic hemorrhage is of venous origin, less elevation of the intracranial pressure and less perfusion deficits are expected than after aneurysmal subarachnoid hemorrhage.</p></div></div>
<div class="section" id="ijs12021-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>We compared perfusion in the acute stage after perimesencephalic hemorrhage and aneurysmal subarachnoid hemorrhage.</p></div></div>
<div class="section" id="ijs12021-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We included 45 perimesencephalic hemorrhage patients and 45 aneurysmal subarachnoid hemorrhage patients, who were matched on clinical condition at admission and underwent computerized tomographic scanning &lt;72 h after subarachnoid hemorrhage. Cerebral blood flow was assessed in 12 predefined regions of interest. Differences in cerebral blood flow values with corresponding 95% confidence intervals were calculated. Sub-group analyses were performed stratified on comparable amounts of blood and location of blood (posterior circulation aneurysms and additionally in infratentorial and supratentorial aneurysms).</p></div></div>
<div class="section" id="ijs12021-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Cerebral blood flow was higher in perimesencephalic hemorrhage patients (mean: 63·8) than in aneurysmal sub-arachnoid hemorrhage patients (mean: 55·9; difference of means: −7·9 [95% confidence interval: −10·7 to −5·2]) and also in the sub-group with comparable amounts of blood (mean cerebral blood flow: 56·4; difference of means: −7·4 [95% confidence interval: −10·4 to −4·3]). Cerebral blood flow was comparable with perimesencephalic hemorrhage patients for the sub-group with posterior circulation aneurysms (difference of means: −0·7 [95% confidence interval: −5·2 to 3·8]); however, differences diverged after stratifying posterior circulation aneurysms into supratentorial (difference of means −3·9 [95% confidence interval: −9·3 to 1·4]) and infratentorial aneurysms (difference of means 3·0 [95% confidence interval: −2·8 to 8·8]).</p></div></div>
<div class="section" id="ijs12021-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Perimesencephalic hemorrhage patients have a higher cerebral blood flow than aneurysmal subarachnoid hemorrhage patients. The findings of this study further support a venous origin of bleeding in perimesencephalic hemorrhage patients. Future studies should further elaborate on cerebral blood flow in posterior circulation aneurysms.</p></div></div>
]]></content:encoded><description>

Background
The cause of perimesencephalic hemorrhage is unknown, but a venous source is suggested. If perimesencephalic hemorrhage is of venous origin, less elevation of the intracranial pressure and less perfusion deficits are expected than after aneurysmal subarachnoid hemorrhage.


Aims
We compared perfusion in the acute stage after perimesencephalic hemorrhage and aneurysmal subarachnoid hemorrhage.


Methods
We included 45 perimesencephalic hemorrhage patients and 45 aneurysmal subarachnoid hemorrhage patients, who were matched on clinical condition at admission and underwent computerized tomographic scanning &lt;72 h after subarachnoid hemorrhage. Cerebral blood flow was assessed in 12 predefined regions of interest. Differences in cerebral blood flow values with corresponding 95% confidence intervals were calculated. Sub-group analyses were performed stratified on comparable amounts of blood and location of blood (posterior circulation aneurysms and additionally in infratentorial and supratentorial aneurysms).


Results
Cerebral blood flow was higher in perimesencephalic hemorrhage patients (mean: 63·8) than in aneurysmal sub-arachnoid hemorrhage patients (mean: 55·9; difference of means: −7·9 [95% confidence interval: −10·7 to −5·2]) and also in the sub-group with comparable amounts of blood (mean cerebral blood flow: 56·4; difference of means: −7·4 [95% confidence interval: −10·4 to −4·3]). Cerebral blood flow was comparable with perimesencephalic hemorrhage patients for the sub-group with posterior circulation aneurysms (difference of means: −0·7 [95% confidence interval: −5·2 to 3·8]); however, differences diverged after stratifying posterior circulation aneurysms into supratentorial (difference of means −3·9 [95% confidence interval: −9·3 to 1·4]) and infratentorial aneurysms (difference of means 3·0 [95% confidence interval: −2·8 to 8·8]).


Conclusions
Perimesencephalic hemorrhage patients have a higher cerebral blood flow than aneurysmal subarachnoid hemorrhage patients. The findings of this study further support a venous origin of bleeding in perimesencephalic hemorrhage patients. Future studies should further elaborate on cerebral blood flow in posterior circulation aneurysms.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12000" xmlns="http://purl.org/rss/1.0/"><title>Stroke incidence and 30-day and six-month case fatality rates in Udine, Italy: a population-based prospective study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12000</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Stroke incidence and 30-day and six-month case fatality rates in Udine, Italy: a population-based prospective study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Francesco Janes, Gian Luigi Gigli, Lucio D'Anna, Iacopo Cancelli, Anna Perelli, Giessica Canal, Valentina Russo, Barbara Zanchettin, Mariarosaria Valente</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-21T21:21:54.050584-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12000</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12000</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12000</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12000-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Stroke incidence in high-income countries is reported to decrease, and new data on stroke incidence and outcome are needed to design stroke services and to ameliorate stroke management.</p></div></div>
<div class="section" id="ijs12000-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>This study is part of a two-year prospective community-based registry of all cerebrovascular events in the district of Udine (153 312 inhabitants), Friuli-Venezia Giulia region, northeast of Italy, between 1 April 2007 and 31 March 2009. Overlapping sources for case finding were used, combining hot and cold pursuit.</p></div></div>
<div class="section" id="ijs12000-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>We identified 784 stroke cases, 640 (81·6%) incident. The crude overall annual incidence rate per 100 000 residents was 256 (95% confidence interval 241–271) for all strokes and 209 (95% confidence interval 195–223) for first-ever strokes. Incidence rate for first-ever strokes was 181 (95% confidence interval 155–211) after adjustment to the 2007 Italian population and 104 (95% confidence interval 88–122) compared with the European standard population. Incidence rates for first-ever strokes was 215 (196–235) for women, 202 (183–223) for men. Crude annual incidence rates per 100 000 population were 167 (153–178) for ischemic stroke, 31 (26–37) for intracerebral hemorrhage, 8·1 (5·7–11·4) for sub-arachnoid hemorrage, and 4·6 (2·8–7·1) for undetermined stroke. Overall case fatality rates for first-ever stroke were 20·6% at 28 days and 30·2% at 180 days.</p></div></div>
<div class="section" id="ijs12000-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Our study shows incidence rates higher than previously reported in our region but not supporting the view of higher incidence rates in Northern than in Southern Italy. Results contribute to time-trends analysis on epidemiology, useful for dimensioning services in Italy and show the persistence of a gap between the outcome of stroke in Italy and that of the best performing European countries, urging to adopt better stroke management plans.</p></div></div>
]]></content:encoded><description>

Background
Stroke incidence in high-income countries is reported to decrease, and new data on stroke incidence and outcome are needed to design stroke services and to ameliorate stroke management.


Methods
This study is part of a two-year prospective community-based registry of all cerebrovascular events in the district of Udine (153 312 inhabitants), Friuli-Venezia Giulia region, northeast of Italy, between 1 April 2007 and 31 March 2009. Overlapping sources for case finding were used, combining hot and cold pursuit.


Results
We identified 784 stroke cases, 640 (81·6%) incident. The crude overall annual incidence rate per 100 000 residents was 256 (95% confidence interval 241–271) for all strokes and 209 (95% confidence interval 195–223) for first-ever strokes. Incidence rate for first-ever strokes was 181 (95% confidence interval 155–211) after adjustment to the 2007 Italian population and 104 (95% confidence interval 88–122) compared with the European standard population. Incidence rates for first-ever strokes was 215 (196–235) for women, 202 (183–223) for men. Crude annual incidence rates per 100 000 population were 167 (153–178) for ischemic stroke, 31 (26–37) for intracerebral hemorrhage, 8·1 (5·7–11·4) for sub-arachnoid hemorrage, and 4·6 (2·8–7·1) for undetermined stroke. Overall case fatality rates for first-ever stroke were 20·6% at 28 days and 30·2% at 180 days.


Conclusions
Our study shows incidence rates higher than previously reported in our region but not supporting the view of higher incidence rates in Northern than in Southern Italy. Results contribute to time-trends analysis on epidemiology, useful for dimensioning services in Italy and show the persistence of a gap between the outcome of stroke in Italy and that of the best performing European countries, urging to adopt better stroke management plans.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12045" xmlns="http://purl.org/rss/1.0/"><title>The Stroke Hyperglycemia Insulin Network Effort (SHINE) trial protocol: a randomized, blinded, efficacy trial of standard vs. intensive hyperglycemia management in acute stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12045</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The Stroke Hyperglycemia Insulin Network Effort (SHINE) trial protocol: a randomized, blinded, efficacy trial of standard vs. intensive hyperglycemia management in acute stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Askiel Bruno, Valerie L. Durkalski, Christiana E. Hall, Rattan Juneja, William G. Barsan, Scott Janis, William J. Meurer, Amy Fansler, Karen C. Johnston, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-19T04:58:18.088884-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12045</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12045</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12045</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocol</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12045-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Patients with acute ischemic stroke and hyperglycemia have worse outcomes than those without hyperglycemia. Intensive glucose control during acute stroke is feasible and can be accomplished safely but has not been fully assessed for efficacy.</p></div></div>
<div class="section" id="ijs12045-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The Stroke Hyperglycemia Insulin Network Effort trial aims to determine the safety and efficacy of standard vs. intensive glucose control with insulin in hyperglycemic acute ischemic stroke patients.</p></div></div>
<div class="section" id="ijs12045-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>This is a randomized, blinded, multicenter, phase III trial of approximately 1400 hyperglycemic patients who receive either standard sliding scale subcutaneous insulin (blood glucose range 80–179 mg/dL, 4·44-9·93 mmol/L) or continuous intravenous insulin (target blood glucose 80–130 mg/dL, 4·44-7·21 mmol/L) for up to 72 h, starting within 12 h of stroke symptom onset. The acute treatment phase is single blind (for the patients), but the final outcome assessment is double blind. The study is powered to detect a 7% absolute difference in favorable outcome at 90 days.</p></div></div>
<div class="section" id="ijs12045-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study outcomes</h4><div class="para"><p>The primary outcome is a baseline severity adjusted 90-day modified Rankin Scale score, defined as 0, 0–1, or 0–2, if the baseline National Institutes of Health Stroke Scale score is 3–7, 8–14, or 15–22, respectively. The primary safety outcome is the rate of severe hypoglycemia (&lt;40 mg/dL, &lt;2·22 mmol/L).</p></div></div>
<div class="section" id="ijs12045-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Discussion</h4><div class="para"><p>This trial will provide important novel information about preferred management of acute ischemic stroke patients with hyperglycemia. It will determine the potential benefits and risks of intensive glucose control during acute stroke.</p></div></div>
]]></content:encoded><description>

Rationale
Patients with acute ischemic stroke and hyperglycemia have worse outcomes than those without hyperglycemia. Intensive glucose control during acute stroke is feasible and can be accomplished safely but has not been fully assessed for efficacy.


Aims
The Stroke Hyperglycemia Insulin Network Effort trial aims to determine the safety and efficacy of standard vs. intensive glucose control with insulin in hyperglycemic acute ischemic stroke patients.


Design
This is a randomized, blinded, multicenter, phase III trial of approximately 1400 hyperglycemic patients who receive either standard sliding scale subcutaneous insulin (blood glucose range 80–179 mg/dL, 4·44-9·93 mmol/L) or continuous intravenous insulin (target blood glucose 80–130 mg/dL, 4·44-7·21 mmol/L) for up to 72 h, starting within 12 h of stroke symptom onset. The acute treatment phase is single blind (for the patients), but the final outcome assessment is double blind. The study is powered to detect a 7% absolute difference in favorable outcome at 90 days.


Study outcomes
The primary outcome is a baseline severity adjusted 90-day modified Rankin Scale score, defined as 0, 0–1, or 0–2, if the baseline National Institutes of Health Stroke Scale score is 3–7, 8–14, or 15–22, respectively. The primary safety outcome is the rate of severe hypoglycemia (&lt;40 mg/dL, &lt;2·22 mmol/L).


Discussion
This trial will provide important novel information about preferred management of acute ischemic stroke patients with hyperglycemia. It will determine the potential benefits and risks of intensive glucose control during acute stroke.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12043" xmlns="http://purl.org/rss/1.0/"><title>Representation of people with aphasia in randomized controlled trials of acute stroke interventions</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12043</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Representation of people with aphasia in randomized controlled trials of acute stroke interventions</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Myzoon Ali, Philip M. Bath, Patrick D. Lyden, J. Bernhardt, Marian Brady, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-19T04:58:07.821069-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12043</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12043</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12043</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12043-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Aphasia affects up to a third of the stroke population and is associated with poor social participation and quality of life. Yet people with aphasia may be excluded from some types of stroke research due to challenges in informing, consenting, and conducting follow-up in this population.</p></div></div>
<div class="section" id="ijs12043-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims and/or hypothesis</h4><div class="para"><p>We described the representation of those with aphasia in acute stroke clinical research, the level of inclusion across international trial sites, and whether there have been improvements in the inclusion of this population in recent clinical trials.</p></div></div>
<div class="section" id="ijs12043-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We conducted a retrospective analysis of clinical trial data from the Virtual International Stroke Trials Archive (VISTA), defining aphasia using the Best Language (item 9) domain of the National Institutes of Health Stroke Scale. We used proportional odds modeling, adjusting for age, gender, ethnicity, stroke severity, medical history, hemisphere affected by stroke, and trial eligibility criteria, to examine the associations between year, location of enrollment, inclusion, and attrition of those with aphasia.</p></div></div>
<div class="section" id="ijs12043-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Data were available for 8904 patients from 10 trials; no trials listed aphasia as an exclusion criterion. At baseline, aphasia was present in 4039 (45·4%); severe/global aphasia was present in 2688 (30·2%). We observed no geographic or longitudinal disparity in the attrition of these patients at three-months. Centers in the Philippines recruited fewer people [<em>P</em> = 0·05, odds ratio = 0·5, 95% confidence interval (0·2, 1·0)], while centers in Central and South America included more people with severe/global aphasia [<em>P</em> = 0·0004, odds ratio = 2·4, 95% confidence interval (1·3, 4·3)], when compared with centers in the USA and Canada.</p></div></div>
<div class="section" id="ijs12043-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Acute stroke trials have demonstrated the feasibility of including people with aphasia in stroke research; we observed geographic variations that were not entirely explained by case mix or trial eligibility criteria. Similar levels of inclusion should be sought in nonemergency stroke trials to improve the applicability of research findings to this population.</p></div></div>
]]></content:encoded><description>

Background
Aphasia affects up to a third of the stroke population and is associated with poor social participation and quality of life. Yet people with aphasia may be excluded from some types of stroke research due to challenges in informing, consenting, and conducting follow-up in this population.


Aims and/or hypothesis
We described the representation of those with aphasia in acute stroke clinical research, the level of inclusion across international trial sites, and whether there have been improvements in the inclusion of this population in recent clinical trials.


Methods
We conducted a retrospective analysis of clinical trial data from the Virtual International Stroke Trials Archive (VISTA), defining aphasia using the Best Language (item 9) domain of the National Institutes of Health Stroke Scale. We used proportional odds modeling, adjusting for age, gender, ethnicity, stroke severity, medical history, hemisphere affected by stroke, and trial eligibility criteria, to examine the associations between year, location of enrollment, inclusion, and attrition of those with aphasia.


Results
Data were available for 8904 patients from 10 trials; no trials listed aphasia as an exclusion criterion. At baseline, aphasia was present in 4039 (45·4%); severe/global aphasia was present in 2688 (30·2%). We observed no geographic or longitudinal disparity in the attrition of these patients at three-months. Centers in the Philippines recruited fewer people [P = 0·05, odds ratio = 0·5, 95% confidence interval (0·2, 1·0)], while centers in Central and South America included more people with severe/global aphasia [P = 0·0004, odds ratio = 2·4, 95% confidence interval (1·3, 4·3)], when compared with centers in the USA and Canada.


Conclusions
Acute stroke trials have demonstrated the feasibility of including people with aphasia in stroke research; we observed geographic variations that were not entirely explained by case mix or trial eligibility criteria. Similar levels of inclusion should be sought in nonemergency stroke trials to improve the applicability of research findings to this population.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12034" xmlns="http://purl.org/rss/1.0/"><title>Evaluation of plasma d-dimer plus fibrinogen in predicting acute CVST</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12034</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Evaluation of plasma d-dimer plus fibrinogen in predicting acute CVST</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ran Meng, Xiaoying Wang, Mohammed Hussain, David Dornbos, Lu Meng, Yu Liu, Yan Wu, Mingming Ning, Buonanno Ferdinando S, Eng H. Lo, Yuchuan Ding, Xunming Ji</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-19T04:58:00.017083-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12034</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12034</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12034</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12034-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Prompt diagnosis of cerebral venous sinus thrombosis is a challenge owing in part to its complex and non-specific early clinical symptoms.</p></div></div>
<div class="section" id="ijs12034-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>This study aims to evaluate the value of clinically useful biomarkers (<span class="smallCaps">d</span>-dimer and fibrinogen) for cerebral venous sinus thrombosis prediction.</p></div></div>
<div class="section" id="ijs12034-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Two-hundred and thirty-three suspected cerebral venous sinus thrombosis patients were enrolled in this prospective study. Thirty-four cases confirmed as cerebral venous sinus thrombosis using imaging modalities, whereas the other 199 cases served as mimic controls. Plasma samples of 34 healthy controls were further collected from age- and gender-matched volunteers. <span class="smallCaps">d</span>-dimer and fibrinogen levels of all patients and controls were measured before imaging and treatment. The dynamic <span class="smallCaps">d</span>-dimer and fibrinogen levels in cerebral venous sinus thrombosis cases after anticoagulation were monitored for up to 180 consecutive days.</p></div></div>
<div class="section" id="ijs12034-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>At admission before treatment the average <span class="smallCaps">d</span>-dimer and fibrinogen levels in cerebral venous sinus thrombosis group were 968·9 ± 160·1 μg/l and 6·9 ± 1·3 g/l, both of which were significantly elevated when compared with that of the controls. In cerebral venous sinus thrombosis patients, 94·1% had <span class="smallCaps">d</span>-dimer elevation, 73·5% had fibrinogen elevation, and 67·6% had both elevated <span class="smallCaps">d</span>-dimer and fibrinogen. During acute phase, the sensitivity and specificity of predicting cerebral venous sinus thrombosis using only <span class="smallCaps">d</span>-dimer were 94·1% and 97·5%, whereas that of <span class="smallCaps">d</span>-dimer in combination with fibrinogen were 67·6% and 98·9%. After administering anticoagulation, <span class="smallCaps">d</span>-dimer levels gradually recovered; however, fibrinogen levels fluctuated with 33·3% of the patients still exhibiting elevated values up until 180 days.</p></div></div>
<div class="section" id="ijs12034-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p><span class="smallCaps">d</span>-dimer may serve as an important screening tool to determine the urgency of obtaining magnetic resonance imaging/magnetic resonance venography or digital subtraction angiography in patients presenting with clinical symptoms that are suspected of cerebral venous sinus thrombosis. Furthermore, <span class="smallCaps">d</span>-dimer in combination with fibrinogen may increase the predictive value of acute cerebral venous sinus thrombosis.</p></div></div>
]]></content:encoded><description>

Background
Prompt diagnosis of cerebral venous sinus thrombosis is a challenge owing in part to its complex and non-specific early clinical symptoms.


Objective
This study aims to evaluate the value of clinically useful biomarkers (d-dimer and fibrinogen) for cerebral venous sinus thrombosis prediction.


Methods
Two-hundred and thirty-three suspected cerebral venous sinus thrombosis patients were enrolled in this prospective study. Thirty-four cases confirmed as cerebral venous sinus thrombosis using imaging modalities, whereas the other 199 cases served as mimic controls. Plasma samples of 34 healthy controls were further collected from age- and gender-matched volunteers. d-dimer and fibrinogen levels of all patients and controls were measured before imaging and treatment. The dynamic d-dimer and fibrinogen levels in cerebral venous sinus thrombosis cases after anticoagulation were monitored for up to 180 consecutive days.


Results
At admission before treatment the average d-dimer and fibrinogen levels in cerebral venous sinus thrombosis group were 968·9 ± 160·1 μg/l and 6·9 ± 1·3 g/l, both of which were significantly elevated when compared with that of the controls. In cerebral venous sinus thrombosis patients, 94·1% had d-dimer elevation, 73·5% had fibrinogen elevation, and 67·6% had both elevated d-dimer and fibrinogen. During acute phase, the sensitivity and specificity of predicting cerebral venous sinus thrombosis using only d-dimer were 94·1% and 97·5%, whereas that of d-dimer in combination with fibrinogen were 67·6% and 98·9%. After administering anticoagulation, d-dimer levels gradually recovered; however, fibrinogen levels fluctuated with 33·3% of the patients still exhibiting elevated values up until 180 days.


Conclusions
d-dimer may serve as an important screening tool to determine the urgency of obtaining magnetic resonance imaging/magnetic resonance venography or digital subtraction angiography in patients presenting with clinical symptoms that are suspected of cerebral venous sinus thrombosis. Furthermore, d-dimer in combination with fibrinogen may increase the predictive value of acute cerebral venous sinus thrombosis.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12044" xmlns="http://purl.org/rss/1.0/"><title>CHIMES-I: sub-group analyzes of the effects of NeuroAiD according to baseline brain imaging characteristics among patients randomized in the CHIMES study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12044</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">CHIMES-I: sub-group analyzes of the effects of NeuroAiD according to baseline brain imaging characteristics among patients randomized in the CHIMES study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jose C. Navarro, Christopher Li Hsian Chen, Pedro Danilo J. Lagamayo, Melodia B. Geslani, Gaik Bee Eow, Niphon Poungvarin, Asita Silva, Lawrence K. S. Wong, N. Venketasubramanian, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-19T04:47:08.38008-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12044</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12044</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12044</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocol</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12044-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>The clinical effects of neuroprotective and/or neurorestorative therapies may vary according to location and size of the ischemic injury. Imaging techniques can be useful in stratifying patients for trials that may be beneficial against particular ischemic lesion characteristics.</p></div></div>
<div class="section" id="ijs12044-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>To test the hypothesis that the efficacy of NeuroAiD compared with placebo in improving functional outcome and reducing neurological deficit in patients with cerebral infarction of intermediate severity varies between sub-groups of patients randomized in the main Chinese Medicine Neuroaid Efficacy on Stroke study when categorized according to baseline imaging characteristics.</p></div></div>
<div class="section" id="ijs12044-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>This is a retrospective cohort sub-group analysis of patients who participated in the main Chinese Medicine Neuroaid Efficacy on Stroke study, a multicenter, double-blind, placebo-controlled trial that recruited 1100 patients within 72 h of ischemic stroke onset with National Institutes of Health Stroke Scale 6–14 and were randomized to either NeuroAiD or placebo taken four capsules three times daily for three months. Review of the baseline images to classify the acute stroke lesions in terms of size, location, and extent of involvement will be performed retrospectively by two readers who will remain blinded as to treatment allocation and outcomes of the subjects.</p></div></div>
<div class="section" id="ijs12044-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study outcomes</h4><div class="para"><p>The primary efficacy end-point in the main Chinese Medicine Neuroaid Efficacy on Stroke study is the modified Rankin Scale grades at three-months. Secondary efficacy end-points are the National Institutes of Health Stroke Scale score at three-months; difference of National Institutes of Health Stroke Scale scores between baseline and 10 days and between baseline and three-months; difference of National Institutes of Health Stroke Scale sub-scores between baseline and 10 days and between baseline and three-months; modified Rankin Scale at 10 days, one-month, and three-months; Barthel index at three-months; and Mini Mental State Examination at 10 days and three-months. Analysis of these primary and secondary end-points will be performed for sub-groups defined in this study after review of the baseline brain imaging: nonlacunar and lacunar, cortical and sub-cortical, hemispheric vs. brainstem, Alberta Stroke Program Early CT score &lt;7 and 7–10, and score &lt;8 and 8–10.</p></div></div>
]]></content:encoded><description>

Rationale
The clinical effects of neuroprotective and/or neurorestorative therapies may vary according to location and size of the ischemic injury. Imaging techniques can be useful in stratifying patients for trials that may be beneficial against particular ischemic lesion characteristics.


Aim
To test the hypothesis that the efficacy of NeuroAiD compared with placebo in improving functional outcome and reducing neurological deficit in patients with cerebral infarction of intermediate severity varies between sub-groups of patients randomized in the main Chinese Medicine Neuroaid Efficacy on Stroke study when categorized according to baseline imaging characteristics.


Design
This is a retrospective cohort sub-group analysis of patients who participated in the main Chinese Medicine Neuroaid Efficacy on Stroke study, a multicenter, double-blind, placebo-controlled trial that recruited 1100 patients within 72 h of ischemic stroke onset with National Institutes of Health Stroke Scale 6–14 and were randomized to either NeuroAiD or placebo taken four capsules three times daily for three months. Review of the baseline images to classify the acute stroke lesions in terms of size, location, and extent of involvement will be performed retrospectively by two readers who will remain blinded as to treatment allocation and outcomes of the subjects.


Study outcomes
The primary efficacy end-point in the main Chinese Medicine Neuroaid Efficacy on Stroke study is the modified Rankin Scale grades at three-months. Secondary efficacy end-points are the National Institutes of Health Stroke Scale score at three-months; difference of National Institutes of Health Stroke Scale scores between baseline and 10 days and between baseline and three-months; difference of National Institutes of Health Stroke Scale sub-scores between baseline and 10 days and between baseline and three-months; modified Rankin Scale at 10 days, one-month, and three-months; Barthel index at three-months; and Mini Mental State Examination at 10 days and three-months. Analysis of these primary and secondary end-points will be performed for sub-groups defined in this study after review of the baseline brain imaging: nonlacunar and lacunar, cortical and sub-cortical, hemispheric vs. brainstem, Alberta Stroke Program Early CT score &lt;7 and 7–10, and score &lt;8 and 8–10.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12036" xmlns="http://purl.org/rss/1.0/"><title>Efficacy and safety of warfarin vs. antiplatelet therapy in patients with systolic heart failure and sinus rhythm: a systematic review and meta-analysis of randomized controlled trials</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12036</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Efficacy and safety of warfarin vs. antiplatelet therapy in patients with systolic heart failure and sinus rhythm: a systematic review and meta-analysis of randomized controlled trials</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Aaron YL. Liew, John W. Eikelboom, Stuart J. Connolly, Martin O' Donnell, Robert G. Hart</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-19T04:47:03.582932-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12036</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12036</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12036</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Systematic Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12036-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and purpose</h4><div class="para"><p>Heart failure is an independent risk factor for stroke. Anticoagulation is effective for prevention of cardio-embolic stroke secondary to atrial fibrillation or mechanical heart valves but is of uncertain benefit in heart failure patients. We performed this meta-analysis to obtain the best estimates of the efficacy and safety of warfarin as compared with antiplatelet therapy in patients with systolic heart failure who are in sinus rhythm.</p></div></div>
<div class="section" id="ijs12036-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods and results</h4><div class="para"><p>A systematic search was performed using PubMed and Central Register of Controlled Trials databases for all randomized controlled trials, which compare warfarin with antiplatelet therapy given for at least one-month in heart failure patients with sinus rhythm and report at least one of the following outcomes: ischemic stroke, death, myocardial infarction, hospitalization due to worsening heart failure, intracranial hemorrhage, and major hemorrhage. Four randomized controlled trials involving adjusted-dose warfarin (4187 subjects) were included. When compared with antiplatelet therapy, warfarin reduced ischemic stroke by 0·74% per year (RR 0·49; 95% CI: 0·32–0·73: <em>P</em> = 0·0006; Number needed to treat = 135) but increased major hemorrhage by 0·99% per year (RR 2·15; 95% CI: 1·55–2·99: <em>P</em> &lt; 0·00001; Number needed to harm = 101). Warfarin did not significantly affect the risk of death, myocardial infarction, hospitalization due to heart failure or intracranial hemorrhage as compared with antiplatelet therapy.</p></div></div>
<div class="section" id="ijs12036-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Warfarin as compared with antiplatelet therapy reduces risk of ischemic stroke, does not significantly affect death, myocardial infarction, hospitalization due to heart failure or intracranial hemorrhage and increases major hemorrhage in heart failure patients who are in sinus rhythm.</p></div></div>
]]></content:encoded><description>

Background and purpose
Heart failure is an independent risk factor for stroke. Anticoagulation is effective for prevention of cardio-embolic stroke secondary to atrial fibrillation or mechanical heart valves but is of uncertain benefit in heart failure patients. We performed this meta-analysis to obtain the best estimates of the efficacy and safety of warfarin as compared with antiplatelet therapy in patients with systolic heart failure who are in sinus rhythm.


Methods and results
A systematic search was performed using PubMed and Central Register of Controlled Trials databases for all randomized controlled trials, which compare warfarin with antiplatelet therapy given for at least one-month in heart failure patients with sinus rhythm and report at least one of the following outcomes: ischemic stroke, death, myocardial infarction, hospitalization due to worsening heart failure, intracranial hemorrhage, and major hemorrhage. Four randomized controlled trials involving adjusted-dose warfarin (4187 subjects) were included. When compared with antiplatelet therapy, warfarin reduced ischemic stroke by 0·74% per year (RR 0·49; 95% CI: 0·32–0·73: P = 0·0006; Number needed to treat = 135) but increased major hemorrhage by 0·99% per year (RR 2·15; 95% CI: 1·55–2·99: P &lt; 0·00001; Number needed to harm = 101). Warfarin did not significantly affect the risk of death, myocardial infarction, hospitalization due to heart failure or intracranial hemorrhage as compared with antiplatelet therapy.


Conclusions
Warfarin as compared with antiplatelet therapy reduces risk of ischemic stroke, does not significantly affect death, myocardial infarction, hospitalization due to heart failure or intracranial hemorrhage and increases major hemorrhage in heart failure patients who are in sinus rhythm.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12033" xmlns="http://purl.org/rss/1.0/"><title>Functional connectivity magnetic resonance imaging in stroke: an evidence-based clinical review</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12033</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Functional connectivity magnetic resonance imaging in stroke: an evidence-based clinical review</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ourania Varsou, Mary Joan Macleod, Christian Schwarzbauer</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-19T04:46:57.785269-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12033</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12033</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12033</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Stroke is a common condition that may lead to various degrees of neurological deficit and long-term disability. It has become increasingly recognized that cortical reorganization of neuronal networks plays a significant role in regaining function following a focal brain injury. However, the mechanisms involved in this process are still not fully understood. Resting-state functional connectivity magnetic resonance imaging is a rapidly evolving scanning technique that has the potential to shed light into this neuronal rearrangement. A better understanding of the underlying neurological pathways may contribute to the development of targeted treatment that will promote repair and reduce poststroke deficit. The aim of this review is to provide an up-to-date summary of the available scientific data evaluating the clinical application of functional connectivity magnetic resonance imaging among stroke survivors.</p></div>
]]></content:encoded><description>
Stroke is a common condition that may lead to various degrees of neurological deficit and long-term disability. It has become increasingly recognized that cortical reorganization of neuronal networks plays a significant role in regaining function following a focal brain injury. However, the mechanisms involved in this process are still not fully understood. Resting-state functional connectivity magnetic resonance imaging is a rapidly evolving scanning technique that has the potential to shed light into this neuronal rearrangement. A better understanding of the underlying neurological pathways may contribute to the development of targeted treatment that will promote repair and reduce poststroke deficit. The aim of this review is to provide an up-to-date summary of the available scientific data evaluating the clinical application of functional connectivity magnetic resonance imaging among stroke survivors.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12032" xmlns="http://purl.org/rss/1.0/"><title>Emergency transfer of acute stroke patients within the East Saxony telemedicine stroke network: a descriptive analysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12032</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Emergency transfer of acute stroke patients within the East Saxony telemedicine stroke network: a descriptive analysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jessica Kepplinger, Imanuel Dzialowski, Kristian Barlinn, Volker Puetz, Claudia Wojciechowski, Hauke Schneider, Georg Gahn, Tobias Back, Gabriele Schackert, Heinz Reichmann, Ruediger Kummer, Ulf Bodechtel</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-19T04:46:50.616138-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12032</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12032</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12032</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12032-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Telemedicine may facilitate the selection of stroke patients who require emergency transfer to a comprehensive stroke center to receive additional therapies other than intravenous tissue plasminogen activator.</p></div></div>
<div class="section" id="ijs12032-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims and/or hypothesis</h4><div class="para"><p>We sought to analyze frequency, patient characteristics, and specific therapies among emergently transferred patients within the telemedical Stroke East Saxony Network.</p></div></div>
<div class="section" id="ijs12032-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We reviewed consecutive patients who were transferred emergently from remote spoke sites to hub sites. Certified stroke neurologists performed teleconsultations 24/7, with access to high-speed videoconferencing and transfer of brain images. Emergent transfers were initiated when considered necessary by the stroke neurologist.</p></div></div>
<div class="section" id="ijs12032-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>In 2009 and 2010, we conducted 1413 teleconsultations and subsequently recommended transfer in 339 (24%) patients [mean age 64 ± 14 years, 54% males, median National Institutes of Health Stroke Scale score 5 (interquartile range, IQR 12). The mean teleconsultation-to-arrival time was 1·7 ± 0·8 h (median 1·6 h). Sixty-eight (20%) transferred patients had a nonstroke diagnosis. The remaining 271 (80%) patients had stroke diagnoses [ischemic stroke, 114 (34%); transient ischemic attack, 8 (2%); and intracranial haemorrhage, 149 (44%)]. Forty (35%) ischemic stroke patients received tissue plasminogen activator at spoke sites (‘drip and ship’). Of the 240 stroke patients emergently transferred to the main hub site, 119 (49·6%) received at least one specific stroke therapy.</p></div></div>
<div class="section" id="ijs12032-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>A remarkable number of stroke patients can be transferred within a telemedical network to enable the delivery of specific stroke therapies that require advanced multispecialty expertise. Whether associated logistic efforts and costs have an impact on patients' clinical outcomes needs to be evaluated.</p></div></div>
]]></content:encoded><description>

Background
Telemedicine may facilitate the selection of stroke patients who require emergency transfer to a comprehensive stroke center to receive additional therapies other than intravenous tissue plasminogen activator.


Aims and/or hypothesis
We sought to analyze frequency, patient characteristics, and specific therapies among emergently transferred patients within the telemedical Stroke East Saxony Network.


Methods
We reviewed consecutive patients who were transferred emergently from remote spoke sites to hub sites. Certified stroke neurologists performed teleconsultations 24/7, with access to high-speed videoconferencing and transfer of brain images. Emergent transfers were initiated when considered necessary by the stroke neurologist.


Results
In 2009 and 2010, we conducted 1413 teleconsultations and subsequently recommended transfer in 339 (24%) patients [mean age 64 ± 14 years, 54% males, median National Institutes of Health Stroke Scale score 5 (interquartile range, IQR 12). The mean teleconsultation-to-arrival time was 1·7 ± 0·8 h (median 1·6 h). Sixty-eight (20%) transferred patients had a nonstroke diagnosis. The remaining 271 (80%) patients had stroke diagnoses [ischemic stroke, 114 (34%); transient ischemic attack, 8 (2%); and intracranial haemorrhage, 149 (44%)]. Forty (35%) ischemic stroke patients received tissue plasminogen activator at spoke sites (‘drip and ship’). Of the 240 stroke patients emergently transferred to the main hub site, 119 (49·6%) received at least one specific stroke therapy.


Conclusions
A remarkable number of stroke patients can be transferred within a telemedical network to enable the delivery of specific stroke therapies that require advanced multispecialty expertise. Whether associated logistic efforts and costs have an impact on patients' clinical outcomes needs to be evaluated.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12031" xmlns="http://purl.org/rss/1.0/"><title>Is the rate of cerebral hemorrhages declining among stroke patients in South America?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12031</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Is the rate of cerebral hemorrhages declining among stroke patients in South America?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Oscar H. Del Brutto, Victor J. Del Brutto</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-19T04:46:44.917207-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12031</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12031</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12031</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Panorama</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Recent stroke registries suggest that the rate of cerebral hemorrhages is declining among stroke patients in South America. High rates of cerebral hemorrhages (approaching 40% of stroke cases) reported in pioneer registries during the 1990s have not been duplicated in more recent studies. In contrast, almost all studies recruiting patients from 2003 on, reported less than 20% of cerebral hemorrhages among their stroke patients. Intermediate rates of hemorrhagic strokes (from 25% to 27%) were noted among registries recruiting patients by the end of the 20th century and the start of the new Millennium. We also noted a significant declining rate of hemorrhagic stroke over the past 20 years at our Institution. In a series of 651 consecutive first-ever stroke patients included in the Hospital-Clínica Kennedy stroke registry (Guayaquil), cerebral hemorrhages accounted for 26·3% of patients recruited between 1990 and 1994 but for only 16·5% of those seen between 2005 and 2009 (<em>P</em> = 0·03). More longitudinal studies are needed to confirm these findings and to determine whether the reported declining rate of hemorrhagic strokes in South America is related to increase life expectancy of the population, or to changes in lifestyle, dietary habits, or some other specific stroke risk factors not well evaluated so far.</p></div>
]]></content:encoded><description>
Recent stroke registries suggest that the rate of cerebral hemorrhages is declining among stroke patients in South America. High rates of cerebral hemorrhages (approaching 40% of stroke cases) reported in pioneer registries during the 1990s have not been duplicated in more recent studies. In contrast, almost all studies recruiting patients from 2003 on, reported less than 20% of cerebral hemorrhages among their stroke patients. Intermediate rates of hemorrhagic strokes (from 25% to 27%) were noted among registries recruiting patients by the end of the 20th century and the start of the new Millennium. We also noted a significant declining rate of hemorrhagic stroke over the past 20 years at our Institution. In a series of 651 consecutive first-ever stroke patients included in the Hospital-Clínica Kennedy stroke registry (Guayaquil), cerebral hemorrhages accounted for 26·3% of patients recruited between 1990 and 1994 but for only 16·5% of those seen between 2005 and 2009 (P = 0·03). More longitudinal studies are needed to confirm these findings and to determine whether the reported declining rate of hemorrhagic strokes in South America is related to increase life expectancy of the population, or to changes in lifestyle, dietary habits, or some other specific stroke risk factors not well evaluated so far.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12030" xmlns="http://purl.org/rss/1.0/"><title>Door-to-door survey of cardiovascular health, stroke, and ischemic heart disease in rural coastal Ecuador – the Atahualpa Project: methodology and operational definitions</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12030</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Door-to-door survey of cardiovascular health, stroke, and ischemic heart disease in rural coastal Ecuador – the Atahualpa Project: methodology and operational definitions</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Oscar H. Del Brutto, Ernesto Peñaherrera, Elio Ochoa, Milton Santamaría, Mauricio Zambrano, Victor J. Del Brutto, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-19T04:46:41.135814-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12030</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12030</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12030</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12030-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Stroke and cardiovascular diseases will be the next health epidemics in Latin America due to increased life expectancy and changes in the lifestyle and dietary habits of the population. Knowledge of the cardiovascular health status of the inhabitants will allow the implementation of policies directed to reduce the burden of stroke and cardiovascular diseases in the region.</p></div></div>
<div class="section" id="ijs12030-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>To evaluate the cardiovascular health status of the inhabitants of Atahualpa (a rural village in coastal Ecuador) and to determine the prevalence and incidence of stroke and ischemic heart disease in the region.</p></div></div>
<div class="section" id="ijs12030-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Three-phase epidemiologic survey. During <em>phase I</em>, Atahualpa residents aged ≥40 years will be screened with standardized questionnaires to evaluate their cardiovascular health and to identify those with suspected stroke or ischemic heart disease. In <em>phase II</em>, neurologists and cardiologists will examine suspected cases of stroke or ischemic heart disease, as well as a random sample of matched negative individuals, to assess the prevalence and incidence of these conditions. In <em>phase III</em>, patients with a diagnosis of stroke and ischemic heart disease will undergo complementary tests for achieving a more specific diagnosis.</p></div></div>
<div class="section" id="ijs12030-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Discussion</h4><div class="para"><p>Implementation of public health strategies directed to improve the cardiovascular health status of a given population must be based on studies evaluating specific risk factors at regional levels. Epidemiologic surveys such as the Atahualpa Project may prove cost-effective in improving the cardiovascular health status of people living in Latin American rural villages by increasing the knowledge on the particular needs of these populations.</p></div></div>
]]></content:encoded><description>

Rationale
Stroke and cardiovascular diseases will be the next health epidemics in Latin America due to increased life expectancy and changes in the lifestyle and dietary habits of the population. Knowledge of the cardiovascular health status of the inhabitants will allow the implementation of policies directed to reduce the burden of stroke and cardiovascular diseases in the region.


Aims
To evaluate the cardiovascular health status of the inhabitants of Atahualpa (a rural village in coastal Ecuador) and to determine the prevalence and incidence of stroke and ischemic heart disease in the region.


Design
Three-phase epidemiologic survey. During phase I, Atahualpa residents aged ≥40 years will be screened with standardized questionnaires to evaluate their cardiovascular health and to identify those with suspected stroke or ischemic heart disease. In phase II, neurologists and cardiologists will examine suspected cases of stroke or ischemic heart disease, as well as a random sample of matched negative individuals, to assess the prevalence and incidence of these conditions. In phase III, patients with a diagnosis of stroke and ischemic heart disease will undergo complementary tests for achieving a more specific diagnosis.


Discussion
Implementation of public health strategies directed to improve the cardiovascular health status of a given population must be based on studies evaluating specific risk factors at regional levels. Epidemiologic surveys such as the Atahualpa Project may prove cost-effective in improving the cardiovascular health status of people living in Latin American rural villages by increasing the knowledge on the particular needs of these populations.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12025" xmlns="http://purl.org/rss/1.0/"><title>Stroke education in the Philippines</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12025</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Stroke education in the Philippines</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jose C. Navarro, Alejandro C. Baroque, Johnny K. Lokin</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-19T04:46:27.185112-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12025</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12025</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12025</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Panorama</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Education is paramount in effectively reducing the significant burden of stroke in the Philippines. Dedicated academic institutions and dynamic professional organizations in the Philippines have collaborated to involve themselves in the plight against stroke through systematic curriculum development for undergraduates, continuous regulation of quality residency and fellowship training program, hosting up-to-date Continuing Medical Education (CME) activities for local and international audience, and active participation in clinical stroke trials. Most recently, the University of Santo Tomas Faculty of Medicine &amp; Surgery and the Department of Neurology &amp; Psychiatry offered a 72-hour Certification Course in Stroke Medicine that commenced in 2011 in anticipation of the Master on Health Sciences in Stroke Medicine course being prepared for 2013.</p></div>
]]></content:encoded><description>
Education is paramount in effectively reducing the significant burden of stroke in the Philippines. Dedicated academic institutions and dynamic professional organizations in the Philippines have collaborated to involve themselves in the plight against stroke through systematic curriculum development for undergraduates, continuous regulation of quality residency and fellowship training program, hosting up-to-date Continuing Medical Education (CME) activities for local and international audience, and active participation in clinical stroke trials. Most recently, the University of Santo Tomas Faculty of Medicine &amp; Surgery and the Department of Neurology &amp; Psychiatry offered a 72-hour Certification Course in Stroke Medicine that commenced in 2011 in anticipation of the Master on Health Sciences in Stroke Medicine course being prepared for 2013.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12024" xmlns="http://purl.org/rss/1.0/"><title>What is stroke symptom knowledge?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12024</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">What is stroke symptom knowledge?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ian Mosley, Marcus Nicol, Geoffrey Donnan, Amanda G. Thrift, Helen M. Dewey</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-19T04:46:23.413408-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12024</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12024</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12024</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12024-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>No commonly agreed definition exists for ‘stroke symptom knowledge’ among members of the general public. Recalling at least one correct stroke symptom has been used in the past. However, this criterion was not associated with rapid presentation to hospital. Rapid presentation is vital in order to provide effective acute stroke treatment.</p></div></div>
<div class="section" id="ijs12024-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims and/or hypothesis</h4><div class="para"><p>We sought to identify a base level of community stroke symptom knowledge associated with stroke recognition when symptoms occur, an immediate ambulance call, and ‘stroke recognition and immediately calling an ambulance’ as a single sequence of events.</p></div></div>
<div class="section" id="ijs12024-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>For six-months in 2004–2005, we identified all patients with stroke living in a defined region of Melbourne and who were transported by ambulance to one of the three hospitals. The person who called the ambulance (caller) was interviewed.</p></div></div>
<div class="section" id="ijs12024-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>One hundred ninety-eight patients were identified and 150 callers interviewed. Symptoms reported most frequently were limb weakness (67%), speech problems (57%), and facial weakness (24%). Reporting at least two of the symptoms – facial weakness, limb weakness, or speech problems (62% of callers) – was associated with stroke recognition (<em>P</em> = 0·004), immediately calling an ambulance (<em>P</em> = 0·065), and both ‘stroke recognition and immediately calling an ambulance’ (<em>P</em> = 0·053).</p></div></div>
<div class="section" id="ijs12024-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Knowing at least two of the symptoms – facial weakness, limb weakness, and speech problems – appears to be an appropriate indicator of stroke symptom knowledge as it is associated with stroke recognition and appropriate action. Recognizing stroke symptoms and immediately calling an ambulance increase the potential to reduce prehospital time delays and improve eligibility of acute stroke patients for rapid treatment.</p></div></div>
]]></content:encoded><description>

Background
No commonly agreed definition exists for ‘stroke symptom knowledge’ among members of the general public. Recalling at least one correct stroke symptom has been used in the past. However, this criterion was not associated with rapid presentation to hospital. Rapid presentation is vital in order to provide effective acute stroke treatment.


Aims and/or hypothesis
We sought to identify a base level of community stroke symptom knowledge associated with stroke recognition when symptoms occur, an immediate ambulance call, and ‘stroke recognition and immediately calling an ambulance’ as a single sequence of events.


Methods
For six-months in 2004–2005, we identified all patients with stroke living in a defined region of Melbourne and who were transported by ambulance to one of the three hospitals. The person who called the ambulance (caller) was interviewed.


Results
One hundred ninety-eight patients were identified and 150 callers interviewed. Symptoms reported most frequently were limb weakness (67%), speech problems (57%), and facial weakness (24%). Reporting at least two of the symptoms – facial weakness, limb weakness, or speech problems (62% of callers) – was associated with stroke recognition (P = 0·004), immediately calling an ambulance (P = 0·065), and both ‘stroke recognition and immediately calling an ambulance’ (P = 0·053).


Conclusions
Knowing at least two of the symptoms – facial weakness, limb weakness, and speech problems – appears to be an appropriate indicator of stroke symptom knowledge as it is associated with stroke recognition and appropriate action. Recognizing stroke symptoms and immediately calling an ambulance increase the potential to reduce prehospital time delays and improve eligibility of acute stroke patients for rapid treatment.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12023" xmlns="http://purl.org/rss/1.0/"><title>Safety and feasibiLIty of Metformin in patients with Impaired glucose Tolerance and a recent TIA or minor ischemic stroke (LIMIT) trial – a multicenter, randomized, open-label phase II trial</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12023</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Safety and feasibiLIty of Metformin in patients with Impaired glucose Tolerance and a recent TIA or minor ischemic stroke (LIMIT) trial – a multicenter, randomized, open-label phase II trial</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Heleen M. Hertog, S. E. Vermeer, A. A. M. Zandbergen, Sefanja Achterberg, Diederik W. J. Dippel, Ale Algra, L. J. Kappelle, Peter J. Koudstaal</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-15T03:07:53.06237-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12023</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12023</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12023</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12023-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and purpose</h4><div class="para"><p>We aimed to assess the safety, feasibility, and effects on glucose metabolism of treatment with metformin in patients with TIA or minor ischemic stroke and impaired glucose tolerance.</p></div></div>
<div class="section" id="ijs12023-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We performed a multicenter, randomized, controlled, open-label phase II trial with blinded outcome assessment. Patients with TIA or minor ischemic stroke in the previous six months and impaired glucose tolerance (2-hour post-load glucose levels of 7.8–11.0 mmol/l) were randomized to metformin, in a daily dose of 2 g, or no metformin, for three months. Primary outcome measures were safety and feasibility of metformin, and the adjusted difference in 2-hour post-load glucose levels at three months. This trial is registered as an International Standard Randomized Controlled Trial Number 54960762.</p></div></div>
<div class="section" id="ijs12023-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Forty patients were enrolled; 19 patients were randomly assigned metformin. Nine patients in the metformin group had side effects, mostly gastrointestinal, leading to permanent discontinuation in four patients after 3–10 weeks. Treatment with metformin was associated with a significant reduction in 2-hour post-load glucose levels of 0·97 mmol/l (95% CI 0·11–1·83) in the on-treatment analysis, but not in the intention-to-treat analysis (0·71 mmol/l; 95% CI −0·36 to 1·78).</p></div></div>
<div class="section" id="ijs12023-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Treatment with metformin in patients with TIA or minor ischemic stroke and impaired glucose tolerance is safe, but leads to minor side effects. If tolerated, it may lead to a significant reduction in post-load glucose levels. This suggests that the role of metformin as potential therapeutic agent for secondary stroke prevention should be further explored.</p></div></div>
]]></content:encoded><description>

Background and purpose
We aimed to assess the safety, feasibility, and effects on glucose metabolism of treatment with metformin in patients with TIA or minor ischemic stroke and impaired glucose tolerance.


Methods
We performed a multicenter, randomized, controlled, open-label phase II trial with blinded outcome assessment. Patients with TIA or minor ischemic stroke in the previous six months and impaired glucose tolerance (2-hour post-load glucose levels of 7.8–11.0 mmol/l) were randomized to metformin, in a daily dose of 2 g, or no metformin, for three months. Primary outcome measures were safety and feasibility of metformin, and the adjusted difference in 2-hour post-load glucose levels at three months. This trial is registered as an International Standard Randomized Controlled Trial Number 54960762.


Results
Forty patients were enrolled; 19 patients were randomly assigned metformin. Nine patients in the metformin group had side effects, mostly gastrointestinal, leading to permanent discontinuation in four patients after 3–10 weeks. Treatment with metformin was associated with a significant reduction in 2-hour post-load glucose levels of 0·97 mmol/l (95% CI 0·11–1·83) in the on-treatment analysis, but not in the intention-to-treat analysis (0·71 mmol/l; 95% CI −0·36 to 1·78).


Conclusions
Treatment with metformin in patients with TIA or minor ischemic stroke and impaired glucose tolerance is safe, but leads to minor side effects. If tolerated, it may lead to a significant reduction in post-load glucose levels. This suggests that the role of metformin as potential therapeutic agent for secondary stroke prevention should be further explored.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12019" xmlns="http://purl.org/rss/1.0/"><title>Optimal medical treatment versus carotid endarterectomy: the rationale and design of the Aggressive Medical Treatment Evaluation for Asymptomatic Carotid Artery Stenosis (AMTEC) study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12019</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Optimal medical treatment versus carotid endarterectomy: the rationale and design of the Aggressive Medical Treatment Evaluation for Asymptomatic Carotid Artery Stenosis (AMTEC) study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Igor Kolos, Mikhail Loukianov, Nikolay Dupik, Sergey Boytsov, Alexandr Deev</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-15T03:06:49.556013-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12019</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12019</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12019</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12019-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Carotid endarterectomy and medical therapy (aspirin) were shown superior to medical therapy alone for asymptomatic (≥60%) carotid stenosis. The role of modern medical therapy (statins, antihypertensive treatment, and aspirin) in the treatment of such patients is undefined. Establishing the safety, efficacy, and durability of optimal medical therapy and lifestyle modification requires rigorous comparison with carotid endarterectomy in asymptomatic patients.</p></div></div>
<div class="section" id="ijs12019-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The objective is to compare the efficacy of carotid endarterectomy + optimal medical therapy versus optimal medical therapy alone in patients with asymptomatic (70–79%) extracranial carotid stenosis.</p></div></div>
<div class="section" id="ijs12019-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>The Aggressive Medical Treatment Evaluation for Asymptomatic Carotid Artery Stenosis study is a prospective, randomized, parallel, two-arm, multicenter trial. Primary end-points will be analyzed using standard time-to-event statistical modeling with adjustment for major baseline covariates. The primary analysis is on an intent-to-treat basis.</p></div></div>
<div class="section" id="ijs12019-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study Outcomes</h4><div class="para"><p>The primary outcome is nonfatal stroke, nonfatal myocardial infarction, and death during follow-up of up to five-years, and the secondary outcome includes death from any cause and stroke.</p></div></div>
]]></content:encoded><description>

Rationale
Carotid endarterectomy and medical therapy (aspirin) were shown superior to medical therapy alone for asymptomatic (≥60%) carotid stenosis. The role of modern medical therapy (statins, antihypertensive treatment, and aspirin) in the treatment of such patients is undefined. Establishing the safety, efficacy, and durability of optimal medical therapy and lifestyle modification requires rigorous comparison with carotid endarterectomy in asymptomatic patients.


Aims
The objective is to compare the efficacy of carotid endarterectomy + optimal medical therapy versus optimal medical therapy alone in patients with asymptomatic (70–79%) extracranial carotid stenosis.


Design
The Aggressive Medical Treatment Evaluation for Asymptomatic Carotid Artery Stenosis study is a prospective, randomized, parallel, two-arm, multicenter trial. Primary end-points will be analyzed using standard time-to-event statistical modeling with adjustment for major baseline covariates. The primary analysis is on an intent-to-treat basis.


Study Outcomes
The primary outcome is nonfatal stroke, nonfatal myocardial infarction, and death during follow-up of up to five-years, and the secondary outcome includes death from any cause and stroke.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12018" xmlns="http://purl.org/rss/1.0/"><title>The Know Your Numbers (KYN) program 2008 to 2010: impact on knowledge and health promotion behavior among participants</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12018</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The Know Your Numbers (KYN) program 2008 to 2010: impact on knowledge and health promotion behavior among participants</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">D. A. Cadilhac, M. F. Kilkenny, R. Johnson, B. Wilkinson, B. Amatya, E. Lalor</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-12T05:25:54.005552-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12018</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12018</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12018</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12018-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Since 2007, the National Stroke Foundation in Australia has undertaken a community-based ‘Know Your Numbers’ program on blood pressure and other stroke risk factors.</p></div></div>
<div class="section" id="ijs12018-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The aims of this study are to assess, in a sample of registrants participating in a three-month follow-up survey, retention of knowledge of risk factors and health conditions associated with hypertension, and whether those who were advised to see their doctor sought treatment or performed other health promotion actions.</p></div></div>
<div class="section" id="ijs12018-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Various organizations (mainly pharmacies) were recruited to offer a ‘free’ standardized blood pressure check and educational resources for one-week/year between 2008 and 2010. Data collection was done thru registration log and detailed questionnaires for a sample of registrants at baseline and three-months. Descriptive statistics were used for comparison of baseline and three-month data.</p></div></div>
<div class="section" id="ijs12018-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>There were 59 817 registrants over three-years. A total of 2044/2283 (90%) registrants completed a baseline survey (66% female, 50% aged &gt;55 years); 43% had blood pressure ≥140/90 mmHg whereby 32% were unaware of their blood pressure status. Follow-up surveys were obtained from 510/805 (63%) baseline participants who provided consent. At three-months, improved knowledge was found for 9 of 11 risk factors for hypertension (e.g. lack of exercise baseline 73%; three-months 85%, <em>P</em> &lt; 0·001). Knowledge for all the health conditions assessed that are associated with hypertension improved (e.g. stroke baseline 72%; three-months 87%, <em>P</em> &lt; 0·001, heart attack baseline 69%; three-months 84%, <em>P</em> &lt; 0·001). All respondents reported at least one health promotion action. Among 141/510 advised to visit their doctor, 114 (81%) did.</p></div></div>
<div class="section" id="ijs12018-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Know Your Numbers is a successful health promotion program and encourages people to be reviewed by their doctor.</p></div></div>
]]></content:encoded><description>

Background
Since 2007, the National Stroke Foundation in Australia has undertaken a community-based ‘Know Your Numbers’ program on blood pressure and other stroke risk factors.


Aims
The aims of this study are to assess, in a sample of registrants participating in a three-month follow-up survey, retention of knowledge of risk factors and health conditions associated with hypertension, and whether those who were advised to see their doctor sought treatment or performed other health promotion actions.


Methods
Various organizations (mainly pharmacies) were recruited to offer a ‘free’ standardized blood pressure check and educational resources for one-week/year between 2008 and 2010. Data collection was done thru registration log and detailed questionnaires for a sample of registrants at baseline and three-months. Descriptive statistics were used for comparison of baseline and three-month data.


Results
There were 59 817 registrants over three-years. A total of 2044/2283 (90%) registrants completed a baseline survey (66% female, 50% aged &gt;55 years); 43% had blood pressure ≥140/90 mmHg whereby 32% were unaware of their blood pressure status. Follow-up surveys were obtained from 510/805 (63%) baseline participants who provided consent. At three-months, improved knowledge was found for 9 of 11 risk factors for hypertension (e.g. lack of exercise baseline 73%; three-months 85%, P &lt; 0·001). Knowledge for all the health conditions assessed that are associated with hypertension improved (e.g. stroke baseline 72%; three-months 87%, P &lt; 0·001, heart attack baseline 69%; three-months 84%, P &lt; 0·001). All respondents reported at least one health promotion action. Among 141/510 advised to visit their doctor, 114 (81%) did.


Conclusion
Know Your Numbers is a successful health promotion program and encourages people to be reviewed by their doctor.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12017" xmlns="http://purl.org/rss/1.0/"><title>The China Stroke Secondary Prevention Trial (CSSPT) protocol: a double-blinded, randomized, controlled trial of combined folic acid and B vitamins for secondary prevention of stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12017</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The China Stroke Secondary Prevention Trial (CSSPT) protocol: a double-blinded, randomized, controlled trial of combined folic acid and B vitamins for secondary prevention of stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Xuedong Liu, Ming Shi, Feng Xia, Junliang Han, Zhirong Liu, Bo Wang, Fang Yang, Li Li, Songdi Wu, Ling Wang, Nan Liu, Yali Lv, Gang Zhao</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-12T05:25:48.665658-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12017</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12017</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12017</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12017-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Epidemiological studies suggest that elevated homocysteine is linked to stroke and heart disease. However, the results of lowering homocysteine levels in reducing the risk of stroke recurrence are controversial.</p></div></div>
<div class="section" id="ijs12017-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The study aims to evaluate whether homocysteine-lowering therapy with folic acid and vitamins B<sub>6</sub> and B<sub>12</sub> reduces recurrent stroke events and other combined incidence of recurrent vascular events and vascular death in ischemic stroke patients of low folate regions.</p></div></div>
<div class="section" id="ijs12017-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>This is a multicenter, randomized, double-blinded, placebo-controlled trial. Patients (<em>n</em> = 8000, <em>α</em> = 0·05, <em>β</em> = 0·10) within one-month of ischemic stroke (large-artery atherosclerosis or small-vessel occlusion) or hypertensive intracerebral haemorrhage with plasma homocysteine level ≥15 μmol/l will be enrolled. Eligible patients will be randomized by a web-based, random allocation system to receive multivitamins (folic acid 0·8 mg, vitamin B<sub>6</sub> 10 mg, and vitamin B<sub>12</sub> 500 μg) or matching placebo daily with a median follow-up of three-years.</p></div></div>
<div class="section" id="ijs12017-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study Outcomes</h4><div class="para"><p>Patients will be evaluated at six monthly intervals. The primary outcome event is the composite event ‘stroke, myocardial infarction, or death from any vascular cause’, whichever occurs first. Secondary outcome measures include nonvascular death, transient ischemic attack, depression, dementia, unstable angina, revascularization procedures of the coronary, and cerebral and peripheral circulations.</p></div></div>
<div class="section" id="ijs12017-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Discussion</h4><div class="para"><p>This is the first multicenter randomized trial of secondary prevention for ischemic stroke in a Chinese population with a higher homocysteine level but without folate food fortification.</p></div></div>
]]></content:encoded><description>

Rationale
Epidemiological studies suggest that elevated homocysteine is linked to stroke and heart disease. However, the results of lowering homocysteine levels in reducing the risk of stroke recurrence are controversial.


Aims
The study aims to evaluate whether homocysteine-lowering therapy with folic acid and vitamins B6 and B12 reduces recurrent stroke events and other combined incidence of recurrent vascular events and vascular death in ischemic stroke patients of low folate regions.


Design
This is a multicenter, randomized, double-blinded, placebo-controlled trial. Patients (n = 8000, α = 0·05, β = 0·10) within one-month of ischemic stroke (large-artery atherosclerosis or small-vessel occlusion) or hypertensive intracerebral haemorrhage with plasma homocysteine level ≥15 μmol/l will be enrolled. Eligible patients will be randomized by a web-based, random allocation system to receive multivitamins (folic acid 0·8 mg, vitamin B6 10 mg, and vitamin B12 500 μg) or matching placebo daily with a median follow-up of three-years.


Study Outcomes
Patients will be evaluated at six monthly intervals. The primary outcome event is the composite event ‘stroke, myocardial infarction, or death from any vascular cause’, whichever occurs first. Secondary outcome measures include nonvascular death, transient ischemic attack, depression, dementia, unstable angina, revascularization procedures of the coronary, and cerebral and peripheral circulations.


Discussion
This is the first multicenter randomized trial of secondary prevention for ischemic stroke in a Chinese population with a higher homocysteine level but without folate food fortification.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12016" xmlns="http://purl.org/rss/1.0/"><title>The obesity paradox in stroke: Lower mortality and lower risk of readmission for recurrent stroke in obese stroke patients</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12016</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The obesity paradox in stroke: Lower mortality and lower risk of readmission for recurrent stroke in obese stroke patients</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Klaus Kaae Andersen, Tom Skyhøj Olsen</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-12T05:25:44.907286-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12016</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12016</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12016</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12016-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Although associated with excess mortality and morbidity, obesity is associated with lower mortality after stroke. The association between obesity and risk of recurrent stroke is unclear.</p></div></div>
<div class="section" id="ijs12016-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The study aims to investigate the association in stroke patients between body mass index and risk of death and readmission for recurrent stroke.</p></div></div>
<div class="section" id="ijs12016-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>An administrative Danish quality-control registry designed to collect a predefined dataset on all hospitalized stroke patients in Denmark 2000–2010 includes 45 615 acute first-ever stroke patients with information on body mass index in 29 326. Data include age, gender, civil status, stroke severity, computed tomography, and cardiovascular risk factors. Patients were followed up to 9·8 years (median 2·6 years). We used Cox regression models to compare risk of death and readmission for recurrent stroke in the four body mass index groups: underweight (body mass index &lt; 18·5), normal weight (body mass index 18·5–24·9), overweight (body mass index 25·0–29·9), obese (body mass index ≥ 30·0).</p></div></div>
<div class="section" id="ijs12016-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Mean age 72·3 years, 48% women. Mean body mass index 23·0. Within follow-up, 7902 (26·9%) patients had died; 2437 (8·3%) were readmitted because of recurrent stroke. Mortality was significantly lower in overweight (hazard ratio 0·72; confidence interval 0·68–0·78) and obese (hazard ratio 0·80; confidence interval 0·73–0·88) patients while significantly higher in underweight patients (hazard ratio 1·66; confidence interval 1·49–1·84) compared with normal weight patients. Risk of readmission for recurrent stroke was significantly lower in obese than in normal weight patients (hazard ratio 0·84; confidence interval 0·72–0·92).</p></div></div>
<div class="section" id="ijs12016-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusionsx</h4><div class="para"><p>Obesity was not only associated with reduced mortality relative to normal weight patients. Compared with normal weight, risk of readmission for recurrent stroke was also lower in obese stroke patients.</p></div></div>
]]></content:encoded><description>

Background
Although associated with excess mortality and morbidity, obesity is associated with lower mortality after stroke. The association between obesity and risk of recurrent stroke is unclear.


Aims
The study aims to investigate the association in stroke patients between body mass index and risk of death and readmission for recurrent stroke.


Methods
An administrative Danish quality-control registry designed to collect a predefined dataset on all hospitalized stroke patients in Denmark 2000–2010 includes 45 615 acute first-ever stroke patients with information on body mass index in 29 326. Data include age, gender, civil status, stroke severity, computed tomography, and cardiovascular risk factors. Patients were followed up to 9·8 years (median 2·6 years). We used Cox regression models to compare risk of death and readmission for recurrent stroke in the four body mass index groups: underweight (body mass index &lt; 18·5), normal weight (body mass index 18·5–24·9), overweight (body mass index 25·0–29·9), obese (body mass index ≥ 30·0).


Results
Mean age 72·3 years, 48% women. Mean body mass index 23·0. Within follow-up, 7902 (26·9%) patients had died; 2437 (8·3%) were readmitted because of recurrent stroke. Mortality was significantly lower in overweight (hazard ratio 0·72; confidence interval 0·68–0·78) and obese (hazard ratio 0·80; confidence interval 0·73–0·88) patients while significantly higher in underweight patients (hazard ratio 1·66; confidence interval 1·49–1·84) compared with normal weight patients. Risk of readmission for recurrent stroke was significantly lower in obese than in normal weight patients (hazard ratio 0·84; confidence interval 0·72–0·92).


Conclusionsx
Obesity was not only associated with reduced mortality relative to normal weight patients. Compared with normal weight, risk of readmission for recurrent stroke was also lower in obese stroke patients.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12013" xmlns="http://purl.org/rss/1.0/"><title>Long-term mortality in patients with coexisting potential causes of ischemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12013</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Long-term mortality in patients with coexisting potential causes of ischemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Young Dae Kim, Myoung-Jin Cha, Jinkwon Kim, Dong Hyun Lee, Hye Sun Lee, Chung Mo Nam, Hyo Suk Nam, Ji Hoe Heo</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-12T05:25:41.099975-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12013</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12013</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12013</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12013-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Multiple potential causes of stroke may coexist in ischemic stroke patients, which may affect long-term outcome.</p></div></div>
<div class="section" id="ijs12013-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>We investigated whether there are differences in long-term mortality among stroke patients with coexisting potential causes.</p></div></div>
<div class="section" id="ijs12013-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We evaluated the long-term all-cause mortality and stroke or cardiovascular mortality of ischemic stroke patients with multiple potential stroke mechanisms, large artery atherosclerosis, cardioembolism, small vessel occlusion, and negative evaluation admitted to a single center between January 1996 and December 2008. Mortality data were obtained from a National Death Certificate system.</p></div></div>
<div class="section" id="ijs12013-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Total 3533 patients were included in this study: 286 multiple potential mechanisms (138 large artery atherosclerosis + cardioembolism, 105 small vessel occlusion + large artery atherosclerosis, 43 small vessel occlusion + cardioembolism), 1045 large artery atherosclerosis, 701 cardioembolism, 606 small vessel occlusion, and 895 negative evaluation. During a mean follow-up of 3·9 years, as referenced to small vessel occlusion mortality rate, the adjusted mortality hazard ratio was 4·387 (95% confidence interval 3·157–6·096) for large artery atherosclerosis + cardioembolism group, 3·903 (95% confidence interval 3·032–5·024) for cardioembolism group, and 2·121 (95% confidence interval 1·655–2·717) for large artery atherosclerosis. The risk of long-term ischemic stroke mortality or cardiovascular mortality also showed comparable findings: highest in the large artery atherosclerosis + cardioembolism, followed by cardioembolism, and large artery atherosclerosis groups. However, the outcome of small vessel occlusion + large artery atherosclerosis or small vessel occlusion + cardioembolism group was not significantly different from that of small vessel occlusion.</p></div></div>
<div class="section" id="ijs12013-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Coexisting potential causes of ischemic stroke impact on long-term mortality. Identification of coexisting potential causes may help to predict stroke outcomes and to guide planning secondary prevention strategies.</p></div></div>
]]></content:encoded><description>

Background
Multiple potential causes of stroke may coexist in ischemic stroke patients, which may affect long-term outcome.


Aim
We investigated whether there are differences in long-term mortality among stroke patients with coexisting potential causes.


Methods
We evaluated the long-term all-cause mortality and stroke or cardiovascular mortality of ischemic stroke patients with multiple potential stroke mechanisms, large artery atherosclerosis, cardioembolism, small vessel occlusion, and negative evaluation admitted to a single center between January 1996 and December 2008. Mortality data were obtained from a National Death Certificate system.


Results
Total 3533 patients were included in this study: 286 multiple potential mechanisms (138 large artery atherosclerosis + cardioembolism, 105 small vessel occlusion + large artery atherosclerosis, 43 small vessel occlusion + cardioembolism), 1045 large artery atherosclerosis, 701 cardioembolism, 606 small vessel occlusion, and 895 negative evaluation. During a mean follow-up of 3·9 years, as referenced to small vessel occlusion mortality rate, the adjusted mortality hazard ratio was 4·387 (95% confidence interval 3·157–6·096) for large artery atherosclerosis + cardioembolism group, 3·903 (95% confidence interval 3·032–5·024) for cardioembolism group, and 2·121 (95% confidence interval 1·655–2·717) for large artery atherosclerosis. The risk of long-term ischemic stroke mortality or cardiovascular mortality also showed comparable findings: highest in the large artery atherosclerosis + cardioembolism, followed by cardioembolism, and large artery atherosclerosis groups. However, the outcome of small vessel occlusion + large artery atherosclerosis or small vessel occlusion + cardioembolism group was not significantly different from that of small vessel occlusion.


Conclusions
Coexisting potential causes of ischemic stroke impact on long-term mortality. Identification of coexisting potential causes may help to predict stroke outcomes and to guide planning secondary prevention strategies.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12012" xmlns="http://purl.org/rss/1.0/"><title>Postthrombolysis outcomes in acute ischemic stroke patients of Asian race-ethnicity</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12012</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Postthrombolysis outcomes in acute ischemic stroke patients of Asian race-ethnicity</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Nishant K. Mishra, Bernard P. L. Chan, Hock-Luen Teoh, Chang-Hui Meng, Kennedy R. Lees, Christopher Chen, Vijay K. Sharma, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-12T05:25:38.65043-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12012</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12012</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12012</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12012-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Race-ethnic differences may influence postthrombolysis outcomes in acute ischemic stroke patients. Guidelines for thrombolytic therapy to treat Asian stroke patients are based mostly on extrapolated western data.</p></div></div>
<div class="section" id="ijs12012-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>We undertook to examine outcomes among Asians by comparing a propensity-matched cohort of thrombolyzed patients from a tertiary center in Singapore with nonthrombolyzed Asian comparators collated from Virtual International Stroke Trials Archives (control).</p></div></div>
<div class="section" id="ijs12012-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We identified propensity scores-matched patients between thrombolyzed and control Asian patients lodged in the Virtual International Stroke Trials Archives by employing propensity scores method. We compared matched patients for their distributions of three-month functional (modified Rankin scores) and neurological outcomes (National Institute of Health Stroke Scale) by employing Cochran–Mantel–Haenszel test and proportional odds logistic regression analysis. We report odds ratio and 95% confidence interval for improved outcomes on day 90.</p></div></div>
<div class="section" id="ijs12012-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Virtual International Stroke Trials Archives and National University Hospital, Singapore, contributed 517 and 133 patients of Asian race-ethnicity (<em>n</em> = 650), respectively. After propensity matching, sample size reduced to 237 patients; 104 were from Virtual International Stroke Trials Archives. Age (59·7 vs. 61·5 years, <em>P</em> = 0·2) and mean baseline National Institute of Health Stroke Scale scores were similar (14) between thrombolyzed and control. The odds ratio for shift toward improved modified Rankin scores and National Institute of Health Stroke Scale distributions after tissue plasminogen activator therapy were 2·8 (95% confidence interval 1·8-4·5, <em>P</em> &lt; 0·0001, <em>n</em> = 233; Cochran–Mantel–Haenszel <em>P</em> &lt; 0·0001) and 2·8 (95% confidence interval 1·7–4·7, <em>P</em> = 0·0008, <em>n</em> = 201; Cochran–Mantel–Haenszel <em>P</em> = 0·0001).</p></div></div>
<div class="section" id="ijs12012-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Our data indicate that Asian patients derive benefit from thrombolytic therapy.</p></div></div>
]]></content:encoded><description>

Background
Race-ethnic differences may influence postthrombolysis outcomes in acute ischemic stroke patients. Guidelines for thrombolytic therapy to treat Asian stroke patients are based mostly on extrapolated western data.


Aims
We undertook to examine outcomes among Asians by comparing a propensity-matched cohort of thrombolyzed patients from a tertiary center in Singapore with nonthrombolyzed Asian comparators collated from Virtual International Stroke Trials Archives (control).


Methods
We identified propensity scores-matched patients between thrombolyzed and control Asian patients lodged in the Virtual International Stroke Trials Archives by employing propensity scores method. We compared matched patients for their distributions of three-month functional (modified Rankin scores) and neurological outcomes (National Institute of Health Stroke Scale) by employing Cochran–Mantel–Haenszel test and proportional odds logistic regression analysis. We report odds ratio and 95% confidence interval for improved outcomes on day 90.


Results
Virtual International Stroke Trials Archives and National University Hospital, Singapore, contributed 517 and 133 patients of Asian race-ethnicity (n = 650), respectively. After propensity matching, sample size reduced to 237 patients; 104 were from Virtual International Stroke Trials Archives. Age (59·7 vs. 61·5 years, P = 0·2) and mean baseline National Institute of Health Stroke Scale scores were similar (14) between thrombolyzed and control. The odds ratio for shift toward improved modified Rankin scores and National Institute of Health Stroke Scale distributions after tissue plasminogen activator therapy were 2·8 (95% confidence interval 1·8-4·5, P &lt; 0·0001, n = 233; Cochran–Mantel–Haenszel P &lt; 0·0001) and 2·8 (95% confidence interval 1·7–4·7, P = 0·0008, n = 201; Cochran–Mantel–Haenszel P = 0·0001).


Conclusions
Our data indicate that Asian patients derive benefit from thrombolytic therapy.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12011" xmlns="http://purl.org/rss/1.0/"><title>A multicenter, randomized, double-blind, placebo-controlled trial to test efficacy and safety of magnetic resonance imaging-based thrombolysis in wake-up stroke (WAKE-UP)</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12011</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A multicenter, randomized, double-blind, placebo-controlled trial to test efficacy and safety of magnetic resonance imaging-based thrombolysis in wake-up stroke (WAKE-UP)</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Götz Thomalla, Jochen B. Fiebach, Leif Østergaard, Salvador Pedraza, Vincent Thijs, Norbert Nighoghossian, Pascal Roy, Keith W. Muir, Martin Ebinger, Bastian Cheng, Ivana Galinovic, Tae-Hee Cho, Josep Puig, Florent Boutitie, Claus Z. Simonsen, Matthias Endres, Jens Fiehler, Christian Gerloff, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-12T05:24:24.310075-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12011</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12011</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12011</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12011-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>In about 20% of acute ischemic stroke patients stroke occurs during sleep. These patients are generally excluded from intravenous thrombolysis. MRI can identify patients within the time-window for thrombolysis (≤4·5 h from symptom onset) by a mismatch between the acute ischemic lesion visible on diffusion weighted imaging (DWI) but not visible on fluid-attenuated inversion recovery (FLAIR) imaging.</p></div></div>
<div class="section" id="ijs12011-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims and hypothesis</h4><div class="para"><p>The study aims to test the efficacy and safety of MRI-guided thrombolysis with tissue plasminogen activator (rtPA) in ischemic stroke patients with unknown time of symptom onset, e.g., waking up with stroke symptoms. We hypothesize that stroke patients with unknown time of symptom onset with a DWI-FLAIR-mismatch pattern on MRI will have improved outcome when treated with rtPA compared to placebo.</p></div></div>
<div class="section" id="ijs12011-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>WAKE-UP is an investigator initiated, European, multicentre, randomized, double-blind, placebo-controlled clinical trial. Patients with unknown time of symptom onset who fulfil clinical inclusion criteria (disabling neurological deficit, no contraindications against thrombolysis) will be studied by MRI. Patients with MRI findings of a DWI-FLAIR-mismatch will be randomised to either treatment with rtPA or placebo.</p></div></div>
<div class="section" id="ijs12011-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study outcome</h4><div class="para"><p>The primary efficacy endpoint will be favourable outcome defined by modified Rankin Scale 0–1 at day 90. The primary safety outcome measures will be mortality and death or dependency defined by modified Rankin Scale 4–6 at 90 days.</p></div></div>
<div class="section" id="ijs12011-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Discussion</h4><div class="para"><p>If positive, WAKE-UP is expected to change clinical practice making effective and safe treatment available for a large group of acute stroke patients currently excluded from specific acute therapy.</p></div></div>
]]></content:encoded><description>

Rationale
In about 20% of acute ischemic stroke patients stroke occurs during sleep. These patients are generally excluded from intravenous thrombolysis. MRI can identify patients within the time-window for thrombolysis (≤4·5 h from symptom onset) by a mismatch between the acute ischemic lesion visible on diffusion weighted imaging (DWI) but not visible on fluid-attenuated inversion recovery (FLAIR) imaging.


Aims and hypothesis
The study aims to test the efficacy and safety of MRI-guided thrombolysis with tissue plasminogen activator (rtPA) in ischemic stroke patients with unknown time of symptom onset, e.g., waking up with stroke symptoms. We hypothesize that stroke patients with unknown time of symptom onset with a DWI-FLAIR-mismatch pattern on MRI will have improved outcome when treated with rtPA compared to placebo.


Design
WAKE-UP is an investigator initiated, European, multicentre, randomized, double-blind, placebo-controlled clinical trial. Patients with unknown time of symptom onset who fulfil clinical inclusion criteria (disabling neurological deficit, no contraindications against thrombolysis) will be studied by MRI. Patients with MRI findings of a DWI-FLAIR-mismatch will be randomised to either treatment with rtPA or placebo.


Study outcome
The primary efficacy endpoint will be favourable outcome defined by modified Rankin Scale 0–1 at day 90. The primary safety outcome measures will be mortality and death or dependency defined by modified Rankin Scale 4–6 at 90 days.


Discussion
If positive, WAKE-UP is expected to change clinical practice making effective and safe treatment available for a large group of acute stroke patients currently excluded from specific acute therapy.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12007" xmlns="http://purl.org/rss/1.0/"><title>Worse stroke outcome in atrial fibrillation is explained by more severe hypoperfusion, infarct growth, and hemorrhagic transformation</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12007</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Worse stroke outcome in atrial fibrillation is explained by more severe hypoperfusion, infarct growth, and hemorrhagic transformation</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hans T. H. Tu, Bruce C. V. Campbell, Soren Christensen, Patricia M. Desmond, Deidre A. De Silva, Mark W. Parsons, Leonid Churilov, Maarten G. Lansberg, Michael Mlynash, Jean-Marc Olivot, Matus Straka, Roland Bammer, Gregory W. Albers, Geoffrey A. Donnan, Stephen M. Davis, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-12T05:24:20.543702-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12007</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12007</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12007</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12007-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Atrial fibrillation is associated with greater baseline neurological impairment and worse outcomes following ischemic stroke. Previous studies suggest that greater volumes of more severe baseline hypoperfusion in patients with history of atrial fibrillation may explain this association. We further investigated this association by comparing patients with and without atrial fibrillation on initial examination following stroke using pooled multimodal magnetic resonance imaging and clinical data from the Echoplanar Imaging Thrombolytic Evaluation Trial and the Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution studies.</p></div></div>
<div class="section" id="ijs12007-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Echoplanar Imaging Thrombolytic Evaluation Trial was a trial of 101 ischemic stroke patients randomized to intravenous tissue plasminogen activator or placebo, and Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution was a prospective cohort of 74 ischemic stroke patients treated with intravenous tissue plasminogen activator at three to six hours following symptom onset. Patients underwent multimodal magnetic resonance imaging before treatment, at three to five days and three-months after stroke in Echoplanar Imaging Thrombolytic Evaluation Trial; before treatment, three to six hours after treatment and one-month after stroke in Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution. Patients were assessed with the National Institutes of Health Stroke Scale and the modified Rankin scale before treatment and at three-months after stroke. Patients were categorized into definite atrial fibrillation (present on initial examination), probable atrial fibrillation (history but no atrial fibrillation on initial examination), and no atrial fibrillation. Perfusion data were reprocessed with automated magnetic resonance imaging analysis software (RAPID, Stanford University, Stanford, CA, USA). Hypoperfusion volumes were defined using time to maximum delays in two-second increments from &gt;4 to &gt;8 s. Hemorrhagic transformation was classified according to the European Cooperative Acute Stroke Studies criteria.</p></div></div>
<div class="section" id="ijs12007-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Of the 175 patients, 28 had definite atrial fibrillation, 30 probable atrial fibrillation, 111 no atrial fibrillation, and six were excluded due to insufficient imaging data. At baseline, patients with definite atrial fibrillation had more severe hypoperfusion (median time to maximum &gt;8 s, volume 48 vs. 29 ml, <em>P</em> = 0·02) compared with patients with no atrial fibrillation. At outcome, patients with definite atrial fibrillation had greater infarct growth (median volume 47 vs. 8 ml, <em>P</em> = 0·001), larger infarcts (median volume 75 vs. 23 ml, <em>P</em> = 0·001), more frequent parenchymal hematoma grade hemorrhagic transformation (30% vs. 10%, <em>P</em> = 0·03), worse functional outcomes (median modified Rankin scale score 4 vs. 3, <em>P</em> = 0·03), and higher mortality (36% vs. 16%, <em>P</em> = 0·03) compared with patients with no atrial fibrillation. Definite atrial fibrillation was independently associated with increased parenchymal hematoma (odds ratio = 6·05, 95% confidence interval 1·60–22·83) but not poor functional outcome (modified Rankin scale 3–6, odds ratio = 0·99, 95% confidence interval 0·35–2·80) or mortality (odds ratio = 2·54, 95% confidence interval 0·86–7·49) three-months following stroke, after adjusting for other baseline imbalances.</p></div></div>
<div class="section" id="ijs12007-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Atrial fibrillation is associated with greater volumes of more severe baseline hypoperfusion, leading to higher infarct growth, more frequent severe hemorrhagic transformation and worse stroke outcomes.</p></div></div>
]]></content:encoded><description>

Background
Atrial fibrillation is associated with greater baseline neurological impairment and worse outcomes following ischemic stroke. Previous studies suggest that greater volumes of more severe baseline hypoperfusion in patients with history of atrial fibrillation may explain this association. We further investigated this association by comparing patients with and without atrial fibrillation on initial examination following stroke using pooled multimodal magnetic resonance imaging and clinical data from the Echoplanar Imaging Thrombolytic Evaluation Trial and the Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution studies.


Methods
Echoplanar Imaging Thrombolytic Evaluation Trial was a trial of 101 ischemic stroke patients randomized to intravenous tissue plasminogen activator or placebo, and Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution was a prospective cohort of 74 ischemic stroke patients treated with intravenous tissue plasminogen activator at three to six hours following symptom onset. Patients underwent multimodal magnetic resonance imaging before treatment, at three to five days and three-months after stroke in Echoplanar Imaging Thrombolytic Evaluation Trial; before treatment, three to six hours after treatment and one-month after stroke in Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution. Patients were assessed with the National Institutes of Health Stroke Scale and the modified Rankin scale before treatment and at three-months after stroke. Patients were categorized into definite atrial fibrillation (present on initial examination), probable atrial fibrillation (history but no atrial fibrillation on initial examination), and no atrial fibrillation. Perfusion data were reprocessed with automated magnetic resonance imaging analysis software (RAPID, Stanford University, Stanford, CA, USA). Hypoperfusion volumes were defined using time to maximum delays in two-second increments from &gt;4 to &gt;8 s. Hemorrhagic transformation was classified according to the European Cooperative Acute Stroke Studies criteria.


Results
Of the 175 patients, 28 had definite atrial fibrillation, 30 probable atrial fibrillation, 111 no atrial fibrillation, and six were excluded due to insufficient imaging data. At baseline, patients with definite atrial fibrillation had more severe hypoperfusion (median time to maximum &gt;8 s, volume 48 vs. 29 ml, P = 0·02) compared with patients with no atrial fibrillation. At outcome, patients with definite atrial fibrillation had greater infarct growth (median volume 47 vs. 8 ml, P = 0·001), larger infarcts (median volume 75 vs. 23 ml, P = 0·001), more frequent parenchymal hematoma grade hemorrhagic transformation (30% vs. 10%, P = 0·03), worse functional outcomes (median modified Rankin scale score 4 vs. 3, P = 0·03), and higher mortality (36% vs. 16%, P = 0·03) compared with patients with no atrial fibrillation. Definite atrial fibrillation was independently associated with increased parenchymal hematoma (odds ratio = 6·05, 95% confidence interval 1·60–22·83) but not poor functional outcome (modified Rankin scale 3–6, odds ratio = 0·99, 95% confidence interval 0·35–2·80) or mortality (odds ratio = 2·54, 95% confidence interval 0·86–7·49) three-months following stroke, after adjusting for other baseline imbalances.


Conclusion
Atrial fibrillation is associated with greater volumes of more severe baseline hypoperfusion, leading to higher infarct growth, more frequent severe hemorrhagic transformation and worse stroke outcomes.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12006" xmlns="http://purl.org/rss/1.0/"><title>Age- and gender-specific time trend in risk of death of patients admitted with aneurysmal subarachnoid hemorrhage in the Netherlands</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12006</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Age- and gender-specific time trend in risk of death of patients admitted with aneurysmal subarachnoid hemorrhage in the Netherlands</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Dennis J. Nieuwkamp, Ilonca Vaartjes, Ale Algra, Michiel L. Bots, Gabriël J. E. Rinkel</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-12T05:23:46.219086-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12006</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12006</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12006</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12006-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and aim</h4><div class="para"><p>In a meta-analysis of population-based studies, case-fatality rates of subarachnoid hemorrhage have decreased worldwide by 17% between 1973 and 2002. However, age- and gender-specific decreases could not be determined. Because &gt;10% of patients with subarachnoid hemorrhage die before reaching the hospital, this suggests that the prognosis for hospitalized subarachnoid hemorrhage patients has improved even more. We assessed age- and gender-specific time trends of the risk of death for hospitalized subarachnoid hemorrhage patients.</p></div></div>
<div class="section" id="ijs12006-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>From the Dutch hospital discharge register (nationwide coverage), we identified 9403 patients admitted with subarachnoid hemorrhage in the Netherlands between 1997 and 2006. Changes in risk of death within this time frame and influence of age and gender were quantified with Poisson regression.</p></div></div>
<div class="section" id="ijs12006-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The overall 30-day risk of death was 34·0% (95% confidence interval 33·1↔35·0%). After adjustment for age and gender, the annual decrease was 1·6% (95% confidence interval 0·5↔2·6%), which confers to a decrease of 13·4% (95% confidence interval4·8↔21·2%) in the study period. The one-year risk of death decreased 2·0% per year (95% confidence interval1·1↔2·9%). The decrease in risk of death was mainly found in the period 2003–2005, was not found for patients ≥65 years and was statistically significant for men, but not for women.</p></div></div>
<div class="section" id="ijs12006-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The decrease in risk of death for patients admitted in the Netherlands with subarachnoid hemorrhage is overall considerable, but unevenly distributed over age and gender. Further research should focus on reasons for improved survival (improved diagnostics, improved treatment) and reasons why improvement has not occurred for women and for patients in older age categories.</p></div></div>
]]></content:encoded><description>

Background and aim
In a meta-analysis of population-based studies, case-fatality rates of subarachnoid hemorrhage have decreased worldwide by 17% between 1973 and 2002. However, age- and gender-specific decreases could not be determined. Because &gt;10% of patients with subarachnoid hemorrhage die before reaching the hospital, this suggests that the prognosis for hospitalized subarachnoid hemorrhage patients has improved even more. We assessed age- and gender-specific time trends of the risk of death for hospitalized subarachnoid hemorrhage patients.


Methods
From the Dutch hospital discharge register (nationwide coverage), we identified 9403 patients admitted with subarachnoid hemorrhage in the Netherlands between 1997 and 2006. Changes in risk of death within this time frame and influence of age and gender were quantified with Poisson regression.


Results
The overall 30-day risk of death was 34·0% (95% confidence interval 33·1↔35·0%). After adjustment for age and gender, the annual decrease was 1·6% (95% confidence interval 0·5↔2·6%), which confers to a decrease of 13·4% (95% confidence interval4·8↔21·2%) in the study period. The one-year risk of death decreased 2·0% per year (95% confidence interval1·1↔2·9%). The decrease in risk of death was mainly found in the period 2003–2005, was not found for patients ≥65 years and was statistically significant for men, but not for women.


Conclusions
The decrease in risk of death for patients admitted in the Netherlands with subarachnoid hemorrhage is overall considerable, but unevenly distributed over age and gender. Further research should focus on reasons for improved survival (improved diagnostics, improved treatment) and reasons why improvement has not occurred for women and for patients in older age categories.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12005" xmlns="http://purl.org/rss/1.0/"><title>Type of admission is associated with outcome of spontaneous subarachnoid hemorrhage</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12005</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Type of admission is associated with outcome of spontaneous subarachnoid hemorrhage</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Doniel Drazin, Jack Rosner, Miriam Nuño, Michael J. Alexander, Wouter I. Schievink, David Palestrant, Patrick D. Lyden, Chad Miller</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-12T05:23:44.205816-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12005</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12005</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12005</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12005-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Admitting facility may significantly affect outcome for spontaneous subarachnoid hemorrhage patients. We assessed outcomes of patients admitted directly to a comprehensive stroke center with those initially admitted to a general hospital and subsequently transferred. The comprehensive stroke center included a neurocritical care ICU, cerebrovascular neurosurgeons and endovascular specialists.</p></div></div>
<div class="section" id="ijs12005-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We identified 107 consecutive spontaneous subarachnoid hemorrhage cases. Of these cases, 31 (29%) patients were admitted directly and 76 (71%) were transferred from general hospitals. Univariate and multivariate analyses evaluated differences in mortality, complications, discharge disposition, and in-hospital length of stay.</p></div></div>
<div class="section" id="ijs12005-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Differences in baseline parameters (age, gender, admission Glasgow Coma Scale, Fisher grade, admission Hunt and Hess grade) were not statistically significant between direct-admit and transfer patients at our institution. Transferred patients developed vasospasm more frequently (58% vs. 32%; <em>P</em> &lt; 0·05) and had a longer delay time to surgery (3·9-days vs. 2·4-days: <em>P</em> &lt; 0·05). Multivariate analysis showed that the likelihood of vasospasm was significantly higher for transfer patients (OR 3·46, CI: 1·2–10·3, <em>P</em> = 0·03). In addition, longer in-hospital stays and higher odds of non-routine discharge were observed in transferred patients (<em>P</em> &lt; 0·01). No differences in outcome could be identified for surgical vs. endovascular treatment rates between direct-admit and transfer patients. An association, but no causative link, can be made between the effect of transfer and the outcomes of SAH patients due to the retrospective nature of our study.</p></div></div>
<div class="section" id="ijs12005-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Spontaneous subarachnoid hemorrhage patients admitted directly to our comprehensive stroke center showed less complications compared to those transferred from general hospitals. This improvement was independent of time to treatment. Additional research in multiple centers using prospective analysis should be conducted to confirm that preferential direct transport to a comprehensive stroke center would likely yield considerable improvements in public health.</p></div></div>
]]></content:encoded><description>

Background
Admitting facility may significantly affect outcome for spontaneous subarachnoid hemorrhage patients. We assessed outcomes of patients admitted directly to a comprehensive stroke center with those initially admitted to a general hospital and subsequently transferred. The comprehensive stroke center included a neurocritical care ICU, cerebrovascular neurosurgeons and endovascular specialists.


Methods
We identified 107 consecutive spontaneous subarachnoid hemorrhage cases. Of these cases, 31 (29%) patients were admitted directly and 76 (71%) were transferred from general hospitals. Univariate and multivariate analyses evaluated differences in mortality, complications, discharge disposition, and in-hospital length of stay.


Results
Differences in baseline parameters (age, gender, admission Glasgow Coma Scale, Fisher grade, admission Hunt and Hess grade) were not statistically significant between direct-admit and transfer patients at our institution. Transferred patients developed vasospasm more frequently (58% vs. 32%; P &lt; 0·05) and had a longer delay time to surgery (3·9-days vs. 2·4-days: P &lt; 0·05). Multivariate analysis showed that the likelihood of vasospasm was significantly higher for transfer patients (OR 3·46, CI: 1·2–10·3, P = 0·03). In addition, longer in-hospital stays and higher odds of non-routine discharge were observed in transferred patients (P &lt; 0·01). No differences in outcome could be identified for surgical vs. endovascular treatment rates between direct-admit and transfer patients. An association, but no causative link, can be made between the effect of transfer and the outcomes of SAH patients due to the retrospective nature of our study.


Conclusions
Spontaneous subarachnoid hemorrhage patients admitted directly to our comprehensive stroke center showed less complications compared to those transferred from general hospitals. This improvement was independent of time to treatment. Additional research in multiple centers using prospective analysis should be conducted to confirm that preferential direct transport to a comprehensive stroke center would likely yield considerable improvements in public health.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12003" xmlns="http://purl.org/rss/1.0/"><title>Dual antiplatelets reduce microembolic signals in patients with transient ischemic attack and minor stroke: subgroup analysis of CLAIR study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12003</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Dual antiplatelets reduce microembolic signals in patients with transient ischemic attack and minor stroke: subgroup analysis of CLAIR study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Alexander Y. Lau, Yudong Zhao, Christopher Chen, Thomas W. Leung, Jianhui Fu, Yining Huang, Nijasri C. Suwanwela, Zhao Han, Kay Sin Tan, Disya Ratanakorn, Hugh S. Markus, Ka Sing Wong, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-12T05:23:41.229694-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12003</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12003</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12003</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Trial</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12003-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Short course of dual antiplatelet therapy for early secondary prevention is a promising treatment for patients with minor stroke or transient ischemic attack at high risk of recurrence.</p></div></div>
<div class="section" id="ijs12003-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We examined the efficacy and safety of dual antiplatelets in patients with transient ischemic attack or minor stroke, defined as National Institute of Health Stroke Scale scores 0–3, in a subgroup analysis of Clopidogrel plus aspirin versus Aspirin alone for Reducing embolization in patients with acute symptomatic cerebral or carotid artery stenosis (CLAIR) study. Microembolic signals on transcranial Doppler monitoring was used as surrogate marker for recurrent stroke risk. Patients with ≥1 microembolic signals at baseline were randomized to receive dual therapy (aspirin 75–160 mg daily and clopidogrel 300 mg day 1 then 75 mg daily) or monotherapy (aspirin 75–160 mg daily) for seven-days.</p></div></div>
<div class="section" id="ijs12003-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Sixty-five of 100 patients recruited had transient ischemic attack or minor stroke: 30 received dual therapy and 35 received monotherapy. Mean onset-to-randomization was 2·3 days in dual therapy group and 3·2 days in monotherapy group (<em>P</em> = 0·03). At day 7, the proportion of patients with ≥1 microembolic signals was 9 of 29 patients in dual therapy group and 18 of 34 patients in monotherapy group (adjusted relative risk reduction 41·4%, 95% CI 29·8–51·1, <em>P</em> &lt; 0·001). The median number of microembolic signals on day 7 was 0 in dual therapy group and 1·0 in monotherapy group (<em>P</em> = 0·046). No patients had intracranial or severe systemic hemorrhage.</p></div></div>
<div class="section" id="ijs12003-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Early dual therapy with clopidogrel and aspirin reduces microembolic signals in patients with minor ischemic stroke or transient ischemic attack, without causing significant bleeding complications.</p></div></div>
]]></content:encoded><description>

Background
Short course of dual antiplatelet therapy for early secondary prevention is a promising treatment for patients with minor stroke or transient ischemic attack at high risk of recurrence.


Methods
We examined the efficacy and safety of dual antiplatelets in patients with transient ischemic attack or minor stroke, defined as National Institute of Health Stroke Scale scores 0–3, in a subgroup analysis of Clopidogrel plus aspirin versus Aspirin alone for Reducing embolization in patients with acute symptomatic cerebral or carotid artery stenosis (CLAIR) study. Microembolic signals on transcranial Doppler monitoring was used as surrogate marker for recurrent stroke risk. Patients with ≥1 microembolic signals at baseline were randomized to receive dual therapy (aspirin 75–160 mg daily and clopidogrel 300 mg day 1 then 75 mg daily) or monotherapy (aspirin 75–160 mg daily) for seven-days.


Results
Sixty-five of 100 patients recruited had transient ischemic attack or minor stroke: 30 received dual therapy and 35 received monotherapy. Mean onset-to-randomization was 2·3 days in dual therapy group and 3·2 days in monotherapy group (P = 0·03). At day 7, the proportion of patients with ≥1 microembolic signals was 9 of 29 patients in dual therapy group and 18 of 34 patients in monotherapy group (adjusted relative risk reduction 41·4%, 95% CI 29·8–51·1, P &lt; 0·001). The median number of microembolic signals on day 7 was 0 in dual therapy group and 1·0 in monotherapy group (P = 0·046). No patients had intracranial or severe systemic hemorrhage.


Conclusions
Early dual therapy with clopidogrel and aspirin reduces microembolic signals in patients with minor ischemic stroke or transient ischemic attack, without causing significant bleeding complications.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12001" xmlns="http://purl.org/rss/1.0/"><title>Inflammatory markers and their association with post stroke cognitive decline</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12001</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Inflammatory markers and their association with post stroke cognitive decline</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kaavya Narasimhalu, Jasinda Lee, Yi-Lin Leong, Lu Ma, Deidre A. De Silva, Meng-Cheong Wong, Hui-Meng Chang, Christopher Chen</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-12T05:23:38.621044-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12001</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12001</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12001</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12001-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Population-based studies have demonstrated the association of inflammation and cognitive impairment. However, few studies to date have examined this association in ischemic stroke patients.</p></div></div>
<div class="section" id="ijs12001-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The study aims to determine the association between inflammatory markers and cognitive impairment.</p></div></div>
<div class="section" id="ijs12001-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Ischemic stroke patients with baseline neuropsychological assessments at three-months poststroke were followed up with annual neuropsychological assessments for up to five-years. Inflammatory markers (C-reactive protein, interleukin 1<em>β</em>, interleukin 6, interleukin 8, interleukin 10, interleukin 12, and tumor necrosis factor-<em>α</em>) were assayed, and logistic regression analyses were performed to determine associations between inflammatory markers and both baseline cognitive status and subsequent cognitive decline.</p></div></div>
<div class="section" id="ijs12001-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>There were 243 ischemic stroke patients in the study. In multivariable ordinal logistic regression analysis, age, education, ethnicity, stroke subtype, and interleukin 8 (OR 1·23 CI 1·05–1·44) levels were independently associated with baseline cognitive status. In multivariable logistic regression analyses, age, gender, recurrent strokes, and interleukin 12 (OR 25·02 CI 3·73 to 168·03) were independent predictors of subsequent cognitive decline.</p></div></div>
<div class="section" id="ijs12001-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Following ischemic stroke, higher serum interleukin 8 is independently associated with baseline cognitive impairment while higher serum interleukin 12 is associated with subsequent cognitive decline.</p></div></div>
]]></content:encoded><description>

Background
Population-based studies have demonstrated the association of inflammation and cognitive impairment. However, few studies to date have examined this association in ischemic stroke patients.


Aims
The study aims to determine the association between inflammatory markers and cognitive impairment.


Methods
Ischemic stroke patients with baseline neuropsychological assessments at three-months poststroke were followed up with annual neuropsychological assessments for up to five-years. Inflammatory markers (C-reactive protein, interleukin 1β, interleukin 6, interleukin 8, interleukin 10, interleukin 12, and tumor necrosis factor-α) were assayed, and logistic regression analyses were performed to determine associations between inflammatory markers and both baseline cognitive status and subsequent cognitive decline.


Results
There were 243 ischemic stroke patients in the study. In multivariable ordinal logistic regression analysis, age, education, ethnicity, stroke subtype, and interleukin 8 (OR 1·23 CI 1·05–1·44) levels were independently associated with baseline cognitive status. In multivariable logistic regression analyses, age, gender, recurrent strokes, and interleukin 12 (OR 25·02 CI 3·73 to 168·03) were independent predictors of subsequent cognitive decline.


Conclusions
Following ischemic stroke, higher serum interleukin 8 is independently associated with baseline cognitive impairment while higher serum interleukin 12 is associated with subsequent cognitive decline.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12014" xmlns="http://purl.org/rss/1.0/"><title>Referral and triage of patients with transient ischemic attacks to an acute access clinic: risk stratification in an Australian setting</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12014</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Referral and triage of patients with transient ischemic attacks to an acute access clinic: risk stratification in an Australian setting</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Parker Magin, Daniel Lasserson, Mark Parsons, Neil Spratt, Malcolm Evans, Michelle Russell, Angela Royan, Susan Goode, Patrick McElduff, Christopher Levi</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-12T03:26:35.82972-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12014</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12014</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12014</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12014-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Transient ischemic attacks and minor stroke entail considerable risk of completed stroke but this risk is reduced by prompt assessment and treatment. Risk can be stratified according to the ABCD2 prediction score. Current guidelines suggest specialist assessment and treatment within 24 h for high-risk event (ABCD2 score 4–7) and seven-days for low-risk event (ABCD2 score ≤ 3).</p></div></div>
<div class="section" id="ijs12014-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The study aims to establish paths to care and outcomes for patients referred by general practitioners and emergency departments to an Australian acute access transient ischemic attack service.</p></div></div>
<div class="section" id="ijs12014-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>This is a prospective audit. Primary outcomes were time from event to referral, from referral to clinic appointment, and from event to appointment. ABCD2 score was calculated for each event. Time from event was modeled using Cox proportional hazards regression.</p></div></div>
<div class="section" id="ijs12014-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>There were 231 clinic attendees (general practitioner: 127; emergency department: 104). Mean time from event to referral was 9·2 days (SD 23·7, median 2), from referral to being seen in the clinic was 13·6 days (SD 19·0, median 7), and from event to being seen in the clinic was 17·2 days (SD 27·1, median 10). Of low-risk patients, 38·5% were seen within seven-days of event. Of high-risk patients, 36·7% were seen within one-day. ABCD2 score was not a significant predictor of any time interval from event to clinic attendance. There were no completed strokes prior to clinic attendance.</p></div></div>
<div class="section" id="ijs12014-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Times from event to clinic assessment were in excess of current recommendations and risk stratification was suboptimal, though short-term outcomes were good. Improvements in referral mechanisms may enhance risk-stratification and triage.</p></div></div>
]]></content:encoded><description>

Background
Transient ischemic attacks and minor stroke entail considerable risk of completed stroke but this risk is reduced by prompt assessment and treatment. Risk can be stratified according to the ABCD2 prediction score. Current guidelines suggest specialist assessment and treatment within 24 h for high-risk event (ABCD2 score 4–7) and seven-days for low-risk event (ABCD2 score ≤ 3).


Aims
The study aims to establish paths to care and outcomes for patients referred by general practitioners and emergency departments to an Australian acute access transient ischemic attack service.


Methods
This is a prospective audit. Primary outcomes were time from event to referral, from referral to clinic appointment, and from event to appointment. ABCD2 score was calculated for each event. Time from event was modeled using Cox proportional hazards regression.


Results
There were 231 clinic attendees (general practitioner: 127; emergency department: 104). Mean time from event to referral was 9·2 days (SD 23·7, median 2), from referral to being seen in the clinic was 13·6 days (SD 19·0, median 7), and from event to being seen in the clinic was 17·2 days (SD 27·1, median 10). Of low-risk patients, 38·5% were seen within seven-days of event. Of high-risk patients, 36·7% were seen within one-day. ABCD2 score was not a significant predictor of any time interval from event to clinic attendance. There were no completed strokes prior to clinic attendance.


Conclusions
Times from event to clinic assessment were in excess of current recommendations and risk stratification was suboptimal, though short-term outcomes were good. Improvements in referral mechanisms may enhance risk-stratification and triage.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00951.x" xmlns="http://purl.org/rss/1.0/"><title>Anaemia on admission is associated with more severe intracerebral haemorrhage and worse outcomes</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00951.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Anaemia on admission is associated with more severe intracerebral haemorrhage and worse outcomes</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Miguel Bussière, Meera Gupta, Mukul Sharma, Dar Dowlatshahi, Jiming Fang, Rajat Dhar, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-07T03:46:21.449347-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00951.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00951.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00951.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs951-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Lower haemoglobin levels may impair cerebral oxygen delivery and threaten tissue viability in the setting of acute brain injury. Few studies have examined the association between haemoglobin levels and outcomes after spontaneous intracerebral haemorrhage.</p></div></div>
<div class="section" id="ijs951-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>We evaluated whether anaemia on admission was associated with greater intracerebral haemorrhage severity and worse outcome.</p></div></div>
<div class="section" id="ijs951-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Consecutive patients with spontaneous intracerebral haemorrhage were analyzed from the Registry of the Canadian Stroke Network. Admission haemoglobin was related to stroke severity (using the Canadian Neurological Scale), modified Rankin score at discharge, and one-year mortality. Adjustment was made for potential confounders including age, gender, medical history, warfarin use, glucose, creatinine, blood pressure, and intraventricular haemorrhage.</p></div></div>
<div class="section" id="ijs951-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Two thousand four hundred six patients with intracerebral haemorrhage were studied of whom 23% had anaemia (haemoglobin &lt;120 g/l) on admission, including 4% with haemoglobin &lt;100 g/l. Patients with anaemia were more likely to have severe neurological deficits at presentation [haemoglobin ≤100 g/l, adjusted odds ratio 4·04 (95% confidence interval 2·39, 6·84); haemoglobin 101–120 g/l, adjusted odds ratio 1·93 (95% confidence interval 1·43, 2·59), both <em>P</em> &lt; 0·0001]. In nonanticoagulated patients, severe anaemia was also associated with poor outcome (modified Rankin score 4–6) at discharge [haemoglobin ≤100 g/l, adjusted odds ratio 2·42 (95% confidence interval 1·07–5·47), <em>P</em> = 0·034] and increased mortality at one-year [haemoglobin ≤100 g/l, adjusted hazard ratio 1·73 (95% confidence interval 1·22–2·45), <em>P</em> = 0·002].</p></div></div>
<div class="section" id="ijs951-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Anaemia on admission is associated with greater intracerebral haemorrhage severity and worse outcomes. The utility of transfusion remains unclear in this setting.</p></div></div>
]]></content:encoded><description>

Background
Lower haemoglobin levels may impair cerebral oxygen delivery and threaten tissue viability in the setting of acute brain injury. Few studies have examined the association between haemoglobin levels and outcomes after spontaneous intracerebral haemorrhage.


Aims
We evaluated whether anaemia on admission was associated with greater intracerebral haemorrhage severity and worse outcome.


Methods
Consecutive patients with spontaneous intracerebral haemorrhage were analyzed from the Registry of the Canadian Stroke Network. Admission haemoglobin was related to stroke severity (using the Canadian Neurological Scale), modified Rankin score at discharge, and one-year mortality. Adjustment was made for potential confounders including age, gender, medical history, warfarin use, glucose, creatinine, blood pressure, and intraventricular haemorrhage.


Results
Two thousand four hundred six patients with intracerebral haemorrhage were studied of whom 23% had anaemia (haemoglobin &lt;120 g/l) on admission, including 4% with haemoglobin &lt;100 g/l. Patients with anaemia were more likely to have severe neurological deficits at presentation [haemoglobin ≤100 g/l, adjusted odds ratio 4·04 (95% confidence interval 2·39, 6·84); haemoglobin 101–120 g/l, adjusted odds ratio 1·93 (95% confidence interval 1·43, 2·59), both P &lt; 0·0001]. In nonanticoagulated patients, severe anaemia was also associated with poor outcome (modified Rankin score 4–6) at discharge [haemoglobin ≤100 g/l, adjusted odds ratio 2·42 (95% confidence interval 1·07–5·47), P = 0·034] and increased mortality at one-year [haemoglobin ≤100 g/l, adjusted hazard ratio 1·73 (95% confidence interval 1·22–2·45), P = 0·002].


Conclusions
Anaemia on admission is associated with greater intracerebral haemorrhage severity and worse outcomes. The utility of transfusion remains unclear in this setting.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00934.x" xmlns="http://purl.org/rss/1.0/"><title>Randomized trial of treadmill training to improve walking in community-dwelling people after stroke: the AMBULATE trial</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00934.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Randomized trial of treadmill training to improve walking in community-dwelling people after stroke: the AMBULATE trial</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Louise Ada, Catherine M Dean, Richard Lindley</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-07T03:46:02.736073-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00934.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00934.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00934.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs934-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Residual walking deficits are common in community-dwelling people after stroke.</p></div></div>
<div class="section" id="ijs934-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The aim of this study was to determine if a four-month treadmill and overground walking program is more effective than a two-month program, compared with control, at improving walking in community-dwelling people with stroke who walk slowly.</p></div></div>
<div class="section" id="ijs934-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Method</h4><div class="para"><p>A three-arm randomized trial with concealed allocation, assessor blinding, and intention-to-treat analysis involving 102 people with stroke living in the community who walked slowly was undertaken. Experimental group 1 undertook 30 min of treadmill and overground walking thrice per week for four-months, experimental group 2 undertook training for two-months, while the control group had no intervention. The primary outcome was walking measured as the distance covered during the six-min walk test. Other outcomes were walking speed, step length and cadence, health status, community participation, self-efficacy and falls.</p></div></div>
<div class="section" id="ijs934-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>By two-months, the experimental groups, who were both undergoing training, had improved their six-min walk distance compared with the control group. The four-month training group continued training beyond two-months and improved further so that by four months they walked 38 m (95% confidence interval 15–60) more than the control group and 29 m (95% confidence interval 4–53) more than the two-month training group. However, by 12 months, well after the cessation of training, both experimental groups had returned to near baseline levels, and there was no difference between the groups.</p></div></div>
<div class="section" id="ijs934-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Four months of treadmill training results in better walking. However, these effects disappear once training ceases. Therefore, training should be ongoing.</p></div></div>
]]></content:encoded><description>

Background
Residual walking deficits are common in community-dwelling people after stroke.


Aims
The aim of this study was to determine if a four-month treadmill and overground walking program is more effective than a two-month program, compared with control, at improving walking in community-dwelling people with stroke who walk slowly.


Method
A three-arm randomized trial with concealed allocation, assessor blinding, and intention-to-treat analysis involving 102 people with stroke living in the community who walked slowly was undertaken. Experimental group 1 undertook 30 min of treadmill and overground walking thrice per week for four-months, experimental group 2 undertook training for two-months, while the control group had no intervention. The primary outcome was walking measured as the distance covered during the six-min walk test. Other outcomes were walking speed, step length and cadence, health status, community participation, self-efficacy and falls.


Results
By two-months, the experimental groups, who were both undergoing training, had improved their six-min walk distance compared with the control group. The four-month training group continued training beyond two-months and improved further so that by four months they walked 38 m (95% confidence interval 15–60) more than the control group and 29 m (95% confidence interval 4–53) more than the two-month training group. However, by 12 months, well after the cessation of training, both experimental groups had returned to near baseline levels, and there was no difference between the groups.


Conclusion
Four months of treadmill training results in better walking. However, these effects disappear once training ceases. Therefore, training should be ongoing.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12038" xmlns="http://purl.org/rss/1.0/"><title>Protocol of a cluster randomized trial evaluation of a patient and carer-centered system of longer-term stroke care (LoTS care)</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12038</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Protocol of a cluster randomized trial evaluation of a patient and carer-centered system of longer-term stroke care (LoTS care)</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Anne Forster, John Young, Jane Nixon, Katie Chapman, Jenni Murray, Anita Patel, Martin Knapp, Shamaila Anwar, Rachel Breen, Kirste Mellish, Ivana Holloway, Amanda Farrin</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-02-19T01:10:28.528319-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12038</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12038</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12038</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12038-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Despite recognition of the importance of the longer-term consequences of stroke, services addressing these needs remain poorly developed. There are persuasive arguments that a community-based orientation to poststroke care, to assess, support, and coordinate relevant services, might be more helpful in minimizing longer-term stroke morbidity. To address this, an evidence-based system of care has been developed that aims to meet the longer-term needs for stroke survivors and their carers living at home in the community.</p></div></div>
<div class="section" id="ijs12038-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The study aims to evaluate the clinical and cost-effectiveness of a purposely developed system of care for stroke patients and their carers living in the community.</p></div></div>
<div class="section" id="ijs12038-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>This is a cluster randomized, controlled trial. The trial aimed to recruit 800 patients (and their carers, if appropriate) in 32 stroke services across the United Kingdom. The system of care is delivered by health professionals undertaking a community-based liaison or coordinating role for stroke patients (termed ‘stroke care coordinators’). Stroke care coordinators in stroke services randomized to the intervention group were trained to deliver the system of care, while those randomised to the control group continued to deliver current practice.</p></div></div>
<div class="section" id="ijs12038-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study outcomes</h4><div class="para"><p>The primary outcome is patient emotional health measured using the General Health Questionnaire 12 at six-months after recruitment. Secondary outcomes include cost-effectiveness, patient functional health and carer emotional health, with final follow-up at 12 months.</p></div></div>
<div class="section" id="ijs12038-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Current status</h4><div class="para"><p>Thirty-two stroke services were randomized and 800 patients and 208 carers were recruited from 29 services. Follow-up is ongoing, and trial results are expected in early 2013.</p></div></div>
]]></content:encoded><description>

Rationale
Despite recognition of the importance of the longer-term consequences of stroke, services addressing these needs remain poorly developed. There are persuasive arguments that a community-based orientation to poststroke care, to assess, support, and coordinate relevant services, might be more helpful in minimizing longer-term stroke morbidity. To address this, an evidence-based system of care has been developed that aims to meet the longer-term needs for stroke survivors and their carers living at home in the community.


Aims
The study aims to evaluate the clinical and cost-effectiveness of a purposely developed system of care for stroke patients and their carers living in the community.


Design
This is a cluster randomized, controlled trial. The trial aimed to recruit 800 patients (and their carers, if appropriate) in 32 stroke services across the United Kingdom. The system of care is delivered by health professionals undertaking a community-based liaison or coordinating role for stroke patients (termed ‘stroke care coordinators’). Stroke care coordinators in stroke services randomized to the intervention group were trained to deliver the system of care, while those randomised to the control group continued to deliver current practice.


Study outcomes
The primary outcome is patient emotional health measured using the General Health Questionnaire 12 at six-months after recruitment. Secondary outcomes include cost-effectiveness, patient functional health and carer emotional health, with final follow-up at 12 months.


Current status
Thirty-two stroke services were randomized and 800 patients and 208 carers were recruited from 29 services. Follow-up is ongoing, and trial results are expected in early 2013.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00946.x" xmlns="http://purl.org/rss/1.0/"><title>Protocol for the perfusion and angiography imaging sub-study of the Third International Stroke Trial (IST-3) of alteplase treatment within six-hours of acute ischemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00946.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Protocol for the perfusion and angiography imaging sub-study of the Third International Stroke Trial (IST-3) of alteplase treatment within six-hours of acute ischemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Joanna M. Wardlaw, Rudiger Kummer, Trevor Carpenter, Mark Parsons, Richard I. Lindley, Geoff Cohen, Veronica Murray, Adam Kobayashi, Andre Peeters, Francesca Chappell, Peter A. G. Sandercock</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-22T02:57:00.454996-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00946.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00946.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00946.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs946-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Intravenous thrombolysis with recombinant tissue Plasminogen Activator improves outcomes in patients treated early after stroke but at the risk of causing intracranial hemorrhage. Restricting recombinant tissue Plasminogen Activator use to patients with evidence of still salvageable tissue, or with definite arterial occlusion, might help reduce risk, increase benefit and identify patients for treatment at late time windows.</p></div></div>
<div class="section" id="ijs946-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>To determine if perfusion or angiographic imaging with computed tomography or magnetic resonance help identify patients who are more likely to benefit from recombinant tissue Plasminogen Activator in the context of a large multicenter randomized trial of recombinant tissue Plasminogen Activator given within six-hours of onset of acute ischemic stroke, the Third International Stroke Trial.</p></div></div>
<div class="section" id="ijs946-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Third International Stroke Trial is a prospective multicenter randomized controlled trial testing recombinant tissue Plasminogen Activator (0·9 mg/kg, maximum dose 90 mg) started up to six-hours after onset of acute ischemic stroke, in patients with no clear indication for or contraindication to recombinant tissue Plasminogen Activator. Brain imaging (computed tomography or magnetic resonance) was mandatory pre-randomization to exclude hemorrhage. Scans were read centrally, blinded to treatment and clinical information. In centers where perfusion and/or angiography imaging were used routinely in stroke, these images were also collected centrally, processed and assessed using validated visual scores and computational measures.</p></div></div>
<div class="section" id="ijs946-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study outcomes</h4><div class="para"><p>The primary outcome in Third International Stroke Trial is alive and independent (Oxford Handicap Score 0–2) at 6 months; secondary outcomes are symptomatic and fatal intracranial hemorrhage, early and late death. The perfusion and angiography study additionally will examine interactions between recombinant tissue Plasminogen Activator and clinical outcomes, infarct growth and recanalization in the presence or absence of perfusion lesions and/or arterial occlusion at presentation. The study is registered ISRCTN25765518.</p></div></div>
]]></content:encoded><description>

Rationale
Intravenous thrombolysis with recombinant tissue Plasminogen Activator improves outcomes in patients treated early after stroke but at the risk of causing intracranial hemorrhage. Restricting recombinant tissue Plasminogen Activator use to patients with evidence of still salvageable tissue, or with definite arterial occlusion, might help reduce risk, increase benefit and identify patients for treatment at late time windows.


Aims
To determine if perfusion or angiographic imaging with computed tomography or magnetic resonance help identify patients who are more likely to benefit from recombinant tissue Plasminogen Activator in the context of a large multicenter randomized trial of recombinant tissue Plasminogen Activator given within six-hours of onset of acute ischemic stroke, the Third International Stroke Trial.


Design
Third International Stroke Trial is a prospective multicenter randomized controlled trial testing recombinant tissue Plasminogen Activator (0·9 mg/kg, maximum dose 90 mg) started up to six-hours after onset of acute ischemic stroke, in patients with no clear indication for or contraindication to recombinant tissue Plasminogen Activator. Brain imaging (computed tomography or magnetic resonance) was mandatory pre-randomization to exclude hemorrhage. Scans were read centrally, blinded to treatment and clinical information. In centers where perfusion and/or angiography imaging were used routinely in stroke, these images were also collected centrally, processed and assessed using validated visual scores and computational measures.


Study outcomes
The primary outcome in Third International Stroke Trial is alive and independent (Oxford Handicap Score 0–2) at 6 months; secondary outcomes are symptomatic and fatal intracranial hemorrhage, early and late death. The perfusion and angiography study additionally will examine interactions between recombinant tissue Plasminogen Activator and clinical outcomes, infarct growth and recanalization in the presence or absence of perfusion lesions and/or arterial occlusion at presentation. The study is registered ISRCTN25765518.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00923.x" xmlns="http://purl.org/rss/1.0/"><title>Thrombolysis in the developing world: is there a role for streptokinase?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00923.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Thrombolysis in the developing world: is there a role for streptokinase?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ken Butcher, Ashfaq Shuaib, Jeffrey Saver, Geoffrey Donnan, Stephen M. Davis, Bo Norrving, K. S. Lawrence Wong, Foad Abd-Allah, Rohit Bhatia, Adnan Khan</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-21T21:42:24.261864-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00923.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00923.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00923.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Intravenous thrombolysis with tissue plasminogen activator is the only proven acute therapy for ischemic stroke. This therapy has not been translated into clinical practice in the developing world primarily due to economic constraints. Streptokinase, a lower cost alternative thrombolytic agent, is widely available in developing countries where it is utilized to treat patients with acute coronary syndromes. Although this drug has previously been found to be ineffective in ischemic stroke, the lack of benefit may have been related to a number of factors related to trial design rather than the drug itself. Specific features of prior trial designs that may have adversely affected outcomes include a prolonged treatment window, inclusion of patients with established infarction on computed tomography scan, failure to treat excessive arterial pressures, a fixed dose of streptokinase, and concomitant use of antithrombotic medications. Given the lack of therapeutic alternatives in developing countries, a new trial of streptokinase in acute stroke, utilizing stricter inclusion criteria similar to those in more recent thrombolytic studies, appears warranted.</p></div>
]]></content:encoded><description>
Intravenous thrombolysis with tissue plasminogen activator is the only proven acute therapy for ischemic stroke. This therapy has not been translated into clinical practice in the developing world primarily due to economic constraints. Streptokinase, a lower cost alternative thrombolytic agent, is widely available in developing countries where it is utilized to treat patients with acute coronary syndromes. Although this drug has previously been found to be ineffective in ischemic stroke, the lack of benefit may have been related to a number of factors related to trial design rather than the drug itself. Specific features of prior trial designs that may have adversely affected outcomes include a prolonged treatment window, inclusion of patients with established infarction on computed tomography scan, failure to treat excessive arterial pressures, a fixed dose of streptokinase, and concomitant use of antithrombotic medications. Given the lack of therapeutic alternatives in developing countries, a new trial of streptokinase in acute stroke, utilizing stricter inclusion criteria similar to those in more recent thrombolytic studies, appears warranted.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00957.x" xmlns="http://purl.org/rss/1.0/"><title>Determinants of early case-fatality among stroke patients in Maputo, Mozambique and impact of in-hospital complications</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00957.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Determinants of early case-fatality among stroke patients in Maputo, Mozambique and impact of in-hospital complications</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Joana Gomes, Albertino Damasceno, Carla Carrilho, Vitória Lobo, Hélder Lopes, Tavares Madede, Pius Pravinrai, Carla Silva-Matos, Domingos Diogo, Ana Azevedo, Nuno Lunet</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-20T20:02:06.718318-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00957.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00957.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00957.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Panorama</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs957-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><div class="para"><p>The burden of stroke is increasing in developing countries that struggle to manage it efficiently. We identified determinants of early case-fatality among stroke patients in Maputo, Mozambique, to assess the impact of in-hospital complications. Patients admitted to any hospital in Maputo with a new stroke event were prospectively registered (<em>n</em> = 651) according to the World Health Organization's STEPwise approach, in 2005–2006. We assessed the determinants of in-hospital and 28-day fatality, independently of age, gender and education, and computed population attributable fractions. In-hospital mortality was higher among patients with Glasgow score at admission ≤6 (more than fivefold) or needing cardiopulmonary resuscitation during hospitalization (approximately 2·5-fold). Pneumonia and deep vein thrombosis/other cardiovascular complications during hospitalization were responsible for 19·6% (95% confidence interval, 5·3 to 31·7) of ischaemic stroke and 15·9% (95% confidence interval, 5·8 to 24·9) of haemorrhagic stroke deaths until the 28th day. Ischaemic stroke patients with systolic blood pressure 160–200 mmHg had lower in-hospital mortality (relative risk = 0·32, 95% confidence interval, 0·13 to 0·78), and, for those with haemorrhagic events (haemorrhagic stroke), 28-day mortality was higher when systolic blood pressure was over 200 mmHg (hazard ratio = 3·42; 95% confidence interval, 1·02 to 11·51), compared with systolic blood pressure 121–140 mmHg. Regarding diastolic blood pressure, the risk was lowest at 121–150 mmHg for ischaemic stroke and at 61–90 mmHg for haemorrhagic stroke. Early case-fatality was mostly influenced by stroke severity and in-hospital complications. The allocation of resources to the latter may have a large impact on the reduction of the burden of stroke in this setting.</p></div></div>
]]></content:encoded><description>

The burden of stroke is increasing in developing countries that struggle to manage it efficiently. We identified determinants of early case-fatality among stroke patients in Maputo, Mozambique, to assess the impact of in-hospital complications. Patients admitted to any hospital in Maputo with a new stroke event were prospectively registered (n = 651) according to the World Health Organization's STEPwise approach, in 2005–2006. We assessed the determinants of in-hospital and 28-day fatality, independently of age, gender and education, and computed population attributable fractions. In-hospital mortality was higher among patients with Glasgow score at admission ≤6 (more than fivefold) or needing cardiopulmonary resuscitation during hospitalization (approximately 2·5-fold). Pneumonia and deep vein thrombosis/other cardiovascular complications during hospitalization were responsible for 19·6% (95% confidence interval, 5·3 to 31·7) of ischaemic stroke and 15·9% (95% confidence interval, 5·8 to 24·9) of haemorrhagic stroke deaths until the 28th day. Ischaemic stroke patients with systolic blood pressure 160–200 mmHg had lower in-hospital mortality (relative risk = 0·32, 95% confidence interval, 0·13 to 0·78), and, for those with haemorrhagic events (haemorrhagic stroke), 28-day mortality was higher when systolic blood pressure was over 200 mmHg (hazard ratio = 3·42; 95% confidence interval, 1·02 to 11·51), compared with systolic blood pressure 121–140 mmHg. Regarding diastolic blood pressure, the risk was lowest at 121–150 mmHg for ischaemic stroke and at 61–90 mmHg for haemorrhagic stroke. Early case-fatality was mostly influenced by stroke severity and in-hospital complications. The allocation of resources to the latter may have a large impact on the reduction of the burden of stroke in this setting.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00968.x" xmlns="http://purl.org/rss/1.0/"><title>Leucocyte count in young adults with first-ever ischaemic stroke: associated factors and association on prognosis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00968.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Leucocyte count in young adults with first-ever ischaemic stroke: associated factors and association on prognosis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Terttu Heikinheimo, Jukka Putaala, Elena Haapaniemi, Markku Kaste, Turgut Tatlisumak</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-07T10:09:32.950554-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00968.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00968.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00968.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs968-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Limited data exist on the associated factors and correlation of leucocyte count to outcome in young adults with first-ever ischaemic stroke.</p></div></div>
<div class="section" id="ijs968-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>Our objectives were to investigate factors associated with elevated leucocyte count and whether there is correlation between leucocyte count and short- and long-term outcomes.</p></div></div>
<div class="section" id="ijs968-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Of our database of 1008 consecutive patients aged 15 to 49, we included those with leucocyte count measured within the first two days from stroke onset. Outcomes were three-month and long-term disability, death, and vascular events. Linear regression was used to explore baseline variables associated with leucocyte count. Logistic regression and Cox proportional models studied the association between leucocyte count and clinical outcomes.</p></div></div>
<div class="section" id="ijs968-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>In our study cohort of 797 patients (61·7% males; mean age 41·4 years), mean leucocyte count was high: 8·8 ± 3·1 × 10<sup>9</sup> cells/L (Reference range: 3·4–8·2 × 10<sup>9</sup> cells/L). Higher leucocyte levels were associated with dyslipidaemia, smoking, peripheral arterial disease, stroke severity, and lesion size. After adjustment for age, gender, relevant risk factors, both continuous leucocyte count and the highest quartile of leucocyte count were independently associated with unfavourable three-month outcome. Regarding events in the long-term (follow-up 8·1 ± 4·2 years in survivors), no association between leucocyte count and the event risks appeared.</p></div></div>
<div class="section" id="ijs968-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Among young stroke patients, high leucocyte count was a common finding. It was associated with vascular disease and its risk factors as well as severity of stroke, but it was also independently associated with unfavourable three-month outcome in these patients. There was no association with the long-term outcome.</p></div></div>
]]></content:encoded><description>

Background
Limited data exist on the associated factors and correlation of leucocyte count to outcome in young adults with first-ever ischaemic stroke.


Aims
Our objectives were to investigate factors associated with elevated leucocyte count and whether there is correlation between leucocyte count and short- and long-term outcomes.


Methods
Of our database of 1008 consecutive patients aged 15 to 49, we included those with leucocyte count measured within the first two days from stroke onset. Outcomes were three-month and long-term disability, death, and vascular events. Linear regression was used to explore baseline variables associated with leucocyte count. Logistic regression and Cox proportional models studied the association between leucocyte count and clinical outcomes.


Results
In our study cohort of 797 patients (61·7% males; mean age 41·4 years), mean leucocyte count was high: 8·8 ± 3·1 × 109 cells/L (Reference range: 3·4–8·2 × 109 cells/L). Higher leucocyte levels were associated with dyslipidaemia, smoking, peripheral arterial disease, stroke severity, and lesion size. After adjustment for age, gender, relevant risk factors, both continuous leucocyte count and the highest quartile of leucocyte count were independently associated with unfavourable three-month outcome. Regarding events in the long-term (follow-up 8·1 ± 4·2 years in survivors), no association between leucocyte count and the event risks appeared.


Conclusions
Among young stroke patients, high leucocyte count was a common finding. It was associated with vascular disease and its risk factors as well as severity of stroke, but it was also independently associated with unfavourable three-month outcome in these patients. There was no association with the long-term outcome.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00955.x" xmlns="http://purl.org/rss/1.0/"><title>The disability adjusted life years due to stroke in South Africa in 2008</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00955.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The disability adjusted life years due to stroke in South Africa in 2008</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Melanie Y. Bertram, Judith Katzenellenbogen, Theo Vos, Debbie Bradshaw, Karen J. Hofman</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-07T10:09:30.411778-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00955.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00955.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00955.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs955-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>South Africa is experiencing epidemiological transition, with the burden of chronic diseases increasing. Stroke is currently the second leading cause of death in South Africa; however, limited data are available on incidence, prevalence and resulting disability. Quantifying the epidemiological parameters and disease burden is important in the planning of health services.</p></div></div>
<div class="section" id="ijs955-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>To synthesize the data surrounding stroke in South Africa and calculate disability adjusted life years attributable to stroke in South Africa in 2008.</p></div></div>
<div class="section" id="ijs955-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We undertook a systematic review to identify studies on the prevalence and mortality of stroke in South Africa. We used the DisMod program to calculate missing epidemiological parameters, in particular incidence and duration. Using these values, we calculated the burden of disease in years of life lost (YLL), years lived with disability (YLD) and disability adjusted life years (DALY).</p></div></div>
<div class="section" id="ijs955-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Data on prevalence and mortality of stroke in South Africa are scarce. We estimate there are 75 000 strokes in South Africa each year, with 25 000 of these fatal within the first month. The burden of disease due to stroke in South Africa was 564 000 DALYs. Of this, 17% is contributed by YLD (14–20% in sensitivity analysis).</p></div></div>
<div class="section" id="ijs955-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>This study provides information on prevalence, incidence and disease burden of stroke at the national level in South Africa. The results of this analysis will enable further work on priority setting and health service planning for primary and secondary prevention of stroke in South Africa.</p></div></div>
]]></content:encoded><description>

Background
South Africa is experiencing epidemiological transition, with the burden of chronic diseases increasing. Stroke is currently the second leading cause of death in South Africa; however, limited data are available on incidence, prevalence and resulting disability. Quantifying the epidemiological parameters and disease burden is important in the planning of health services.


Aims
To synthesize the data surrounding stroke in South Africa and calculate disability adjusted life years attributable to stroke in South Africa in 2008.


Methods
We undertook a systematic review to identify studies on the prevalence and mortality of stroke in South Africa. We used the DisMod program to calculate missing epidemiological parameters, in particular incidence and duration. Using these values, we calculated the burden of disease in years of life lost (YLL), years lived with disability (YLD) and disability adjusted life years (DALY).


Results
Data on prevalence and mortality of stroke in South Africa are scarce. We estimate there are 75 000 strokes in South Africa each year, with 25 000 of these fatal within the first month. The burden of disease due to stroke in South Africa was 564 000 DALYs. Of this, 17% is contributed by YLD (14–20% in sensitivity analysis).


Conclusions
This study provides information on prevalence, incidence and disease burden of stroke at the national level in South Africa. The results of this analysis will enable further work on priority setting and health service planning for primary and secondary prevention of stroke in South Africa.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00931.x" xmlns="http://purl.org/rss/1.0/"><title>The 2010 British Association of Stroke Physicians Survey of interventional treatments for stroke in the United Kingdom</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00931.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The 2010 British Association of Stroke Physicians Survey of interventional treatments for stroke in the United Kingdom</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">R. Sanyal, J. Barrick, A. Bhalla, T. Cassidy, D. Collas, G. Cloud, P. Fearon, P. Gompertz, S. Keir, P. Khanna, M. Power, P. White, C. Roffe</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-07T10:09:26.959465-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00931.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00931.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00931.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs931-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Introduction</h4><div class="para"><p>The UK National Stroke Strategy (Department of Health 2007) states that patients should have access to a stroke service with neurointerventional capacity. This survey was conducted by the Clinical Standards Committee of the British Association of Stroke Physicians to get a snapshot of the availability of interventional treatments for stroke in the United Kingdom.</p></div></div>
<div class="section" id="ijs931-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Questionnaires covering availability of endovascular treatments for stroke, e.g. intra-arterial thrombolysis and mechanical thrombectomy, were emailed to all British Association of Stroke Physicians members in October 2010. Where more than one response was received from the same hospital, the data were only entered once. If there was a discrepancy between different respondents for the same hospital, details were cross-checked with the respondents to ensure accuracy.</p></div></div>
<div class="section" id="ijs931-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Responses were received from 58 hospitals in England, Scotland, Wales, and Northern Ireland. Intra-arterial thrombolysis and/or mechanical thrombectomy were available in 23 hospitals. Of these, three had not performed any procedures in 2010. Twenty centres had conducted a mean (range) of eight (2–20) procedures during the 10-month period. Thirty-five hospitals were not offering endovascular treatments. Sixteen of these were not referring patients to centres which could provide interventional treatments. Hospitals offering endovascular treatments had a mean (range) of 5·2 (2–12) stroke physicians, 2·3 (0–4) interventional neuroradiologists, and 3·6 (0–9) noninterventional neuroradiologists. Only two hospitals providing interventions had four or more interventional neuroradiologists.</p></div></div>
<div class="section" id="ijs931-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Only a small number of hospitals in the United Kingdom provide interventional treatments for stroke. Almost 50% of hospitals not providing interventions had no processes in place for referral to providers.</p></div></div>
]]></content:encoded><description>

Introduction
The UK National Stroke Strategy (Department of Health 2007) states that patients should have access to a stroke service with neurointerventional capacity. This survey was conducted by the Clinical Standards Committee of the British Association of Stroke Physicians to get a snapshot of the availability of interventional treatments for stroke in the United Kingdom.


Methods
Questionnaires covering availability of endovascular treatments for stroke, e.g. intra-arterial thrombolysis and mechanical thrombectomy, were emailed to all British Association of Stroke Physicians members in October 2010. Where more than one response was received from the same hospital, the data were only entered once. If there was a discrepancy between different respondents for the same hospital, details were cross-checked with the respondents to ensure accuracy.


Results
Responses were received from 58 hospitals in England, Scotland, Wales, and Northern Ireland. Intra-arterial thrombolysis and/or mechanical thrombectomy were available in 23 hospitals. Of these, three had not performed any procedures in 2010. Twenty centres had conducted a mean (range) of eight (2–20) procedures during the 10-month period. Thirty-five hospitals were not offering endovascular treatments. Sixteen of these were not referring patients to centres which could provide interventional treatments. Hospitals offering endovascular treatments had a mean (range) of 5·2 (2–12) stroke physicians, 2·3 (0–4) interventional neuroradiologists, and 3·6 (0–9) noninterventional neuroradiologists. Only two hospitals providing interventions had four or more interventional neuroradiologists.


Conclusions
Only a small number of hospitals in the United Kingdom provide interventional treatments for stroke. Almost 50% of hospitals not providing interventions had no processes in place for referral to providers.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00914.x" xmlns="http://purl.org/rss/1.0/"><title>Intra-arterial thrombolysis vs. standard treatment or intravenous thrombolysis in adults with acute ischemic stroke: a systematic review and meta-analysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00914.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Intra-arterial thrombolysis vs. standard treatment or intravenous thrombolysis in adults with acute ischemic stroke: a systematic review and meta-analysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Julian Nam, He Jing, Daria O'Reilly</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-07T10:09:18.66569-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00914.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00914.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00914.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Systematic Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs914-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background </h4><div class="para"><p>Recent evidence has suggested that intra-arterial thrombolysis may provide benefit beyond intravenous thrombolysis in ischemic stroke patients. Previous meta-analyses have only compared intra-arterial thrombolysis with standard treatment without thrombolysis. The objective was to review the benefits and harms of intra-arterial thrombolysis in ischemic stroke patients.</p></div></div>
<div class="section" id="ijs914-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods </h4><div class="para"><p>We undertook a meta-analysis of randomized controlled trials comparing the efficacy and safety of intra-arterial thrombolysis with either standard treatment or intravenous thrombolysis following acute ischemic stroke. Primary outcomes included poor functional outcomes (modified Rankin Scale 3–6), mortality, and symptomatic intracranial hemorrhage. Study quality was assessed, and outcomes were stratified by comparison treatment received.</p></div></div>
<div class="section" id="ijs914-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results </h4><div class="para"><p>Four trials (n = 351) comparing intra-arterial thrombolysis with standard treatment were identified. Intra-arterial thrombolysis reduced the risk of poor functional outcomes (modified Rankin Scale 3–6) [relative risk (RR) = 0·80; 95% confidence interval = 0·67–0·95; <em>P</em> = 0·01]. Mortality was not increased (RR = 0·82; 95% confidence interval = 0·56–1·21; <em>P</em> = 0·32); however, risk of symptomatic intracranial hemorrhage was nearly four times more likely (RR = 3·90; 95% confidence interval = 1·41–10·76; <em>P</em> = 0·006). Two trials (n = 81) comparing intra-arterial thrombolysis with intravenous thrombolysis were identified. Intra-arterial thrombolysis was not found to reduce poor functional outcomes (modified Rankin Scale 3–6) (RR = 0·68; 95% confidence interval = 0·46–1·00; <em>P</em> = 0·05). Mortality was not increased (RR = 1·12; 95% confidence interval = 0·47–2·68; <em>P</em> = 0·79); neither was symptomatic intracranial hemorrhage (RR = 1·13; 95% confidence interval = 0·32–3·99; <em>P</em> = 0·85). Differences in time from symptom onset-to-treatment and type of thrombolytic administered were found across the trials.</p></div></div>
<div class="section" id="ijs914-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions </h4><div class="para"><p>This analysis finds a modest benefit of intra-arterial thrombolysis over standard treatment, although it does not find a clear benefit of intra-arterial thrombolysis over intravenous thrombolysis in acute ischemic stroke patients. However, few trials, small sample sizes, and indirectness limit the strength of evidence.</p></div></div>
]]></content:encoded><description>

Background 
Recent evidence has suggested that intra-arterial thrombolysis may provide benefit beyond intravenous thrombolysis in ischemic stroke patients. Previous meta-analyses have only compared intra-arterial thrombolysis with standard treatment without thrombolysis. The objective was to review the benefits and harms of intra-arterial thrombolysis in ischemic stroke patients.


Methods 
We undertook a meta-analysis of randomized controlled trials comparing the efficacy and safety of intra-arterial thrombolysis with either standard treatment or intravenous thrombolysis following acute ischemic stroke. Primary outcomes included poor functional outcomes (modified Rankin Scale 3–6), mortality, and symptomatic intracranial hemorrhage. Study quality was assessed, and outcomes were stratified by comparison treatment received.


Results 
Four trials (n = 351) comparing intra-arterial thrombolysis with standard treatment were identified. Intra-arterial thrombolysis reduced the risk of poor functional outcomes (modified Rankin Scale 3–6) [relative risk (RR) = 0·80; 95% confidence interval = 0·67–0·95; P = 0·01]. Mortality was not increased (RR = 0·82; 95% confidence interval = 0·56–1·21; P = 0·32); however, risk of symptomatic intracranial hemorrhage was nearly four times more likely (RR = 3·90; 95% confidence interval = 1·41–10·76; P = 0·006). Two trials (n = 81) comparing intra-arterial thrombolysis with intravenous thrombolysis were identified. Intra-arterial thrombolysis was not found to reduce poor functional outcomes (modified Rankin Scale 3–6) (RR = 0·68; 95% confidence interval = 0·46–1·00; P = 0·05). Mortality was not increased (RR = 1·12; 95% confidence interval = 0·47–2·68; P = 0·79); neither was symptomatic intracranial hemorrhage (RR = 1·13; 95% confidence interval = 0·32–3·99; P = 0·85). Differences in time from symptom onset-to-treatment and type of thrombolytic administered were found across the trials.


Conclusions 
This analysis finds a modest benefit of intra-arterial thrombolysis over standard treatment, although it does not find a clear benefit of intra-arterial thrombolysis over intravenous thrombolysis in acute ischemic stroke patients. However, few trials, small sample sizes, and indirectness limit the strength of evidence.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00897.x" xmlns="http://purl.org/rss/1.0/"><title>An epidemiological survey of stroke among rural Chinese adults results from the Liaoning province</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00897.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">An epidemiological survey of stroke among rural Chinese adults results from the Liaoning province</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Zhaoqing Sun, Liqiang Zheng, Robert Detrano, Xingang Zhang, Jue Li, Dayi Hu, Yingxian Sun</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-07T10:09:11.324847-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00897.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00897.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00897.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs897-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The aim of this study was to describe the incidence, clinical sub-types, and associated risk factors of stroke among rural Chinese adults.</p></div></div>
<div class="section" id="ijs897-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>A population-based sample of 38 949 rural Chinese adults, aged ≥35 years and free from stroke at baseline, were followed from 2004–2006 to 2010. Stroke was defined by the World Health Organization diagnosis criteria.</p></div></div>
<div class="section" id="ijs897-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The age-standardized incidence rates per 100 000 person-years of overall, first ever stroke was 601·9 (95% confidence interval, 528·3 to 675·5), and mortality rate was 276·7 (95% confidence interval, 251·6 to 301·9). The age-standardized incidence rate was higher in men (775·9 per 100 000 person-years) than in women (435·6 per 100 000 person-years). Among 858 first ever stroke events, 56·3% were ischemic strokes, 40·6% were hemorrhagic strokes, and 3·1% were undetermined strokes. Hypertension and lipid disorder were common modifiable risk factors in the ischemic stroke and hemorrhagic stroke groups.</p></div></div>
<div class="section" id="ijs897-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The annual incidence of stroke and resulting mortality has increased at an accelerated rate. Furthermore, the incidence of stroke in rural China was higher than that found in urban China and Western countries. Hypertension and lipid disorder were important modifiable risk factors. The primary sub-type of stroke observed in rural China was ischemic stroke. These findings underscored the need for more aggressive efforts to control the risk factors of stroke and other cardiovascular diseases in rural areas.</p></div></div>
]]></content:encoded><description>

Background
The aim of this study was to describe the incidence, clinical sub-types, and associated risk factors of stroke among rural Chinese adults.


Methods
A population-based sample of 38 949 rural Chinese adults, aged ≥35 years and free from stroke at baseline, were followed from 2004–2006 to 2010. Stroke was defined by the World Health Organization diagnosis criteria.


Results
The age-standardized incidence rates per 100 000 person-years of overall, first ever stroke was 601·9 (95% confidence interval, 528·3 to 675·5), and mortality rate was 276·7 (95% confidence interval, 251·6 to 301·9). The age-standardized incidence rate was higher in men (775·9 per 100 000 person-years) than in women (435·6 per 100 000 person-years). Among 858 first ever stroke events, 56·3% were ischemic strokes, 40·6% were hemorrhagic strokes, and 3·1% were undetermined strokes. Hypertension and lipid disorder were common modifiable risk factors in the ischemic stroke and hemorrhagic stroke groups.


Conclusions
The annual incidence of stroke and resulting mortality has increased at an accelerated rate. Furthermore, the incidence of stroke in rural China was higher than that found in urban China and Western countries. Hypertension and lipid disorder were important modifiable risk factors. The primary sub-type of stroke observed in rural China was ischemic stroke. These findings underscored the need for more aggressive efforts to control the risk factors of stroke and other cardiovascular diseases in rural areas.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00953.x" xmlns="http://purl.org/rss/1.0/"><title>The progressive course of neurological symptoms in anterior choroidal artery infarcts</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00953.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The progressive course of neurological symptoms in anterior choroidal artery infarcts</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sabine Derflinger, Jochen B. Fiebach, Stefanie Böttger, Roman L. Haberl, Heinrich J. Audebert</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-07T09:50:36.32399-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00953.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00953.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00953.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Short Report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs953-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Infarctions of the anterior choroidal artery affect multiple anatomical structures, leading to a wide spectrum of neurological deficits with frequent symptom fluctuation or progression.</p></div></div>
<div class="section" id="ijs953-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>To assess etiological mechanisms, frequency, and predictors of symptom progression, as well as its impact on prognosis.</p></div></div>
<div class="section" id="ijs953-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Anterior choroidal artery infarct patients were prospectively identified via predefined infarct locations with ischemic lesions ≥1·5 cm vertical diameter in cerebral imaging. Definition of neurological progression was ≥2 National Institutes of Health Stroke Scale points in motor function or ≥4 in total National Institutes of Health Stroke Scale. Stroke etiology was determined according to Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification. We assessed demographical data, risk factors, and acute phase parameters in order to find predictors of neurological progression.</p></div></div>
<div class="section" id="ijs953-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Thirty patients fulfilled the inclusion criteria. Eighteen patients (60%) had neurological progression during days 1–3. Despite similar stroke severity at admission (median National Institutes of Health Stroke Scale in progressive infarcts 4·5 versus 4; <em>P</em> = 0·72), patients with progression had more severe deficits at day 3 (median National Institutes of Health Stroke Scale 9 vs. 3·5; <em>P</em> = 0·04) and worse three-month outcome. Only 31% of patients with progression scored &lt;2 in the modified Rankin Scale compared with 89% without progression (<em>P</em> = 0·01) after three-months. No statistically significant differences regarding possible predictors of progression were found. Magnetic resonance imaging findings and etiological assessment suggest overlapping mechanisms of small and large vessel disease.</p></div></div>
<div class="section" id="ijs953-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Neurological deterioration is frequent in anterior choroidal artery infarcts and is associated with worse outcome. While mechanisms of small and large vessel disease seem to overlap in anterior choroidal artery infarction, we were not able to identify predictors of neurological progression.</p></div></div>
]]></content:encoded><description>

Background
Infarctions of the anterior choroidal artery affect multiple anatomical structures, leading to a wide spectrum of neurological deficits with frequent symptom fluctuation or progression.


Aims
To assess etiological mechanisms, frequency, and predictors of symptom progression, as well as its impact on prognosis.


Methods
Anterior choroidal artery infarct patients were prospectively identified via predefined infarct locations with ischemic lesions ≥1·5 cm vertical diameter in cerebral imaging. Definition of neurological progression was ≥2 National Institutes of Health Stroke Scale points in motor function or ≥4 in total National Institutes of Health Stroke Scale. Stroke etiology was determined according to Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification. We assessed demographical data, risk factors, and acute phase parameters in order to find predictors of neurological progression.


Results
Thirty patients fulfilled the inclusion criteria. Eighteen patients (60%) had neurological progression during days 1–3. Despite similar stroke severity at admission (median National Institutes of Health Stroke Scale in progressive infarcts 4·5 versus 4; P = 0·72), patients with progression had more severe deficits at day 3 (median National Institutes of Health Stroke Scale 9 vs. 3·5; P = 0·04) and worse three-month outcome. Only 31% of patients with progression scored &lt;2 in the modified Rankin Scale compared with 89% without progression (P = 0·01) after three-months. No statistically significant differences regarding possible predictors of progression were found. Magnetic resonance imaging findings and etiological assessment suggest overlapping mechanisms of small and large vessel disease.


Conclusions
Neurological deterioration is frequent in anterior choroidal artery infarcts and is associated with worse outcome. While mechanisms of small and large vessel disease seem to overlap in anterior choroidal artery infarction, we were not able to identify predictors of neurological progression.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00943.x" xmlns="http://purl.org/rss/1.0/"><title>Selection for delayed intravenous alteplase treatment based on a prognostic score</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00943.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Selection for delayed intravenous alteplase treatment based on a prognostic score</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Rachael L Fulton, Kennedy R Lees, Erich Bluhmki, Gabriele Biegert, Gregory W Albers, Stephen M Davis, Geoffrey A Donnan, James C Grotta, Werner Hacke, Markku Kaste, Rüdiger von Kummer, Ashfaq Shuaib, Danilo Toni, , A. Alexandrov, P.W. Bath, L. Claesson, J. Curram, H.C. Diener, M. Fisher, B. Gregson, M.G. Hennerici, M. Hommel, P. Lyden, J. Marler, K. Muir, R. Sacco, P. Teal, N.G. Wahlgren, S. Warach, C. Weimar</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-07T09:50:32.992144-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00943.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00943.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00943.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs943-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and Purpose</h4><div class="para"><p>Approved use of intravenous alteplase for ischemic stroke offers net benefit. Pooled randomized controlled trial analysis suggests additional patients could benefit but others be harmed with treatment initiated beyond 4·5 h after stroke onset. We proposed prognostic scoring methods to identify a strategy for patient selection.</p></div></div>
<div class="section" id="ijs943-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We selected 500 patients treated by intravenous alteplase and 500 controls from Virtual International Stroke Trials Archive, matching modified Rankin score outcomes to those from pooled randomized controlled trial 4·5–6 h data. We ranked patients by prognostic score. We chose limits to optimize our sample for a net treatment benefit significant at <em>P</em> = 0·01 by Cochran–Mantel–Haenszel test and by ordinal regression. For validation, we had these applied to the pooled randomized controlled trial data for 4·5–6 h, testing for net benefit by Cochran–Mantel–Haenszel test, ordinal regression, and also by dichotomized outcomes: modified Rankin score 0–1, mortality and parenchymal hemorrhage type 2 bleeds. All analyses were adjusted for age and National Institutes of Health Stroke Scale.</p></div></div>
<div class="section" id="ijs943-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>In the training dataset, limits of 56–95 on a prognostic score retained 714 patients in whom there was net benefit significant at <em>P </em>= 0·01. When applied to the 1120 patients in the pooled randomized controlled trial 4·5–6 h dataset, score limits of 56–95 retained 711 patients and gave odds ratio for improved modified Rankin score distribution of 1·13, 95% confidence interval 0·87–1·47, Cochran–Mantel–Haenszel <em>P </em>= 0·89. More patients achieved modified Rankin score 0–1 (odds ratio 1·44, 1·02–2·05, <em>P</em> = 0·04) but mortality and parenchymal hemorrhage type 2 bleeds were increased: odds ratio 1·56, 1·01–2·40, <em>P</em> = 0·04; odds ratio 15·6, 3·7–65·8, <em>P</em> = 0·0002, respectively.</p></div></div>
<div class="section" id="ijs943-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Selection of patients between 4·5 and 6 h based on simple clinical measures failed to deliver a population in whom the alteplase effect would be safe and effective.</p></div></div>
]]></content:encoded><description>

Background and Purpose
Approved use of intravenous alteplase for ischemic stroke offers net benefit. Pooled randomized controlled trial analysis suggests additional patients could benefit but others be harmed with treatment initiated beyond 4·5 h after stroke onset. We proposed prognostic scoring methods to identify a strategy for patient selection.


Methods
We selected 500 patients treated by intravenous alteplase and 500 controls from Virtual International Stroke Trials Archive, matching modified Rankin score outcomes to those from pooled randomized controlled trial 4·5–6 h data. We ranked patients by prognostic score. We chose limits to optimize our sample for a net treatment benefit significant at P = 0·01 by Cochran–Mantel–Haenszel test and by ordinal regression. For validation, we had these applied to the pooled randomized controlled trial data for 4·5–6 h, testing for net benefit by Cochran–Mantel–Haenszel test, ordinal regression, and also by dichotomized outcomes: modified Rankin score 0–1, mortality and parenchymal hemorrhage type 2 bleeds. All analyses were adjusted for age and National Institutes of Health Stroke Scale.


Results
In the training dataset, limits of 56–95 on a prognostic score retained 714 patients in whom there was net benefit significant at P = 0·01. When applied to the 1120 patients in the pooled randomized controlled trial 4·5–6 h dataset, score limits of 56–95 retained 711 patients and gave odds ratio for improved modified Rankin score distribution of 1·13, 95% confidence interval 0·87–1·47, Cochran–Mantel–Haenszel P = 0·89. More patients achieved modified Rankin score 0–1 (odds ratio 1·44, 1·02–2·05, P = 0·04) but mortality and parenchymal hemorrhage type 2 bleeds were increased: odds ratio 1·56, 1·01–2·40, P = 0·04; odds ratio 15·6, 3·7–65·8, P = 0·0002, respectively.


Conclusion
Selection of patients between 4·5 and 6 h based on simple clinical measures failed to deliver a population in whom the alteplase effect would be safe and effective.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12004" xmlns="http://purl.org/rss/1.0/"><title>Statistical analysis plan for the second INTEnsive blood pressure Reduction in Acute Cerebral hemorrhage Trial (INTERACT2): a large-scale investigation to solve longstanding controversy over the most appropriate management of elevated blood pressure in the hyperacute phase of intracerebral hemorrhage</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12004</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Statistical analysis plan for the second INTEnsive blood pressure Reduction in Acute Cerebral hemorrhage Trial (INTERACT2): a large-scale investigation to solve longstanding controversy over the most appropriate management of elevated blood pressure in the hyperacute phase of intracerebral hemorrhage</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Craig Anderson, Emma Heeley, Stephane Heritier, Hisatomi Arima, Mark Woodward, Richard Lindley, Bruce Neal, Yining Huang, Ji-Guang Wang, Mark Parsons, Christian Stapf, Tom Robinson, Pablo Lavados, Candice Delcourt, Stephen Davis, John Chalmers, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-07T09:46:32.341543-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12004</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12004</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12004</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>The Statistical analysis plan (SAP) for the second INTEnsive blood pressure Reduction in Acute Cerebral hemorrhage Trial (INTERACT2).</p></div>
]]></content:encoded><description>
The Statistical analysis plan (SAP) for the second INTEnsive blood pressure Reduction in Acute Cerebral hemorrhage Trial (INTERACT2).
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00954.x" xmlns="http://purl.org/rss/1.0/"><title>Predictors of delayed stroke in patients with cervical artery dissection</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00954.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Predictors of delayed stroke in patients with cervical artery dissection</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Christoph Lichy, Antti Metso, Alessandro Pezzini, Didier Leys, Tiina Metso, Philippe Lyrer, Stéphanie Debette, Vincent Thijs, Shérine Abboud, Manja Kloss, Yves Samson, Valeria Caso, Maria Sessa, Simone Beretta, Chantal Lamy, Elizabeth Medeiros, Anna Bersano, Emmanuel Touze, Turgut Tatlisumak, Armin Grau, Tobias Brandt, Stefan Engelter, Caspar Grond-Ginsbach, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:52:48.208848-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00954.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00954.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00954.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs954-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Stroke in patients with acute cervical artery dissection may be anticipated by initial transient ischemic or nonischemic symptoms.</p></div></div>
<div class="section" id="ijs954-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>Identifying risk factors for delayed stroke upon cervical artery dissection.</p></div></div>
<div class="section" id="ijs954-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Cervical artery dissection patients from the multicenter Cervical Artery Dissection and Ischemic Stroke Patients study were classified as patients without stroke (<em>n</em> = 339), with stroke preceded by nonstroke symptoms (delayed stroke, <em>n</em> = 244), and with stroke at onset (<em>n</em> = 382). Demographics, clinical, and vascular findings were compared between the three groups.</p></div></div>
<div class="section" id="ijs954-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Patients with delayed stroke were more likely to present with occlusive cervical artery dissection (<em>P </em>&lt;<em> </em>0·001), multiple cervical artery dissection (<em>P</em> = 0·031), and vertebral artery dissection (<em>P </em>&lt;<em> </em>0·001) than patients without stroke. No differences were observed in age, smoking, arterial hypertension, hypercholesterolemia, migraine, body mass index, infections during the last week, and trauma during the last month, but patients with delayed stroke had less often transient ischemic attack (<em>P </em>&lt;<em> </em>0·001) and local signs (Horner syndrome and cranial nerve palsy; <em>P </em>&lt;<em> </em>0·001).</p></div></div>
<div class="section" id="ijs954-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Occlusive cervical artery dissection, multiple cervical artery dissection, and vertebral artery dissection were associated with an increased risk for delayed stroke. No other risk factors for delayed stroke were identified. Immediate cervical imaging of cervical artery dissection patients without ischemic stroke is needed to identify patients at increased risk for delayed ischemia.</p></div></div>
]]></content:encoded><description>

Background
Stroke in patients with acute cervical artery dissection may be anticipated by initial transient ischemic or nonischemic symptoms.


Aim
Identifying risk factors for delayed stroke upon cervical artery dissection.


Methods
Cervical artery dissection patients from the multicenter Cervical Artery Dissection and Ischemic Stroke Patients study were classified as patients without stroke (n = 339), with stroke preceded by nonstroke symptoms (delayed stroke, n = 244), and with stroke at onset (n = 382). Demographics, clinical, and vascular findings were compared between the three groups.


Results
Patients with delayed stroke were more likely to present with occlusive cervical artery dissection (P &lt; 0·001), multiple cervical artery dissection (P = 0·031), and vertebral artery dissection (P &lt; 0·001) than patients without stroke. No differences were observed in age, smoking, arterial hypertension, hypercholesterolemia, migraine, body mass index, infections during the last week, and trauma during the last month, but patients with delayed stroke had less often transient ischemic attack (P &lt; 0·001) and local signs (Horner syndrome and cranial nerve palsy; P &lt; 0·001).


Conclusions
Occlusive cervical artery dissection, multiple cervical artery dissection, and vertebral artery dissection were associated with an increased risk for delayed stroke. No other risk factors for delayed stroke were identified. Immediate cervical imaging of cervical artery dissection patients without ischemic stroke is needed to identify patients at increased risk for delayed ischemia.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00950.x" xmlns="http://purl.org/rss/1.0/"><title>A critical review of Early Supported Discharge for stroke patients: from evidence to implementation into practice</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00950.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A critical review of Early Supported Discharge for stroke patients: from evidence to implementation into practice</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Miquel Àngel Mas, Marco Inzitari</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:52:26.441819-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00950.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00950.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00950.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>After an acute stroke, a multidimensional approach based on multidisciplinary work and rehabilitation is required in order to promote functional independence and social reinsertion and to maintain medical stability. These activities are usually developed in the hospital setting as a continuum of the acute phase, but hospitalization is resource consuming and resources are limited. Early Support Discharge strategies base postacute care and rehabilitation at home after an early discharge planning and represent possible alternatives to conventional hospitalization. Recent evidence suggests that Early Supported Discharge might be superior to hospitalization from both the clinical-functional and the economic viewpoints. Moreover, home-based rehabilitation might potentiate important determinants of effectiveness, such as patient's motivation and goal-directed rehabilitation. However, hitherto produced evidence and recommendations show a number of limitations related to the organization models, the inclusion/exclusion criteria, and the questionable applicability of results to any healthcare setting worldwide. In this article, we critically review different methodological and organizational aspects of the available studies. For example in the definition of the target population, based mainly on residual disability and medical stability, we suggest that other relevant aspects, such as premorbid functional status, cognitive function, and previous institutionalization, should be better defined. Focusing on the outcomes, we suggest that, besides strong outcomes such as global functioning, surrogate outcomes, such as physical function, could help to refine the specific interventions. Finally, considering that the majority of studies were conducted in northern Europe, further studies are needed to test the implementation of Early Supported Discharge in different regions.</p></div>
]]></content:encoded><description>
After an acute stroke, a multidimensional approach based on multidisciplinary work and rehabilitation is required in order to promote functional independence and social reinsertion and to maintain medical stability. These activities are usually developed in the hospital setting as a continuum of the acute phase, but hospitalization is resource consuming and resources are limited. Early Support Discharge strategies base postacute care and rehabilitation at home after an early discharge planning and represent possible alternatives to conventional hospitalization. Recent evidence suggests that Early Supported Discharge might be superior to hospitalization from both the clinical-functional and the economic viewpoints. Moreover, home-based rehabilitation might potentiate important determinants of effectiveness, such as patient's motivation and goal-directed rehabilitation. However, hitherto produced evidence and recommendations show a number of limitations related to the organization models, the inclusion/exclusion criteria, and the questionable applicability of results to any healthcare setting worldwide. In this article, we critically review different methodological and organizational aspects of the available studies. For example in the definition of the target population, based mainly on residual disability and medical stability, we suggest that other relevant aspects, such as premorbid functional status, cognitive function, and previous institutionalization, should be better defined. Focusing on the outcomes, we suggest that, besides strong outcomes such as global functioning, surrogate outcomes, such as physical function, could help to refine the specific interventions. Finally, considering that the majority of studies were conducted in northern Europe, further studies are needed to test the implementation of Early Supported Discharge in different regions.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00949.x" xmlns="http://purl.org/rss/1.0/"><title>Excessive work and risk of haemorrhagic stroke: a nationwide case-control study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00949.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Excessive work and risk of haemorrhagic stroke: a nationwide case-control study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Beom Joon Kim, Seung-Hoon Lee, Wi-Sun Ryu, Chi Kyung Kim, Jong-Won Chung, Dohoung Kim, Hong-Kyun Park, Hee-Joon Bae, Byung-Joo Park, Byung-Woo Yoon, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:52:04.795648-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00949.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00949.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00949.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs949-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Adverse effect of excessive work on health has been suggested previously, but it was not documented in cerebrovascular diseases.</p></div></div>
<div class="section" id="ijs949-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>The authors investigated whether excessive working conditions would associate with increased risk of haemorrhagic stroke.</p></div></div>
<div class="section" id="ijs949-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>A nationwide matched case-control study database, which contains 940 cases of incident haemorrhagic stroke (498 intracerebral haemorrhages and 442 sub-arachnoid haemorrhages) with 1880 gender- and age- (±5-year) matched controls, was analysed. Work-related information based on the regular job situation, including type of occupation, regular working time, duration of strenuous activity during regular work and shift work, was gathered through face-to-face interviews. Conditional logistic regression analyses were used for the multivariable analyses.</p></div></div>
<div class="section" id="ijs949-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Compared with white-collar workers, blue-collar workers had a higher risk for haemorrhagic stroke (odds ratio, 1·33 [95% confidence interval, 1·06–1·66]). Longer regular working time was associated with increased risk of haemorrhagic stroke [odds ratio, 1·38 (95% confidence interval, 1·05–1·81) for 8–12 h/day; odds ratio, 1·95 (95% confidence interval, 1·33–2·86) for ≥13 h/day; compared with ≤4 h/day]. Exposure to ≥8 h/week of strenuous activity also associated haemorrhagic stroke risk [odds ratio, 1·61 (95% confidence interval, 1·26–2·05); compared with no strenuous activity]. Shift work was not associated with haemorrhagic stroke (<em>P</em> = 0·98). Positive associations between working condition indices and haemorrhagic stroke risk were consistent regardless of haemorrhagic stroke sub-types and current employment status.</p></div></div>
<div class="section" id="ijs949-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Blue-collar occupation, longer regular working time and extended duration of strenuous activity during work may relate to an increased risk of haemorrhagic stroke.</p></div></div>
]]></content:encoded><description>

Background
Adverse effect of excessive work on health has been suggested previously, but it was not documented in cerebrovascular diseases.


Aim
The authors investigated whether excessive working conditions would associate with increased risk of haemorrhagic stroke.


Methods
A nationwide matched case-control study database, which contains 940 cases of incident haemorrhagic stroke (498 intracerebral haemorrhages and 442 sub-arachnoid haemorrhages) with 1880 gender- and age- (±5-year) matched controls, was analysed. Work-related information based on the regular job situation, including type of occupation, regular working time, duration of strenuous activity during regular work and shift work, was gathered through face-to-face interviews. Conditional logistic regression analyses were used for the multivariable analyses.


Results
Compared with white-collar workers, blue-collar workers had a higher risk for haemorrhagic stroke (odds ratio, 1·33 [95% confidence interval, 1·06–1·66]). Longer regular working time was associated with increased risk of haemorrhagic stroke [odds ratio, 1·38 (95% confidence interval, 1·05–1·81) for 8–12 h/day; odds ratio, 1·95 (95% confidence interval, 1·33–2·86) for ≥13 h/day; compared with ≤4 h/day]. Exposure to ≥8 h/week of strenuous activity also associated haemorrhagic stroke risk [odds ratio, 1·61 (95% confidence interval, 1·26–2·05); compared with no strenuous activity]. Shift work was not associated with haemorrhagic stroke (P = 0·98). Positive associations between working condition indices and haemorrhagic stroke risk were consistent regardless of haemorrhagic stroke sub-types and current employment status.


Conclusions
Blue-collar occupation, longer regular working time and extended duration of strenuous activity during work may relate to an increased risk of haemorrhagic stroke.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00948.x" xmlns="http://purl.org/rss/1.0/"><title>Diagnostic procedures in ischaemic stroke patients with dementia. a population-based study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00948.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Diagnostic procedures in ischaemic stroke patients with dementia. a population-based study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yannick Béjot, Agnès Jacquin, Odile Troisgros, Olivier Rouaud, Corine Aboa-Eboulé, Marie Hervieu, Guy-Victor Osseby, Maurice Giroud</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:51:44.971281-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00948.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00948.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00948.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Short Report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs948-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Dementia is a frequent condition in stroke patients.</p></div></div>
<div class="section" id="ijs948-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>To investigate the effect of dementia on access to diagnostic procedures in ischaemic stroke patients.</p></div></div>
<div class="section" id="ijs948-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>All cases of ischaemic stroke from 2006 to 2010 were identified from the population-based Stroke Registry of Dijon, France. Patients' characteristics were recorded, as was the use of brain computed tomography scans, brain magnetic resonance imaging, electrocardiogram, echocardiography, and Doppler ultrasonography of the cervical arteries. Dementia was diagnosed according to Diagnostic and Statistical Manual of Mental Disorders-IV criteria. Logistic regression models were used to evaluate the associations between dementia and the use of the diagnostic procedures.</p></div></div>
<div class="section" id="ijs948-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Of the 907 patients recorded, 104 were excluded because of death and inability to test cognition. Among the remaining 803 patients, 149 (18·5%) had dementia. Almost all of the patients underwent a brain computed tomography scan and an electrocardiogram during their stay. In contrast, the use of both Doppler ultrasonography of the cervical arteries (79·2% versus 90·2%, <em>P</em> &lt; 0·001), echocardiography (32·9% versus 43·6%, <em>P</em> = 0·02), and brain magnetic resonance imaging (21·5% versus 34·4%, <em>P</em> &lt; 0·001) were significantly lower in stroke patients with dementia than in those without. In multivariate logistic regression, dementia was associated with a lower use of both Doppler ultrasonography (odds ratio = 0·49; 95% confidence interval: 0·29–0·81, <em>P</em> = 0·005), echocardiography (odds ratio = 0·57; 95% confidence interval: 0·37–0·89, <em>P</em> = 0·012), brain magnetic resonance imaging (odds ratio = 0·55; 95% confidence interval: 0·34–0·89, <em>P</em> = 0·015), and a comprehensive assessment (odds ratio = 0·62; 95% confidence interval: 0·40–0·96, <em>P</em> = 0·033).</p></div></div>
<div class="section" id="ijs948-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Demented patients were less likely to undergo diagnostic procedures after ischaemic stroke. Further studies are needed to determine whether this lower utilization could account for the reported excess in recurrent events in these patients.</p></div></div>
]]></content:encoded><description>

Background
Dementia is a frequent condition in stroke patients.


Aims
To investigate the effect of dementia on access to diagnostic procedures in ischaemic stroke patients.


Methods
All cases of ischaemic stroke from 2006 to 2010 were identified from the population-based Stroke Registry of Dijon, France. Patients' characteristics were recorded, as was the use of brain computed tomography scans, brain magnetic resonance imaging, electrocardiogram, echocardiography, and Doppler ultrasonography of the cervical arteries. Dementia was diagnosed according to Diagnostic and Statistical Manual of Mental Disorders-IV criteria. Logistic regression models were used to evaluate the associations between dementia and the use of the diagnostic procedures.


Results
Of the 907 patients recorded, 104 were excluded because of death and inability to test cognition. Among the remaining 803 patients, 149 (18·5%) had dementia. Almost all of the patients underwent a brain computed tomography scan and an electrocardiogram during their stay. In contrast, the use of both Doppler ultrasonography of the cervical arteries (79·2% versus 90·2%, P &lt; 0·001), echocardiography (32·9% versus 43·6%, P = 0·02), and brain magnetic resonance imaging (21·5% versus 34·4%, P &lt; 0·001) were significantly lower in stroke patients with dementia than in those without. In multivariate logistic regression, dementia was associated with a lower use of both Doppler ultrasonography (odds ratio = 0·49; 95% confidence interval: 0·29–0·81, P = 0·005), echocardiography (odds ratio = 0·57; 95% confidence interval: 0·37–0·89, P = 0·012), brain magnetic resonance imaging (odds ratio = 0·55; 95% confidence interval: 0·34–0·89, P = 0·015), and a comprehensive assessment (odds ratio = 0·62; 95% confidence interval: 0·40–0·96, P = 0·033).


Conclusion
Demented patients were less likely to undergo diagnostic procedures after ischaemic stroke. Further studies are needed to determine whether this lower utilization could account for the reported excess in recurrent events in these patients.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00945.x" xmlns="http://purl.org/rss/1.0/"><title>Patient refusal of thrombolytic therapy for suspected acute ischemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00945.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Patient refusal of thrombolytic therapy for suspected acute ischemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">F. S. Vahidy, M. H. Rahbar, A. P. Lal, J. C. Grotta, S. I. Savitz</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:51:24.505652-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00945.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00945.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00945.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs945-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>To determine factors associated with patients refusing IV t-PA for suspected acute ischemic stroke (AIS), and to compare the outcomes of patients who refused t-PA (RT) with those treated with t-PA.</p></div></div>
<div class="section" id="ijs945-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Patients who were treated with and refused t-PA at our stroke center were identified retrospectively. Demographics, clinical presentation, and outcome measures were collected and compared. Clinical outcome was defined as excellent (mRS: 0–1), good (mRS: 0–2), and poor (mRS: 3–6).</p></div></div>
<div class="section" id="ijs945-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Over 7·5 years, 30 (4·2%) patients refused t-PA. There were no demographic differences between the treated and RT groups. The rate of RT decreased over time (OR 0·63, 95% CI 0·50–0·79). Factors associated with refusal included a later symptom onset to emergency department presentation time (OR 1·02, 95% CI 1·01–1·03), lower NIHSS (OR 1·11, 95% CI 1·03–1·18), a higher proportion of stroke mimics (OR 17·61, 95% CI 6·20–50·02) and shorter hospital stay (OR 1·32, 95% CI 1·09–1·61). Among patients who were subsequently diagnosed with ischemic stroke, only length of stay was significantly shorter for refusal patients (OR 1·37, 95% CI 1·06–1·78). After controlling for mild strokes and stroke mimics, clinical outcome was not different between the groups (OR 1·61, 95% CI 0·69–3·73).</p></div></div>
<div class="section" id="ijs945-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>The incidence of patients refusing t-PA has decreased over time, yet it may be a cause for t-PA under-utilization. Patients with milder symptoms were more likely to refuse t-PA. Refusal patients presented later to the hospital and had shorter hospital stays. One out of six refusal patients (16·6%) had a stroke mimic.</p></div></div>
]]></content:encoded><description>

Objective
To determine factors associated with patients refusing IV t-PA for suspected acute ischemic stroke (AIS), and to compare the outcomes of patients who refused t-PA (RT) with those treated with t-PA.


Methods
Patients who were treated with and refused t-PA at our stroke center were identified retrospectively. Demographics, clinical presentation, and outcome measures were collected and compared. Clinical outcome was defined as excellent (mRS: 0–1), good (mRS: 0–2), and poor (mRS: 3–6).


Results
Over 7·5 years, 30 (4·2%) patients refused t-PA. There were no demographic differences between the treated and RT groups. The rate of RT decreased over time (OR 0·63, 95% CI 0·50–0·79). Factors associated with refusal included a later symptom onset to emergency department presentation time (OR 1·02, 95% CI 1·01–1·03), lower NIHSS (OR 1·11, 95% CI 1·03–1·18), a higher proportion of stroke mimics (OR 17·61, 95% CI 6·20–50·02) and shorter hospital stay (OR 1·32, 95% CI 1·09–1·61). Among patients who were subsequently diagnosed with ischemic stroke, only length of stay was significantly shorter for refusal patients (OR 1·37, 95% CI 1·06–1·78). After controlling for mild strokes and stroke mimics, clinical outcome was not different between the groups (OR 1·61, 95% CI 0·69–3·73).


Conclusion
The incidence of patients refusing t-PA has decreased over time, yet it may be a cause for t-PA under-utilization. Patients with milder symptoms were more likely to refuse t-PA. Refusal patients presented later to the hospital and had shorter hospital stays. One out of six refusal patients (16·6%) had a stroke mimic.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00942.x" xmlns="http://purl.org/rss/1.0/"><title>Top 10 research priorities relating to life after stroke – consensus from stroke survivors, caregivers, and health professionals</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00942.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Top 10 research priorities relating to life after stroke – consensus from stroke survivors, caregivers, and health professionals</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Alex Pollock, Bridget St George, Mark Fenton, Lester Firkins</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:51:05.253785-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00942.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00942.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00942.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs942-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Research resources should address the issues that are most important to people affected by a particular healthcare problem. Systematic identification of stroke survivor, caregiver, and health professional priorities would ensure that scarce research resources are directed to areas that matter most to people affected by stroke.</p></div></div>
<div class="section" id="ijs942-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>We aimed to identify the top 10 research priorities relating to life after stroke, as agreed by stroke survivors, caregivers, and health professionals.</p></div></div>
<div class="section" id="ijs942-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Key stages involved establishing a priority setting partnership; gathering treatment uncertainties from stroke survivors, caregivers, and health professionals relating to life after stroke (using surveys administered by e-mail, post, and at face-to-face meetings); checking submitted treatment uncertainties to ensure that they were clear, unanswered questions about the effects of a treatment/intervention; interim prioritization to identify the highest priority questions (objectively identified from ranking of personal priorities by original survey respondents); and a final consensus meeting to reach agreement on the top 10 research priorities.</p></div></div>
<div class="section" id="ijs942-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>We gathered 548 research questions that were refined into 226 unique unanswered treatment uncertainties. Ninety-seven respondents completed the interim prioritization process, objectively identifying 24 shared priority treatment uncertainties. A representative group of 28 stroke survivors, caregivers, and health professionals attended a final meeting, reaching consensus on the top 10 research priorities relating to life after stroke.</p></div><div class="para"><p>Six of the agreed top 10 research priorities related to specific stroke-related impairments, including cognition, aphasia, vision, upper limb, mobility, and fatigue. Three related to more social aspects of ‘living with stroke’ including coming to terms with long-term consequences, confidence, and helping stroke survivors and their families ‘cope’ with speech problems. One related to the secondary consequences of stroke and subsequent stroke prevention.</p></div></div>
<div class="section" id="ijs942-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The top 10 research priorities relating to life after stroke have been identified using a rigorous and person-centered approach. These should be used to inform the prioritization and funding of future research relating to life after stroke.</p></div></div>
]]></content:encoded><description>

Background
Research resources should address the issues that are most important to people affected by a particular healthcare problem. Systematic identification of stroke survivor, caregiver, and health professional priorities would ensure that scarce research resources are directed to areas that matter most to people affected by stroke.


Aims
We aimed to identify the top 10 research priorities relating to life after stroke, as agreed by stroke survivors, caregivers, and health professionals.


Methods
Key stages involved establishing a priority setting partnership; gathering treatment uncertainties from stroke survivors, caregivers, and health professionals relating to life after stroke (using surveys administered by e-mail, post, and at face-to-face meetings); checking submitted treatment uncertainties to ensure that they were clear, unanswered questions about the effects of a treatment/intervention; interim prioritization to identify the highest priority questions (objectively identified from ranking of personal priorities by original survey respondents); and a final consensus meeting to reach agreement on the top 10 research priorities.


Results
We gathered 548 research questions that were refined into 226 unique unanswered treatment uncertainties. Ninety-seven respondents completed the interim prioritization process, objectively identifying 24 shared priority treatment uncertainties. A representative group of 28 stroke survivors, caregivers, and health professionals attended a final meeting, reaching consensus on the top 10 research priorities relating to life after stroke.
Six of the agreed top 10 research priorities related to specific stroke-related impairments, including cognition, aphasia, vision, upper limb, mobility, and fatigue. Three related to more social aspects of ‘living with stroke’ including coming to terms with long-term consequences, confidence, and helping stroke survivors and their families ‘cope’ with speech problems. One related to the secondary consequences of stroke and subsequent stroke prevention.


Conclusions
The top 10 research priorities relating to life after stroke have been identified using a rigorous and person-centered approach. These should be used to inform the prioritization and funding of future research relating to life after stroke.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00941.x" xmlns="http://purl.org/rss/1.0/"><title>Yield of CT perfusion for the evaluation of transient ischaemic attack</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00941.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Yield of CT perfusion for the evaluation of transient ischaemic attack</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jonathan T. Kleinman, Michael Mlynash, Greg Zaharchuk, Alyshia A. Ogdie, Matus Straka, Maarten G. Lansberg, Neil E. Schwartz, Paul Singh, Stephanie Kemp, Roland Bammer, Gregory W. Albers, Jean-Marc Olivot</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:50:42.700994-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00941.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00941.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00941.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs941-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Magnetic resonance diffusion-weighted imaging and perfusion-weighted imaging are able to identify ischaemic ‘footprints’ in transient ischaemic attack. Computed tomography perfusion (CTP) may be useful for patient triage and subsequent management. To date, less than 100 cases have been reported, and none have compared computed tomography perfusion to perfusion-weighted imaging (PWI). We sought to define the yield of computed tomography perfusion for the evaluation of transient ischaemic attack.</p></div></div>
<div class="section" id="ijs941-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Consecutive patients with a discharge diagnosis of possible or definite transient ischaemic event who underwent computed tomography perfusion were included in this study. The presence of an ischaemic lesion was assessed on noncontrast computed tomography, automatically deconvolved CTP<sub>TMax</sub> (Time till the residue function reaches its maximum), and when available on diffusion-weighted imaging and PWI<sub>TMax</sub> maps.</p></div></div>
<div class="section" id="ijs941-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Thirty-four patients were included and 17 underwent magnetic resonance imaging. Median delay between onset and computed tomography perfusion was 4·4 h (Interquartile range [IQR]: 1·9–9·6), and between computed tomography perfusion and magnetic resonance imaging was 11 h (Interquartile range: 3·8–22). Noncontrast computed tomography was negative in all cases, while CTP<sub>TMax</sub> identified an ischaemic lesion in 12/34 patients (35%). In the subgroup of patients with multimodal magnetic resonance imaging, an ischaemic lesion was found in six (35%) patients using CTP<sub>TMax</sub> versus nine (53%) on magnetic resonance imaging (five diffusion-weighted imaging, nine perfusion-weighted imaging). The additional yield of CTP<sub>TMax</sub> over computed tomography angiography was significant in the evaluation of transient ischaemic attack (12 vs. 3, McNemar, <em>P</em> = 0·004).</p></div></div>
<div class="section" id="ijs941-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>CTP<sub>TMax</sub> found an ischaemic lesion in one-third of acute transient ischaemic attack patients. Computed tomography perfusion may be an acceptable substitute when magnetic resonance imaging is unavailable or contraindicated, and has additional yield over computed tomography angiography. Further studies evaluating the outcome of patients with computed tomography perfusion lesions in transient ischaemic attack are justified at this time.</p></div></div>
]]></content:encoded><description>

Background
Magnetic resonance diffusion-weighted imaging and perfusion-weighted imaging are able to identify ischaemic ‘footprints’ in transient ischaemic attack. Computed tomography perfusion (CTP) may be useful for patient triage and subsequent management. To date, less than 100 cases have been reported, and none have compared computed tomography perfusion to perfusion-weighted imaging (PWI). We sought to define the yield of computed tomography perfusion for the evaluation of transient ischaemic attack.


Methods
Consecutive patients with a discharge diagnosis of possible or definite transient ischaemic event who underwent computed tomography perfusion were included in this study. The presence of an ischaemic lesion was assessed on noncontrast computed tomography, automatically deconvolved CTPTMax (Time till the residue function reaches its maximum), and when available on diffusion-weighted imaging and PWITMax maps.


Results
Thirty-four patients were included and 17 underwent magnetic resonance imaging. Median delay between onset and computed tomography perfusion was 4·4 h (Interquartile range [IQR]: 1·9–9·6), and between computed tomography perfusion and magnetic resonance imaging was 11 h (Interquartile range: 3·8–22). Noncontrast computed tomography was negative in all cases, while CTPTMax identified an ischaemic lesion in 12/34 patients (35%). In the subgroup of patients with multimodal magnetic resonance imaging, an ischaemic lesion was found in six (35%) patients using CTPTMax versus nine (53%) on magnetic resonance imaging (five diffusion-weighted imaging, nine perfusion-weighted imaging). The additional yield of CTPTMax over computed tomography angiography was significant in the evaluation of transient ischaemic attack (12 vs. 3, McNemar, P = 0·004).


Conclusions
CTPTMax found an ischaemic lesion in one-third of acute transient ischaemic attack patients. Computed tomography perfusion may be an acceptable substitute when magnetic resonance imaging is unavailable or contraindicated, and has additional yield over computed tomography angiography. Further studies evaluating the outcome of patients with computed tomography perfusion lesions in transient ischaemic attack are justified at this time.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00935.x" xmlns="http://purl.org/rss/1.0/"><title>Gender differences in the association between parental divorce during childhood and stroke in adulthood: findings from a population-based survey</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00935.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Gender differences in the association between parental divorce during childhood and stroke in adulthood: findings from a population-based survey</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Esme Fuller-Thomson, Angela D. Dalton</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:50:21.605305-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00935.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00935.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00935.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs935-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Although there is a substantial literature examining the mental health consequences of parental divorce, less attention has been paid to possible long-term physical health outcomes.</p></div></div>
<div class="section" id="ijs935-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The aim of this study was to examine the gender-specific association between childhood parental divorce and later incidence of stroke, while controlling for age, race ethnicity, socioeconomic status, health behaviors, diabetes, social support, marital status, mental health, and health care utilization.</p></div></div>
<div class="section" id="ijs935-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Secondary analysis of the population-based Behavioral Risk Factor Surveillance System survey; logistic regression analyses were conducted. The final sample included 4074 males and 5886 females. Respondents were excluded if they had experienced parental addictions to drugs or alcohol, any form of childhood abuse (physical, sexual, or emotional), or witnessed domestic violence.</p></div></div>
<div class="section" id="ijs935-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>A threefold risk of stroke was found for males who had experienced parental divorce before the age of 18 in comparison with males whose parents had not divorced [age- and race ethnicity-adjusted model odds ratio (OR) = 2·99, 95% confidence interval (CI) = 1·79, 4·98; fully adjusted model OR = 3·01, 95% CI = 1·68, 5·39]. Parental divorce was not significantly associated with stroke among women (fully adjusted OR = 1·64, 95% CI = 0·89, 3·02).</p></div></div>
<div class="section" id="ijs935-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>There is a robust association between parental divorce and stroke among males, even after adjustment for many known risk factors and the exclusion of respondents who had experienced parental addictions or family violence. Further research is needed to investigate plausible pathways linking parental divorce and stroke in males.</p></div></div>
]]></content:encoded><description>

Background
Although there is a substantial literature examining the mental health consequences of parental divorce, less attention has been paid to possible long-term physical health outcomes.


Aims
The aim of this study was to examine the gender-specific association between childhood parental divorce and later incidence of stroke, while controlling for age, race ethnicity, socioeconomic status, health behaviors, diabetes, social support, marital status, mental health, and health care utilization.


Methods
Secondary analysis of the population-based Behavioral Risk Factor Surveillance System survey; logistic regression analyses were conducted. The final sample included 4074 males and 5886 females. Respondents were excluded if they had experienced parental addictions to drugs or alcohol, any form of childhood abuse (physical, sexual, or emotional), or witnessed domestic violence.


Results
A threefold risk of stroke was found for males who had experienced parental divorce before the age of 18 in comparison with males whose parents had not divorced [age- and race ethnicity-adjusted model odds ratio (OR) = 2·99, 95% confidence interval (CI) = 1·79, 4·98; fully adjusted model OR = 3·01, 95% CI = 1·68, 5·39]. Parental divorce was not significantly associated with stroke among women (fully adjusted OR = 1·64, 95% CI = 0·89, 3·02).


Conclusions
There is a robust association between parental divorce and stroke among males, even after adjustment for many known risk factors and the exclusion of respondents who had experienced parental addictions or family violence. Further research is needed to investigate plausible pathways linking parental divorce and stroke in males.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00933.x" xmlns="http://purl.org/rss/1.0/"><title>Risk factor management in survivors of stroke: a double-blind, cluster-randomized, controlled trial</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00933.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Risk factor management in survivors of stroke: a double-blind, cluster-randomized, controlled trial</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Amanda G. Thrift, Velandai K. Srikanth, Mark R. Nelson, Joosup Kim, Sharyn M. Fitzgerald, Richard P. Gerraty, Christopher F. Bladin, Thanh G. Phan, Dominique A. Cadilhac</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:49:44.293684-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00933.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00933.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00933.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs933-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Comprehensive community care has the potential to improve risk factor management of patients with stroke or transient ischaemic attack.</p></div></div>
<div class="section" id="ijs933-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>The primary aim is to determine the effectiveness of an individualized management program on risk factor management for patients discharged from hospital after stroke.</p></div></div>
<div class="section" id="ijs933-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Multicentre, cluster-randomized, controlled trial, with clusters by general practice. Participants are randomized to receive intervention or control after a baseline assessment undertaken after discharge from hospital. The general practice they attend is marked as an intervention or control accordingly. All subsequent participants attending those practices are automatically assigned as intervention or control. Baseline and all outcome assessments, including an analysis of risk factors, are undertaken by assessors blinded to patient randomization.</p></div></div>
<div class="section" id="ijs933-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Intervention Details</h4><div class="para"><p>Based on the results of blinded assessments, the individualized management program group will receive targeted advice on how to manage their risk factors using a standardized, evidence-based template to communicate ‘ideal’ management with their general practitioner. In addition, patients randomized to the individualized management program group will receive counselling and education about stroke risk factor management by an intervention study nurse. Individualized management programs will be reviewed at three-months, six-months, 12 months, and 18 months after stroke, at which times they will be modified if appropriate. Stroke risk management will be evaluated using changes in the Framingham cardiovascular risk score. Analysis will be on an intention-to-treat basis using analysis of covariance or generalized linear model to adjust for baseline risk score and other relevant confounding factors.</p></div></div>
]]></content:encoded><description>

Background
Comprehensive community care has the potential to improve risk factor management of patients with stroke or transient ischaemic attack.


Aim
The primary aim is to determine the effectiveness of an individualized management program on risk factor management for patients discharged from hospital after stroke.


Design
Multicentre, cluster-randomized, controlled trial, with clusters by general practice. Participants are randomized to receive intervention or control after a baseline assessment undertaken after discharge from hospital. The general practice they attend is marked as an intervention or control accordingly. All subsequent participants attending those practices are automatically assigned as intervention or control. Baseline and all outcome assessments, including an analysis of risk factors, are undertaken by assessors blinded to patient randomization.


Intervention Details
Based on the results of blinded assessments, the individualized management program group will receive targeted advice on how to manage their risk factors using a standardized, evidence-based template to communicate ‘ideal’ management with their general practitioner. In addition, patients randomized to the individualized management program group will receive counselling and education about stroke risk factor management by an intervention study nurse. Individualized management programs will be reviewed at three-months, six-months, 12 months, and 18 months after stroke, at which times they will be modified if appropriate. Stroke risk management will be evaluated using changes in the Framingham cardiovascular risk score. Analysis will be on an intention-to-treat basis using analysis of covariance or generalized linear model to adjust for baseline risk score and other relevant confounding factors.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00932.x" xmlns="http://purl.org/rss/1.0/"><title>Do lacunar strokes benefit from thrombolysis? Evidence from the Registry of the Canadian Stroke Network</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00932.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Do lacunar strokes benefit from thrombolysis? Evidence from the Registry of the Canadian Stroke Network</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Nandavar Shobha, Jiming Fang, Michael D. Hill</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:49:26.796155-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00932.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00932.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00932.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs932-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Lacunar infarcts constitute up to 25% of all ischaemic strokes. As acute intracranial vascular imaging has become widely available with computed tomographic angiography, thrombolysis of lacunar strokes has become contentious because an intracranial vascular lesion cannot be visualized. We studied the effect of thrombolysis on lacunar strokes compared to other clinical ischaemic stroke sub-types.</p></div></div>
<div class="section" id="ijs932-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Ischaemic stroke patients from phase 3 of the Registry of the Canadian Stroke Network data (July 2003–March 2008) were included. Lacunar stroke was defined as a lacunar syndrome supported by computed tomography brain showing a subcortical hypodense lesion with a diameter &lt;20 mm. Clinical syndromes were used to define other stroke sub-types. The outcomes were mortality at 90 days, modified Rankin Scale score 0–2 at discharge, occurrence of intracranial haemorrhage as a complication of stroke in-hospital, and discharge disposition to home.</p></div></div>
<div class="section" id="ijs932-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>A total of 11 503 patients of ischaemic stroke were included from the Registry of the Canadian Stroke Network 3 between July 2003 and March 2008. Lacunar strokes formed 19·1% of the total strokes. The total number of patients who received tissue plasminogen activator was 1630 (14·2%). A significant association was found between tissue plasminogen activator treatment and outcomes after controlling Oxfordshire Community Stroke Project types – for modified Rankin Scale at discharge and discharge to home, but not for mortality. A thrombolysis-by-Oxfordshire Community Stroke Project stroke sub-type interaction was observed due to lack of benefit among the posterior circulation stroke sub-types. Patients with lacunar strokes, partial anterior circulation stroke, and total anterior circulation strokes all benefited approximately equally from thrombolysis.</p></div></div>
<div class="section" id="ijs932-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Thrombolysis is associated with clinically improved outcome among patients with lacunar stroke syndromes.</p></div></div>
]]></content:encoded><description>

Background
Lacunar infarcts constitute up to 25% of all ischaemic strokes. As acute intracranial vascular imaging has become widely available with computed tomographic angiography, thrombolysis of lacunar strokes has become contentious because an intracranial vascular lesion cannot be visualized. We studied the effect of thrombolysis on lacunar strokes compared to other clinical ischaemic stroke sub-types.


Methods
Ischaemic stroke patients from phase 3 of the Registry of the Canadian Stroke Network data (July 2003–March 2008) were included. Lacunar stroke was defined as a lacunar syndrome supported by computed tomography brain showing a subcortical hypodense lesion with a diameter &lt;20 mm. Clinical syndromes were used to define other stroke sub-types. The outcomes were mortality at 90 days, modified Rankin Scale score 0–2 at discharge, occurrence of intracranial haemorrhage as a complication of stroke in-hospital, and discharge disposition to home.


Results
A total of 11 503 patients of ischaemic stroke were included from the Registry of the Canadian Stroke Network 3 between July 2003 and March 2008. Lacunar strokes formed 19·1% of the total strokes. The total number of patients who received tissue plasminogen activator was 1630 (14·2%). A significant association was found between tissue plasminogen activator treatment and outcomes after controlling Oxfordshire Community Stroke Project types – for modified Rankin Scale at discharge and discharge to home, but not for mortality. A thrombolysis-by-Oxfordshire Community Stroke Project stroke sub-type interaction was observed due to lack of benefit among the posterior circulation stroke sub-types. Patients with lacunar strokes, partial anterior circulation stroke, and total anterior circulation strokes all benefited approximately equally from thrombolysis.


Conclusions
Thrombolysis is associated with clinically improved outcome among patients with lacunar stroke syndromes.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00929.x" xmlns="http://purl.org/rss/1.0/"><title>Aspirin resistance in Chinese stroke patients increased the rate of recurrent stroke and other vascular events</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00929.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Aspirin resistance in Chinese stroke patients increased the rate of recurrent stroke and other vascular events</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Xingyang Yi, Qiang Zhou, Jing Lin, LiFen Chi</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:49:09.996765-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00929.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00929.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00929.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs929-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Introduction</h4><div class="para"><p>To investigate the prevalent of aspirin resistance (AR) in Chinese stroke patients and its association with recurrent stroke and other vascular events, including cardiovascular disease and death.</p></div></div>
<div class="section" id="ijs929-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We prospectively enrolled 634 Chinese stroke patients. Aspirin was administrated to every patient from the first day of admission. Whole blood samples were collected for platelet aggregation testing after aspirin was administered for 7–10 days. A follow-up period of 12–24 months was performed to record vascular events and hemorrhagic side effects.</p></div></div>
<div class="section" id="ijs929-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Aspirin resistance (AR) was detected in 129 patients (20·4%), aspirin semi-resistance (ASR) in 28 patients (4·4%) and aspirin sensitivity (AS) in 477 patients (75·2%). Logistic regression analysis found that diabetes and high levels of low density lipoprotein cholesterol (LDL) were independent risk factors for ASR and AR. During a median follow-up period of 19·4 months, the prevalence of recurrent stroke, death from all causes, myocardial infarction and vascular events overall were higher in patients with AR + ASR than in patients with AS. Cox regression analysis found that diabetes and AR were independent risk factors for vascular events.</p></div></div>
<div class="section" id="ijs929-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Aspirin resistance is common in Chinese patient taking antiplatelet medications. Diabetes and high LDL may induce platelet activation and thrombosis and increase the occurrence of aspirin resistance. Patients who are detected to be aspirin resistant are at a greater risk of clinically important vascular events.</p></div></div>
]]></content:encoded><description>

Introduction
To investigate the prevalent of aspirin resistance (AR) in Chinese stroke patients and its association with recurrent stroke and other vascular events, including cardiovascular disease and death.


Methods
We prospectively enrolled 634 Chinese stroke patients. Aspirin was administrated to every patient from the first day of admission. Whole blood samples were collected for platelet aggregation testing after aspirin was administered for 7–10 days. A follow-up period of 12–24 months was performed to record vascular events and hemorrhagic side effects.


Results
Aspirin resistance (AR) was detected in 129 patients (20·4%), aspirin semi-resistance (ASR) in 28 patients (4·4%) and aspirin sensitivity (AS) in 477 patients (75·2%). Logistic regression analysis found that diabetes and high levels of low density lipoprotein cholesterol (LDL) were independent risk factors for ASR and AR. During a median follow-up period of 19·4 months, the prevalence of recurrent stroke, death from all causes, myocardial infarction and vascular events overall were higher in patients with AR + ASR than in patients with AS. Cox regression analysis found that diabetes and AR were independent risk factors for vascular events.


Conclusion
Aspirin resistance is common in Chinese patient taking antiplatelet medications. Diabetes and high LDL may induce platelet activation and thrombosis and increase the occurrence of aspirin resistance. Patients who are detected to be aspirin resistant are at a greater risk of clinically important vascular events.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00927.x" xmlns="http://purl.org/rss/1.0/"><title>Social position and chronic conditions across the life span and risk of stroke: a life course epidemiological analysis of 22 847 American adults in ages over 50</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00927.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Social position and chronic conditions across the life span and risk of stroke: a life course epidemiological analysis of 22 847 American adults in ages over 50</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Longjian Liu, Fuzhong Xue, Jixiang Ma, Marshal Ma, Yong Long, Craig J. Newschaffer</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:48:54.227896-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00927.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00927.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00927.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs927-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Evidence is limited on the impact of childhood socioeconomic status, adulthood socioeconomic status and chronic conditions on risk of incident stroke in later life. We aimed to examine these associations using data from a nationally representative sample of the Health and Retirement Study.</p></div></div>
<div class="section" id="ijs927-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Stroke-free participants (<em>n</em> = 22 847) aged &gt; 50 years in the Health and Retirement Study (1992–2008) were analyzed. Childhood and adulthood socioeconomic status were assessed using parental and participant's education attainments. Incident stroke was defined as self-reported first incident stroke.</p></div></div>
<div class="section" id="ijs927-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Of the study sample, 2298 subjects experienced first incident stroke (10·06%). Cox's regression models indicate that subjects with low childhood socioeconomic status had 1·36 times higher risk (95% confidence interval: 1·18–1·57) of first incident stroke than those with high childhood socioeconomic status. There was an 8% reduction of this association after adjustment for adulthood socioeconomic status. Adults with diabetes mellitus had the highest hazard ratio (1·91, 95% confidence interval: 1·63–2·23) for incident stroke, followed by heart disease (1·69, 1·48–1·93), and then hypertension (1·56, 1·40–1·75). Significant interaction effect of childhood socioeconomic status and diabetes mellitus, and combined effects of socioeconomic status and chronic conditions on risk of incident stroke were observed.</p></div></div>
<div class="section" id="ijs927-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Both low socioeconomic status in childhood and adulthood socioeconomic status predict the risk of stroke. There are significantly combined effects of socioeconomic status and chronic conditions on the risk of stroke. Improving socioeconomic status across the life span and aggressive control of chronic conditions may play pivotal roles in the prevention of stroke development.</p></div></div>
]]></content:encoded><description>

Background
Evidence is limited on the impact of childhood socioeconomic status, adulthood socioeconomic status and chronic conditions on risk of incident stroke in later life. We aimed to examine these associations using data from a nationally representative sample of the Health and Retirement Study.


Methods
Stroke-free participants (n = 22 847) aged &gt; 50 years in the Health and Retirement Study (1992–2008) were analyzed. Childhood and adulthood socioeconomic status were assessed using parental and participant's education attainments. Incident stroke was defined as self-reported first incident stroke.


Results
Of the study sample, 2298 subjects experienced first incident stroke (10·06%). Cox's regression models indicate that subjects with low childhood socioeconomic status had 1·36 times higher risk (95% confidence interval: 1·18–1·57) of first incident stroke than those with high childhood socioeconomic status. There was an 8% reduction of this association after adjustment for adulthood socioeconomic status. Adults with diabetes mellitus had the highest hazard ratio (1·91, 95% confidence interval: 1·63–2·23) for incident stroke, followed by heart disease (1·69, 1·48–1·93), and then hypertension (1·56, 1·40–1·75). Significant interaction effect of childhood socioeconomic status and diabetes mellitus, and combined effects of socioeconomic status and chronic conditions on risk of incident stroke were observed.


Conclusions
Both low socioeconomic status in childhood and adulthood socioeconomic status predict the risk of stroke. There are significantly combined effects of socioeconomic status and chronic conditions on the risk of stroke. Improving socioeconomic status across the life span and aggressive control of chronic conditions may play pivotal roles in the prevention of stroke development.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00926.x" xmlns="http://purl.org/rss/1.0/"><title>Improved survival of patients with warfarin-associated intracerebral haemorrhage: a retrospective longitudinal population-based study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00926.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Improved survival of patients with warfarin-associated intracerebral haemorrhage: a retrospective longitudinal population-based study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Juha Huhtakangas, Sami Tetri, Seppo Juvela, Pertti Saloheimo, Michaela K Bode, Vesa Karttunen, Anni Käräjämäki, Matti Hillbom</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:48:34.596743-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00926.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00926.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00926.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs926-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Warfarin-associated intracerebral haemorrhage carries poor outcome due to rapid haemorrhage growth. Reversal of warfarin anticoagulation with prothrombin complex concentrate has been implemented as an acute treatment option for these subjects.</p></div></div>
<div class="section" id="ijs926-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>We investigated whether survival of subjects with warfarin-associated intracerebral haemorrhage had improved after implementation of reversal of warfarin anticoagulation with prothrombin complex concentrate.</p></div></div>
<div class="section" id="ijs926-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We identified all subjects with warfarin-associated intracerebral haemorrhage during 1993–2008 among the population of Northern Ostrobothnia, Finland. From 2004 onwards, prothrombin complex concentrate was used in Oulu University Hospital, the only hospital treating intracerebral haemorrhage subjects in the region, to counteract the effect of warfarin in subjects with warfarin-associated intracerebral haemorrhage. We compared the outcomes of subjects admitted during 1993–2003 and 2004–2008 and those treated and not treated with prothrombin complex concentrate. We also explored the predictors for one-year survival of the warfarin-associated intracerebral haemorrhage subjects.</p></div></div>
<div class="section" id="ijs926-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>We identified altogether 181 subjects who had intracerebral haemorrhage while on warfarin. One-year survival was significantly (<em>P</em> = 0·031) higher for the 60 subjects admitted during 2004–2008 (43·3%) than for the 121 admitted before 2004 (30·6%). In multivariable analysis, prothrombin complex concentrate treatment reduced one-year case fatality (hazard ratio 0·52, 95% confidence interval 0·29–0·93). Thromboembolic complications did not occur more frequently among those treated with prothrombin complex concentrate.</p></div></div>
<div class="section" id="ijs926-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>The survival of warfarin-associated intracerebral haemorrhage subjects among the population of Northern Ostrobothnia has improved likely because of introduction of prothrombin complex concentrate.</p></div></div>
]]></content:encoded><description>

Background
Warfarin-associated intracerebral haemorrhage carries poor outcome due to rapid haemorrhage growth. Reversal of warfarin anticoagulation with prothrombin complex concentrate has been implemented as an acute treatment option for these subjects.


Aim
We investigated whether survival of subjects with warfarin-associated intracerebral haemorrhage had improved after implementation of reversal of warfarin anticoagulation with prothrombin complex concentrate.


Methods
We identified all subjects with warfarin-associated intracerebral haemorrhage during 1993–2008 among the population of Northern Ostrobothnia, Finland. From 2004 onwards, prothrombin complex concentrate was used in Oulu University Hospital, the only hospital treating intracerebral haemorrhage subjects in the region, to counteract the effect of warfarin in subjects with warfarin-associated intracerebral haemorrhage. We compared the outcomes of subjects admitted during 1993–2003 and 2004–2008 and those treated and not treated with prothrombin complex concentrate. We also explored the predictors for one-year survival of the warfarin-associated intracerebral haemorrhage subjects.


Results
We identified altogether 181 subjects who had intracerebral haemorrhage while on warfarin. One-year survival was significantly (P = 0·031) higher for the 60 subjects admitted during 2004–2008 (43·3%) than for the 121 admitted before 2004 (30·6%). In multivariable analysis, prothrombin complex concentrate treatment reduced one-year case fatality (hazard ratio 0·52, 95% confidence interval 0·29–0·93). Thromboembolic complications did not occur more frequently among those treated with prothrombin complex concentrate.


Conclusion
The survival of warfarin-associated intracerebral haemorrhage subjects among the population of Northern Ostrobothnia has improved likely because of introduction of prothrombin complex concentrate.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00925.x" xmlns="http://purl.org/rss/1.0/"><title>International Paediatric Stroke Study: stroke associated with cardiac disorders</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00925.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">International Paediatric Stroke Study: stroke associated with cardiac disorders</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Michael M. Dowling, Linda S. Hynan, Warren Lo, Daniel J. Licht, Chalmer McClure, Jerome Y. Yager, Nomazulu Dlamini, Fenella J. Kirkham, Gabrielle deVeber, Steve Pavlakis, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-11T05:48:18.544614-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00925.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00925.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00925.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs925-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and hypothesis</h4><div class="para"><p>The aetiologies of arterial ischaemic stroke in children are diverse and often multifactorial. A large proportion occurs in children with cardiac disorders. We hypothesized that the clinical and radiographic features of children with arterial ischaemic stroke attributed to cardiac disorders would differ from those with other causes.</p></div></div>
<div class="section" id="ijs925-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Using the large population collected in the prospective International Paediatric Stroke Study, we analysed the characteristics, clinical presentations, imaging findings, and early outcomes of children with and without cardiac disorders.</p></div></div>
<div class="section" id="ijs925-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Aetiological data were available for 667 children with arterial ischaemic stroke (ages 29 days to 19 years). Cardiac disorders were indentified in 204/667 (30·6%), congenital defects in 121/204 (59·3%), acquired in 40/204 (19·6%), and isolated patent foramen ovale in 31/204 (15·2%). Compared to other children with stroke, those with cardiac disorders were younger (median age 3·1 vs. 6·5 years; <em>P</em> &lt; 0·001) and less likely to present with headache (25·6% vs. 44·6%; <em>P</em> &lt; 0·001), but were similar in terms of gender and presentation with focal deficits, seizures, or recent infection. Analysis of imaging data identified significant differences (<em>P</em> = 0·005) in the vascular distribution (anterior vs. posterior circulation or both) between groups. Bilateral strokes and haemorrhagic conversion were more prevalent in the cardiac disorders group.</p></div></div>
<div class="section" id="ijs925-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Cardiac disorders were identified in almost one-third of children with arterial ischaemic stroke. They had similar clinical presentations to those without cardiac disorders but differed in age and headache prevalence. Children with cardiac disorders more frequently had a ‘cardioembolic stroke pattern’ with a higher prevalence of bilateral strokes in both the anterior and posterior circulations, and a greater tendency to haemorrhagic transformation.</p></div></div>
]]></content:encoded><description>

Background and hypothesis
The aetiologies of arterial ischaemic stroke in children are diverse and often multifactorial. A large proportion occurs in children with cardiac disorders. We hypothesized that the clinical and radiographic features of children with arterial ischaemic stroke attributed to cardiac disorders would differ from those with other causes.


Methods
Using the large population collected in the prospective International Paediatric Stroke Study, we analysed the characteristics, clinical presentations, imaging findings, and early outcomes of children with and without cardiac disorders.


Results
Aetiological data were available for 667 children with arterial ischaemic stroke (ages 29 days to 19 years). Cardiac disorders were indentified in 204/667 (30·6%), congenital defects in 121/204 (59·3%), acquired in 40/204 (19·6%), and isolated patent foramen ovale in 31/204 (15·2%). Compared to other children with stroke, those with cardiac disorders were younger (median age 3·1 vs. 6·5 years; P &lt; 0·001) and less likely to present with headache (25·6% vs. 44·6%; P &lt; 0·001), but were similar in terms of gender and presentation with focal deficits, seizures, or recent infection. Analysis of imaging data identified significant differences (P = 0·005) in the vascular distribution (anterior vs. posterior circulation or both) between groups. Bilateral strokes and haemorrhagic conversion were more prevalent in the cardiac disorders group.


Conclusions
Cardiac disorders were identified in almost one-third of children with arterial ischaemic stroke. They had similar clinical presentations to those without cardiac disorders but differed in age and headache prevalence. Children with cardiac disorders more frequently had a ‘cardioembolic stroke pattern’ with a higher prevalence of bilateral strokes in both the anterior and posterior circulations, and a greater tendency to haemorrhagic transformation.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00947.x" xmlns="http://purl.org/rss/1.0/"><title>Characteristics of cerebral ischemia in major rat stroke models of middle cerebral artery ligation through craniectomy</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00947.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Characteristics of cerebral ischemia in major rat stroke models of middle cerebral artery ligation through craniectomy</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Alexey Shmonin, Elena Melnikova, Michael Galagudza, Timur Vlasov</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-04T04:10:41.806035-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00947.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00947.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00947.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs947-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The refinement of experimental stroke models is important for further development of neuroprotective interventions.</p></div></div>
<div class="section" id="ijs947-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims and/or hypothesis</h4><div class="para"><p>Our goal was to study the reproducibility of outcomes obtained in five rat models of middle cerebral artery (MCA) ligation in order to identify the optimal model for the preclinical studies.</p></div></div>
<div class="section" id="ijs947-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>In Part 1 of the experiments, systolic blood flow velocity (sBFV) and cerebral area at risk (AR) were determined immediately after the onset of brain ischemia induced in different ways in Wistar rats. After that, another set of experiments was performed (Part 2 of the experiments), now aimed at the assessment of the delayed outcome of five different models of cerebral ischemia designated as Versions 1–5.</p></div><div class="para"><p>The versions were: Version 1 – 40-minute left MCA (LMCA) occlusion with reperfusion; Version 2 – permanent LMCA ligation; Version 3 – permanent ligation of both LMCA and left common carotid artery (CCA); Version 4 – permanent LMCA and bilateral CCA (bCCA) ligation; Version 5 – permanent LMCA ligation and 40-minute bCCA occlusion. The infarct size (IS) was quantified using triphenyltetrazolium chloride staining. The severity of neurological deficit was assessed by the Garcia score. The extent of brain edema was determined by calculating the difference in volumes of affected and contralateral hemispheres.</p></div></div>
<div class="section" id="ijs947-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Within a relatively big AR, Versions 1 and 2 resulted in a small IS [0·2 (0·0; 0·4)% and 0·3 (0·0; 0·7)%, respectively, <em>P</em> &gt; 0·05]. Unlike that and comparable with AR, Version 3 resulted in a greater, albeit more variable IS [5·9 (2·1; 8·3)%, <em>P</em> &lt; 0·0001 vs. Version 2]. Also comparable with AR, Versions 4 and 5 produced greatest values of IS [14·5 (11·4; 17·9)% and 11·3 (10·1; 14·2)%, respectively]; this parameter was most reproducible in Version 5. A significant decrease in neurological deficit score was found in Versions 4 and 5. Again, the reproducibility of the data on neurological outcome was higher in Version 5 versus Version 4.</p></div></div>
<div class="section" id="ijs947-sec-0006" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Comparative analysis of several Versions of focal cerebral ischemia within a single study might be helpful in better understanding of the mechanisms underlying the development and aftermath of stroke. Permanent LMCA ligation plus transient bilateral CCA occlusion produced most consistent results and might be recommended for preclinical studies.</p></div></div>
]]></content:encoded><description>

Background
The refinement of experimental stroke models is important for further development of neuroprotective interventions.


Aims and/or hypothesis
Our goal was to study the reproducibility of outcomes obtained in five rat models of middle cerebral artery (MCA) ligation in order to identify the optimal model for the preclinical studies.


Methods
In Part 1 of the experiments, systolic blood flow velocity (sBFV) and cerebral area at risk (AR) were determined immediately after the onset of brain ischemia induced in different ways in Wistar rats. After that, another set of experiments was performed (Part 2 of the experiments), now aimed at the assessment of the delayed outcome of five different models of cerebral ischemia designated as Versions 1–5.
The versions were: Version 1 – 40-minute left MCA (LMCA) occlusion with reperfusion; Version 2 – permanent LMCA ligation; Version 3 – permanent ligation of both LMCA and left common carotid artery (CCA); Version 4 – permanent LMCA and bilateral CCA (bCCA) ligation; Version 5 – permanent LMCA ligation and 40-minute bCCA occlusion. The infarct size (IS) was quantified using triphenyltetrazolium chloride staining. The severity of neurological deficit was assessed by the Garcia score. The extent of brain edema was determined by calculating the difference in volumes of affected and contralateral hemispheres.


Results
Within a relatively big AR, Versions 1 and 2 resulted in a small IS [0·2 (0·0; 0·4)% and 0·3 (0·0; 0·7)%, respectively, P &gt; 0·05]. Unlike that and comparable with AR, Version 3 resulted in a greater, albeit more variable IS [5·9 (2·1; 8·3)%, P &lt; 0·0001 vs. Version 2]. Also comparable with AR, Versions 4 and 5 produced greatest values of IS [14·5 (11·4; 17·9)% and 11·3 (10·1; 14·2)%, respectively]; this parameter was most reproducible in Version 5. A significant decrease in neurological deficit score was found in Versions 4 and 5. Again, the reproducibility of the data on neurological outcome was higher in Version 5 versus Version 4.


Conclusions
Comparative analysis of several Versions of focal cerebral ischemia within a single study might be helpful in better understanding of the mechanisms underlying the development and aftermath of stroke. Permanent LMCA ligation plus transient bilateral CCA occlusion produced most consistent results and might be recommended for preclinical studies.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00928.x" xmlns="http://purl.org/rss/1.0/"><title>Multifactorial vascular risk factor intervention to prevent cognitive impairment after stroke and TIA: a 12-month randomized controlled trial</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00928.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Multifactorial vascular risk factor intervention to prevent cognitive impairment after stroke and TIA: a 12-month randomized controlled trial</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hege Ihle-Hansen, Bente Thommessen, Morten W. Fagerland, Anne R. Øksengård, Torgeir B. Wyller, Knut Engedal, Brynjar Fure</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-04T04:10:37.749979-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00928.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00928.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00928.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs928-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Objectives</h4><div class="para"><p>Vascular risk factor control may not only prevent stroke but also reduce the risk of dementia. We investigated whether a multifactorial intervention program reduces the incidence of cognitive symptoms one-year after stroke and transient ischemic attack in first ever stroke patients without cognitive decline prior to the stroke.</p></div></div>
<div class="section" id="ijs928-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Materials and methods</h4><div class="para"><p>Patients suffering their first ever stroke were included in this randomized, evaluator-blinded, controlled trial with two parallel groups. Baseline examination included extensive assessment of exposure to vascular risk factors and cognitive assessments regarding memory, attention, and executive function. After discharge, patients were allocated to either intensive vascular risk factor intervention or care as usual. The primary end points were changes in trailmaking test A and 10-word test from baseline to 12 months follow-up.</p></div></div>
<div class="section" id="ijs928-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>One hundred ninety-five patients were randomized. The difference between groups in trail-making test A, adjusted for baseline measurements, was 3·8 s (95% confidence interval: −4·2 to 11·9; P = 0·35) in favor of the intervention group. The difference between groups in the 10-word recall test was 1·1 words (95% confidence interval: −0·5 to 2·7; P = 0·17) in favor of the intervention group. We did not observe any differences in the secondary outcomes of incident dementia or mild cognitive impairment.</p></div></div>
<div class="section" id="ijs928-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>We could not demonstrate cognitive effects of an intensive risk factor intervention at one-year poststroke. Longer follow-up and a more heterogeneous study sample might have lead to larger effects. More effective methods for managing the risk of further cognitive decline after stroke are needed.</p></div></div>
]]></content:encoded><description>

Objectives
Vascular risk factor control may not only prevent stroke but also reduce the risk of dementia. We investigated whether a multifactorial intervention program reduces the incidence of cognitive symptoms one-year after stroke and transient ischemic attack in first ever stroke patients without cognitive decline prior to the stroke.


Materials and methods
Patients suffering their first ever stroke were included in this randomized, evaluator-blinded, controlled trial with two parallel groups. Baseline examination included extensive assessment of exposure to vascular risk factors and cognitive assessments regarding memory, attention, and executive function. After discharge, patients were allocated to either intensive vascular risk factor intervention or care as usual. The primary end points were changes in trailmaking test A and 10-word test from baseline to 12 months follow-up.


Results
One hundred ninety-five patients were randomized. The difference between groups in trail-making test A, adjusted for baseline measurements, was 3·8 s (95% confidence interval: −4·2 to 11·9; P = 0·35) in favor of the intervention group. The difference between groups in the 10-word recall test was 1·1 words (95% confidence interval: −0·5 to 2·7; P = 0·17) in favor of the intervention group. We did not observe any differences in the secondary outcomes of incident dementia or mild cognitive impairment.


Conclusions
We could not demonstrate cognitive effects of an intensive risk factor intervention at one-year poststroke. Longer follow-up and a more heterogeneous study sample might have lead to larger effects. More effective methods for managing the risk of further cognitive decline after stroke are needed.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00924.x" xmlns="http://purl.org/rss/1.0/"><title>The influence of bolus to infusion delays on plasma Tissue Plasminogen Activator levels</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00924.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The influence of bolus to infusion delays on plasma Tissue Plasminogen Activator levels</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Curtis Smith, Yusur Al-Nuaimi, Jane Wainwright, Charles Sherrington, Arun Singh, Jouher Kallingal, Christopher Douglass, Adrian Parry-Jones, Craig Smith, Anand Dixit, Arshad Majid</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-04T04:10:26.725216-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00924.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00924.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00924.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Short report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs924-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Estimates of neuronal loss in acute ischemic stroke show that the typical patient may lose 1·9 million neurons each minute that treatment is delayed. Consequently, significant emphasis has been placed on early evaluation and thrombolysis with tissue plasminogen activator (TPA), the only approved thrombolytic therapy. TPA should be administered as a bolus followed by an immediate infusion because of its short half life. However, in the real life clinical situation, delays in starting the infusion after the bolus can occur. Similarly, once infusion has started, interruptions in the infusion of TPA can also occur. These scenarios may result in lower serum concentrations which could decrease the effectiveness of thrombolysis. We sought to simulate, the influence of bolus infusion delays and also the influence of different intervals of interruptions in the infusion of TPA on serum TPA concentrations.</p></div></div>
<div class="section" id="ijs924-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We simulated the effect of multiple intervals of delay after the bolus on serum TPA concentrations using known pharmacokinetics parameters of TPA. The effect of different intervals of interruptions in the infusion of TPA was also determined. The effect of rebolusing with TPA on serum concentrations in the event of significant bolus to infusion delays or significant infusion interruption was also simulated.</p></div></div>
<div class="section" id="ijs924-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Our data show that delays in starting the infusion may have significant effects on serum TPA concentrations. After the initial bolus, there is a rapid decrease in serum TPA concentrations unless the infusion is started immediately. Greater than 5 min delays in starting the infusion results in a slow gradual increase in serum TPA levels and levels stay well below the target concentrations for significant periods of time. Similarly, interruptions in the infusion of TPA lasting longer than 5 min can also significantly influence TPA levels. Rebolusing with TPA in these scenarios rapidly restores TPA levels to target concentrations.</p></div></div>
<div class="section" id="ijs924-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Because of its short half life, TPA should be administered as a bolus followed by an immediate infusion. Bolus to infusion delays or interruptions in the infusion of TPA after the bolus may significantly impact serum TPA levels and may reduce the efficacy of thrombolysis. Protocols or administration regimens should be employed to prevent delays or interruptions in the infusion. When delays do occur, rebolusing of TPA may be needed to rapidly restore TPA to target levels.</p></div></div>
]]></content:encoded><description>

Background
Estimates of neuronal loss in acute ischemic stroke show that the typical patient may lose 1·9 million neurons each minute that treatment is delayed. Consequently, significant emphasis has been placed on early evaluation and thrombolysis with tissue plasminogen activator (TPA), the only approved thrombolytic therapy. TPA should be administered as a bolus followed by an immediate infusion because of its short half life. However, in the real life clinical situation, delays in starting the infusion after the bolus can occur. Similarly, once infusion has started, interruptions in the infusion of TPA can also occur. These scenarios may result in lower serum concentrations which could decrease the effectiveness of thrombolysis. We sought to simulate, the influence of bolus infusion delays and also the influence of different intervals of interruptions in the infusion of TPA on serum TPA concentrations.


Methods
We simulated the effect of multiple intervals of delay after the bolus on serum TPA concentrations using known pharmacokinetics parameters of TPA. The effect of different intervals of interruptions in the infusion of TPA was also determined. The effect of rebolusing with TPA on serum concentrations in the event of significant bolus to infusion delays or significant infusion interruption was also simulated.


Results
Our data show that delays in starting the infusion may have significant effects on serum TPA concentrations. After the initial bolus, there is a rapid decrease in serum TPA concentrations unless the infusion is started immediately. Greater than 5 min delays in starting the infusion results in a slow gradual increase in serum TPA levels and levels stay well below the target concentrations for significant periods of time. Similarly, interruptions in the infusion of TPA lasting longer than 5 min can also significantly influence TPA levels. Rebolusing with TPA in these scenarios rapidly restores TPA levels to target concentrations.


Conclusion
Because of its short half life, TPA should be administered as a bolus followed by an immediate infusion. Bolus to infusion delays or interruptions in the infusion of TPA after the bolus may significantly impact serum TPA levels and may reduce the efficacy of thrombolysis. Protocols or administration regimens should be employed to prevent delays or interruptions in the infusion. When delays do occur, rebolusing of TPA may be needed to rapidly restore TPA to target levels.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00856.x" xmlns="http://purl.org/rss/1.0/"><title>SOLITAIRE™ with the intention for thrombectomy (SWIFT) trial: design of a randomized, controlled, multicenter study comparing the SOLITAIRE™ Flow Restoration device and the MERCI Retriever in acute ischaemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00856.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">SOLITAIRE™ with the intention for thrombectomy (SWIFT) trial: design of a randomized, controlled, multicenter study comparing the SOLITAIRE™ Flow Restoration device and the MERCI Retriever in acute ischaemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">J. L. Saver, R. Jahan, E. I. Levy, T. G. Jovin, B. Baxter, R. Nogueira, W. Clark, R. Budzik, O. O. Zaidat, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-11-06T22:38:02.768359-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00856.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00856.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00856.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocol</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs856-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale </h4><div class="para"><p>Self-expanding stent retrievers are a promising new device class designed for rapid flow restoration in acute cerebral ischaemia. The SOLITAIRE™ Flow Restoration device (SOLITAIRE) has shown high rates of recanalization in preclinical models and in uncontrolled clinical series.</p></div></div>
<div class="section" id="ijs856-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims </h4><div class="para"><p>(1) To demonstrate non-inferiority of SOLITAIRE compared with a legally marketed device, the MERCI Retrieval System®; (2) To demonstrate safety, feasibility, and efficacy of SOLITAIRE in subjects requiring mechanical thrombectomy diagnosed with acute ischaemic stroke.</p></div></div>
<div class="section" id="ijs856-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design </h4><div class="para"><p>Multicenter, randomized, prospective, controlled trial with blinded primary end-point ascertainment.</p></div></div>
<div class="section" id="ijs856-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study Procedures </h4><div class="para"><p>Key entry criteria include: age 22–85; National Institute of Health Stroke Scale (NIHSS) ≥8 and &lt;30; clinical and imaging findings consistent with acute ischaemic stroke; patient ineligible or failed intravenous tissue plasminogen activator; accessible occlusion in M1 or M2 middle cerebral artery, internal carotid artery, basilar artery, or vertebral artery; and patient able to be treated within 8 h of onset. Sites first participate in a roll-in phase, treating two patients with the SOLITAIRE device, before proceeding to the randomized phase. In patients unresponsive to the initially assigned therapy, after the angiographic component of the primary end-point is ascertained (reperfusion with the initial assigned device), rescue therapy with other reperfusion techniques is permitted.</p></div></div>
<div class="section" id="ijs856-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Outcomes </h4><div class="para"><p>The primary efficacy end-point is successful recanalization with the assigned study device (no use of rescue therapy) and with no symptomatic intracranial haemorrhage. Successful recanalization is defined as achieving Thrombolysis In Myocardial Ischemia 2 or 3 flow in all treatable vessels. The primary safety end-point is the incidence of device-related and procedure-related serious adverse events. A major secondary efficacy end-point is time to achieve initial recanalization. Additional secondary end-points include clinical outcomes at 90 days and radiologic haemorrhagic transformation.</p></div></div>
]]></content:encoded><description>

Rationale 
Self-expanding stent retrievers are a promising new device class designed for rapid flow restoration in acute cerebral ischaemia. The SOLITAIRE™ Flow Restoration device (SOLITAIRE) has shown high rates of recanalization in preclinical models and in uncontrolled clinical series.


Aims 
(1) To demonstrate non-inferiority of SOLITAIRE compared with a legally marketed device, the MERCI Retrieval System®; (2) To demonstrate safety, feasibility, and efficacy of SOLITAIRE in subjects requiring mechanical thrombectomy diagnosed with acute ischaemic stroke.


Design 
Multicenter, randomized, prospective, controlled trial with blinded primary end-point ascertainment.


Study Procedures 
Key entry criteria include: age 22–85; National Institute of Health Stroke Scale (NIHSS) ≥8 and &lt;30; clinical and imaging findings consistent with acute ischaemic stroke; patient ineligible or failed intravenous tissue plasminogen activator; accessible occlusion in M1 or M2 middle cerebral artery, internal carotid artery, basilar artery, or vertebral artery; and patient able to be treated within 8 h of onset. Sites first participate in a roll-in phase, treating two patients with the SOLITAIRE device, before proceeding to the randomized phase. In patients unresponsive to the initially assigned therapy, after the angiographic component of the primary end-point is ascertained (reperfusion with the initial assigned device), rescue therapy with other reperfusion techniques is permitted.


Outcomes 
The primary efficacy end-point is successful recanalization with the assigned study device (no use of rescue therapy) and with no symptomatic intracranial haemorrhage. Successful recanalization is defined as achieving Thrombolysis In Myocardial Ischemia 2 or 3 flow in all treatable vessels. The primary safety end-point is the incidence of device-related and procedure-related serious adverse events. A major secondary efficacy end-point is time to achieve initial recanalization. Additional secondary end-points include clinical outcomes at 90 days and radiologic haemorrhagic transformation.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00930.x" xmlns="http://purl.org/rss/1.0/"><title>Secondary prevention of stroke in Saskatchewan, Canada: hypertension control</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00930.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Secondary prevention of stroke in Saskatchewan, Canada: hypertension control</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Janelle Ann Bartsch, Gary F. Teare, Anne Neufeld, Nedeene Hudema, Nazeem Muhajarine</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-10-23T04:05:56.225977-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00930.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00930.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00930.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs930-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>In the province of Saskatchewan, Canada, stroke is the third leading cause of death as well as the major cause of adult disability. Once a person suffers a stroke or transient ischemic attack (TIA), they are at high risk for having a secondary stroke. Hypertension (elevated blood pressure) is the single most important modifiable risk factor for both first and recurrent stroke, and is thus an important risk factor to be controlled. According to the Canadian Stroke Strategy (CSS) Best Practice Recommendations, blood pressure lowering treatment should be initiated before discharge from hospital for all stroke/TIA patients. The purpose of this study was to examine the quality of medically driven secondary stroke prevention care in Saskatchewan as applied to hypertension control.</p></div></div>
<div class="section" id="ijs930-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The objectives of the study were to: (1) develop methodology and calculate a secondary stroke process of care measure using available data in Saskatchewan, based on an appropriate hypertension therapy indicator recommendation from the CSS Performance Measurement Manual; (2) examine variation in secondary stroke prevention hypertensive care among the Saskatchewan Regional Health Authorities; and (3) investigate factors associated with receiving evidence-based hypertensive secondary stroke prevention.</p></div></div>
<div class="section" id="ijs930-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>This multi-year cross-sectional study was an analysis of deidentified health data derived from linkage of administrative health data. A select indicator from the CSS Performance Measurement Manual that measures adherence to a CSS Best Practice Guidelines concerning use of antihypertensive medications for secondary stroke prevention was calculated. Logistic regression was used to quantify the association of patient demographic and socioeconomic characteristics and geographic location of care with receipt of guideline-recommended hypertensive secondary stroke prevention. The target population was all Saskatchewan residents who were hospitalized in Saskatchewan for a stroke or TIA between April 1, 2001 and March 31, 2008.</p></div></div>
<div class="section" id="ijs930-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The results of this study indicate that the management of hypertension for secondary stroke prevention is sub-optimal in Saskatchewan. Although there was some improvement over the time period, approximately 40% of patients were not taking antihypertensives at 90 days after discharge from acute care. The correlates, urban/non-urban, previous use of antihypertensive drugs and effect of age modified by sex, were found to be significantly associated with receiving hypertensive secondary stroke prevention, suggesting there are modifiable factors that contribute to variations in this form of secondary stroke care quality in Saskatchewan.</p></div></div>
<div class="section" id="ijs930-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The results of this study suggest that there is a need for province-wide improvement to secondary stroke prevention in Saskatchewan, Canada.</p></div></div>
]]></content:encoded><description>

Background
In the province of Saskatchewan, Canada, stroke is the third leading cause of death as well as the major cause of adult disability. Once a person suffers a stroke or transient ischemic attack (TIA), they are at high risk for having a secondary stroke. Hypertension (elevated blood pressure) is the single most important modifiable risk factor for both first and recurrent stroke, and is thus an important risk factor to be controlled. According to the Canadian Stroke Strategy (CSS) Best Practice Recommendations, blood pressure lowering treatment should be initiated before discharge from hospital for all stroke/TIA patients. The purpose of this study was to examine the quality of medically driven secondary stroke prevention care in Saskatchewan as applied to hypertension control.


Aims
The objectives of the study were to: (1) develop methodology and calculate a secondary stroke process of care measure using available data in Saskatchewan, based on an appropriate hypertension therapy indicator recommendation from the CSS Performance Measurement Manual; (2) examine variation in secondary stroke prevention hypertensive care among the Saskatchewan Regional Health Authorities; and (3) investigate factors associated with receiving evidence-based hypertensive secondary stroke prevention.


Methods
This multi-year cross-sectional study was an analysis of deidentified health data derived from linkage of administrative health data. A select indicator from the CSS Performance Measurement Manual that measures adherence to a CSS Best Practice Guidelines concerning use of antihypertensive medications for secondary stroke prevention was calculated. Logistic regression was used to quantify the association of patient demographic and socioeconomic characteristics and geographic location of care with receipt of guideline-recommended hypertensive secondary stroke prevention. The target population was all Saskatchewan residents who were hospitalized in Saskatchewan for a stroke or TIA between April 1, 2001 and March 31, 2008.


Results
The results of this study indicate that the management of hypertension for secondary stroke prevention is sub-optimal in Saskatchewan. Although there was some improvement over the time period, approximately 40% of patients were not taking antihypertensives at 90 days after discharge from acute care. The correlates, urban/non-urban, previous use of antihypertensive drugs and effect of age modified by sex, were found to be significantly associated with receiving hypertensive secondary stroke prevention, suggesting there are modifiable factors that contribute to variations in this form of secondary stroke care quality in Saskatchewan.


Conclusions
The results of this study suggest that there is a need for province-wide improvement to secondary stroke prevention in Saskatchewan, Canada.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00922.x" xmlns="http://purl.org/rss/1.0/"><title>Impact of collateral circulation on early outcome and risk of hemorrhagic complications after systemic thrombolysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00922.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Impact of collateral circulation on early outcome and risk of hemorrhagic complications after systemic thrombolysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Freimuth Brunner, Bernd Tomandl, Katrin Hanken, Helmut Hildebrandt, Andreas Kastrup</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-10-23T04:05:53.362697-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00922.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00922.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00922.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs922-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>In stroke patients, collateral flow can rapidly be assessed on computed tomography angiography (CTA).</p></div></div>
<div class="section" id="ijs922-sec-1001" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>In this study, the impact of baseline collaterals on early outcome and risk of symptomatic intracerebral hemorrhages after systemic thrombolysis in patients with proximal arterial occlusions within the anterior circulation were analyzed.</p></div></div>
<div class="section" id="ijs922-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Collateralization scores were determined on the CT angiography source images (0 = absent; 1 ≤ 50%, 2 &gt; 50% but &lt;100%, and 3 = 100% collateral filling) of patients with distal intracranial carotid artery and/or M1 segment occlusions treated from 2008 to December 2011. A collateral score of 0 to 1 was designated as poor and 2 to 3 as good collateral vessel status. Outcome variables included in hospital mortality, favorable outcome at discharge (modified Rankin score ≤ 2), and rates of symptomatic intracerebral hemorrhage based on the European–Australasian Acute Stroke Study II definition.</p></div></div>
<div class="section" id="ijs922-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Among 246 subjects (mean age of 74 years; median National Institutes of Health Stroke Scale N at admission 14), 205 patients (83%) had good collaterals, whereas 41 patients (17%) had poor collaterals, respectively. Patients with poor collaterals had significantly higher rates of in-hospital mortality (41% vs. 12%, <em>P</em> &lt; 0·001), of symptomatic intracerebral hemorrhage (15% vs. 4·9%, <em>P</em> &lt; 0·05) and had significantly lower rates of favorable early clinical outcome (0% vs. 28%, <em>P</em> &lt; 0·001) compared with those with good collaterals. The grade of collateralization was independently associated with in-hospital mortality (<em>P</em> &lt; 0·001), early clinical outcome (<em>P</em> &lt; 0·01), and rates of symptomatic intracerebral hemorrhage (<em>P</em> &lt; 0·01).</p></div></div>
<div class="section" id="ijs922-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Patients with proximal arterial occlusions within the anterior circulation and poor baseline collaterals have a poor early functional outcome and high rates of symptomatic intracerebral hemorrhage after systemic thrombolysis. Since similar findings have also been reported after endovascular therapy, strategies to improve collateral blood flow should be assessed in this patient population.</p></div></div>
]]></content:encoded><description>

Background
In stroke patients, collateral flow can rapidly be assessed on computed tomography angiography (CTA).

 Aims
In this study, the impact of baseline collaterals on early outcome and risk of symptomatic intracerebral hemorrhages after systemic thrombolysis in patients with proximal arterial occlusions within the anterior circulation were analyzed.

 Methods
Collateralization scores were determined on the CT angiography source images (0 = absent; 1 ≤ 50%, 2 &gt; 50% but &lt;100%, and 3 = 100% collateral filling) of patients with distal intracranial carotid artery and/or M1 segment occlusions treated from 2008 to December 2011. A collateral score of 0 to 1 was designated as poor and 2 to 3 as good collateral vessel status. Outcome variables included in hospital mortality, favorable outcome at discharge (modified Rankin score ≤ 2), and rates of symptomatic intracerebral hemorrhage based on the European–Australasian Acute Stroke Study II definition.


Results
Among 246 subjects (mean age of 74 years; median National Institutes of Health Stroke Scale N at admission 14), 205 patients (83%) had good collaterals, whereas 41 patients (17%) had poor collaterals, respectively. Patients with poor collaterals had significantly higher rates of in-hospital mortality (41% vs. 12%, P &lt; 0·001), of symptomatic intracerebral hemorrhage (15% vs. 4·9%, P &lt; 0·05) and had significantly lower rates of favorable early clinical outcome (0% vs. 28%, P &lt; 0·001) compared with those with good collaterals. The grade of collateralization was independently associated with in-hospital mortality (P &lt; 0·001), early clinical outcome (P &lt; 0·01), and rates of symptomatic intracerebral hemorrhage (P &lt; 0·01).


Conclusion
Patients with proximal arterial occlusions within the anterior circulation and poor baseline collaterals have a poor early functional outcome and high rates of symptomatic intracerebral hemorrhage after systemic thrombolysis. Since similar findings have also been reported after endovascular therapy, strategies to improve collateral blood flow should be assessed in this patient population.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00920.x" xmlns="http://purl.org/rss/1.0/"><title>A prospective test of the late effects of potentially antineuroplastic drugs in a stroke rehabilitation study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00920.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A prospective test of the late effects of potentially antineuroplastic drugs in a stroke rehabilitation study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Stephen E. Nadeau, Xiaomin Lu, Bruce Dobkin, Samuel S. Wu, Yunfeng E. Dai, Pamela W. Duncan, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-10-23T04:05:48.754989-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00920.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00920.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00920.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs920-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Extensive data, primarily from animal studies, suggest that several classes of drugs may have antineuroplastic effects that could impede recovery from brain injury or reduce the efficacy of rehabilitation.</p></div></div>
<div class="section" id="ijs920-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The Locomotor Experience Applied Post-Stroke trial, a randomized controlled study of 408 subjects that tested the relative efficacy of two rehabilitation techniques on functional walking level at one-year poststroke, provided us the opportunity to prospectively assess the potential antineuroplastic effects of several classes of drug.</p></div></div>
<div class="section" id="ijs920-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Subjects were randomized to receive one of the two rehabilitation therapies at two-months poststroke. Drugs taken were recorded at time of randomization. Outcome was assessed at one-year poststroke. Regression models were used to determine the amount of variance in success in improving functional walking level, gains in walking speed, and declines in lower extremity, upper extremity, and cognitive impairment accounted for by <em>α</em>1 noradrenergic blockers + <em>α</em>2 noradrenergic agonists, benzodiazepines, voltage-sensitive sodium channel anticonvulsants, and <em>α</em>2<em>δ</em> voltage-sensitive calcium channel blockers.</p></div></div>
<div class="section" id="ijs920-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The maximum variance accounted for by any drug class was 1·66%. Drug effects were not statistically significant when using even our most lenient standard for correction for multiple comparisons.</p></div></div>
<div class="section" id="ijs920-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Drugs in the classes we were able to assess do not appear to exert a clinically important effect on outcome over the period between two- and 12 months poststroke. However, the potential antineuroplastic effects of certain drugs remain an incompletely settled scientific question.</p></div></div>
]]></content:encoded><description>

Background
Extensive data, primarily from animal studies, suggest that several classes of drugs may have antineuroplastic effects that could impede recovery from brain injury or reduce the efficacy of rehabilitation.


Aims
The Locomotor Experience Applied Post-Stroke trial, a randomized controlled study of 408 subjects that tested the relative efficacy of two rehabilitation techniques on functional walking level at one-year poststroke, provided us the opportunity to prospectively assess the potential antineuroplastic effects of several classes of drug.


Methods
Subjects were randomized to receive one of the two rehabilitation therapies at two-months poststroke. Drugs taken were recorded at time of randomization. Outcome was assessed at one-year poststroke. Regression models were used to determine the amount of variance in success in improving functional walking level, gains in walking speed, and declines in lower extremity, upper extremity, and cognitive impairment accounted for by α1 noradrenergic blockers + α2 noradrenergic agonists, benzodiazepines, voltage-sensitive sodium channel anticonvulsants, and α2δ voltage-sensitive calcium channel blockers.


Results
The maximum variance accounted for by any drug class was 1·66%. Drug effects were not statistically significant when using even our most lenient standard for correction for multiple comparisons.


Conclusions
Drugs in the classes we were able to assess do not appear to exert a clinically important effect on outcome over the period between two- and 12 months poststroke. However, the potential antineuroplastic effects of certain drugs remain an incompletely settled scientific question.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00915.x" xmlns="http://purl.org/rss/1.0/"><title>Illustrating problems faced by stroke researchers: a review of cluster-randomized controlled trials</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00915.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Illustrating problems faced by stroke researchers: a review of cluster-randomized controlled trials</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Christopher J. Sutton, Caroline L. Watkins, Paola Dey</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-10-23T04:05:44.932679-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00915.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00915.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00915.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>The cluster-randomized controlled trial is a design increasingly used in prevention and health care evaluation studies and is highly relevant to stroke research. However, there are methodological issues that make it complex to implement. These are not always fully appreciated, with reviews continuing to reveal deficiencies. We searched PUBMED and CENTRAL databases to March 31, 2011 for cluster-randomized controlled trials in stroke. Two investigators independently reviewed citations for eligibility and extracted data on key aspects of each trial. Fifteen trials met the eligibility criteria. No trial fully met CONSORT cluster-randomized controlled trial guidelines, although good design and reporting practice were usually present. Twelve trials included the term ‘cluster-randomized’ (or ‘group-randomized’) in the title, and 12 trials stated the intraclass correlation coefficient used to plan the number of clusters and cluster size. However, few provided a clear, evidence-based justification for the choice of intraclass correlation coefficient, and only two-thirds reported the intraclass correlation coefficient for primary outcomes. Several trials appeared underpowered because of problems in determining an appropriate sample size, defining appropriate clusters, and recruiting and retaining clusters and patients. Cluster-randomized controlled trials are difficult to design and perform due to the combination of methodological and practical difficulties. It is important that further improvements are made to reporting cluster-randomized trials and intraclass correlation coefficients should be estimated using a standardized approach and reported consistently; this would be beneficial for stroke researchers when designing future cluster-randomized trials.</p></div>
]]></content:encoded><description>
The cluster-randomized controlled trial is a design increasingly used in prevention and health care evaluation studies and is highly relevant to stroke research. However, there are methodological issues that make it complex to implement. These are not always fully appreciated, with reviews continuing to reveal deficiencies. We searched PUBMED and CENTRAL databases to March 31, 2011 for cluster-randomized controlled trials in stroke. Two investigators independently reviewed citations for eligibility and extracted data on key aspects of each trial. Fifteen trials met the eligibility criteria. No trial fully met CONSORT cluster-randomized controlled trial guidelines, although good design and reporting practice were usually present. Twelve trials included the term ‘cluster-randomized’ (or ‘group-randomized’) in the title, and 12 trials stated the intraclass correlation coefficient used to plan the number of clusters and cluster size. However, few provided a clear, evidence-based justification for the choice of intraclass correlation coefficient, and only two-thirds reported the intraclass correlation coefficient for primary outcomes. Several trials appeared underpowered because of problems in determining an appropriate sample size, defining appropriate clusters, and recruiting and retaining clusters and patients. Cluster-randomized controlled trials are difficult to design and perform due to the combination of methodological and practical difficulties. It is important that further improvements are made to reporting cluster-randomized trials and intraclass correlation coefficients should be estimated using a standardized approach and reported consistently; this would be beneficial for stroke researchers when designing future cluster-randomized trials.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00881.x" xmlns="http://purl.org/rss/1.0/"><title>The Alberta Stroke Prevention in TIAs and mild strokes (ASPIRE) intervention: rationale and design for evaluating the implementation of a province-wide TIA Triaging system</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00881.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The Alberta Stroke Prevention in TIAs and mild strokes (ASPIRE) intervention: rationale and design for evaluating the implementation of a province-wide TIA Triaging system</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Thomas Jeerakathil, Ashfaq Shuaib, Sumit R. Majumdar, Andrew M. Demchuk, Kenneth S. Butcher, Tim J. Watson, Naeem Dean, Deb Gordon, Cathy Edmond, Shelagh B. Coutts, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-10-23T04:05:41.362342-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00881.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00881.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00881.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs881-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Stroke risk after transient ischaemic attack is high and, it is a challenge worldwide to provide urgent assessment and preventive services to entire populations.</p></div></div>
<div class="section" id="ijs881-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>To determine whether a province-wide transient ischaemic attack Triaging algorithm and transient ischaemic attack hotline (the Alberta Stroke Prevention in transient ischaemic attacks and mild strokes intervention) can reduce the rate of stroke recurrence following transient ischaemic attack across the population of Alberta, Canada (population 3·7 million, 90-day rate of post-stroke transient ischaemic attack currently 9·5%). It also seeks to improve upon current transient ischaemic attack triaging rules by incorporating time from symptom onset as a predictive variable.</p></div></div>
<div class="section" id="ijs881-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>The transient ischaemic attack algorithm and hotline were developed with a broad consensus of clinicians, patients, policy-makers, and researchers and based on local adaptation of the work of others and research and insights developed within the province. Because neither patient-level nor region-level randomization was possible, we conducted a quasi-experimental design examining changes in the post-transient ischaemic attack rate of stroke recurrence before and after the 15-month implementation period using an interrupted time-series regression analysis. The design controls for changes in case-mix, co-interventions, and secular trends. A prospective transient ischaemic attack cohort will also be concurrently created with telephone follow-up at seven-days and 90 days as well as passive follow-up over the longer term using linkages to provincial healthcare administrative databases.</p></div></div>
<div class="section" id="ijs881-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study Outcomes</h4><div class="para"><p>The primary outcome measure is the change in recurrence rate of stroke following transient ischaemic attack at seven-days and 90 days, comparing a period of two-years before vs. two-years after the intervention is implemented. All cases of recurrent stroke will be validated. Secondary outcomes include functional status, hospitalizations, morbidity, and mortality.</p></div></div>
<div class="section" id="ijs881-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>We are undertaking a rigorous evaluation of a population-based approach to improving quality of transient ischaemic attack care. Whether positive or negative, our work should provide important insights for all potential stakeholders.</p></div></div>
]]></content:encoded><description>

Rationale
Stroke risk after transient ischaemic attack is high and, it is a challenge worldwide to provide urgent assessment and preventive services to entire populations.


Aims
To determine whether a province-wide transient ischaemic attack Triaging algorithm and transient ischaemic attack hotline (the Alberta Stroke Prevention in transient ischaemic attacks and mild strokes intervention) can reduce the rate of stroke recurrence following transient ischaemic attack across the population of Alberta, Canada (population 3·7 million, 90-day rate of post-stroke transient ischaemic attack currently 9·5%). It also seeks to improve upon current transient ischaemic attack triaging rules by incorporating time from symptom onset as a predictive variable.


Design
The transient ischaemic attack algorithm and hotline were developed with a broad consensus of clinicians, patients, policy-makers, and researchers and based on local adaptation of the work of others and research and insights developed within the province. Because neither patient-level nor region-level randomization was possible, we conducted a quasi-experimental design examining changes in the post-transient ischaemic attack rate of stroke recurrence before and after the 15-month implementation period using an interrupted time-series regression analysis. The design controls for changes in case-mix, co-interventions, and secular trends. A prospective transient ischaemic attack cohort will also be concurrently created with telephone follow-up at seven-days and 90 days as well as passive follow-up over the longer term using linkages to provincial healthcare administrative databases.


Study Outcomes
The primary outcome measure is the change in recurrence rate of stroke following transient ischaemic attack at seven-days and 90 days, comparing a period of two-years before vs. two-years after the intervention is implemented. All cases of recurrent stroke will be validated. Secondary outcomes include functional status, hospitalizations, morbidity, and mortality.


Conclusions
We are undertaking a rigorous evaluation of a population-based approach to improving quality of transient ischaemic attack care. Whether positive or negative, our work should provide important insights for all potential stakeholders.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00863.x" xmlns="http://purl.org/rss/1.0/"><title>Use of nonsteroidal anti-inflammatory drugs among healthy people and specific cerebrovascular safety</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00863.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Use of nonsteroidal anti-inflammatory drugs among healthy people and specific cerebrovascular safety</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Emil L. Fosbøl, Anne-Marie Schjerning Olsen, Jonas Bjerring Olesen, Charlotte Andersson, Lars Kober, Christian Torp-Pedersen, Gunnar H. Gislason</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-10-23T04:05:38.704747-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00863.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00863.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00863.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Short Report</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs863-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Nonsteroidal anti-inflammatory drugs can increase bleeding and thrombosis, but little is known about the cerebrovascular safety of these drugs, especially among healthy people.</p></div></div>
<div class="section" id="ijs863-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The aim of this study was to examine the risk of ischemic and hemorrhagic stroke associated with the use of nonsteroidal anti-inflammatory drugs in healthy people.</p></div></div>
<div class="section" id="ijs863-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>By individual-level linkage of nationwide administrative registers in Denmark, information on hospital admissions, prescription claims, vital status, and cause of death were obtained. A cohort of healthy people without hospital admissions for five-years and no important prescription claims for two-years was selected. Case crossover and Cox proportional hazard models were used to analyze the relationship between nonsteroidal anti-inflammatory drug utilization and specific cerebrovascular risk (fatal or non-fatal ischemic or hemorrhagic stroke).</p></div></div>
<div class="section" id="ijs863-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>We selected 1 028 437 healthy individuals (median age 39 years). At least one nonsteroidal anti-inflammatory drug was claimed by 44·7% of the study population, and the drugs were generally used for a short period of time and in low doses. High-dose ibuprofen and diclofenac were associated with increased risk of ischemic stroke [hazard ratio 2·15 (95% confidence interval 1·66–2·79) and 2·37 (confidence interval 1·99–2·81), respectively]. Diclofenac was also associated with increased risk of hemorrhagic stroke and so was naproxen [hazard ratio 2·15 (confidence interval 1·35–3·42)].</p></div></div>
<div class="section" id="ijs863-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>In healthy individuals, use of commonly available nonsteroidal anti-inflammatory drugs such as ibuprofen, diclofenac, and naproxen was associated with increased risk of stroke.</p></div></div>
]]></content:encoded><description>

Background
Nonsteroidal anti-inflammatory drugs can increase bleeding and thrombosis, but little is known about the cerebrovascular safety of these drugs, especially among healthy people.


Aims
The aim of this study was to examine the risk of ischemic and hemorrhagic stroke associated with the use of nonsteroidal anti-inflammatory drugs in healthy people.


Methods
By individual-level linkage of nationwide administrative registers in Denmark, information on hospital admissions, prescription claims, vital status, and cause of death were obtained. A cohort of healthy people without hospital admissions for five-years and no important prescription claims for two-years was selected. Case crossover and Cox proportional hazard models were used to analyze the relationship between nonsteroidal anti-inflammatory drug utilization and specific cerebrovascular risk (fatal or non-fatal ischemic or hemorrhagic stroke).


Results
We selected 1 028 437 healthy individuals (median age 39 years). At least one nonsteroidal anti-inflammatory drug was claimed by 44·7% of the study population, and the drugs were generally used for a short period of time and in low doses. High-dose ibuprofen and diclofenac were associated with increased risk of ischemic stroke [hazard ratio 2·15 (95% confidence interval 1·66–2·79) and 2·37 (confidence interval 1·99–2·81), respectively]. Diclofenac was also associated with increased risk of hemorrhagic stroke and so was naproxen [hazard ratio 2·15 (confidence interval 1·35–3·42)].


Conclusions
In healthy individuals, use of commonly available nonsteroidal anti-inflammatory drugs such as ibuprofen, diclofenac, and naproxen was associated with increased risk of stroke.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00860.x" xmlns="http://purl.org/rss/1.0/"><title>Improvement in stroke risk prediction: role of C-reactive protein and lipoprotein-associated phospholipase A2 in the women's health initiative</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00860.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Improvement in stroke risk prediction: role of C-reactive protein and lipoprotein-associated phospholipase A2 in the women's health initiative</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sylvia Wassertheil-Smoller, Aileen McGinn, Matthew Allison, Tianxi Ca, David Curb, Charles Eaton, Susan Hendrix, Robert Kaplan, Marcia Ko, Lisa W. Martin, Xiaonan Xue</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-10-23T04:05:33.917706-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00860.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00860.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00860.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs860-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and Purpose</h4><div class="para"><p>Classification of risk of ischemic stroke is important for medical care and public health reasons. Whether addition of biomarkers adds to predictive power of the Framingham Stroke Risk or other traditional risk factors has not been studied in older women.</p></div></div>
<div class="section" id="ijs860-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The Hormones and Biomarkers Predicting Stroke Study is a case-control study of blood biomarkers assayed in 972 ischemic stroke cases and 972 controls, nested in the Women's Health Initiative Observational Study of 93 676 postmenopausal women followed for an average of eight-years. We evaluated additive predictive value of two commercially available biomarkers: C-reactive protein and lipoprotein-associated phospholipase A<sub>2</sub> to determine if they added to risk prediction by the Framingham Stroke Risk Score or by traditional risk factors, which included lipids and other variables not included in the Framingham Stroke Risk Score. As measures of additive predictive value, we used the C-statistic, net reclassification improvement, category-less net reclassification improvement, and integrated discrimination improvement index.</p></div></div>
<div class="section" id="ijs860-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Addition of C-reactive protein to Framingham risk models or additional traditional risk factors overall modestly improved prediction of ischemic stroke and resulted in overall net reclassification improvement of 6·3%, (case net reclassification improvement = 3·9%, control net reclassification improvement = 2·4%). In particular, high-sensitivity C-reactive protein was useful in prediction of cardioembolic strokes (net reclassification improvement = 12·0%; 95% confidence interval 4·3–19·6%) and in strokes occurring in less than three-years (net reclassification improvement = 7·9%, 95% confidence interval 0·8–14·9%). Lipoprotein-associated phospholipase A<sub>2</sub> was useful in risk prediction of large artery strokes (net reclassification improvement = 19·8%, 95% confidence interval 7·4−32·1%) and in early strokes (net reclassification improvement = 5·8%, 95% confidence interval 0·4–11·2%).</p></div></div>
<div class="section" id="ijs860-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>C-reactive protein and lipoprotein-associated phospholipase A<sub>2</sub> can improve prediction of certain subtypes of ischemic stroke in older women, over the Framingham stroke risk model and traditional risk factors, and may help to guide surveillance and treatment of women at risk.</p></div></div>
]]></content:encoded><description>

Background and Purpose
Classification of risk of ischemic stroke is important for medical care and public health reasons. Whether addition of biomarkers adds to predictive power of the Framingham Stroke Risk or other traditional risk factors has not been studied in older women.


Methods
The Hormones and Biomarkers Predicting Stroke Study is a case-control study of blood biomarkers assayed in 972 ischemic stroke cases and 972 controls, nested in the Women's Health Initiative Observational Study of 93 676 postmenopausal women followed for an average of eight-years. We evaluated additive predictive value of two commercially available biomarkers: C-reactive protein and lipoprotein-associated phospholipase A2 to determine if they added to risk prediction by the Framingham Stroke Risk Score or by traditional risk factors, which included lipids and other variables not included in the Framingham Stroke Risk Score. As measures of additive predictive value, we used the C-statistic, net reclassification improvement, category-less net reclassification improvement, and integrated discrimination improvement index.


Results
Addition of C-reactive protein to Framingham risk models or additional traditional risk factors overall modestly improved prediction of ischemic stroke and resulted in overall net reclassification improvement of 6·3%, (case net reclassification improvement = 3·9%, control net reclassification improvement = 2·4%). In particular, high-sensitivity C-reactive protein was useful in prediction of cardioembolic strokes (net reclassification improvement = 12·0%; 95% confidence interval 4·3–19·6%) and in strokes occurring in less than three-years (net reclassification improvement = 7·9%, 95% confidence interval 0·8–14·9%). Lipoprotein-associated phospholipase A2 was useful in risk prediction of large artery strokes (net reclassification improvement = 19·8%, 95% confidence interval 7·4−32·1%) and in early strokes (net reclassification improvement = 5·8%, 95% confidence interval 0·4–11·2%).


Conclusions
C-reactive protein and lipoprotein-associated phospholipase A2 can improve prediction of certain subtypes of ischemic stroke in older women, over the Framingham stroke risk model and traditional risk factors, and may help to guide surveillance and treatment of women at risk.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00913.x" xmlns="http://purl.org/rss/1.0/"><title>ImProving Outcomes after STroke (POST): results from the randomized clinical pilot trial</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00913.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">ImProving Outcomes after STroke (POST): results from the randomized clinical pilot trial</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Maree L. Hackett, Greg Carter, Denis Crimmins, Tracy Clarke, Lucy Arblaster, Laurent Billot, Jayanthi Mysore, Jonathan Sturm</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-10-18T01:58:27.386932-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00913.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00913.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00913.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs913-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>One in three patients experience depression after stroke. An effective strategy to prevent depression after stroke that could be economically delivered to most patients with a low likelihood of adverse events is needed.</p></div></div>
<div class="section" id="ijs913-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>In a randomized trial conducted in New South Wales, Australia, a postcard was sent monthly to participants (<em>n</em> = 100) for five-months following hospital discharge after stroke (plus usual care) and compared with usual care (<em>n</em> = 101). Ethical approval was obtained to withhold information about the intervention and primary outcome from participants during the consent process.</p></div></div>
<div class="section" id="ijs913-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>No significant difference was seen in the proportion of participants with depression in the intervention group (1/88) vs. the control group (3/76) (relative risk 0·29, 95% confidence interval 0·03–2·71) at six-months. No significant differences were seen on Hospital Anxiety Depression Scale (HADS) depression and anxiety sub-scale scores, quality of life, or activities of daily living; however, many (47/100) responded positively to the postcards.</p></div></div>
<div class="section" id="ijs913-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Although this simple postcard intervention did not significantly reduce the proportion of participants experiencing high HADS depression sub-scale scores after stroke, it may be an effective way to engage with people after stroke following hospital discharge.</p></div></div>
]]></content:encoded><description>

Background
One in three patients experience depression after stroke. An effective strategy to prevent depression after stroke that could be economically delivered to most patients with a low likelihood of adverse events is needed.


Methods
In a randomized trial conducted in New South Wales, Australia, a postcard was sent monthly to participants (n = 100) for five-months following hospital discharge after stroke (plus usual care) and compared with usual care (n = 101). Ethical approval was obtained to withhold information about the intervention and primary outcome from participants during the consent process.


Results
No significant difference was seen in the proportion of participants with depression in the intervention group (1/88) vs. the control group (3/76) (relative risk 0·29, 95% confidence interval 0·03–2·71) at six-months. No significant differences were seen on Hospital Anxiety Depression Scale (HADS) depression and anxiety sub-scale scores, quality of life, or activities of daily living; however, many (47/100) responded positively to the postcards.


Conclusions
Although this simple postcard intervention did not significantly reduce the proportion of participants experiencing high HADS depression sub-scale scores after stroke, it may be an effective way to engage with people after stroke following hospital discharge.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00919.x" xmlns="http://purl.org/rss/1.0/"><title>Thromboelastography in patients with acute ischemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00919.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Thromboelastography in patients with acute ischemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Andrea Elliott, Jeremy Wetzel, Tiffany Roper, Evan Pivalizza, James McCarthy, Cristina Wallace, Mary Jane Hess, Hui Peng, Mohammad H. Rahbar, Navdeep Sangha, James C. Grotta</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:33:58.400939-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00919.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00919.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00919.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs919-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Thromboelastography measures the dynamics of coagulation. There are limited data about thromboelastography in acute ischemic stroke other than a single study from 1974 suggesting that acute ischemic stroke patients are hypercoagulable. There have been no studies of thromboelastography in the thrombolytic era despite its potential usefulness as a measure of clot lysis. This study was designed to provide initial thromboelastography data in stroke patients before and after tissue plasminogen activator therapy and to provide the necessary preliminary data for further study of thromboelastography's ability to identify clot subtype and predict response to tissue plasminogen activator therapy.</p></div></div>
<div class="section" id="ijs919-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>All acute ischemic stroke patients presenting between 11/2009 and 2/2011 eligible for tissue plasminogen activator therapy were screened and 56 enrolled. Blood was drawn before (52 patients) and 10 mins after tissue plasminogen activator bolus (30 patients). Demographics, vitals, labs, 24 h National Institutes of Health Stroke Scale, and computed tomography scan results were collected. Patients were compared with normal controls.</p></div></div>
<div class="section" id="ijs919-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Acute ischemic stroke patients had shorter R (4·8 ± 1·5 vs. 6·0 ± 1·7 min, <em>P</em> = 0·0004), greater <em>α</em> Angle (65·0 ± 7·6 vs. 61·5 ± 5·9°, <em>P</em> = 0·01), and shorter K (1·7 ± 0·7 vs. 2·1 ± 0·7 min, <em>P</em> = 0·002) indicating faster clotting. Additionally, a subset formed clots with stronger platelet-fibrin matrices. Treatment with tissue plasminogen activator resulted in reduction in all indices of clot strength (LY30 = 0 (0–0·4) vs. 94·4 (15·2–95·3) <em>P</em> &lt; 0·0001); however, there was considerable variability in response.</p></div></div>
<div class="section" id="ijs919-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Thromboelastography demonstrates that many acute ischemic stroke patients are hypercoaguable. Thromboelastography values reflect variable clot subtype and response to tissue plasminogen activator. Further study based on these data will determine if thromboelastography is useful for measuring the dynamic aspects of clot formation and monitoring lytic therapy.</p></div></div>
]]></content:encoded><description>

Background
Thromboelastography measures the dynamics of coagulation. There are limited data about thromboelastography in acute ischemic stroke other than a single study from 1974 suggesting that acute ischemic stroke patients are hypercoagulable. There have been no studies of thromboelastography in the thrombolytic era despite its potential usefulness as a measure of clot lysis. This study was designed to provide initial thromboelastography data in stroke patients before and after tissue plasminogen activator therapy and to provide the necessary preliminary data for further study of thromboelastography's ability to identify clot subtype and predict response to tissue plasminogen activator therapy.


Methods
All acute ischemic stroke patients presenting between 11/2009 and 2/2011 eligible for tissue plasminogen activator therapy were screened and 56 enrolled. Blood was drawn before (52 patients) and 10 mins after tissue plasminogen activator bolus (30 patients). Demographics, vitals, labs, 24 h National Institutes of Health Stroke Scale, and computed tomography scan results were collected. Patients were compared with normal controls.


Results
Acute ischemic stroke patients had shorter R (4·8 ± 1·5 vs. 6·0 ± 1·7 min, P = 0·0004), greater α Angle (65·0 ± 7·6 vs. 61·5 ± 5·9°, P = 0·01), and shorter K (1·7 ± 0·7 vs. 2·1 ± 0·7 min, P = 0·002) indicating faster clotting. Additionally, a subset formed clots with stronger platelet-fibrin matrices. Treatment with tissue plasminogen activator resulted in reduction in all indices of clot strength (LY30 = 0 (0–0·4) vs. 94·4 (15·2–95·3) P &lt; 0·0001); however, there was considerable variability in response.


Conclusions
Thromboelastography demonstrates that many acute ischemic stroke patients are hypercoaguable. Thromboelastography values reflect variable clot subtype and response to tissue plasminogen activator. Further study based on these data will determine if thromboelastography is useful for measuring the dynamic aspects of clot formation and monitoring lytic therapy.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00918.x" xmlns="http://purl.org/rss/1.0/"><title>Intravenous alteplase versus rescue endovascular procedure in patients with proximal middle cerebral artery occlusion</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00918.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Intravenous alteplase versus rescue endovascular procedure in patients with proximal middle cerebral artery occlusion</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Daniel Strbian, Satu Mustanoja, Johanna Pekkola, Jukka Putaala, Elena Haapaniemi, Tapio Paananen, Markku Kaste, Kimmo Lappalainen, Turgut Tatlisumak</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:33:07.811771-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00918.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00918.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00918.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs918-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Objectives</h4><div class="para"><p>To compare outcome of ischaemic stroke patients undergoing rescue endovascular procedure for proximal middle cerebral artery occlusion with matched patients without endovascular procedure after unsuccessful intravenous thrombolysis.</p></div></div>
<div class="section" id="ijs918-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Endovascularly treated patients with middle cerebral artery occlusion (<em>n</em> = 41) were matched by propensity score with similar patients treated by intravenous thrombolysis and having a considerable post-thrombolysis neurological deficit (<em>n</em> = 82). We compared their three-month outcome (modified Rankin Scale) and frequency of symptomatic intracerebral haemorrhage. For the endovascular group, we report onset-to-puncture time, onset-to-recanalization time, and recanalization rates.</p></div></div>
<div class="section" id="ijs918-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>In age, gender, time from onset, admission National Institutes of Health Stroke Scale, systolic and diastolic blood pressure, blood glucose, history of hypertension, diabetes mellitus, hyperlipidaemia, atrial fibrillation, and congestive heart failure, and in aetiology, the groups were similar. Endovascular group patients had a recanalization rate of 90%, and more often reached three-month modified Rankin Scale 0–2 (36·6% vs. 18·3%, <em>P</em> = 0·03). Mortality was equally common (19·5%) in both groups, and frequency of symptomatic intracerebral haemorrhage was 9·8% vs. 14·6% (<em>P</em> = 0·45). The endovascular group's median onset-to-puncture time was four-hours and six-minutes and onset-to-recanalization time was five-hours and 12 min. The latter time was more than one-hour longer in patients treated under general anaesthesia compared with patients treated under conscious sedation (median four-hours 50 min vs. five-hours 58 min; <em>P</em> &lt; 0·01).</p></div></div>
<div class="section" id="ijs918-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Rescue endovascular approach increases likelihood of recanalization and may improve functional outcome in acute ischaemic stroke patients with proximal middle cerebral artery occlusion who did not respond to intravenous thrombolysis.</p></div></div>
]]></content:encoded><description>

Objectives
To compare outcome of ischaemic stroke patients undergoing rescue endovascular procedure for proximal middle cerebral artery occlusion with matched patients without endovascular procedure after unsuccessful intravenous thrombolysis.


Methods
Endovascularly treated patients with middle cerebral artery occlusion (n = 41) were matched by propensity score with similar patients treated by intravenous thrombolysis and having a considerable post-thrombolysis neurological deficit (n = 82). We compared their three-month outcome (modified Rankin Scale) and frequency of symptomatic intracerebral haemorrhage. For the endovascular group, we report onset-to-puncture time, onset-to-recanalization time, and recanalization rates.


Results
In age, gender, time from onset, admission National Institutes of Health Stroke Scale, systolic and diastolic blood pressure, blood glucose, history of hypertension, diabetes mellitus, hyperlipidaemia, atrial fibrillation, and congestive heart failure, and in aetiology, the groups were similar. Endovascular group patients had a recanalization rate of 90%, and more often reached three-month modified Rankin Scale 0–2 (36·6% vs. 18·3%, P = 0·03). Mortality was equally common (19·5%) in both groups, and frequency of symptomatic intracerebral haemorrhage was 9·8% vs. 14·6% (P = 0·45). The endovascular group's median onset-to-puncture time was four-hours and six-minutes and onset-to-recanalization time was five-hours and 12 min. The latter time was more than one-hour longer in patients treated under general anaesthesia compared with patients treated under conscious sedation (median four-hours 50 min vs. five-hours 58 min; P &lt; 0·01).


Conclusions
Rescue endovascular approach increases likelihood of recanalization and may improve functional outcome in acute ischaemic stroke patients with proximal middle cerebral artery occlusion who did not respond to intravenous thrombolysis.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00917.x" xmlns="http://purl.org/rss/1.0/"><title>Comparison of stroke warning sign campaigns in Australia, England, and Canada</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00917.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Comparison of stroke warning sign campaigns in Australia, England, and Canada</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kym Trobbiani, Kate Freeman, Manuel Arango, Erin Lalor, Damian Jenkinson, Amanda G. Thrift</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:32:49.648458-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00917.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00917.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00917.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs917-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Public awareness of the signs of stroke is essential to ensure that those affected by stroke arrive at the hospital in time for lifesaving therapies. It is unclear how well stroke awareness campaigns improve awareness of stroke signs and whether people translate this into action.</p></div></div>
<div class="section" id="ijs917-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We evaluated stroke awareness campaigns conducted in England, Australia, and Canada using pre- and post-campaign surveys. We assessed the proportion of people who could name the main signs of stroke, and compared the proportion naming these correctly between locations. We also assessed whether people would call emergency services in the event of a stroke. Proportion responding correctly was compared using chi-square analysis.</p></div></div>
<div class="section" id="ijs917-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The amount spent on the campaigns was different in each country. The post-campaign survey was conducted among 400 people in Australia, 1921 in England, and 2703 in Canada. Sixty-eight per cent of people in Australia and 57% in Canada could name two or more signs of stroke (<em>P</em> &lt; 0·001). After the campaign, knowledge of each of the elements of the campaign (face, arm, speech, time) was significantly greater in England than in Australia (<em>P</em> &lt; 0·001 for each item). A high proportion of participants reported that they would call emergency services in the event of a stroke (97% in England, 90% in Australia, and 67% in Canada).</p></div></div>
<div class="section" id="ijs917-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Knowledge of stroke signs and the action to be taken can be improved with awareness campaigns. The effectiveness of these campaigns may be enhanced by spend on media, media mix, and key messages. It is critical to ensure that campaigns provide the clear and bold message that prompt action is an essential ingredient to reduce death and disability following stroke.</p></div></div>
]]></content:encoded><description>

Background
Public awareness of the signs of stroke is essential to ensure that those affected by stroke arrive at the hospital in time for lifesaving therapies. It is unclear how well stroke awareness campaigns improve awareness of stroke signs and whether people translate this into action.


Methods
We evaluated stroke awareness campaigns conducted in England, Australia, and Canada using pre- and post-campaign surveys. We assessed the proportion of people who could name the main signs of stroke, and compared the proportion naming these correctly between locations. We also assessed whether people would call emergency services in the event of a stroke. Proportion responding correctly was compared using chi-square analysis.


Results
The amount spent on the campaigns was different in each country. The post-campaign survey was conducted among 400 people in Australia, 1921 in England, and 2703 in Canada. Sixty-eight per cent of people in Australia and 57% in Canada could name two or more signs of stroke (P &lt; 0·001). After the campaign, knowledge of each of the elements of the campaign (face, arm, speech, time) was significantly greater in England than in Australia (P &lt; 0·001 for each item). A high proportion of participants reported that they would call emergency services in the event of a stroke (97% in England, 90% in Australia, and 67% in Canada).


Conclusion
Knowledge of stroke signs and the action to be taken can be improved with awareness campaigns. The effectiveness of these campaigns may be enhanced by spend on media, media mix, and key messages. It is critical to ensure that campaigns provide the clear and bold message that prompt action is an essential ingredient to reduce death and disability following stroke.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00916.x" xmlns="http://purl.org/rss/1.0/"><title>A comparative study of neuroprotective effect of single and combined blockade of AT1 receptor and PARP-1 in focal cerebral ischaemia in rat</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00916.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A comparative study of neuroprotective effect of single and combined blockade of AT1 receptor and PARP-1 in focal cerebral ischaemia in rat</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Neetu Singh, Gaurav Sharma, Nilendra Singh, Kashif Hanif</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:32:46.993053-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00916.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00916.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00916.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs916-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Cerebral ischaemia results in enhanced expression of type 1 angiotensin receptor and oxidative stress. Free radicals due to oxidative stress lead to excessive DNA damage causing overactivation of poly (ADP-ribose) polymerase-1 resulting in neuronal death. Activation of both type 1 angiotensin receptors and poly (ADP-ribose) polymerase-1 following cerebral ischaemia takes place simultaneously, but until now, no study has explored the effect of combined blockade of both angiotensin type 1 angiotensin receptor and poly (ADP-ribose) polymerase-1 in cerebral ischaemia.</p></div></div>
<div class="section" id="ijs916-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>Our purpose was to compare the effect of single and combined treatment with angiotensin type 1 angiotensin receptor blocker, candesartan, and the poly (ADP-ribose) polymerase-1 inhibitor, 1, 5 isoquinolinediol, on brain damage and oxidative stress in transient focal cerebral ischaemia in rats.</p></div></div>
<div class="section" id="ijs916-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Method</h4><div class="para"><p>Transient focal cerebral ischaemia was induced in Sprague-Dawley rats by an intraluminal technique for two-hours following 48 h of reperfusion. Candesartan (0·05 mg/kg) was administered just after initiation of ischaemia followed by a repeat administration at 24 h while 1, 5 isoquinolinediol (0·1 mg/kg) was given one-hour after of ischaemia. After 24 h of reperfusion, neurological deficit was evaluated in the different treatment groups. After 48 h of reperfusion, the rats were sacrificed and the brain was isolated. Ischaemic brain damage by 2,3,5 triphenyl tetrazolium chloride staining, oxidative stress markers, and levels of reactive oxygen species were determined biochemically.</p></div></div>
<div class="section" id="ijs916-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Result</h4><div class="para"><p>Single treatment with candesartan and 1, 5 isoquinolinediol significantly reduced neurological deficit, infarct, and oedema volume as compared to ischaemic control and different vehicle groups for each of the drugs. However, treatment with candesartan + 1, 5 isoquinolinediol offered greater reduction in neurological deficit, cerebral infarct volume, and oedema as compared to single-drug treatments. Furthermore, treatment with candesartan + 1, 5 isoquinolinediol significantly decreased oxidative stress as compared to single treatments with each drug.</p></div></div>
<div class="section" id="ijs916-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>The study suggests that blockade of either type 1 angiotensin receptor or poly (ADP-ribose) polymerase-1 alone provides neuroprotection, but the better result was achieved when both type 1 angiotensin receptor and poly (ADP-ribose) polymerase-1 were blocked together by the combined use of their pharmacological inhibitor in transient cerebral ischaemia in rat.</p></div></div>
]]></content:encoded><description>

Background
Cerebral ischaemia results in enhanced expression of type 1 angiotensin receptor and oxidative stress. Free radicals due to oxidative stress lead to excessive DNA damage causing overactivation of poly (ADP-ribose) polymerase-1 resulting in neuronal death. Activation of both type 1 angiotensin receptors and poly (ADP-ribose) polymerase-1 following cerebral ischaemia takes place simultaneously, but until now, no study has explored the effect of combined blockade of both angiotensin type 1 angiotensin receptor and poly (ADP-ribose) polymerase-1 in cerebral ischaemia.


Aim
Our purpose was to compare the effect of single and combined treatment with angiotensin type 1 angiotensin receptor blocker, candesartan, and the poly (ADP-ribose) polymerase-1 inhibitor, 1, 5 isoquinolinediol, on brain damage and oxidative stress in transient focal cerebral ischaemia in rats.


Method
Transient focal cerebral ischaemia was induced in Sprague-Dawley rats by an intraluminal technique for two-hours following 48 h of reperfusion. Candesartan (0·05 mg/kg) was administered just after initiation of ischaemia followed by a repeat administration at 24 h while 1, 5 isoquinolinediol (0·1 mg/kg) was given one-hour after of ischaemia. After 24 h of reperfusion, neurological deficit was evaluated in the different treatment groups. After 48 h of reperfusion, the rats were sacrificed and the brain was isolated. Ischaemic brain damage by 2,3,5 triphenyl tetrazolium chloride staining, oxidative stress markers, and levels of reactive oxygen species were determined biochemically.


Result
Single treatment with candesartan and 1, 5 isoquinolinediol significantly reduced neurological deficit, infarct, and oedema volume as compared to ischaemic control and different vehicle groups for each of the drugs. However, treatment with candesartan + 1, 5 isoquinolinediol offered greater reduction in neurological deficit, cerebral infarct volume, and oedema as compared to single-drug treatments. Furthermore, treatment with candesartan + 1, 5 isoquinolinediol significantly decreased oxidative stress as compared to single treatments with each drug.


Conclusion
The study suggests that blockade of either type 1 angiotensin receptor or poly (ADP-ribose) polymerase-1 alone provides neuroprotection, but the better result was achieved when both type 1 angiotensin receptor and poly (ADP-ribose) polymerase-1 were blocked together by the combined use of their pharmacological inhibitor in transient cerebral ischaemia in rat.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00912.x" xmlns="http://purl.org/rss/1.0/"><title>Risk factors, radiological features, and infarct topography of craniocervical arterial dissection</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00912.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Risk factors, radiological features, and infarct topography of craniocervical arterial dissection</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lucy Caroline Thomas, Darren A. Rivett, Mark Parsons, Christopher Levi</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:32:43.857509-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00912.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00912.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00912.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs912-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Craniocervical arterial dissection is a common cause of ischemic stroke in the young to middle-aged population. There have been a number of previous studies where radiological features have been described but few with detailed mapping of infarct topography and none where these features have been related to the reported risk factors.</p></div></div>
<div class="section" id="ijs912-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The aims of this study were to describe the radiological characteristics of dissection patients ≤55 years and relate these to reported risk factors.</p></div></div>
<div class="section" id="ijs912-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Craniocervical arterial dissection cases ≤55 years, and age- and gender-matched controls were identified from a medical records database between 1998 and 2009. Control cases had stroke from another cause than dissection. Records and radiology were reviewed.</p></div></div>
<div class="section" id="ijs912-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Thirty-six radiologically confirmed dissection cases [20 (56%) vertebral artery, 16 (44%) internal carotid], and 43 controls were identified. Dissections were extracranial with intracranial extension in 10 (28%) cases. Infarction was demonstrated in 22 (61%) dissection cases. The most common wall deficit identified was an intimal flap. Twenty-three (64%) dissection cases had a recent history of neck trauma (<em>P</em> &gt; 0·000) and 13 (36%) had vascular variants (<em>P</em> = 0·013).</p></div></div>
<div class="section" id="ijs912-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Craniocervical arterial dissection cases, particularly vertebral artery, were more likely to have a history of neck trauma. Dissections were most commonly extracranial, in the upper cervical region, with intracranial extension in 28%. Dissection cases with trauma more commonly had a dissection flap and evidence of infarction in the lateral medulla, anterior or posterior inferior cerebellar artery territory. Close inspection of the V3 segment of the vertebral or skull base for internal carotid artery may be warranted with a history of neck trauma.</p></div></div>
]]></content:encoded><description>

Background
Craniocervical arterial dissection is a common cause of ischemic stroke in the young to middle-aged population. There have been a number of previous studies where radiological features have been described but few with detailed mapping of infarct topography and none where these features have been related to the reported risk factors.


Aims
The aims of this study were to describe the radiological characteristics of dissection patients ≤55 years and relate these to reported risk factors.


Methods
Craniocervical arterial dissection cases ≤55 years, and age- and gender-matched controls were identified from a medical records database between 1998 and 2009. Control cases had stroke from another cause than dissection. Records and radiology were reviewed.


Results
Thirty-six radiologically confirmed dissection cases [20 (56%) vertebral artery, 16 (44%) internal carotid], and 43 controls were identified. Dissections were extracranial with intracranial extension in 10 (28%) cases. Infarction was demonstrated in 22 (61%) dissection cases. The most common wall deficit identified was an intimal flap. Twenty-three (64%) dissection cases had a recent history of neck trauma (P &gt; 0·000) and 13 (36%) had vascular variants (P = 0·013).


Conclusion
Craniocervical arterial dissection cases, particularly vertebral artery, were more likely to have a history of neck trauma. Dissections were most commonly extracranial, in the upper cervical region, with intracranial extension in 28%. Dissection cases with trauma more commonly had a dissection flap and evidence of infarction in the lateral medulla, anterior or posterior inferior cerebellar artery territory. Close inspection of the V3 segment of the vertebral or skull base for internal carotid artery may be warranted with a history of neck trauma.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00906.x" xmlns="http://purl.org/rss/1.0/"><title>Frequency of anxiety after stroke: a systematic review and meta-analysis of observational studies</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00906.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Frequency of anxiety after stroke: a systematic review and meta-analysis of observational studies</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">C. Alexia Campbell Burton, Jenni Murray, John Holmes, Felicity Astin, Darren Greenwood, Peter Knapp</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:32:39.686802-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00906.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00906.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00906.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Systematic Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs906-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and purpose</h4><div class="para"><p>Negative psychological outcomes occur frequently after stroke; however, there is uncertainty regarding the occurrence of anxiety disorders and anxiety symptoms after stroke. A systematic review of observational studies was conducted that assessed the frequency of anxiety in stroke patients using a diagnostic or screening tool.</p></div></div>
<div class="section" id="ijs906-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Summary of review</h4><div class="para"><p>Databases were searched up to March 2011. A random effects model was used to summarize the pooled estimate. Statistical heterogeneity was assessed using the I<sup>2</sup> statistic. Forty-four published studies comprising 5760 stroke patients were included. The overall pooled estimate of anxiety disorders assessed by clinical interview was 18% (95%confidence interval 8–29%, I<sup>2</sup> = 97%) and was 25% (95% confidence interval 21–28%, I<sup>2</sup> = 90%) for anxiety assessed by rating scale. The Hospital Anxiety and Depression Scale-Anxiety subscale ‘probable’ and ‘possible’ cutoff scores were the most widely used assessment criteria. The combined rate of anxiety by time after stroke was: 20% (95% confidence interval 13–27%, I<sup>2</sup> = 96%) within one-month of stroke; 23% (95% confidence interval 19–27%, I<sup>2</sup> = 84%) one to five-months after stroke; and 24% (95% confidence interval 19–29%, I<sup>2</sup> = 89%) six-months or more after stroke.</p></div></div>
<div class="section" id="ijs906-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Anxiety after stroke occurs frequently although methodological limitations in the primary studies may limit generalizability. Given the association between prevalence rates and the Hospital Anxiety and Depression Scale-Anxiety cutoff used in studies, reported rates could in fact underrepresent the extent of the problem. Additionally, risk factors for anxiety, its impact on patient outcomes, and effects in tangent with depression remain unclear.</p></div></div>
]]></content:encoded><description>

Background and purpose
Negative psychological outcomes occur frequently after stroke; however, there is uncertainty regarding the occurrence of anxiety disorders and anxiety symptoms after stroke. A systematic review of observational studies was conducted that assessed the frequency of anxiety in stroke patients using a diagnostic or screening tool.


Summary of review
Databases were searched up to March 2011. A random effects model was used to summarize the pooled estimate. Statistical heterogeneity was assessed using the I2 statistic. Forty-four published studies comprising 5760 stroke patients were included. The overall pooled estimate of anxiety disorders assessed by clinical interview was 18% (95%confidence interval 8–29%, I2 = 97%) and was 25% (95% confidence interval 21–28%, I2 = 90%) for anxiety assessed by rating scale. The Hospital Anxiety and Depression Scale-Anxiety subscale ‘probable’ and ‘possible’ cutoff scores were the most widely used assessment criteria. The combined rate of anxiety by time after stroke was: 20% (95% confidence interval 13–27%, I2 = 96%) within one-month of stroke; 23% (95% confidence interval 19–27%, I2 = 84%) one to five-months after stroke; and 24% (95% confidence interval 19–29%, I2 = 89%) six-months or more after stroke.


Conclusion
Anxiety after stroke occurs frequently although methodological limitations in the primary studies may limit generalizability. Given the association between prevalence rates and the Hospital Anxiety and Depression Scale-Anxiety cutoff used in studies, reported rates could in fact underrepresent the extent of the problem. Additionally, risk factors for anxiety, its impact on patient outcomes, and effects in tangent with depression remain unclear.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00905.x" xmlns="http://purl.org/rss/1.0/"><title>Ischemic bowel disease and risk of stroke: a one-year follow-up study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00905.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Ischemic bowel disease and risk of stroke: a one-year follow-up study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jiunn-Horng Kang, Joseph J. Keller, Herng-Ching Lin</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:32:35.821178-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00905.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00905.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00905.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs905-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Ischemic bowel disease and stroke have been noted to have shared pathomechanisms. However, data regarding the stroke occurrence following ischemic bowel disease are still lacking.</p></div></div>
<div class="section" id="ijs905-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>The aim of this study is to explore the risk of stroke in patients with ischemic bowel disease during a one-year follow-up period in Taiwan.</p></div></div>
<div class="section" id="ijs905-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Data used in this study were retrieved from the ‘Longitudinal Health Insurance Database 2000. Five hundred sixty-nine patients hospitalized with ischemic bowel disease were included as the study group, and 3414 subjects, matched by age and gender, were randomly extracted as a comparison group. Cox proportional hazards regression analysis was performed to test the relationship of ischemic bowel disease and subsequent stroke during the one-year follow-up period.</p></div></div>
<div class="section" id="ijs905-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The incidence rate of stroke among the sampled subjects during the 30-day, 90-day, and 365-day follow-up period was 1·24, 0·76, and 0·43 per 10 person-years. The adjusted hazard ratio for stroke for those patients with ischemic bowel disease within 30-, 90-, and 365-day follow-up periods was found to be 3·71 (95% confidence interval = 1·89–7·27), 2·11 (95% confidence interval = 1·22–3·66), and 1·70 (95% confidence interval = 1·14–2·52) times that of matched comparisons, respectively. The adjusted hazard ratio of ischemic stroke for patients with ischemic bowel disease was found to be 5·29 during the 30-day follow-up period than comparisons.</p></div></div>
<div class="section" id="ijs905-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>We found ischemic bowel disease to be significantly associated with stroke occurrence.</p></div></div>
]]></content:encoded><description>

Background
Ischemic bowel disease and stroke have been noted to have shared pathomechanisms. However, data regarding the stroke occurrence following ischemic bowel disease are still lacking.


Aim
The aim of this study is to explore the risk of stroke in patients with ischemic bowel disease during a one-year follow-up period in Taiwan.


Methods
Data used in this study were retrieved from the ‘Longitudinal Health Insurance Database 2000. Five hundred sixty-nine patients hospitalized with ischemic bowel disease were included as the study group, and 3414 subjects, matched by age and gender, were randomly extracted as a comparison group. Cox proportional hazards regression analysis was performed to test the relationship of ischemic bowel disease and subsequent stroke during the one-year follow-up period.


Results
The incidence rate of stroke among the sampled subjects during the 30-day, 90-day, and 365-day follow-up period was 1·24, 0·76, and 0·43 per 10 person-years. The adjusted hazard ratio for stroke for those patients with ischemic bowel disease within 30-, 90-, and 365-day follow-up periods was found to be 3·71 (95% confidence interval = 1·89–7·27), 2·11 (95% confidence interval = 1·22–3·66), and 1·70 (95% confidence interval = 1·14–2·52) times that of matched comparisons, respectively. The adjusted hazard ratio of ischemic stroke for patients with ischemic bowel disease was found to be 5·29 during the 30-day follow-up period than comparisons.


Conclusions
We found ischemic bowel disease to be significantly associated with stroke occurrence.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00904.x" xmlns="http://purl.org/rss/1.0/"><title>Haemorrhagic transformation of ischaemic stroke in young adults</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00904.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Haemorrhagic transformation of ischaemic stroke in young adults</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Satu Mustanoja, Elena Haapaniemi, Jukka Putaala, Daniel Strbian, Markku Kaste, Turgut Tatlisumak</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:30:42.609284-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00904.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00904.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00904.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs904-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Frequency, factors associated with, and impact on outcome of haemorrhagic transformation in young adults with ischaemic stroke are unknown.</p></div></div>
<div class="section" id="ijs904-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Consecutive young patients (age 15–49) with first-ever ischaemic stroke were included, having their first brain computed tomography/magnetic resonance imaging within seven-days of stroke onset, and second within seven-days from the first imaging. Haemorrhagic transformation in any imaging was classified as haemorrhagic infarct or parenchymal haemorrhage within or remote from the infarct. Symptomatic haemorrhagic transformation was defined according to the European Cooperative Acute Stroke Study II (ECASS II) criteria as any haemorrhage leading to a National Institutes of Health Stroke Scale score increase of ≥4 points or death. Unfavourable three-month outcome was defined as a modified Rankin Scale 2–6.</p></div></div>
<div class="section" id="ijs904-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>In 636 eligible patients, any haemorrhagic transformation occurred in 79 patients (12·4%; 10·0–15·2%): 66 (10·4%; 8·24–12·9%) had haemorrhagic infarct, and 13 (2·04%; 1·19–3·46%) had parenchymal haemorrhage. Symptomatic haemorrhagic transformation occurred in 16 patients (2·5%; 4·04–1·55%). In logistic regression analysis, independent factors associated with haemorrhagic transformation were large anterior (18·70; 6·72–52·04), large posterior (9·41; 3·13–28·25), medium-sized (odds ratio 3·30; 95% confidence interval 1·14–9·57) lesions, higher low-density lipoprotein level (1·44 per unit increment; 1·10–1·90), and lower platelet count (1·005 per unit decrement; 1·009–1·001). Haemorrhagic infarct (1·76; 0·76–4·11) or parenchymal haemorrhage (2·39; 0·23–24·76) were not associated with unfavourable functional outcome or death at three-months.</p></div></div>
<div class="section" id="ijs904-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>In young adults, haemorrhagic transformation of ischaemic stroke occurred in comparable rates to haemorrhagic transformation in elderly patients. Although haemorrhagic transformation was more common in severe strokes, it was the lesion size and baseline stroke severity that were associated with three-month clinical outcome, not haemorrhagic transformation <em>per se</em>.</p></div></div>
]]></content:encoded><description>

Background
Frequency, factors associated with, and impact on outcome of haemorrhagic transformation in young adults with ischaemic stroke are unknown.


Methods
Consecutive young patients (age 15–49) with first-ever ischaemic stroke were included, having their first brain computed tomography/magnetic resonance imaging within seven-days of stroke onset, and second within seven-days from the first imaging. Haemorrhagic transformation in any imaging was classified as haemorrhagic infarct or parenchymal haemorrhage within or remote from the infarct. Symptomatic haemorrhagic transformation was defined according to the European Cooperative Acute Stroke Study II (ECASS II) criteria as any haemorrhage leading to a National Institutes of Health Stroke Scale score increase of ≥4 points or death. Unfavourable three-month outcome was defined as a modified Rankin Scale 2–6.


Results
In 636 eligible patients, any haemorrhagic transformation occurred in 79 patients (12·4%; 10·0–15·2%): 66 (10·4%; 8·24–12·9%) had haemorrhagic infarct, and 13 (2·04%; 1·19–3·46%) had parenchymal haemorrhage. Symptomatic haemorrhagic transformation occurred in 16 patients (2·5%; 4·04–1·55%). In logistic regression analysis, independent factors associated with haemorrhagic transformation were large anterior (18·70; 6·72–52·04), large posterior (9·41; 3·13–28·25), medium-sized (odds ratio 3·30; 95% confidence interval 1·14–9·57) lesions, higher low-density lipoprotein level (1·44 per unit increment; 1·10–1·90), and lower platelet count (1·005 per unit decrement; 1·009–1·001). Haemorrhagic infarct (1·76; 0·76–4·11) or parenchymal haemorrhage (2·39; 0·23–24·76) were not associated with unfavourable functional outcome or death at three-months.


Conclusions
In young adults, haemorrhagic transformation of ischaemic stroke occurred in comparable rates to haemorrhagic transformation in elderly patients. Although haemorrhagic transformation was more common in severe strokes, it was the lesion size and baseline stroke severity that were associated with three-month clinical outcome, not haemorrhagic transformation per se.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00903.x" xmlns="http://purl.org/rss/1.0/"><title>Stroke mortality variations in South-East Asia: empirical evidence from the field</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00903.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Stroke mortality variations in South-East Asia: empirical evidence from the field</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Damian G. Hoy, Chalapati Rao, Nguyen Phuong Hoa, S. Suhardi, Aye Moe Moe Lwin</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:30:37.387886-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00903.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00903.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00903.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs903-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Stroke is a leading cause of death in Asia; however, many estimates of stroke mortality are based on epidemiological models rather than empirical data. Since 2005, initiatives have been undertaken in a number of Asian countries to strengthen and analyse vital registration data. This has increased the availability of empirical data on stroke mortality.</p></div></div>
<div class="section" id="ijs903-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The aim of this paper is to present estimates of stroke mortality for Indonesia, Myanmar, Viet Nam, Thailand, and Malaysia, which have been derived using these empirical data.</p></div></div>
<div class="section" id="ijs903-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Age-specific stroke mortality rates were calculated in each of the five countries, and adjusted for data completeness or misclassification where feasible. All data were age-standardized and the resulting rates were compared with World Health Organization estimates, which are largely based on epidemiological models.</p></div></div>
<div class="section" id="ijs903-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Using empirical data, stroke ranked as the leading cause of death in all countries except Malaysia, where it ranked as the second leading cause. Age-standardized rates for males ranged from 94 per 100 000 in Thailand, to over 300 per 100 000 in Indonesia. In all countries, rates were higher for males than for females, and those compiled from empirical data were generally higher than modelled estimates published by World Health Organization.</p></div></div>
<div class="section" id="ijs903-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>This study highlights the extent of stroke mortality in selected Asian countries, and provides important baseline information to investigate the aetiology of stroke in Asia and design appropriate public health strategies to address the rapidly growing burden from stroke.</p></div></div>
]]></content:encoded><description>

Background
Stroke is a leading cause of death in Asia; however, many estimates of stroke mortality are based on epidemiological models rather than empirical data. Since 2005, initiatives have been undertaken in a number of Asian countries to strengthen and analyse vital registration data. This has increased the availability of empirical data on stroke mortality.


Aims
The aim of this paper is to present estimates of stroke mortality for Indonesia, Myanmar, Viet Nam, Thailand, and Malaysia, which have been derived using these empirical data.


Methods
Age-specific stroke mortality rates were calculated in each of the five countries, and adjusted for data completeness or misclassification where feasible. All data were age-standardized and the resulting rates were compared with World Health Organization estimates, which are largely based on epidemiological models.


Results
Using empirical data, stroke ranked as the leading cause of death in all countries except Malaysia, where it ranked as the second leading cause. Age-standardized rates for males ranged from 94 per 100 000 in Thailand, to over 300 per 100 000 in Indonesia. In all countries, rates were higher for males than for females, and those compiled from empirical data were generally higher than modelled estimates published by World Health Organization.


Conclusions
This study highlights the extent of stroke mortality in selected Asian countries, and provides important baseline information to investigate the aetiology of stroke in Asia and design appropriate public health strategies to address the rapidly growing burden from stroke.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00902.x" xmlns="http://purl.org/rss/1.0/"><title>Early ischaemic diffusion lesion reduction in patients treated with intravenous tissue plasminogen activator: infrequent, but significantly associated with recanalization</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00902.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Early ischaemic diffusion lesion reduction in patients treated with intravenous tissue plasminogen activator: infrequent, but significantly associated with recanalization</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yuki Sakamoto, Kazumi Kimura, Kensaku Shibazaki, Takeshi Inoue, Jyunichi Uemura, Junya Aoki, Kenichiro Sakai, Yasuyuki Iguchi</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:30:34.493517-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00902.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00902.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00902.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs902-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and purpose</h4><div class="para"><p>Recent studies have shown that thrombolysis could decrease or eliminate ischaemic diffusion-weighted imaging lesions. However, the features of such diffusion-weighted imaging lesion reduction are not well known.</p></div></div>
<div class="section" id="ijs902-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>To clarify, the frequency of and factors associated with lesion reduction were investigated.</p></div></div>
<div class="section" id="ijs902-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Patients given intravenous tissue plasminogen activator therapy within three-hours of onset were prospectively enrolled. Magnetic resonance imaging including diffusion-weighted imaging and magnetic resonance angiography was performed four times: on admission, just after intravenous tissue plasminogen activator, 24 h from intravenous tissue plasminogen activator, and seven-days after intravenous tissue plasminogen activator. The diffusion-weighted imaging lesion volume was measured by manual trace using National Institutes of Health imaging software. All patients were divided into three groups according to the early diffusion-weighted imaging lesion volume change from admission to just after intravenous tissue plasminogen activator: the lesion reduction group (&gt;20% decrease); the lesion growth group (&gt;20% increase); and the lesion unchanged group.</p></div></div>
<div class="section" id="ijs902-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>In total, 105 patients [56 males, median age 77 (interquartile range 70–83) years, and National Institutes of Health Stroke Scale score 16 (10–22)] were enrolled. Early diffusion-weighted imaging lesion reduction was observed in seven (7%) patients. The decreased lesion increased subsequently. On multivariate analysis, the glucose level on admission (odds ratio 0·95, 95% confidence interval 0·91 to 0·99, <em>P</em> = 0·045) and early recanalization (odds ratio 15·7, 95% confidence interval 1·61 to 153, <em>P</em> = 0·018) were independently related to early lesion reduction.</p></div></div>
<div class="section" id="ijs902-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Early diffusion-weighted imaging lesion reduction was observed in 7% of patients treated with intravenous tissue plasminogen activator. The decreased lesion increased subsequently. Initial glucose level and early recanalization were independently associated with early diffusion-weighted imaging lesion reduction.</p></div></div>
]]></content:encoded><description>

Background and purpose
Recent studies have shown that thrombolysis could decrease or eliminate ischaemic diffusion-weighted imaging lesions. However, the features of such diffusion-weighted imaging lesion reduction are not well known.


Aims
To clarify, the frequency of and factors associated with lesion reduction were investigated.


Methods
Patients given intravenous tissue plasminogen activator therapy within three-hours of onset were prospectively enrolled. Magnetic resonance imaging including diffusion-weighted imaging and magnetic resonance angiography was performed four times: on admission, just after intravenous tissue plasminogen activator, 24 h from intravenous tissue plasminogen activator, and seven-days after intravenous tissue plasminogen activator. The diffusion-weighted imaging lesion volume was measured by manual trace using National Institutes of Health imaging software. All patients were divided into three groups according to the early diffusion-weighted imaging lesion volume change from admission to just after intravenous tissue plasminogen activator: the lesion reduction group (&gt;20% decrease); the lesion growth group (&gt;20% increase); and the lesion unchanged group.


Results
In total, 105 patients [56 males, median age 77 (interquartile range 70–83) years, and National Institutes of Health Stroke Scale score 16 (10–22)] were enrolled. Early diffusion-weighted imaging lesion reduction was observed in seven (7%) patients. The decreased lesion increased subsequently. On multivariate analysis, the glucose level on admission (odds ratio 0·95, 95% confidence interval 0·91 to 0·99, P = 0·045) and early recanalization (odds ratio 15·7, 95% confidence interval 1·61 to 153, P = 0·018) were independently related to early lesion reduction.


Conclusion
Early diffusion-weighted imaging lesion reduction was observed in 7% of patients treated with intravenous tissue plasminogen activator. The decreased lesion increased subsequently. Initial glucose level and early recanalization were independently associated with early diffusion-weighted imaging lesion reduction.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00896.x" xmlns="http://purl.org/rss/1.0/"><title>NeuroThera® Efficacy and Safety Trial – 3 (NEST-3): a double-blind, randomized, sham-controlled, parallel group, multicenter, pivotal study to assess the safety and efficacy of transcranial laser therapy with the NeuroThera® Laser System for the treatment of acute ischemic stroke within 24 h of stroke onset</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00896.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">NeuroThera® Efficacy and Safety Trial – 3 (NEST-3): a double-blind, randomized, sham-controlled, parallel group, multicenter, pivotal study to assess the safety and efficacy of transcranial laser therapy with the NeuroThera® Laser System for the treatment of acute ischemic stroke within 24 h of stroke onset</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">J. A. Zivin, R. Sehra, A. Shoshoo, G. W. Albers, N. M. Bornstein, B. Dahlof, S. E. Kasner, G. Howard, A. Shuaib, J. Streeter, S. P. Richieri, W. Hacke, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:30:31.660236-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00896.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00896.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00896.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs896-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Transcranial laser therapy is undergoing clinical trials in patients with acute ischemic stroke. The NeuroThera<sup>®</sup> Efficacy and Safety Trial-1 was strongly positive for 90-day functional benefit with transcranial laser therapy, and post hoc analyses of the subsequent NeuroThera<sup>®</sup> Efficacy and Safety Trial-2 trial suggested a meaningful beneficial effect in patients with moderate to moderately severe ischemic stroke within 24 h of onset. These served as the basis for the NeuroThera<sup>®</sup> Efficacy and Safety Trial-3 randomized controlled trial.</p></div></div>
<div class="section" id="ijs896-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>The purpose of this pivotal study was to demonstrate safety and efficacy of transcranial laser therapy with the NeuroThera<sup>®</sup> Laser System in the treatment of subjects diagnosed with acute ischemic stroke.</p></div></div>
<div class="section" id="ijs896-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>NeuroThera<sup>®</sup> Efficacy and Safety Trial-3 is a double-blind, randomized, sham-controlled, parallel group, multicenter, pivotal study that will enroll 1000 subjects at up to 50 sites. All subjects will receive standard medical management based on the American Stroke Association and European Stroke Organization Guidelines. In addition to standard medical management, both groups will undergo the transcranial laser therapy procedure between 4·5 and 24 h of stroke onset. The study population will be randomized into two arms: the sham control group will receive a sham transcranial laser therapy procedure and the transcranial laser therapy group will receive an active transcranial laser therapy procedure. The randomization ratio will be 1:1 and will be stratified to ensure a balanced subject distribution between study arms.</p></div></div>
<div class="section" id="ijs896-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study Outcomes</h4><div class="para"><p>The primary efficacy end point is disability at 90 days (or the last rating), as assessed on the modified Rankin Scale, dichotomized as a success (a score of 0–2) or a failure (a score of 3 to 6).</p></div></div>
]]></content:encoded><description>

Rationale
Transcranial laser therapy is undergoing clinical trials in patients with acute ischemic stroke. The NeuroThera® Efficacy and Safety Trial-1 was strongly positive for 90-day functional benefit with transcranial laser therapy, and post hoc analyses of the subsequent NeuroThera® Efficacy and Safety Trial-2 trial suggested a meaningful beneficial effect in patients with moderate to moderately severe ischemic stroke within 24 h of onset. These served as the basis for the NeuroThera® Efficacy and Safety Trial-3 randomized controlled trial.


Aim
The purpose of this pivotal study was to demonstrate safety and efficacy of transcranial laser therapy with the NeuroThera® Laser System in the treatment of subjects diagnosed with acute ischemic stroke.


Design
NeuroThera® Efficacy and Safety Trial-3 is a double-blind, randomized, sham-controlled, parallel group, multicenter, pivotal study that will enroll 1000 subjects at up to 50 sites. All subjects will receive standard medical management based on the American Stroke Association and European Stroke Organization Guidelines. In addition to standard medical management, both groups will undergo the transcranial laser therapy procedure between 4·5 and 24 h of stroke onset. The study population will be randomized into two arms: the sham control group will receive a sham transcranial laser therapy procedure and the transcranial laser therapy group will receive an active transcranial laser therapy procedure. The randomization ratio will be 1:1 and will be stratified to ensure a balanced subject distribution between study arms.


Study Outcomes
The primary efficacy end point is disability at 90 days (or the last rating), as assessed on the modified Rankin Scale, dichotomized as a success (a score of 0–2) or a failure (a score of 3 to 6).

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00890.x" xmlns="http://purl.org/rss/1.0/"><title>Combined full-dose IV and endovascular thrombolysis in acute ischaemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00890.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Combined full-dose IV and endovascular thrombolysis in acute ischaemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Rohit Bhatia, Nandavar Shobha, Bijoy K. Menon, Simerpreet P. Bal, Puneet Kochar, Vanessa Palumbo, John H. Wong, William F. Morrish, Mark E. Hudon, William Hu, Shelagh B. Coutts, Phillip A. Barber, Tim Watson, Mayank Goyal, Andrew M. Demchuk, Michael D. Hill</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:29:20.099325-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00890.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00890.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00890.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Clinical Study</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs890-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>There is an increasing trend to treating proximal vessel occlusions with intravenous–inter-arterial (IV-IA) thrombolysis. The best dose of IV tissue plasminogen activator (tPA) remains undetermined. We compared the combination of full-dose IV recombinant tissue plasminogen activator (rtPA) and IA thrombolytic therapy to IA therapy.</p></div></div>
<div class="section" id="ijs890-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Between 2002 and 2009, we reviewed our computed tomographic angiography database for patients who received full-dose intravenous rtPA and endovascular therapy or endovascular therapy alone for acute ischaemic stroke treatment. Details of demographics, risk factors, endovascular procedure, and symptomatic intracranial haemorrhage were noted. Modified Rankin Scale ≤2 at three-months was used as good outcome. Recanalization was defined as Thrombolysis in Myocardial Ischaemia 2–3 flow on angiography.</p></div></div>
<div class="section" id="ijs890-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Among 157 patients, 104 patients received IV-IA treatment and 53 patients underwent direct IA therapy. There was a higher recanalization rate with IV-IA therapy compared with IA alone (71% vs. 60%, <em>P </em>&lt; 0·21) which was driven by early recanalization after IV rtPA. Mortality and independent outcome were comparable between the two groups. Symptomatic intracranial haemorrhage occurred in 8% of patients (12% in the IA group, 7% in the IV-IA group) but was more frequent as the intensity of intervention increased from device alone to thrombolytic drug alone to device plus thrombolytic drug(s). Recanalization was a strong predictor of reduced mortality risk ratio (RR) 0·48 confidence interval<sub>95</sub> 0·27–0·84) and favourable outcome (RR 2·14 confidence interval<sub>95</sub> 1·3–3·5).</p></div></div>
<div class="section" id="ijs890-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Combined IV-IA therapy with full-dose intravenous rtPA was safe and results in good recanalization rates without excess symptomatic intracranial haemorrhage. Testing of full-dose IV tPA followed by endovascular treatment in the IMS3 trial is justified.</p></div></div>
]]></content:encoded><description>

Background
There is an increasing trend to treating proximal vessel occlusions with intravenous–inter-arterial (IV-IA) thrombolysis. The best dose of IV tissue plasminogen activator (tPA) remains undetermined. We compared the combination of full-dose IV recombinant tissue plasminogen activator (rtPA) and IA thrombolytic therapy to IA therapy.


Methods
Between 2002 and 2009, we reviewed our computed tomographic angiography database for patients who received full-dose intravenous rtPA and endovascular therapy or endovascular therapy alone for acute ischaemic stroke treatment. Details of demographics, risk factors, endovascular procedure, and symptomatic intracranial haemorrhage were noted. Modified Rankin Scale ≤2 at three-months was used as good outcome. Recanalization was defined as Thrombolysis in Myocardial Ischaemia 2–3 flow on angiography.


Results
Among 157 patients, 104 patients received IV-IA treatment and 53 patients underwent direct IA therapy. There was a higher recanalization rate with IV-IA therapy compared with IA alone (71% vs. 60%, P &lt; 0·21) which was driven by early recanalization after IV rtPA. Mortality and independent outcome were comparable between the two groups. Symptomatic intracranial haemorrhage occurred in 8% of patients (12% in the IA group, 7% in the IV-IA group) but was more frequent as the intensity of intervention increased from device alone to thrombolytic drug alone to device plus thrombolytic drug(s). Recanalization was a strong predictor of reduced mortality risk ratio (RR) 0·48 confidence interval95 0·27–0·84) and favourable outcome (RR 2·14 confidence interval95 1·3–3·5).


Conclusions
Combined IV-IA therapy with full-dose intravenous rtPA was safe and results in good recanalization rates without excess symptomatic intracranial haemorrhage. Testing of full-dose IV tPA followed by endovascular treatment in the IMS3 trial is justified.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00878.x" xmlns="http://purl.org/rss/1.0/"><title>Stroke radiology and distinguishing characteristics of intracranial atherosclerotic disease in native South Asian Pakistanis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00878.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Stroke radiology and distinguishing characteristics of intracranial atherosclerotic disease in native South Asian Pakistanis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Maria Khan, Asif Rasheed, Saman Hashmi, Moazzam Zaidi, Muhammad Murtaza, Saba Akhtar, Lajpat Bansari, Nabi Shah, Maria Samuel, Sadaf Raza, Umer Rais Khan, Bilal Ahmed, Bilawal Ahmed, Naveeduddin Ahmed, Jamal Ara, Tasnim Ahsan, S. M. Munir, Shoukat Ali, Khalid Mehmood, Karim Ullah Makki, Muhammad Masroor Ahmed, Niaz Sheikh, Abdul Rauf Memon, Philippe M. Frossard, Ayeesha Kamran Kamal</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:29:17.775655-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00878.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00878.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00878.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs878-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>There are no descriptions of stroke mechanisms from intracranial atherosclerotic disease in native South Asian Pakistanis.</p></div></div>
<div class="section" id="ijs878-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Men and women aged ≥18 years with acute stroke presenting to four tertiary care hospitals in Karachi, Pakistan were screened using magnetic resonance angiography/transcranial Doppler scans. Trial of ORG 10172 in Acute Stroke Treatment criteria were applied to identify strokes from intracranial atherosclerotic disease.</p></div></div>
<div class="section" id="ijs878-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>We studied 245 patients with acute stroke due to intracranial atherosclerotic disease. Two hundred thirty scans were reviewed. Also, 206/230 (89·0%) showed acute ischaemia.</p></div><div class="para"><p>The most frequent presentation was with cortically based strokes in 42·2% (87/206) followed by border-zone infarcts (52/206, 25·2%). Increasing degrees of stenosis correlated with the development of both cortical and border-zone strokes (<em>P</em> = 0·002). Important associated findings were frequent atrophy (166/230, 72·2%), silent brain infarcts (66/230, 28%) and a marked lack of severe leukoaraiosis identified in only 68/230 (29·6%).</p></div><div class="para"><p>A total of 1870 arteries were studied individually. Middle cerebral artery was the symptomatic stroke vessel in half, presenting with complete occlusion in 66%. Evidence of biological disease, symptomatic or asymptomatic was identified in 753 (40·2%) vessels of which 543 (72%) were significantly (&gt;50%) stenosed at presentation.</p></div></div>
<div class="section" id="ijs878-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Intracranial atherosclerotic disease is a diffuse process in Pakistani south Asians, with involvement of multiple vessels in addition to the symptomatic vessel. The middle cerebral artery is the most frequent symptomatic vessel presenting with cortical embolic infarcts. There is a relative lack of leukoaraiosis. Concomitant atrophy, silent brain infarcts and recent ischaemia in the symptomatic territory are all frequently associated findings.</p></div></div>
]]></content:encoded><description>

Background
There are no descriptions of stroke mechanisms from intracranial atherosclerotic disease in native South Asian Pakistanis.


Methods
Men and women aged ≥18 years with acute stroke presenting to four tertiary care hospitals in Karachi, Pakistan were screened using magnetic resonance angiography/transcranial Doppler scans. Trial of ORG 10172 in Acute Stroke Treatment criteria were applied to identify strokes from intracranial atherosclerotic disease.


Results
We studied 245 patients with acute stroke due to intracranial atherosclerotic disease. Two hundred thirty scans were reviewed. Also, 206/230 (89·0%) showed acute ischaemia.
The most frequent presentation was with cortically based strokes in 42·2% (87/206) followed by border-zone infarcts (52/206, 25·2%). Increasing degrees of stenosis correlated with the development of both cortical and border-zone strokes (P = 0·002). Important associated findings were frequent atrophy (166/230, 72·2%), silent brain infarcts (66/230, 28%) and a marked lack of severe leukoaraiosis identified in only 68/230 (29·6%).
A total of 1870 arteries were studied individually. Middle cerebral artery was the symptomatic stroke vessel in half, presenting with complete occlusion in 66%. Evidence of biological disease, symptomatic or asymptomatic was identified in 753 (40·2%) vessels of which 543 (72%) were significantly (&gt;50%) stenosed at presentation.


Conclusion
Intracranial atherosclerotic disease is a diffuse process in Pakistani south Asians, with involvement of multiple vessels in addition to the symptomatic vessel. The middle cerebral artery is the most frequent symptomatic vessel presenting with cortical embolic infarcts. There is a relative lack of leukoaraiosis. Concomitant atrophy, silent brain infarcts and recent ischaemia in the symptomatic territory are all frequently associated findings.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00866.x" xmlns="http://purl.org/rss/1.0/"><title>Platelet activation, function, and reactivity in atherosclerotic carotid artery stenosis: a systematic review of the literature</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00866.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Platelet activation, function, and reactivity in atherosclerotic carotid artery stenosis: a systematic review of the literature</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">J. A. Kinsella, W. O. Tobin, G. Hamilton, D. J. H. McCabe</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-27T05:29:15.078898-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00866.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00866.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00866.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>An important proportion of transient ischemic attack or ischemic stroke is attributable to moderate or severe (50–99%) atherosclerotic carotid stenosis or occlusion. Platelet biomarkers have the potential to improve our understanding of the pathogenesis of vascular events in this patient population. A detailed systematic review was performed to collate all available data on <em>ex vivo</em> platelet activation and platelet function/reactivity in patients with carotid stenosis. Two hundred thirteen potentially relevant articles were initially identified; 26 manuscripts met criteria for inclusion in this systematic review. There was no consistent evidence of clinically informative data from urinary or soluble blood markers of platelet activation in patients with symptomatic moderate or severe carotid stenosis who might be considered suitable for carotid intervention. Data from flow cytometry studies revealed evidence of excessive platelet activation in patients in the early, sub-acute, or late phases after transient ischemic attack or stroke in association with moderate or severe carotid stenosis and in asymptomatic moderate or severe carotid stenosis compared with controls. Furthermore, pilot data suggest that platelet activation may be increased in recently symptomatic than in asymptomatic severe carotid stenosis. Excessive platelet activation and platelet hyperreactivity may play a role in the pathogenesis of first or subsequent transient ischemic attack or stroke in patients with moderate or severe carotid stenosis. Larger longitudinal studies assessing platelet activation status with flow cytometry and platelet function/reactivity in symptomatic vs. asymptomatic carotid stenosis are warranted to improve our understanding of the mechanisms responsible for transient ischemic attack or stroke.</p></div>
]]></content:encoded><description>
An important proportion of transient ischemic attack or ischemic stroke is attributable to moderate or severe (50–99%) atherosclerotic carotid stenosis or occlusion. Platelet biomarkers have the potential to improve our understanding of the pathogenesis of vascular events in this patient population. A detailed systematic review was performed to collate all available data on ex vivo platelet activation and platelet function/reactivity in patients with carotid stenosis. Two hundred thirteen potentially relevant articles were initially identified; 26 manuscripts met criteria for inclusion in this systematic review. There was no consistent evidence of clinically informative data from urinary or soluble blood markers of platelet activation in patients with symptomatic moderate or severe carotid stenosis who might be considered suitable for carotid intervention. Data from flow cytometry studies revealed evidence of excessive platelet activation in patients in the early, sub-acute, or late phases after transient ischemic attack or stroke in association with moderate or severe carotid stenosis and in asymptomatic moderate or severe carotid stenosis compared with controls. Furthermore, pilot data suggest that platelet activation may be increased in recently symptomatic than in asymptomatic severe carotid stenosis. Excessive platelet activation and platelet hyperreactivity may play a role in the pathogenesis of first or subsequent transient ischemic attack or stroke in patients with moderate or severe carotid stenosis. Larger longitudinal studies assessing platelet activation status with flow cytometry and platelet function/reactivity in symptomatic vs. asymptomatic carotid stenosis are warranted to improve our understanding of the mechanisms responsible for transient ischemic attack or stroke.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00895.x" xmlns="http://purl.org/rss/1.0/"><title>Thrombolysis for acute ischaemic stroke with alteplase in an Asian population: results of the multicenter, multinational Safe Implementation of Thrombolysis in Stroke-Non-European Union World (SITS-NEW)</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00895.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Thrombolysis for acute ischaemic stroke with alteplase in an Asian population: results of the multicenter, multinational Safe Implementation of Thrombolysis in Stroke-Non-European Union World (SITS-NEW)</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Joung-Ho Rha, Vasantha Padma Shrivastava, Yongjun Wang, Kim En Lee, Niaz Ahmed, Erich Bluhmki, Karin Hermansson, Nils Wahlgren, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-18T19:54:48.752649-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00895.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00895.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00895.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs895-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Safe Implementation of Thrombolysis in Stroke-Non-European Union World was a multinational, prospective, open, monitored, observational study of intravenous alteplase as thrombolytic therapy in clinical practice. Safe Implementation of Thrombolysis in Stroke-Non-European Union World was required to assess the safety of alteplase in an Asian population by comparison with results from the European Safe Implementation of Thrombolysis in Stroke-Monitoring Study and pooled results from randomized controlled trials.</p></div></div>
<div class="section" id="ijs895-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims and/or hypothesis</h4><div class="para"><p>To evaluate the efficacy and safety of intravenous alteplase (0·9 mg/kg) as thrombolytic therapy within three-hours of onset of acute ischaemic stroke in an Asian population.</p></div></div>
<div class="section" id="ijs895-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The 591 patients included were treated at 48 centers in four countries (South Korea, China, India, and Singapore) between 2006 and 2008. Primary outcomes were symptomatic (deterioration in National Institutes of Health Stroke Scale score ≥4 or death within the first 24 h) intracerebral haemorrhage type 2 22–36 h after the thrombolysis and mortality at three-month follow-up. The secondary outcome was functional independence (modified Rankin Scale score 0–2) at three-months. Results were compared with those from Safe Implementation of Thrombolysis in Stroke-Monitoring Study (<em>n</em> = 6483) and pooled results of patients (<em>n</em> = 415) who received intravenous alteplase (0·9 mg/kg) zero- to three-hours from onset of stroke symptoms in four randomized controlled trials (National Institute of Neurological Disorders and Stroke A and B, Altephase Thrombolysis for Acute Noninterventional Therapy in Ischaemic Stroke, and European Cooperative Acute Stroke Study II).</p></div></div>
<div class="section" id="ijs895-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Results are presented as Safe Implementation of Thrombolysis in Stroke-Non-European Union World vs. Safe Implementation of Thrombolysis in Stroke-Monitoring Study vs. pooled randomized controlled trials. Median age was 64 vs. 68 vs. 70 years, National Institutes of Health Stroke Scale score at baseline was 12 vs. 12 vs. 13, time from stroke onset to treatment was 130 vs. 140 vs. 135 mins, and females were 36·4% vs. 39·8% vs. 41·2%. Main outcomes (proportion of patients and 95% confidence intervals) were symptomatic intracerebral haemorrhage: 1·9% (1·1–3·3) vs. 1·7% (1·4–2·0) vs. 3·1% (1·8–5·3); mortality: 10·2% (8·0–12·9) vs. 11·3% (10·5–12·1) vs. 16·4% (13·1–20·3); and functional independence: 62·5% (58·5–66·4) vs. 54·8% (53·5–56·0) vs. 50·1% (45·3–54·9) at three-months. Adjusted odds ratio (95% confidence intervals) between Safe Implementation of Thrombolysis in Stroke-Non-European Union World and Safe Implementation of Thrombolysis in Stroke-Monitoring Study, and between Safe Implementation of Thrombolysis in Stroke-Non-European Union World and the pooled trials were 1·83 (0·89–3·77; <em>P</em> = 0·1156) and 0·63 (0·19–2·07; <em>P</em> = 0·4470) for symptomatic intracerebral haemorrhage, 0·90 (0·64–1·25; <em>P</em> = 0·5092) and 0·93 (0·52–1·64; <em>P</em> = 0·7915) for mortality at three-months, and 1·57 (1·25–1·96; <em>P</em> &lt; 0·0001) and 1·35 (0·91–2·00; <em>P</em> = 0·1325) for functional independence.</p></div></div>
<div class="section" id="ijs895-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>These data demonstrate the safety and efficacy of the standard dose of intravenous alteplase (0·9 mg/kg) in an Asian population, as previously observed in the European population studied in Safe Implementation of Thrombolysis in Stroke-Monitoring Study and the populations in pooled randomized controlled trials, when used in routine clinical practice within three-hours of stroke onset. The findings should encourage wider use of thrombolytic therapy in Asian countries for suitable patients treated in stroke centers.</p></div></div>
]]></content:encoded><description>

Background
Safe Implementation of Thrombolysis in Stroke-Non-European Union World was a multinational, prospective, open, monitored, observational study of intravenous alteplase as thrombolytic therapy in clinical practice. Safe Implementation of Thrombolysis in Stroke-Non-European Union World was required to assess the safety of alteplase in an Asian population by comparison with results from the European Safe Implementation of Thrombolysis in Stroke-Monitoring Study and pooled results from randomized controlled trials.


Aims and/or hypothesis
To evaluate the efficacy and safety of intravenous alteplase (0·9 mg/kg) as thrombolytic therapy within three-hours of onset of acute ischaemic stroke in an Asian population.


Methods
The 591 patients included were treated at 48 centers in four countries (South Korea, China, India, and Singapore) between 2006 and 2008. Primary outcomes were symptomatic (deterioration in National Institutes of Health Stroke Scale score ≥4 or death within the first 24 h) intracerebral haemorrhage type 2 22–36 h after the thrombolysis and mortality at three-month follow-up. The secondary outcome was functional independence (modified Rankin Scale score 0–2) at three-months. Results were compared with those from Safe Implementation of Thrombolysis in Stroke-Monitoring Study (n = 6483) and pooled results of patients (n = 415) who received intravenous alteplase (0·9 mg/kg) zero- to three-hours from onset of stroke symptoms in four randomized controlled trials (National Institute of Neurological Disorders and Stroke A and B, Altephase Thrombolysis for Acute Noninterventional Therapy in Ischaemic Stroke, and European Cooperative Acute Stroke Study II).


Results
Results are presented as Safe Implementation of Thrombolysis in Stroke-Non-European Union World vs. Safe Implementation of Thrombolysis in Stroke-Monitoring Study vs. pooled randomized controlled trials. Median age was 64 vs. 68 vs. 70 years, National Institutes of Health Stroke Scale score at baseline was 12 vs. 12 vs. 13, time from stroke onset to treatment was 130 vs. 140 vs. 135 mins, and females were 36·4% vs. 39·8% vs. 41·2%. Main outcomes (proportion of patients and 95% confidence intervals) were symptomatic intracerebral haemorrhage: 1·9% (1·1–3·3) vs. 1·7% (1·4–2·0) vs. 3·1% (1·8–5·3); mortality: 10·2% (8·0–12·9) vs. 11·3% (10·5–12·1) vs. 16·4% (13·1–20·3); and functional independence: 62·5% (58·5–66·4) vs. 54·8% (53·5–56·0) vs. 50·1% (45·3–54·9) at three-months. Adjusted odds ratio (95% confidence intervals) between Safe Implementation of Thrombolysis in Stroke-Non-European Union World and Safe Implementation of Thrombolysis in Stroke-Monitoring Study, and between Safe Implementation of Thrombolysis in Stroke-Non-European Union World and the pooled trials were 1·83 (0·89–3·77; P = 0·1156) and 0·63 (0·19–2·07; P = 0·4470) for symptomatic intracerebral haemorrhage, 0·90 (0·64–1·25; P = 0·5092) and 0·93 (0·52–1·64; P = 0·7915) for mortality at three-months, and 1·57 (1·25–1·96; P &lt; 0·0001) and 1·35 (0·91–2·00; P = 0·1325) for functional independence.


Conclusions
These data demonstrate the safety and efficacy of the standard dose of intravenous alteplase (0·9 mg/kg) in an Asian population, as previously observed in the European population studied in Safe Implementation of Thrombolysis in Stroke-Monitoring Study and the populations in pooled randomized controlled trials, when used in routine clinical practice within three-hours of stroke onset. The findings should encourage wider use of thrombolytic therapy in Asian countries for suitable patients treated in stroke centers.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00865.x" xmlns="http://purl.org/rss/1.0/"><title>Differing associations of white matter lesions and lacunar infarction with retinal microvascular signs</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00865.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Differing associations of white matter lesions and lacunar infarction with retinal microvascular signs</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Gerald Liew, Michelle L. Baker, Tien Y. Wong, Peter J. Hand, Jie Jin Wang, Paul Mitchell, Deidre A. De Silva, Meng-Cheong Wong, Elena Rochtchina, Richard I. Lindley, Joanna M. Wardlaw, Graeme J. Hankey, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-18T19:54:44.385339-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00865.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00865.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00865.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs865-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>White matter lesions (WML) and lacunar infarcts (LI) are believed to have microvascular etiologies but the exact microvascular changes occurring in each is unclear.</p></div></div>
<div class="section" id="ijs865-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>Using the retina as a proxy, we assessed retinal microvascular changes in WML and LI.</p></div></div>
<div class="section" id="ijs865-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We prospectively recruited 1211 acute stroke patients. Four subgroups were identified from neuroimaging: WML alone, LI alone, both WML and LI, neither WML nor LI. Masked retinal photographs identified retinopathy and retinal arteriolar wall signs and measured retinal vascular caliber.</p></div></div>
<div class="section" id="ijs865-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Compared with 448 controls with neither WML nor LI, 384 patients with only WML were more likely to have retinopathy [odds ratio (OR) 1·5, 95% confidence interval (CI) 1·1 to 2·1] and enhanced arteriolar light reflex (OR 1·6, 95% CI 1·1 to 2·3); 200 patients with only LI were more likely to have arteriolar narrowing (OR 1·6, 95% CI 1·1 to 2·3) and enhanced arteriolar light reflex (OR 1·6, 95% CI 1·0 to 2·4); and 179 patients with both WML and LI were more likely to have arteriovenous nicking (OR 1·7, 95% CI 1·1 to 2·6), enhanced arteriolar light reflex (OR 2·0, 95% CI 1·3 to 3·2) and wider venules (OR 2·3, 95% CI 1·4 to 3·6). All analyses were adjusted for age, gender, study site and cardiovascular risk factors.</p></div></div>
<div class="section" id="ijs865-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Both WML and LI were associated with retinal microvascular signs, supporting a microvascular etiology. Differing patterns of association suggest different mechanisms may predominate, e.g. greater endothelial permeability in WML, and ischemia associated with arteriolar wall disease in LI.</p></div></div>
]]></content:encoded><description>

Background
White matter lesions (WML) and lacunar infarcts (LI) are believed to have microvascular etiologies but the exact microvascular changes occurring in each is unclear.


Aim
Using the retina as a proxy, we assessed retinal microvascular changes in WML and LI.


Methods
We prospectively recruited 1211 acute stroke patients. Four subgroups were identified from neuroimaging: WML alone, LI alone, both WML and LI, neither WML nor LI. Masked retinal photographs identified retinopathy and retinal arteriolar wall signs and measured retinal vascular caliber.


Results
Compared with 448 controls with neither WML nor LI, 384 patients with only WML were more likely to have retinopathy [odds ratio (OR) 1·5, 95% confidence interval (CI) 1·1 to 2·1] and enhanced arteriolar light reflex (OR 1·6, 95% CI 1·1 to 2·3); 200 patients with only LI were more likely to have arteriolar narrowing (OR 1·6, 95% CI 1·1 to 2·3) and enhanced arteriolar light reflex (OR 1·6, 95% CI 1·0 to 2·4); and 179 patients with both WML and LI were more likely to have arteriovenous nicking (OR 1·7, 95% CI 1·1 to 2·6), enhanced arteriolar light reflex (OR 2·0, 95% CI 1·3 to 3·2) and wider venules (OR 2·3, 95% CI 1·4 to 3·6). All analyses were adjusted for age, gender, study site and cardiovascular risk factors.


Conclusion
Both WML and LI were associated with retinal microvascular signs, supporting a microvascular etiology. Differing patterns of association suggest different mechanisms may predominate, e.g. greater endothelial permeability in WML, and ischemia associated with arteriolar wall disease in LI.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00894.x" xmlns="http://purl.org/rss/1.0/"><title>Design and rationale of the Mechanical Retrieval and Recanalization of Stroke Clots Using Embolectomy (MR RESCUE) Trial</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00894.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Design and rationale of the Mechanical Retrieval and Recanalization of Stroke Clots Using Embolectomy (MR RESCUE) Trial</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Chelsea S. Kidwell, Reza Jahan, Jeffry R. Alger, Timothy J. Schaewe, Judy Guzy, Sidney Starkman, Robert Elashoff, Jeffrey Gornbein, Val Nenov, Jeffrey L. Saver, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:50:44.766803-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00894.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00894.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00894.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs894-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Multimodal imaging has the potential to identify acute ischaemic stroke patients most likely to benefit from late recanalization therapies.</p></div></div>
<div class="section" id="ijs894-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The general aim of the Mechanical Retrieval and Recanalization of Stroke Clots Using Embolectomy Trial is to investigate whether multimodal imaging can identify patients who will benefit substantially from mechanical embolectomy for the treatment of acute ischaemic stroke up to eight-hours from symptom onset.</p></div></div>
<div class="section" id="ijs894-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Mechanical Retrieval and Recanalization of Stroke Clots Using Embolectomy is a randomized, controlled, blinded-outcome clinical trial.</p></div></div>
<div class="section" id="ijs894-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Population studied</h4><div class="para"><p>Acute ischaemic stroke patients with large vessel intracranial internal carotid artery or middle cerebral artery M1 or M2 occlusion enrolled within eight-hours of symptom onset are eligible. The study sample size is 120 patients.</p></div></div>
<div class="section" id="ijs894-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Study intervention</h4><div class="para"><p>Patients are randomized to endovascular embolectomy employing the Merci Retriever (Concentric Medical, Mountain View, CA) or the Penumbra System (Penumbra, Alameda, CA) vs. standard medical care, with randomization stratified by penumbral pattern.</p></div></div> <div class="section" id="ijs894-sec-0006" xmlns="http://www.w3.org/1999/xhtml"><h4>Outcomes</h4><div class="para"><p>The primary aim of the trial is to test the hypothesis that the presence of substantial ischaemic penumbral tissue visualized on multimodal imaging (magnetic resonance imaging or computed tomography) predicts patients most likely to respond to mechanical embolectomy for treatment of acute ischaemic stroke due to a large vessel, intracranial occlusion up to eight-hours from symptom onset. This hypothesis will be tested by analysing whether pretreatment imaging pattern has a significant interaction with treatment as a determinant of functional outcome based on the distribution of scores on the modified Rankin Scale measure of global disability assessed 90 days post-stroke. Nested hypotheses test for (1) treatment efficacy in patients with a penumbral pattern pretreatment, and (2) absence of treatment benefit (equivalency) in patients without a penumbral pattern pretreatment. An additional aim will only be tested if the primary hypothesis of an interaction is negative: that patients treated with mechanical embolectomy have improved functional outcome vs. standard medical management.</p></div></div>
]]></content:encoded><description>

Rationale
Multimodal imaging has the potential to identify acute ischaemic stroke patients most likely to benefit from late recanalization therapies.


Aims
The general aim of the Mechanical Retrieval and Recanalization of Stroke Clots Using Embolectomy Trial is to investigate whether multimodal imaging can identify patients who will benefit substantially from mechanical embolectomy for the treatment of acute ischaemic stroke up to eight-hours from symptom onset.


Design
Mechanical Retrieval and Recanalization of Stroke Clots Using Embolectomy is a randomized, controlled, blinded-outcome clinical trial.


Population studied
Acute ischaemic stroke patients with large vessel intracranial internal carotid artery or middle cerebral artery M1 or M2 occlusion enrolled within eight-hours of symptom onset are eligible. The study sample size is 120 patients.


Study intervention
Patients are randomized to endovascular embolectomy employing the Merci Retriever (Concentric Medical, Mountain View, CA) or the Penumbra System (Penumbra, Alameda, CA) vs. standard medical care, with randomization stratified by penumbral pattern.
 
Outcomes
The primary aim of the trial is to test the hypothesis that the presence of substantial ischaemic penumbral tissue visualized on multimodal imaging (magnetic resonance imaging or computed tomography) predicts patients most likely to respond to mechanical embolectomy for treatment of acute ischaemic stroke due to a large vessel, intracranial occlusion up to eight-hours from symptom onset. This hypothesis will be tested by analysing whether pretreatment imaging pattern has a significant interaction with treatment as a determinant of functional outcome based on the distribution of scores on the modified Rankin Scale measure of global disability assessed 90 days post-stroke. Nested hypotheses test for (1) treatment efficacy in patients with a penumbral pattern pretreatment, and (2) absence of treatment benefit (equivalency) in patients without a penumbral pattern pretreatment. An additional aim will only be tested if the primary hypothesis of an interaction is negative: that patients treated with mechanical embolectomy have improved functional outcome vs. standard medical management.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00893.x" xmlns="http://purl.org/rss/1.0/"><title>Demographics, socio-economic characteristics, and risk factor prevalence in patients with non-cardioembolic ischaemic stroke in low- and middle-income countries: the OPTIC registry</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00893.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Demographics, socio-economic characteristics, and risk factor prevalence in patients with non-cardioembolic ischaemic stroke in low- and middle-income countries: the OPTIC registry</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Halim Abboud, Julien Labreuche, Antonio Arauz, Alan Bryer, Pablo G Lavados, Ayrton Massaro, Mario Munoz Collazos, Philippe Gabriel Steg, Bassem I Yamout, Eric Vicaut, Pierre Amarenco, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:50:40.111542-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00893.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00893.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00893.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs893-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>There is a paucity of data on patients with stroke/transient ischaemic attack in low- and middle-income countries. We sought to describe the characteristics and management of patients with an ischaemic stroke and recent transient ischaemic attack or minor ischaemic strokes in low- or middle-income countries.</p></div></div>
<div class="section" id="ijs893-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The Outcomes in Patients with TIA and Cerebrovascular disease registry is an international, prospective study. Patients ≥45 years who required secondary prevention of stroke (either following an acute transient ischaemic attack or minor ischaemic strokes (National Institutes of Health Stroke Scale &lt;4) of &lt;24 h duration, or recent (&lt;6 months), stable, first-ever, non-disabling ischaemic stroke) were enrolled in 17 countries in Latin America, the Middle East, and Africa. The main measures of interest were risk factors, comorbidities, and socio-economic variables.</p></div></div>
<div class="section" id="ijs893-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Between January 2007 and December 2008, 3635 patients were enrolled in Latin America (<em>n</em> = 1543), the Middle East (<em>n</em> = 1041), North Africa (<em>n</em> = 834), and South Africa (<em>n</em> = 217). Of these, 63% had a stable, first-ever ischaemic stroke (median delay from symptom onset to inclusion, 25 days interquartile range, 7–77); 37% had an acute transient ischaemic attack or minor ischaemic stroke (median delay, two-days; interquartile range, 0–6). Prevalence of diabetes was 46% in the Middle East, 29% in Latin America, 35% in South Africa, and 38% in North Africa; 72% had abdominal obesity (range, 65–78%; adjusted <em>P</em> &lt; 0·001); prevalence of metabolic syndrome was 78% (range, 72–84%, <em>P</em> &lt; 0·001). Abnormal ankle brachial index (&lt;0·9) was present in 22%, peripheral artery disease in 7·6%, and coronary artery disease in 13%. Overall, 24% of patients had no health insurance and 27% had a low educational level.</p></div></div>
<div class="section" id="ijs893-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Interpretation</h4><div class="para"><p>In this study, patients in low- and middle-income countries had a high burden of modifiable risk factors. High rates of low educational level and lack of health insurance in certain regions are potential obstacles to risk factor control.</p></div></div>
<div class="section" id="ijs893-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Funding</h4><div class="para"><p>The Outcomes in Patients with TIA and Cerebrovascular disease registry is supported by Sanofi-Aventis, Paris, France.</p></div></div>
]]></content:encoded><description>

Background
There is a paucity of data on patients with stroke/transient ischaemic attack in low- and middle-income countries. We sought to describe the characteristics and management of patients with an ischaemic stroke and recent transient ischaemic attack or minor ischaemic strokes in low- or middle-income countries.


Methods
The Outcomes in Patients with TIA and Cerebrovascular disease registry is an international, prospective study. Patients ≥45 years who required secondary prevention of stroke (either following an acute transient ischaemic attack or minor ischaemic strokes (National Institutes of Health Stroke Scale &lt;4) of &lt;24 h duration, or recent (&lt;6 months), stable, first-ever, non-disabling ischaemic stroke) were enrolled in 17 countries in Latin America, the Middle East, and Africa. The main measures of interest were risk factors, comorbidities, and socio-economic variables.


Results
Between January 2007 and December 2008, 3635 patients were enrolled in Latin America (n = 1543), the Middle East (n = 1041), North Africa (n = 834), and South Africa (n = 217). Of these, 63% had a stable, first-ever ischaemic stroke (median delay from symptom onset to inclusion, 25 days interquartile range, 7–77); 37% had an acute transient ischaemic attack or minor ischaemic stroke (median delay, two-days; interquartile range, 0–6). Prevalence of diabetes was 46% in the Middle East, 29% in Latin America, 35% in South Africa, and 38% in North Africa; 72% had abdominal obesity (range, 65–78%; adjusted P &lt; 0·001); prevalence of metabolic syndrome was 78% (range, 72–84%, P &lt; 0·001). Abnormal ankle brachial index (&lt;0·9) was present in 22%, peripheral artery disease in 7·6%, and coronary artery disease in 13%. Overall, 24% of patients had no health insurance and 27% had a low educational level.


Interpretation
In this study, patients in low- and middle-income countries had a high burden of modifiable risk factors. High rates of low educational level and lack of health insurance in certain regions are potential obstacles to risk factor control.


Funding
The Outcomes in Patients with TIA and Cerebrovascular disease registry is supported by Sanofi-Aventis, Paris, France.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00882.x" xmlns="http://purl.org/rss/1.0/"><title>A longitudinal cohort study on quality of life in stroke patients and their partners: Restore4Stroke Cohort</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00882.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A longitudinal cohort study on quality of life in stroke patients and their partners: Restore4Stroke Cohort</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Maria L. Mierlo, Caroline M. Heugten, Marcel W. M. Post, Eline Lindeman, Paul L. M. Kort, Johanna M.A. Visser-Meily</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:50:28.638044-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00882.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00882.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00882.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs882-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Stroke is a major cause of disability in the Western world. Its long-term consequences have a negative impact on the quality of life of both the patients and their partners.</p></div></div>
<div class="section" id="ijs882-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>The aim of the Restore4Stroke Cohort study is to investigate the changes in quality of life of stroke patients and their partners over time, and to determine factors predicting quality of life in several domains, especially personal and environmental factors.</p></div></div>
<div class="section" id="ijs882-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Method</h4><div class="para"><p>Multicentre prospective longitudinal cohort study. Inclusion and the first assessment take place during hospital stay in the first week post-stroke. Follow-up assessments take place at two months, six months, one year, and two years post-stroke. Recruitment of 500 patients from stroke units in six participation hospitals is foreseen. If the patient has a partner, he or she is also asked to participate in the study.</p></div></div>
<div class="section" id="ijs882-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Outcomes</h4><div class="para"><p>The main outcome is quality of life, considered from a health-related quality of life and domain-specific quality of life perspective. Factors predicting long-term quality of life will be determined by taking into account the health condition (pre-stroke health condition and stroke-related health condition), personal factors (e.g. coping and illness cognitions), and environmental factors (e.g. caregiver burden and social support).</p></div></div>
<div class="section" id="ijs882-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Discussion</h4><div class="para"><p>This study is expected to provide information about the changes in quality of life of stroke patients and their partners over time. Furthermore, the identification of factors predicting quality of life can be used to improve rehabilitation care and develop new interventions for stroke patients and their partners.</p></div></div>
]]></content:encoded><description>

Background
Stroke is a major cause of disability in the Western world. Its long-term consequences have a negative impact on the quality of life of both the patients and their partners.


Aim
The aim of the Restore4Stroke Cohort study is to investigate the changes in quality of life of stroke patients and their partners over time, and to determine factors predicting quality of life in several domains, especially personal and environmental factors.


Method
Multicentre prospective longitudinal cohort study. Inclusion and the first assessment take place during hospital stay in the first week post-stroke. Follow-up assessments take place at two months, six months, one year, and two years post-stroke. Recruitment of 500 patients from stroke units in six participation hospitals is foreseen. If the patient has a partner, he or she is also asked to participate in the study.


Outcomes
The main outcome is quality of life, considered from a health-related quality of life and domain-specific quality of life perspective. Factors predicting long-term quality of life will be determined by taking into account the health condition (pre-stroke health condition and stroke-related health condition), personal factors (e.g. coping and illness cognitions), and environmental factors (e.g. caregiver burden and social support).


Discussion
This study is expected to provide information about the changes in quality of life of stroke patients and their partners over time. Furthermore, the identification of factors predicting quality of life can be used to improve rehabilitation care and develop new interventions for stroke patients and their partners.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00880.x" xmlns="http://purl.org/rss/1.0/"><title>A systematic review of perceived barriers and motivators to physical activity after stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00880.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A systematic review of perceived barriers and motivators to physical activity after stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sarah Nicholson, Falko F. Sniehotta, Frederike Wijck, Carolyn A. Greig, Marie Johnston, Marion E. T. McMurdo, Martin Dennis, Gillian E Mead</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:50:25.574463-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00880.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00880.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00880.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Systematic review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs880-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and purpose</h4><div class="para"><p>Physical fitness is impaired after stroke, may contribute to disability, yet is amenable to improvement through regular physical activity. To facilitate uptake and maintenance of physical activity, it is essential to understand stroke survivors' perceived barriers and motivators. Therefore, we undertook a systematic review of perceived barriers and motivators to physical activity after stroke.</p></div></div>
<div class="section" id="ijs880-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Electronic searches of EMBASE, Medline, CINAHL, and PsychInfo were performed. We included peer-reviewed journal articles, in English, between 1 January 1966 and 30 August 2010 reporting stroke survivors' perceived barriers and motivators to physical activity.</p></div></div>
<div class="section" id="ijs880-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Searches identified 73 807 citations of which 57 full articles were retrieved. Six articles were included, providing data on 174 stroke survivors (range 10 to 83 per article). Two reported barriers and motivators, two reported only motivators, and two reported only barriers. Five were qualitative articles and one was quantitative. The most commonly reported barriers were lack of motivation, environmental factors (e.g. transport), health concerns, and stroke impairments. The most commonly reported motivators were social support and the need to be able to perform daily tasks.</p></div></div>
<div class="section" id="ijs880-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>This review has furthered our understanding of the perceived barriers and motivators to physical activity after a stroke. This review will enable the development of tailored interventions to target barriers, while building upon perceived motivators to increase and maintain stroke survivors' physical activity.</p></div></div>
]]></content:encoded><description>

Background and purpose
Physical fitness is impaired after stroke, may contribute to disability, yet is amenable to improvement through regular physical activity. To facilitate uptake and maintenance of physical activity, it is essential to understand stroke survivors' perceived barriers and motivators. Therefore, we undertook a systematic review of perceived barriers and motivators to physical activity after stroke.


Methods
Electronic searches of EMBASE, Medline, CINAHL, and PsychInfo were performed. We included peer-reviewed journal articles, in English, between 1 January 1966 and 30 August 2010 reporting stroke survivors' perceived barriers and motivators to physical activity.


Results
Searches identified 73 807 citations of which 57 full articles were retrieved. Six articles were included, providing data on 174 stroke survivors (range 10 to 83 per article). Two reported barriers and motivators, two reported only motivators, and two reported only barriers. Five were qualitative articles and one was quantitative. The most commonly reported barriers were lack of motivation, environmental factors (e.g. transport), health concerns, and stroke impairments. The most commonly reported motivators were social support and the need to be able to perform daily tasks.


Conclusion
This review has furthered our understanding of the perceived barriers and motivators to physical activity after a stroke. This review will enable the development of tailored interventions to target barriers, while building upon perceived motivators to increase and maintain stroke survivors' physical activity.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00879.x" xmlns="http://purl.org/rss/1.0/"><title>Impact of admission glucose and diabetes on recanalization and outcome after intra-arterial thrombolysis for ischaemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00879.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Impact of admission glucose and diabetes on recanalization and outcome after intra-arterial thrombolysis for ischaemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Marcel Arnold, Selina Mattle, Aekaterini Galimanis, Liliane Kappeler, Urs Fischer, Simon Jung, GianMarco DeMarchis, Jan Gralla, Marie-Luise Mono, Caspar Brekenfeld, Niklaus Meier, Krassen Nedeltchev, Gerhard Schroth, Heinrich P. Mattle</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:50:24.823501-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00879.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00879.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00879.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs879-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Stroke patients with diabetes and admission hyperglycaemia have worse outcomes than non-diabetics, with or without intravenous thrombolysis. Poor vessel recanalization was reported in diabetics treated with intravenous thrombolysis.</p></div></div>
<div class="section" id="ijs879-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>This study aimed to determine the impact of admission glucose and diabetes on recanalization and outcome after intra-arterial thrombolysis.</p></div></div>
<div class="section" id="ijs879-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We analysed 389 patients (213 men, 176 women) treated with intra-arterial thrombolysis. The association of diabetes and admission glucose value with recanalization, outcome, mortality, and symptomatic intracranial haemorrhage was determined. Recanalization was classified according to thrombolysis in myocardial infarction grades. Outcome was measured using the modified Rankin Scale at three-months and categorized as favourable (modified Rankin Scale 0–2) or poor (modified Rankin Scale 3–6).</p></div></div>
<div class="section" id="ijs879-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The rate of partial or complete recanalization (thrombolysis in myocardial infarction 2–3) did not differ between patients with and without diabetes (67% vs. 66%; <em>P</em> = 1·000). Mean admission glucose values were similar in patients with poor recanalization (thrombolysis in myocardial infarction 0–1) and patients with partial or complete recanalization (thrombolysis in myocardial infarction 2–3; 7·3 vs. 7·3 mmol/l; <em>P</em> = 0·746). Follow-up at three-months was obtained in 388 of 389 patients. Clinical outcome was favourable (modified Rankin Scale 0–2) in 189 patients (49%) and poor (modified Rankin Scale 3–6) in 199 patients (51%). Mortality at three-months was 20%. Diabetics were more likely to have poor outcome (72% vs. 48%; <em>P</em> = 0·001) and to be dead (30% vs. 19%; <em>P</em> = 0·044) at three-months. After multivariable analysis, there remained an independent relationship between diabetes and outcome (<em>P</em> = 0·003; odds ratio 3·033, 95% confidence interval 1·452–6·336), but not with mortality (<em>P</em> = 0·310; odds ratio 1·436; 95% confidence interval 0·714–2·888). Moreover, higher age (<em>P</em> = 0·001; odds ratio 1·039; 95% confidence interval 1·017–1·061), higher baseline National Institutes of Health Stroke Scale score (<em>P</em> &lt; 0·0001; odds ratio 1·130; 95% confidence interval 1·079–1·182), location of vessel occlusion as categorical variable (<em>P</em> &lt; 0·0001), poor collaterals (<em>P</em> = 0·02; odds ratio 1·587; 95% confidence interval 1·076–2·341), poor vessel recanalization (<em>P</em> &lt; 0·0001; odds ratio 4·713; 95% confidence interval 2·627–8·454), and higher leucocyte count (<em>P</em> = 0·032; odds ratio 1·094; 95% confidence interval 1·008–1·188) were independent baseline predictors of poor outcome. Higher admission glucose was associated with poor outcome (<em>P</em> = 0·006) and mortality (<em>P</em> &lt; 0·0001). After multivariate analyses, glucose remained independently associated with poor outcome (<em>P</em> = 0·019; odds ratio 1·150; 95% confidence interval 1·023–1–292) and mortality (<em>P</em> = 0·005; odds ratio 1·183; 95% confidence interval 1052–1·331). The rate of symptomatic intracranial haemorrhage was similar in diabetics and non-diabetics (6·7% vs. 4·6%; <em>P</em> = 0·512). Mean admission glucose was higher in patients with symptomatic intracranial haemorrhage than without (8·58 vs. 7·26 mmol/l; <em>P</em> = 0·010). Multivariable analysis confirmed an independent association between admission glucose and symptomatic intracranial haemorrhage (<em>P</em> = 0·027; odds ratio 1·187; 95% confidence interval 1·020–1·381).</p></div></div>
<div class="section" id="ijs879-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Diabetes and glucose value on admission did not influence recanalization after intra-arterial thrombolysis; nevertheless, they were independent predictors of poor outcome after intra-arterial thrombolysis and a higher admission glucose value was an independent predictor of symptomatic intracranial haemorrhage. This indicates that factors on the capillary, cellular, or metabolic level may account for the worse outcome in patients with elevated glucose value and diabetes.</p></div></div>
]]></content:encoded><description>

Background
Stroke patients with diabetes and admission hyperglycaemia have worse outcomes than non-diabetics, with or without intravenous thrombolysis. Poor vessel recanalization was reported in diabetics treated with intravenous thrombolysis.


Aims
This study aimed to determine the impact of admission glucose and diabetes on recanalization and outcome after intra-arterial thrombolysis.


Methods
We analysed 389 patients (213 men, 176 women) treated with intra-arterial thrombolysis. The association of diabetes and admission glucose value with recanalization, outcome, mortality, and symptomatic intracranial haemorrhage was determined. Recanalization was classified according to thrombolysis in myocardial infarction grades. Outcome was measured using the modified Rankin Scale at three-months and categorized as favourable (modified Rankin Scale 0–2) or poor (modified Rankin Scale 3–6).


Results
The rate of partial or complete recanalization (thrombolysis in myocardial infarction 2–3) did not differ between patients with and without diabetes (67% vs. 66%; P = 1·000). Mean admission glucose values were similar in patients with poor recanalization (thrombolysis in myocardial infarction 0–1) and patients with partial or complete recanalization (thrombolysis in myocardial infarction 2–3; 7·3 vs. 7·3 mmol/l; P = 0·746). Follow-up at three-months was obtained in 388 of 389 patients. Clinical outcome was favourable (modified Rankin Scale 0–2) in 189 patients (49%) and poor (modified Rankin Scale 3–6) in 199 patients (51%). Mortality at three-months was 20%. Diabetics were more likely to have poor outcome (72% vs. 48%; P = 0·001) and to be dead (30% vs. 19%; P = 0·044) at three-months. After multivariable analysis, there remained an independent relationship between diabetes and outcome (P = 0·003; odds ratio 3·033, 95% confidence interval 1·452–6·336), but not with mortality (P = 0·310; odds ratio 1·436; 95% confidence interval 0·714–2·888). Moreover, higher age (P = 0·001; odds ratio 1·039; 95% confidence interval 1·017–1·061), higher baseline National Institutes of Health Stroke Scale score (P &lt; 0·0001; odds ratio 1·130; 95% confidence interval 1·079–1·182), location of vessel occlusion as categorical variable (P &lt; 0·0001), poor collaterals (P = 0·02; odds ratio 1·587; 95% confidence interval 1·076–2·341), poor vessel recanalization (P &lt; 0·0001; odds ratio 4·713; 95% confidence interval 2·627–8·454), and higher leucocyte count (P = 0·032; odds ratio 1·094; 95% confidence interval 1·008–1·188) were independent baseline predictors of poor outcome. Higher admission glucose was associated with poor outcome (P = 0·006) and mortality (P &lt; 0·0001). After multivariate analyses, glucose remained independently associated with poor outcome (P = 0·019; odds ratio 1·150; 95% confidence interval 1·023–1–292) and mortality (P = 0·005; odds ratio 1·183; 95% confidence interval 1052–1·331). The rate of symptomatic intracranial haemorrhage was similar in diabetics and non-diabetics (6·7% vs. 4·6%; P = 0·512). Mean admission glucose was higher in patients with symptomatic intracranial haemorrhage than without (8·58 vs. 7·26 mmol/l; P = 0·010). Multivariable analysis confirmed an independent association between admission glucose and symptomatic intracranial haemorrhage (P = 0·027; odds ratio 1·187; 95% confidence interval 1·020–1·381).


Conclusions
Diabetes and glucose value on admission did not influence recanalization after intra-arterial thrombolysis; nevertheless, they were independent predictors of poor outcome after intra-arterial thrombolysis and a higher admission glucose value was an independent predictor of symptomatic intracranial haemorrhage. This indicates that factors on the capillary, cellular, or metabolic level may account for the worse outcome in patients with elevated glucose value and diabetes.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00875.x" xmlns="http://purl.org/rss/1.0/"><title>Risk of cardiovascular events and death in the life after aneurysmal subarachnoid haemorrhage: a nationwide study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00875.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Risk of cardiovascular events and death in the life after aneurysmal subarachnoid haemorrhage: a nationwide study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Dennis J. Nieuwkamp, Ilonca Vaartjes, Ale Algra, Gabriel J. E. Rinkel, Michiel L. Bots</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:50:22.582549-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00875.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00875.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00875.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs875-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and aim</h4><div class="para"><p>The increased mortality rates of survivors of aneurysmal subarachnoid haemorrhage have been attributed to an increased risk of cardiovascular events in a registry study in Sweden. Swedish registries have however not been validated for subarachnoid haemorrhage and Scandinavian incidences of cardiovascular disease differ from that in Western European countries. We assessed risks of vascular disease and death in subarachnoid haemorrhage survivors in the Netherlands.</p></div></div>
<div class="section" id="ijs875-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>From the Dutch hospital discharge register, we identified all patients with subarachnoid haemorrhage admission between 1997 and 2008. We determined the accuracy of coding of the diagnosis subarachnoid haemorrhage for patients admitted to our centre. Conditional on survival of three-months after the subarachnoid haemorrhage, we calculated standardized incidence and mortality ratios for fatal or nonfatal vascular diseases, vascular death, and all-cause death. Cumulative risks were estimated with survival analysis.</p></div></div>
<div class="section" id="ijs875-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The diagnosis of nontraumatic subarachnoid haemorrhage was correct in 95·4% of 1472 patients. Of 11 263 admitted subarachnoid haemorrhage patients, 6999 survived more than three-months. During follow-up (mean 5·1 years), 874 (12·5%) died. The risks of death were 3·3% within one-year, 11·3% within five-years, and 21·5% within 10 years. The standardized mortality ratio was 3·4 (95% confidence interval: 3·1 to 3·7) for vascular death and 2·2 (95% confidence interval: 2·1 to 2·3) for all-cause death. The standardized incidence ratio for fatal or nonfatal vascular diseases was 2·7 (95% confidence interval: 2·6 to 2·8).</p></div></div>
<div class="section" id="ijs875-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Dutch hospital discharge and cause of death registries are a valid source of data for subarachnoid haemorrhage, and show that the increased mortality rate in subarachnoid haemorrhage survivors is explained by increased risks for vascular diseases and death.</p></div></div>
]]></content:encoded><description>

Background and aim
The increased mortality rates of survivors of aneurysmal subarachnoid haemorrhage have been attributed to an increased risk of cardiovascular events in a registry study in Sweden. Swedish registries have however not been validated for subarachnoid haemorrhage and Scandinavian incidences of cardiovascular disease differ from that in Western European countries. We assessed risks of vascular disease and death in subarachnoid haemorrhage survivors in the Netherlands.


Methods
From the Dutch hospital discharge register, we identified all patients with subarachnoid haemorrhage admission between 1997 and 2008. We determined the accuracy of coding of the diagnosis subarachnoid haemorrhage for patients admitted to our centre. Conditional on survival of three-months after the subarachnoid haemorrhage, we calculated standardized incidence and mortality ratios for fatal or nonfatal vascular diseases, vascular death, and all-cause death. Cumulative risks were estimated with survival analysis.


Results
The diagnosis of nontraumatic subarachnoid haemorrhage was correct in 95·4% of 1472 patients. Of 11 263 admitted subarachnoid haemorrhage patients, 6999 survived more than three-months. During follow-up (mean 5·1 years), 874 (12·5%) died. The risks of death were 3·3% within one-year, 11·3% within five-years, and 21·5% within 10 years. The standardized mortality ratio was 3·4 (95% confidence interval: 3·1 to 3·7) for vascular death and 2·2 (95% confidence interval: 2·1 to 2·3) for all-cause death. The standardized incidence ratio for fatal or nonfatal vascular diseases was 2·7 (95% confidence interval: 2·6 to 2·8).


Conclusions
Dutch hospital discharge and cause of death registries are a valid source of data for subarachnoid haemorrhage, and show that the increased mortality rate in subarachnoid haemorrhage survivors is explained by increased risks for vascular diseases and death.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00869.x" xmlns="http://purl.org/rss/1.0/"><title>Postthrombolysis intracranial hemorrhage risk of cerebral microbleeds in acute stroke patients: a systematic review and meta-analysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00869.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Postthrombolysis intracranial hemorrhage risk of cerebral microbleeds in acute stroke patients: a systematic review and meta-analysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ashkan Shoamanesh, Chun Shing Kwok, Patricia Annabelle Lim, Oscar R. Benavente</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:45:44.119929-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00869.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00869.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00869.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>It has been questioned whether patients with cerebral microbleeds are at a greater risk for the development of symptomatic intracerebral hemorrhage following thrombolytic therapy in the management of acute ischemic stroke. Thus far, observational studies have not shown a statistically significant increased risk; however, these have been limited by small sample size. The aim is to better quantify the risk of postthrombolysis intracerebral hemorrhage in patients with acute ischemic stroke and cerebral microbleeds on magnetic resonance imaging. A systematic review of controlled studies investigating the presence of microbleeds on magnetic resonance imaging as a risk factor for intracerebral hemorrhage following thrombolysis in acute stroke patients was conducted. A random effects model meta-analysis was performed. In pooled analysis of five studies totaling 790 participants, the prevalence of microbleeds was 17%. The presence of microbleeds revealed a trend toward an increased risk of postthrombolysis symptomatic intracerebral hemorrhage [odds ratio: 1·98 (95% confidence interval, 0·90 to 4·35; <em>P</em> = 0·09), <em>I</em><sup>2</sup> = 0%]. Adjusted analysis minimizing potential bias resulted in an increased absolute risk of 4·6% for the development of symptomatic intracerebral hemorrhage in patients with cerebral microbleeds [odds ratio: 2·29 (95% confidence interval, 1·01 to 5·17), <em>I</em><sup>2</sup> = 0%] reaching borderline significance (<em>P</em> = 0·05). A significant relationship between increasing microbleed burden and symptomatic intracerebral hemorrhage (<em>P</em> = 0·0015) was observed. Isolated analysis of studies using exclusively intravenous tissue plasminogen activator was insignificant. Our data suggest that patients with cerebral microbleeds are at increased risk for symptomatic intracerebral hemorrhage following thrombolysis for acute ischemic stroke. However, current data are insufficient to justify withholding thrombolytic therapy from acute ischemic stroke patients solely of the basis of cerebral microbleed presence.</p></div>
]]></content:encoded><description>
It has been questioned whether patients with cerebral microbleeds are at a greater risk for the development of symptomatic intracerebral hemorrhage following thrombolytic therapy in the management of acute ischemic stroke. Thus far, observational studies have not shown a statistically significant increased risk; however, these have been limited by small sample size. The aim is to better quantify the risk of postthrombolysis intracerebral hemorrhage in patients with acute ischemic stroke and cerebral microbleeds on magnetic resonance imaging. A systematic review of controlled studies investigating the presence of microbleeds on magnetic resonance imaging as a risk factor for intracerebral hemorrhage following thrombolysis in acute stroke patients was conducted. A random effects model meta-analysis was performed. In pooled analysis of five studies totaling 790 participants, the prevalence of microbleeds was 17%. The presence of microbleeds revealed a trend toward an increased risk of postthrombolysis symptomatic intracerebral hemorrhage [odds ratio: 1·98 (95% confidence interval, 0·90 to 4·35; P = 0·09), I2 = 0%]. Adjusted analysis minimizing potential bias resulted in an increased absolute risk of 4·6% for the development of symptomatic intracerebral hemorrhage in patients with cerebral microbleeds [odds ratio: 2·29 (95% confidence interval, 1·01 to 5·17), I2 = 0%] reaching borderline significance (P = 0·05). A significant relationship between increasing microbleed burden and symptomatic intracerebral hemorrhage (P = 0·0015) was observed. Isolated analysis of studies using exclusively intravenous tissue plasminogen activator was insignificant. Our data suggest that patients with cerebral microbleeds are at increased risk for symptomatic intracerebral hemorrhage following thrombolysis for acute ischemic stroke. However, current data are insufficient to justify withholding thrombolytic therapy from acute ischemic stroke patients solely of the basis of cerebral microbleed presence.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00868.x" xmlns="http://purl.org/rss/1.0/"><title>Burden of stroke in Cambodia</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00868.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Burden of stroke in Cambodia</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Keat Wei Loo, Siew Hua Gan</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:45:40.629284-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00868.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00868.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00868.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Panorama</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>In Cambodia, stroke is not ranked among the top 10 leading causes of death, but infectious disease are among the top three leading causes of death. This finding could be attributed to a lack of awareness among Cambodians of the signs and symptoms of stroke or to poor reporting, incomplete data, lack of neurologists and neurosurgeons, or low accessibility to the hospitals. The only study of stroke in Cambodia is the Prevalence of Non-Communicable Disease Risk Factors in Cambodia survey, which identified several stroke-related risk factors in the population. Tobacco chewing or smoking is the main risk factor for stroke in Cambodia. Traditional therapies, such as <em>oyt pleung</em> (moxibustion) and <em>jup</em> (cupping), are widely practiced for stroke rehabilitation. In Cambodia, there are few neurologists and few important equipment, such as magnetic resonance imaging machines and computed tomography scanners. The Cambodian government should cooperate with the World Health Organization and the United Nations Children's Fund to attract foreign expertise and technologies to treat stroke patients.</p></div>
]]></content:encoded><description>
In Cambodia, stroke is not ranked among the top 10 leading causes of death, but infectious disease are among the top three leading causes of death. This finding could be attributed to a lack of awareness among Cambodians of the signs and symptoms of stroke or to poor reporting, incomplete data, lack of neurologists and neurosurgeons, or low accessibility to the hospitals. The only study of stroke in Cambodia is the Prevalence of Non-Communicable Disease Risk Factors in Cambodia survey, which identified several stroke-related risk factors in the population. Tobacco chewing or smoking is the main risk factor for stroke in Cambodia. Traditional therapies, such as oyt pleung (moxibustion) and jup (cupping), are widely practiced for stroke rehabilitation. In Cambodia, there are few neurologists and few important equipment, such as magnetic resonance imaging machines and computed tomography scanners. The Cambodian government should cooperate with the World Health Organization and the United Nations Children's Fund to attract foreign expertise and technologies to treat stroke patients.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00864.x" xmlns="http://purl.org/rss/1.0/"><title>Reduced risk of poststroke pneumonia in thrombolyzed stroke patients with continued statin treatment</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00864.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Reduced risk of poststroke pneumonia in thrombolyzed stroke patients with continued statin treatment</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jan F. Scheitz, Matthias Endres, Peter U. Heuschmann, Heinrich J. Audebert, Christian H. Nolte</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:45:37.148424-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00864.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00864.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00864.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs864-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Pneumonia is a frequent complication after stroke with strong impact on clinical outcome. Statins have pleiotropic immunmodulatory properties and were recently shown to exert beneficial effects on the development and clinical course of pneumonia.</p></div></div>
<div class="section" id="ijs864-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>We aimed to investigate whether statin use is associated with a reduced risk of poststroke pneumonia in acute ischemic stroke patients treated with tissue plasminogen activator within 4·5hours.</p></div></div>
<div class="section" id="ijs864-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Data was extracted from a local register including all consecutive stroke patients who received thrombolysis at our institution. Prior statin use was identified retrospectively from clinical records and had to be continued after hospital admission. Poststroke pneumonia was diagnosed according to standardized criteria of US Centers for Disease Control and Prevention. Mortality and functional outcome at three-months were further assessed.</p></div></div>
<div class="section" id="ijs864-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Overall, 481 ischemic stroke patients were analyzed. Continued statin use was documented in 17% of the patients. Frequency of pneumonia was 11%. Patients with statin use were less likely to develop poststroke pneumonia (5% vs. 13%, <em>P</em> = 0·04). After multivariable adjustment for known risk factors for poststroke pneumonia (age, stroke severity, dysphagia, male sex and diabetes), statin treatment was negatively associated with pneumonia (OR 0·31; 95% CI 0·10–0·94). Occurrence of pneumonia independently predicted three-month mortality and functional outcome.</p></div></div>
<div class="section" id="ijs864-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Use of statins in acute ischemic stroke patients who receive thrombolysis might reduce the risk of poststroke pneumonia. Further studies are warranted to validate this finding.</p></div></div>
]]></content:encoded><description>

Background
Pneumonia is a frequent complication after stroke with strong impact on clinical outcome. Statins have pleiotropic immunmodulatory properties and were recently shown to exert beneficial effects on the development and clinical course of pneumonia.


Aims
We aimed to investigate whether statin use is associated with a reduced risk of poststroke pneumonia in acute ischemic stroke patients treated with tissue plasminogen activator within 4·5hours.


Methods
Data was extracted from a local register including all consecutive stroke patients who received thrombolysis at our institution. Prior statin use was identified retrospectively from clinical records and had to be continued after hospital admission. Poststroke pneumonia was diagnosed according to standardized criteria of US Centers for Disease Control and Prevention. Mortality and functional outcome at three-months were further assessed.


Results
Overall, 481 ischemic stroke patients were analyzed. Continued statin use was documented in 17% of the patients. Frequency of pneumonia was 11%. Patients with statin use were less likely to develop poststroke pneumonia (5% vs. 13%, P = 0·04). After multivariable adjustment for known risk factors for poststroke pneumonia (age, stroke severity, dysphagia, male sex and diabetes), statin treatment was negatively associated with pneumonia (OR 0·31; 95% CI 0·10–0·94). Occurrence of pneumonia independently predicted three-month mortality and functional outcome.


Conclusions
Use of statins in acute ischemic stroke patients who receive thrombolysis might reduce the risk of poststroke pneumonia. Further studies are warranted to validate this finding.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00861.x" xmlns="http://purl.org/rss/1.0/"><title>Inpatient stroke care quality for veterans: are there differences between Veterans Affairs medical centers in the stroke belt and other areas?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00861.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Inpatient stroke care quality for veterans: are there differences between Veterans Affairs medical centers in the stroke belt and other areas?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Huanguang Jia, Michael Phipps, Dawn Bravata, Jaime Castro, Xinli Li, Diana Ordin, Jennifer Myers, W. Bruce Vogel, Linda Williams, Neale Chumbler</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:45:32.485501-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00861.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00861.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00861.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs861-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Stroke mortality has been found to be much higher among residents in the stroke belt region than in the rest of United States, but it is not known whether differences exist in the quality of stroke care provided in Department of Veterans Affairs medical centers in states inside and outside this region.</p></div></div>
<div class="section" id="ijs861-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Objective</h4><div class="para"><p>We compared mortality and inpatient stroke care quality between Veterans Affairs medical centers inside and outside the stroke belt region.</p></div></div>
<div class="section" id="ijs861-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Study patients were veterans hospitalized for ischemic stroke at 129 Veterans Affairs medical centers. Inpatient stroke care quality was assessed by 14 quality indicators. Multivariable logistic regression models were fit to examine differences in quality between facilities inside and outside the stroke belt, adjusting for patient characteristics and Veterans Affairs medical centers clustering effect.</p></div></div>
<div class="section" id="ijs861-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Among the 3909 patients, 28·1% received inpatient ischemic stroke care in 28 stroke belt Veterans Affairs medical centers, and 71·9% obtained care in 101 non-stroke belt Veterans Affairs medical centers. Patients cared for in stroke belt Veterans Affairs medical centers were more likely to be younger, Black, married, have a higher stroke severity, and less likely to be ambulatory pre-stroke. We found no statistically significant differences in short- and long-term post-admission mortality and inpatient care quality indicators between the patients cared for in stroke belt and non-stroke belt Veterans Affairs medical centers after risk adjustment.</p></div></div>
<div class="section" id="ijs861-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>These data suggest that a stroke belt does not exist within the Veterans Affairs health care system in terms of either post-admission mortality or inpatient care quality.</p></div></div>
]]></content:encoded><description>

Background
Stroke mortality has been found to be much higher among residents in the stroke belt region than in the rest of United States, but it is not known whether differences exist in the quality of stroke care provided in Department of Veterans Affairs medical centers in states inside and outside this region.


Objective
We compared mortality and inpatient stroke care quality between Veterans Affairs medical centers inside and outside the stroke belt region.


Methods
Study patients were veterans hospitalized for ischemic stroke at 129 Veterans Affairs medical centers. Inpatient stroke care quality was assessed by 14 quality indicators. Multivariable logistic regression models were fit to examine differences in quality between facilities inside and outside the stroke belt, adjusting for patient characteristics and Veterans Affairs medical centers clustering effect.


Results
Among the 3909 patients, 28·1% received inpatient ischemic stroke care in 28 stroke belt Veterans Affairs medical centers, and 71·9% obtained care in 101 non-stroke belt Veterans Affairs medical centers. Patients cared for in stroke belt Veterans Affairs medical centers were more likely to be younger, Black, married, have a higher stroke severity, and less likely to be ambulatory pre-stroke. We found no statistically significant differences in short- and long-term post-admission mortality and inpatient care quality indicators between the patients cared for in stroke belt and non-stroke belt Veterans Affairs medical centers after risk adjustment.


Conclusions
These data suggest that a stroke belt does not exist within the Veterans Affairs health care system in terms of either post-admission mortality or inpatient care quality.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00859.x" xmlns="http://purl.org/rss/1.0/"><title>Time dependence of reliability of noncontrast computed tomography in comparison to computed tomography angiography source image in acute ischemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00859.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Time dependence of reliability of noncontrast computed tomography in comparison to computed tomography angiography source image in acute ischemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Simerpreet Bal, Rohit Bhatia, Bijoy K. Menon, Nandavar Shobha, Volker Puetz, Imanuel Dzialowski, Jayesh Modi, Mayank Goyal, Michael D. Hill, Eric E. Smith, Andrew M. Demchuk</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:45:29.243161-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00859.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00859.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00859.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>There is no consensus on how the reliability and predictive ability of noncontrast computed tomography (NCCT) and computed tomography angiography source image (CTASI) change over time from acute ischemic stroke onset. We hypothesized that the reliability for detecting early ischemic changes (EIC) would be lower in early time periods and that changes identified on CTASI would be more reliable across examiners than changes identified on NCCT. To address this, we compared the relationships between CTASI, NCCT, and final infarct in patients with initial computed tomography (CT) imaging at different time points after stroke onset. Patients with acute ischemic stroke with proximal anterior circulation occlusions (internal carotid artery, middle carotid artery M1, proximal M2) from Calgary CT Angiography (CTA) database were studied. The cohort was categorized in four groups based on time from stroke onset to baseline NCCT/CTA: 0–90 mins (<em>n</em> = 69), 91–180 mins (<em>n</em> = 88), 181–360 mins (<em>n</em> = 46), and &gt;360 mins (<em>n</em> = 58). Median scores of NCCT-Alberta Stroke Program Early CT Score (ASPECTS), CTASI ASPECTS, and follow-up ASPECTS among different time categories were compared. To determine reliability, a subsample of NCCT brain and CTASI were interpreted at separate sessions weeks apart by two neuroradiologists and two stroke neurologists in random order. Median and mean ASPECTS ratings on NCCT and CTASI were higher than final ASPECTS in each time category (<em>P</em> &lt; 0·001 for all comparisons). CTASI ASPECTS was lower than NCCT ASPECTS in each time category, and differences were significant at 0–90 mins and 91–180 mins (<em>P</em> &lt; 0·001). The least agreement among readers was in detection of EIC on NCCT brain in the ultra-early phase (&lt;90 mins) [intraclass correlation coefficient (ICC) = 0·48. By contrast, there was excellent agreement on EIC on CTASI regardless of time period (ICC = 0·87–0·96). Using ASPECTS methodology, CTASI is more reliable than NCCT at predicting final infarct extent particularly in the early time windows.</p></div>
]]></content:encoded><description>
There is no consensus on how the reliability and predictive ability of noncontrast computed tomography (NCCT) and computed tomography angiography source image (CTASI) change over time from acute ischemic stroke onset. We hypothesized that the reliability for detecting early ischemic changes (EIC) would be lower in early time periods and that changes identified on CTASI would be more reliable across examiners than changes identified on NCCT. To address this, we compared the relationships between CTASI, NCCT, and final infarct in patients with initial computed tomography (CT) imaging at different time points after stroke onset. Patients with acute ischemic stroke with proximal anterior circulation occlusions (internal carotid artery, middle carotid artery M1, proximal M2) from Calgary CT Angiography (CTA) database were studied. The cohort was categorized in four groups based on time from stroke onset to baseline NCCT/CTA: 0–90 mins (n = 69), 91–180 mins (n = 88), 181–360 mins (n = 46), and &gt;360 mins (n = 58). Median scores of NCCT-Alberta Stroke Program Early CT Score (ASPECTS), CTASI ASPECTS, and follow-up ASPECTS among different time categories were compared. To determine reliability, a subsample of NCCT brain and CTASI were interpreted at separate sessions weeks apart by two neuroradiologists and two stroke neurologists in random order. Median and mean ASPECTS ratings on NCCT and CTASI were higher than final ASPECTS in each time category (P &lt; 0·001 for all comparisons). CTASI ASPECTS was lower than NCCT ASPECTS in each time category, and differences were significant at 0–90 mins and 91–180 mins (P &lt; 0·001). The least agreement among readers was in detection of EIC on NCCT brain in the ultra-early phase (&lt;90 mins) [intraclass correlation coefficient (ICC) = 0·48. By contrast, there was excellent agreement on EIC on CTASI regardless of time period (ICC = 0·87–0·96). Using ASPECTS methodology, CTASI is more reliable than NCCT at predicting final infarct extent particularly in the early time windows.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00845.x" xmlns="http://purl.org/rss/1.0/"><title>Stroke care in Central Eastern Europe: current problems and call for action</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00845.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Stroke care in Central Eastern Europe: current problems and call for action</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Laura Lenti, Michael Brainin, Ekaterina Titianova, Sandra Morovic, Vida Demarin, Pavel Kalvach, David Skoloudik, Adam Kobayashi, Anna Czlonkowska, Dafin F. Muresanu, Ksenia Shekhovtsova, Veronica I. Skvortsova, Nadezda Sternic, Ljiljana Beslac Bumbasirevic, Viktor Svigelj, Peter Turcani, Dániel Bereczki, László Csiba</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:45:23.861509-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00845.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00845.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00845.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Panorama</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Stroke is a major medical problem and one of the leading causes of mortality and disability all over in Europe. However, there are significant East–West differences in stroke care as well as in stroke mortality and morbidity rates. Central and Eastern European countries that formerly had centralized and socialist health care systems have serious and similar problems in organizing health and stroke care 20 years after the political transition. In Central and Eastern Europe, stroke is more frequent, the mortality rate is higher, and the victims are younger than in Western Europe. High-risk patients live in worse environmental conditions, and the socioeconomic consequences of stroke further weaken the economic development of these countries. To address these issues, a round table conference was organized. The main aim of this conference was to discuss problems to be solved related to acute and chronic stroke care in Central and Eastern European countries, and also, to exchange ideas on possible solutions. In this article, the discussed problems and possible solutions will be summarized, and introduce ‘The Budapest Statement of Stroke Experts of Central and Eastern European countries′.</p></div>
]]></content:encoded><description>
Stroke is a major medical problem and one of the leading causes of mortality and disability all over in Europe. However, there are significant East–West differences in stroke care as well as in stroke mortality and morbidity rates. Central and Eastern European countries that formerly had centralized and socialist health care systems have serious and similar problems in organizing health and stroke care 20 years after the political transition. In Central and Eastern Europe, stroke is more frequent, the mortality rate is higher, and the victims are younger than in Western Europe. High-risk patients live in worse environmental conditions, and the socioeconomic consequences of stroke further weaken the economic development of these countries. To address these issues, a round table conference was organized. The main aim of this conference was to discuss problems to be solved related to acute and chronic stroke care in Central and Eastern European countries, and also, to exchange ideas on possible solutions. In this article, the discussed problems and possible solutions will be summarized, and introduce ‘The Budapest Statement of Stroke Experts of Central and Eastern European countries′.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00870.x" xmlns="http://purl.org/rss/1.0/"><title>Comparison of quantitative estimation of intracerebral hemorrhage and infarct volumes after thromboembolism in an embolic stroke model</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00870.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Comparison of quantitative estimation of intracerebral hemorrhage and infarct volumes after thromboembolism in an embolic stroke model</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Nina Eriksen, Rune S. Rasmussen, Karsten Overgaard, Flemming F. Johansen, Bente Pakkenberg</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-29T04:46:17.371019-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00870.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00870.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00870.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs870-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Strokes have both ischemic and hemorrhagic components, but most studies of experimental stroke only address the ischemic component. This is likely because investigations of hemorrhagic transformation are hindered by the lack of methods based on unbiased principles for volume estimation.</p></div></div>
<div class="section" id="ijs870-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>We evaluated different methods for estimating the volume of infarcts, hemorrhages, after embolic middle cerebral artery occlusion with or without thrombolysis.</p></div></div>
<div class="section" id="ijs870-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>An experimental thromboembolytic rat model was used in this study. The rats underwent surgery and were placed in two groups. Group 1 was treated with saline, and group 2 was treated with 20 mg/kg recombinant tissue plasminogen activator to promote intracerebral hemorrhages. Stereology, semiautomated computer estimation, and manual erythrocyte counting were used to test the precision and efficiency of determining the size of the infarct and intracerebral hemorrhage.</p></div></div>
<div class="section" id="ijs870-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>No differences were observed in the infarct volume or amount of bleeding when comparing the three methods of volume estimation. Although semiautomated computer estimation and manual erythrocyte counting provided similar results as the stereological measurements, the stereological method was the most efficient and advantageous.</p></div></div>
<div class="section" id="ijs870-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>We found that stereology was the superior method for quantification of hemorrhagic volume, especially for rodent petechial bleeding, which is otherwise difficult to measure. Our results suggest the possibility of measuring both the ischemic and the hemorrhagic components of stroke, two parameters that may be differentially regulated when therapeutic regimens are tested.</p></div></div>
]]></content:encoded><description>

Background
Strokes have both ischemic and hemorrhagic components, but most studies of experimental stroke only address the ischemic component. This is likely because investigations of hemorrhagic transformation are hindered by the lack of methods based on unbiased principles for volume estimation.


Aims
We evaluated different methods for estimating the volume of infarcts, hemorrhages, after embolic middle cerebral artery occlusion with or without thrombolysis.


Methods
An experimental thromboembolytic rat model was used in this study. The rats underwent surgery and were placed in two groups. Group 1 was treated with saline, and group 2 was treated with 20 mg/kg recombinant tissue plasminogen activator to promote intracerebral hemorrhages. Stereology, semiautomated computer estimation, and manual erythrocyte counting were used to test the precision and efficiency of determining the size of the infarct and intracerebral hemorrhage.


Results
No differences were observed in the infarct volume or amount of bleeding when comparing the three methods of volume estimation. Although semiautomated computer estimation and manual erythrocyte counting provided similar results as the stereological measurements, the stereological method was the most efficient and advantageous.


Conclusions
We found that stereology was the superior method for quantification of hemorrhagic volume, especially for rodent petechial bleeding, which is otherwise difficult to measure. Our results suggest the possibility of measuring both the ischemic and the hemorrhagic components of stroke, two parameters that may be differentially regulated when therapeutic regimens are tested.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00872.x" xmlns="http://purl.org/rss/1.0/"><title>Validation of the Totaled Heath Risks In Vascular Events (THRIVE) score for outcome prediction in endovascular stroke treatment</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00872.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Validation of the Totaled Heath Risks In Vascular Events (THRIVE) score for outcome prediction in endovascular stroke treatment</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Alexander C. Flint, Hooman Kamel, Vivek A. Rao, Sean P. Cullen, Bonnie S. Faigeles, Wade S. Smith</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-29T04:46:01.523017-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00872.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00872.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00872.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs872-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>We recently developed the Totaled Health Risks In Vascular Events (THRIVE) score to predict outcomes after endovascular stroke treatment. The THRIVE score, which incorporates age, National Institutes of Health Stroke Scale score, and three medical comorbidities (hypertension, diabetes mellitus, and atrial fibrillation), was developed using data from the Mechanical Embolus Removal in Cerebral Ischemia (MERCI) and Multi MERCI trials.</p></div></div>
<div class="section" id="ijs872-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>We set out to perform external validation of the THRIVE score using data from the largest registry of endovascular stroke treatment performed to date, the Merci Registry.</p></div></div>
<div class="section" id="ijs872-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We compared the performance of the THRIVE score in two different data sets: the development cohort (the MERCI and Multi MERCI trials, <em>n</em> = 305) and a validation cohort (the Merci Registry, a prospective multicenter registry of patients undergoing endovascular stroke treatment, <em>n</em> = 1000). We examined the predictive utility of the THRIVE score across the range of clinical outcomes and used receiver–operator characteristics curve analysis to compare score performance in the two data sets.</p></div></div>
<div class="section" id="ijs872-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The THRIVE score predicted good outcome, death, and the full range of the modified Rankin Scale in a similar fashion between the MERCI trials and the Merci Registry. Receiver–operator characteristics curve comparisons showed no statistically significant difference in the performance of the THRIVE score between the two data sets: for good outcome, the receiver–operator characteristics area under the curve was 0·293 for the MERCI trials and 0·266 for the Merci Registry (<em>P</em> = 0·47) and for death, the receiver–operator characteristics area under the curve was 0·692 for the MERCI trials and 0·717 for the Merci Registry (<em>P</em> = 0·48). The THRIVE score and vessel recanalization were also found to be independent and unrelated predictors of clinical outcome.</p></div></div>
<div class="section" id="ijs872-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The THRIVE score reliably predicts outcomes after endovascular stroke treatment and may be useful as a clinical prognostic tool and to perform severity adjustments in stroke clinical research.</p></div></div>
]]></content:encoded><description>

Background
We recently developed the Totaled Health Risks In Vascular Events (THRIVE) score to predict outcomes after endovascular stroke treatment. The THRIVE score, which incorporates age, National Institutes of Health Stroke Scale score, and three medical comorbidities (hypertension, diabetes mellitus, and atrial fibrillation), was developed using data from the Mechanical Embolus Removal in Cerebral Ischemia (MERCI) and Multi MERCI trials.


Aims
We set out to perform external validation of the THRIVE score using data from the largest registry of endovascular stroke treatment performed to date, the Merci Registry.


Methods
We compared the performance of the THRIVE score in two different data sets: the development cohort (the MERCI and Multi MERCI trials, n = 305) and a validation cohort (the Merci Registry, a prospective multicenter registry of patients undergoing endovascular stroke treatment, n = 1000). We examined the predictive utility of the THRIVE score across the range of clinical outcomes and used receiver–operator characteristics curve analysis to compare score performance in the two data sets.


Results
The THRIVE score predicted good outcome, death, and the full range of the modified Rankin Scale in a similar fashion between the MERCI trials and the Merci Registry. Receiver–operator characteristics curve comparisons showed no statistically significant difference in the performance of the THRIVE score between the two data sets: for good outcome, the receiver–operator characteristics area under the curve was 0·293 for the MERCI trials and 0·266 for the Merci Registry (P = 0·47) and for death, the receiver–operator characteristics area under the curve was 0·692 for the MERCI trials and 0·717 for the Merci Registry (P = 0·48). The THRIVE score and vessel recanalization were also found to be independent and unrelated predictors of clinical outcome.


Conclusions
The THRIVE score reliably predicts outcomes after endovascular stroke treatment and may be useful as a clinical prognostic tool and to perform severity adjustments in stroke clinical research.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00871.x" xmlns="http://purl.org/rss/1.0/"><title>Prediction of vascular risk after stroke – protocol and pilot data of the Prospective Cohort with Incident Stroke (PROSCIS)</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00871.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Prediction of vascular risk after stroke – protocol and pilot data of the Prospective Cohort with Incident Stroke (PROSCIS)</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Thomas G. Liman, Vera Zietemann, Silke Wiedmann, Gerhard J. Jungehuelsing, Matthias Endres, Frank A. Wollenweber, Ian Wellwood, Martin Dichgans, Peter U. Heuschmann</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-29T04:45:53.162296-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00871.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00871.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00871.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs871-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Long-term risk of vascular disease is substantially increased after stroke with several models proposed to predict subsequent stroke and other vascular events after an index event. However, recent validation studies demonstrate limited predictive properties of available prognostic models.</p></div></div>
<div class="section" id="ijs871-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>We aim to determine prediction models of different complexity for the combined vascular end-point of stroke, myocardial infarction, and vascular death at three-years after first-ever stroke. An independent external validation of the developed models will be performed.</p></div></div>
<div class="section" id="ijs871-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Prospective observational hospital-based cohort study of patients after first-ever stroke.</p></div></div>
<div class="section" id="ijs871-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The new predictive models will be developed using the following steps: (1) Development of a basic score based on clinical history data (e.g. hypertension, myocardial infarction, and atrial fibrillation); (2) Development of an advanced score including additional factors such as blood-based biomarkers and results of vascular imaging; (3) Comparing the models fit using different methods (discrimination, calibration); (4) Assessment of clinical utility of an advanced score using methods based on reclassification tables (e.g. net reclassification improvement, integrated discrimination improvement, decision curve analysis); and (5) Investigation of external validity.</p></div></div>
<div class="section" id="ijs871-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Outcomes</h4><div class="para"><p>Primary outcome is a combined vascular end-point composed of stroke, myocardial infarction, and vascular death at three-years after stroke. Furthermore, each component of the composite end-point will be investigated individually and the patterns and time points of risk transitions between vascular end-points and stroke sub-types will be determined.</p></div></div>
]]></content:encoded><description>

Rationale
Long-term risk of vascular disease is substantially increased after stroke with several models proposed to predict subsequent stroke and other vascular events after an index event. However, recent validation studies demonstrate limited predictive properties of available prognostic models.


Aims
We aim to determine prediction models of different complexity for the combined vascular end-point of stroke, myocardial infarction, and vascular death at three-years after first-ever stroke. An independent external validation of the developed models will be performed.


Design
Prospective observational hospital-based cohort study of patients after first-ever stroke.


Methods
The new predictive models will be developed using the following steps: (1) Development of a basic score based on clinical history data (e.g. hypertension, myocardial infarction, and atrial fibrillation); (2) Development of an advanced score including additional factors such as blood-based biomarkers and results of vascular imaging; (3) Comparing the models fit using different methods (discrimination, calibration); (4) Assessment of clinical utility of an advanced score using methods based on reclassification tables (e.g. net reclassification improvement, integrated discrimination improvement, decision curve analysis); and (5) Investigation of external validity.


Outcomes
Primary outcome is a combined vascular end-point composed of stroke, myocardial infarction, and vascular death at three-years after stroke. Furthermore, each component of the composite end-point will be investigated individually and the patterns and time points of risk transitions between vascular end-points and stroke sub-types will be determined.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00857.x" xmlns="http://purl.org/rss/1.0/"><title>Mortality and causes of death in the Familial Intracranial Aneurysm study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00857.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Mortality and causes of death in the Familial Intracranial Aneurysm study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Laura Sauerbeck, Richard Hornung, Daniel Woo, Charles J. Moomaw, Craig Anderson, E. Sander Connolly, Guy A. Rouleau, Robert D. Brown, Joseph P. Broderick, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-29T04:45:46.65114-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00857.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00857.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00857.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs857-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Higher mortality for patients with aneurysmal subarachnoid haemorrhage has been reported.</p></div></div>
<div class="section" id="ijs857-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>In families with intracranial aneurysms, we sought to determine whether mortality among subjects with intracranial aneurysm (affected) was higher and related to rupture, compared with unaffected family members.</p></div></div>
<div class="section" id="ijs857-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Subjects enrolled in the Familial Intracranial Aneurysm protocol were contacted yearly and their status was obtained. If reported to be deceased, the cause of death was verified by available records. A Cox proportional hazards model was utilized to compare mortality rates.</p></div></div>
<div class="section" id="ijs857-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Of the 2794 subjects, 1073 were affected and 1721 were unaffected. There were 8525 person-years of follow-up (mean 3·05 ± 1·73 years) and 85 deaths. Age at study entry for the affected (58·4 ± 11·9 years) was significantly older (<em>P</em> &lt; 0·0001) than for the unaffected (52·2 ± 16·1). After adjusting for age, the overall mortality rate for the affected subjects was not significantly different from that for the unaffected (Rate Ratio [RR] 1·26, 95% confidence interval 0·82–1·93, <em>P</em> = 0·292). There was a strong effect modification due to age. The mortality rate ratio of the affected to the unaffected who were ≤60 years of age was RR = 3·48 (95% confidence interval: 1·59–7·63, <em>P</em> = 0·002), the rate for the affected subjects who were ≥60 was less than the rate for the unaffected (RR = 0·69, 95% confidence interval: 0·404–1·19, <em>P</em> = 0·178). The affected who had ruptures had 2·62 times the mortality rate as those without ruptures (95% confidence interval 1·43–4·80, <em>P</em> = 0·002).</p></div></div>
<div class="section" id="ijs857-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>The overall mortality was similar for the affected and unaffected subjects in this cohort. Among the affected only, those with ruptured intracranial aneurysm had a higher mortality rate than those without ruptured.</p></div></div>
]]></content:encoded><description>

Background
Higher mortality for patients with aneurysmal subarachnoid haemorrhage has been reported.


Aims
In families with intracranial aneurysms, we sought to determine whether mortality among subjects with intracranial aneurysm (affected) was higher and related to rupture, compared with unaffected family members.


Methods
Subjects enrolled in the Familial Intracranial Aneurysm protocol were contacted yearly and their status was obtained. If reported to be deceased, the cause of death was verified by available records. A Cox proportional hazards model was utilized to compare mortality rates.


Results
Of the 2794 subjects, 1073 were affected and 1721 were unaffected. There were 8525 person-years of follow-up (mean 3·05 ± 1·73 years) and 85 deaths. Age at study entry for the affected (58·4 ± 11·9 years) was significantly older (P &lt; 0·0001) than for the unaffected (52·2 ± 16·1). After adjusting for age, the overall mortality rate for the affected subjects was not significantly different from that for the unaffected (Rate Ratio [RR] 1·26, 95% confidence interval 0·82–1·93, P = 0·292). There was a strong effect modification due to age. The mortality rate ratio of the affected to the unaffected who were ≤60 years of age was RR = 3·48 (95% confidence interval: 1·59–7·63, P = 0·002), the rate for the affected subjects who were ≥60 was less than the rate for the unaffected (RR = 0·69, 95% confidence interval: 0·404–1·19, P = 0·178). The affected who had ruptures had 2·62 times the mortality rate as those without ruptures (95% confidence interval 1·43–4·80, P = 0·002).


Conclusion
The overall mortality was similar for the affected and unaffected subjects in this cohort. Among the affected only, those with ruptured intracranial aneurysm had a higher mortality rate than those without ruptured.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00855.x" xmlns="http://purl.org/rss/1.0/"><title>Reduced risk of death with warfarin – results of an observational nationwide study of 20 442 patients with atrial fibrillation and ischaemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00855.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Reduced risk of death with warfarin – results of an observational nationwide study of 20 442 patients with atrial fibrillation and ischaemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Signild Åsberg, Marie Eriksson, Karin M. Henriksson, Andreas Terént</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-29T04:45:41.448875-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00855.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00855.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00855.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs855-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Warfarin is demonstrated to be superior in efficacy over antiplatelet agents for the prevention of stroke, but the relationship between warfarin and mortality is less clear. Our aim was to investigate this relationship in a large cohort of unselected patients with atrial fibrillation and ischaemic stroke.</p></div></div>
<div class="section" id="ijs855-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>This observational study was based on patients who were discharged alive and registered in the Swedish Stroke Register in 2001 through 2005. Vital status was retrieved by linkage to the Swedish Cause of Death Register. We calculated a propensity score for the likelihood of warfarin prescription at discharge from hospital. The risk of death and 95% confidence intervals were estimated in Cox regression models.</p></div></div>
<div class="section" id="ijs855-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Out of the 20 442 patients with atrial fibrillation and ischaemic stroke (mean age = 79·5 years), 31% (<em>n</em> = 6399) were prescribed warfarin. After adjustment for the propensity score, warfarin was associated with a reduced risk of death (0·67; 95% confidence interval, 0·63–0·71). The crude rate (per 100 person-years) of fatal non-haemorrhagic stroke was lower in patients who received warfarin (1·60; 95% confidence interval, 1·34–1·89) compared to those who received antiplatelet (6·83; 95% confidence interval, 6·42–7·25). The rates (per 100 person-years) of fatal haemorrhagic stroke were 0·21 (95% confidence interval, 0·12–0·32) and 0·43 (95% confidence interval, 0·34–0·55) in patients prescribed warfarin and antiplatelet therapy, respectively.</p></div></div>
<div class="section" id="ijs855-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>In addition to its established benefit for stroke prevention, warfarin therapy in patients with atrial fibrillation and ischaemic stroke was associated with a reduced risk of death, without an increased risk of fatal haemorrhagic stroke.</p></div></div>
]]></content:encoded><description>

Background
Warfarin is demonstrated to be superior in efficacy over antiplatelet agents for the prevention of stroke, but the relationship between warfarin and mortality is less clear. Our aim was to investigate this relationship in a large cohort of unselected patients with atrial fibrillation and ischaemic stroke.


Methods
This observational study was based on patients who were discharged alive and registered in the Swedish Stroke Register in 2001 through 2005. Vital status was retrieved by linkage to the Swedish Cause of Death Register. We calculated a propensity score for the likelihood of warfarin prescription at discharge from hospital. The risk of death and 95% confidence intervals were estimated in Cox regression models.


Results
Out of the 20 442 patients with atrial fibrillation and ischaemic stroke (mean age = 79·5 years), 31% (n = 6399) were prescribed warfarin. After adjustment for the propensity score, warfarin was associated with a reduced risk of death (0·67; 95% confidence interval, 0·63–0·71). The crude rate (per 100 person-years) of fatal non-haemorrhagic stroke was lower in patients who received warfarin (1·60; 95% confidence interval, 1·34–1·89) compared to those who received antiplatelet (6·83; 95% confidence interval, 6·42–7·25). The rates (per 100 person-years) of fatal haemorrhagic stroke were 0·21 (95% confidence interval, 0·12–0·32) and 0·43 (95% confidence interval, 0·34–0·55) in patients prescribed warfarin and antiplatelet therapy, respectively.


Conclusions
In addition to its established benefit for stroke prevention, warfarin therapy in patients with atrial fibrillation and ischaemic stroke was associated with a reduced risk of death, without an increased risk of fatal haemorrhagic stroke.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00858.x" xmlns="http://purl.org/rss/1.0/"><title>
STRoke Adverse outcome is associated WIth NoSocomial Infections (STRAWINSKI): procalcitonin ultrasensitive-guided antibacterial therapy in severe ischaemic stroke patients – rationale and protocol for a randomized controlled trial</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00858.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">
STRoke Adverse outcome is associated WIth NoSocomial Infections (STRAWINSKI): procalcitonin ultrasensitive-guided antibacterial therapy in severe ischaemic stroke patients – rationale and protocol for a randomized controlled trial</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lena Ulm, Stephanie Ohlraun, Hendrik Harms, Sarah Hoffmann, Juliane Klehmet, Stefan Ebmeyer, Oliver Hartmann, Christian Meisel, Stefan D. Anker, Andreas Meisel</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-28T05:16:58.066781-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00858.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00858.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00858.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs858-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Stroke-associated pneumonia is one of the most common causes of poor outcome in stroke patients. Clinical signs and laboratory parameters of stroke-associated infections are often inconclusive. Biomarkers may help to identify stroke patients at high risk for pneumonia and to guide physicians in an early antibiotic treatment, thereby improving stroke outcome.</p></div></div>
<div class="section" id="ijs858-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>The aim of the present study is to investigate whether procalcitonin ultrasensitive-guided antibiotic treatment improves functional outcome after severe ischaemic stroke by early treatment of pneumonia.</p></div></div>
<div class="section" id="ijs858-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>STRAWINSKI is an investigator-initiated, multicentre, randomized, controlled trial with blinded assessment of outcome comparing procalcitonin ultrasensitive-guided antibiotic treatment with standard care.</p></div></div>
<div class="section" id="ijs858-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study</h4><div class="para"><p>200 patients with ischaemic stroke in the middle cerebral artery territory and a score &gt;9 on the National Institutes of Health Stroke Scale will be included and randomly assigned to two groups. One group will receive procalcitonin-based antibiotic therapy guidance; the other group will receive standard stroke unit care.</p></div></div>
<div class="section" id="ijs858-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Outcomes</h4><div class="para"><p>The primary endpoint is functional outcome at day 90 after stroke on the modified Rankin Scale, dichotomized as favourable (0–4) or unfavourable outcome (5–6). Secondary endpoints are time to first event of death, rehospitalization, or recurrent stroke; death rate, infection rate, and days with fever up to day 7; length of hospital stay and hospital discharge disposition; shift analysis of the modified Rankin Scale; Barthel Index and days alive and out of hospital at day 90; use of antibiotics until day 90; and modified Rankin Scale, Barthel Index, and infarct volume at day 180.</p></div></div>
]]></content:encoded><description>

Rationale
Stroke-associated pneumonia is one of the most common causes of poor outcome in stroke patients. Clinical signs and laboratory parameters of stroke-associated infections are often inconclusive. Biomarkers may help to identify stroke patients at high risk for pneumonia and to guide physicians in an early antibiotic treatment, thereby improving stroke outcome.


Aim
The aim of the present study is to investigate whether procalcitonin ultrasensitive-guided antibiotic treatment improves functional outcome after severe ischaemic stroke by early treatment of pneumonia.


Design
STRAWINSKI is an investigator-initiated, multicentre, randomized, controlled trial with blinded assessment of outcome comparing procalcitonin ultrasensitive-guided antibiotic treatment with standard care.


Study
200 patients with ischaemic stroke in the middle cerebral artery territory and a score &gt;9 on the National Institutes of Health Stroke Scale will be included and randomly assigned to two groups. One group will receive procalcitonin-based antibiotic therapy guidance; the other group will receive standard stroke unit care.


Outcomes
The primary endpoint is functional outcome at day 90 after stroke on the modified Rankin Scale, dichotomized as favourable (0–4) or unfavourable outcome (5–6). Secondary endpoints are time to first event of death, rehospitalization, or recurrent stroke; death rate, infection rate, and days with fever up to day 7; length of hospital stay and hospital discharge disposition; shift analysis of the modified Rankin Scale; Barthel Index and days alive and out of hospital at day 90; use of antibiotics until day 90; and modified Rankin Scale, Barthel Index, and infarct volume at day 180.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00844.x" xmlns="http://purl.org/rss/1.0/"><title>Utilization of intravenous thrombolysis is increasing in the United States</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00844.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Utilization of intravenous thrombolysis is increasing in the United States</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Deena M. Nasr, Waleed Brinjikji, Harry J. Cloft, Alejandro A. Rabinstein</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-09T20:23:49.578067-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00844.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00844.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00844.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs844-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Evaluating recombinant tissue plasminogen activator utilization rates is important, as many studies have demonstrated that administration of recombinant tissue plasminogen activator to qualified patients significantly improves prognosis.</p></div></div>
<div class="section" id="ijs844-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>We investigated recent trends in the utilization and outcomes of administration of intravenous recombinant tissue plasminogen activator in the United States using the National Inpatient Sample between 2001 and 2008.</p></div></div>
<div class="section" id="ijs844-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We identified patients with a primary diagnosis of acute ischemic stroke who underwent treatment with intravenous recombinant tissue plasminogen activator and studied utilization rates and clinical outcomes: discharge to long-term facility (morbidity), in-hospital death (mortality), and intracranial hemorrhage. Information on demographics, hospital characteristics, and comorbidities was collected. A multivariate logistic regression analysis was performed to determine independent predictors of morbidity, mortality, and intracranial hemorrhage.</p></div></div>
<div class="section" id="ijs844-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Intravenous recombinant tissue plasminogen activator utilization increased from 1·3% in 2001 to 3·5% in 2008. On multivariate analysis, variables associated with increased morbidity after intravenous recombinant tissue plasminogen activator administration included advanced age (<em>P</em> &lt; 0·001), female gender (<em>P</em> &lt; 0·001), and comorbidities of atrial fibrillation (<em>P</em> &lt; 0·001) and hypertension (<em>P</em> &lt; 0·001). Increased mortality was associated with increased age (<em>P</em> &lt; 0·001) and comorbidities of atrial fibrillation, congestive heart failure, coronary artery disease, and diabetes (<em>P</em> &lt; 0·001 for all comorbidities).</p></div></div>
<div class="section" id="ijs844-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Intravenous recombinant tissue plasminogen activator utilization rates increased between 2001 and 2008. Advanced age and atrial fibrillation were significantly associated with increased morbidity and mortality among patients treated with intravenous recombinant tissue plasminogen activator.</p></div></div>
]]></content:encoded><description>

Background
Evaluating recombinant tissue plasminogen activator utilization rates is important, as many studies have demonstrated that administration of recombinant tissue plasminogen activator to qualified patients significantly improves prognosis.


Aims
We investigated recent trends in the utilization and outcomes of administration of intravenous recombinant tissue plasminogen activator in the United States using the National Inpatient Sample between 2001 and 2008.


Methods
We identified patients with a primary diagnosis of acute ischemic stroke who underwent treatment with intravenous recombinant tissue plasminogen activator and studied utilization rates and clinical outcomes: discharge to long-term facility (morbidity), in-hospital death (mortality), and intracranial hemorrhage. Information on demographics, hospital characteristics, and comorbidities was collected. A multivariate logistic regression analysis was performed to determine independent predictors of morbidity, mortality, and intracranial hemorrhage.


Results
Intravenous recombinant tissue plasminogen activator utilization increased from 1·3% in 2001 to 3·5% in 2008. On multivariate analysis, variables associated with increased morbidity after intravenous recombinant tissue plasminogen activator administration included advanced age (P &lt; 0·001), female gender (P &lt; 0·001), and comorbidities of atrial fibrillation (P &lt; 0·001) and hypertension (P &lt; 0·001). Increased mortality was associated with increased age (P &lt; 0·001) and comorbidities of atrial fibrillation, congestive heart failure, coronary artery disease, and diabetes (P &lt; 0·001 for all comorbidities).


Conclusions
Intravenous recombinant tissue plasminogen activator utilization rates increased between 2001 and 2008. Advanced age and atrial fibrillation were significantly associated with increased morbidity and mortality among patients treated with intravenous recombinant tissue plasminogen activator.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00843.x" xmlns="http://purl.org/rss/1.0/"><title>The Risk of Paradoxical Embolism (RoPE) Study: initial description of the completed database</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00843.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The Risk of Paradoxical Embolism (RoPE) Study: initial description of the completed database</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">David E. Thaler, Emanuele Di Angelantonio, Marco R. Di Tullio, Jennifer S. Donovan, John Griffith, Shunichi Homma, Cheryl Jaigobin, Jean-Louis Mas, Heinrich P. Mattle, Patrik Michel, Marie-Luise Mono, Krassen Nedeltchev, Federica Papetti, Robin Ruthazer, Joaquín Serena, Christian Weimar, Mitchell S. V. Elkind, David M. Kent</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-09T20:23:45.918203-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00843.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00843.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00843.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs843-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Detecting a benefit from closure of patent foramen ovale in patients with cryptogenic stroke is hampered by low rates of stroke recurrence and uncertainty about the causal role of patent foramen ovale in the index event. A method to predict patent foramen ovale-attributable recurrence risk is needed. However, individual databases generally have too few stroke recurrences to support risk modeling. Prior studies of this population have been limited by low statistical power for examining factors related to recurrence.</p></div></div>
<div class="section" id="ijs843-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The aim of this study was to develop a database to support modeling of patent foramen ovale-attributable recurrence risk by combining extant data sets.</p></div></div>
<div class="section" id="ijs843-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We identified investigators with extant databases including subjects with cryptogenic stroke investigated for patent foramen ovale, determined the availability and characteristics of data in each database, collaboratively specified the variables to be included in the Risk of Paradoxical Embolism database, harmonized the variables across databases, and collected new primary data when necessary and feasible.</p></div></div>
<div class="section" id="ijs843-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The Risk of Paradoxical Embolism database has individual clinical, radiologic, and echocardiographic data from 12 component databases, including subjects with cryptogenic stroke both with (<em>n</em> = 1925) and without (<em>n</em> = 1749) patent foramen ovale. In the patent foramen ovale subjects, a total of 381 outcomes (stroke, transient ischemic attack, death) occurred (median follow-up 2·2 years). While there were substantial variations in data collection between studies, there was sufficient overlap to define a common set of variables suitable for risk modeling.</p></div></div>
<div class="section" id="ijs843-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>While individual studies are inadequate for modeling patent foramen ovale-attributable recurrence risk, collaboration between investigators has yielded a database with sufficient power to identify those patients at highest risk for a patent foramen ovale-related stroke recurrence who may have the greatest potential benefit from patent foramen ovale closure.</p></div></div>
]]></content:encoded><description>

Background
Detecting a benefit from closure of patent foramen ovale in patients with cryptogenic stroke is hampered by low rates of stroke recurrence and uncertainty about the causal role of patent foramen ovale in the index event. A method to predict patent foramen ovale-attributable recurrence risk is needed. However, individual databases generally have too few stroke recurrences to support risk modeling. Prior studies of this population have been limited by low statistical power for examining factors related to recurrence.


Aims
The aim of this study was to develop a database to support modeling of patent foramen ovale-attributable recurrence risk by combining extant data sets.


Methods
We identified investigators with extant databases including subjects with cryptogenic stroke investigated for patent foramen ovale, determined the availability and characteristics of data in each database, collaboratively specified the variables to be included in the Risk of Paradoxical Embolism database, harmonized the variables across databases, and collected new primary data when necessary and feasible.


Results
The Risk of Paradoxical Embolism database has individual clinical, radiologic, and echocardiographic data from 12 component databases, including subjects with cryptogenic stroke both with (n = 1925) and without (n = 1749) patent foramen ovale. In the patent foramen ovale subjects, a total of 381 outcomes (stroke, transient ischemic attack, death) occurred (median follow-up 2·2 years). While there were substantial variations in data collection between studies, there was sufficient overlap to define a common set of variables suitable for risk modeling.


Conclusion
While individual studies are inadequate for modeling patent foramen ovale-attributable recurrence risk, collaboration between investigators has yielded a database with sufficient power to identify those patients at highest risk for a patent foramen ovale-related stroke recurrence who may have the greatest potential benefit from patent foramen ovale closure.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00842.x" xmlns="http://purl.org/rss/1.0/"><title>Types, outcome and risk factors of stroke in Tribal Patients</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00842.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Types, outcome and risk factors of stroke in Tribal Patients</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jittendra K. Singh, Piyush Ranjan, Archana Kumari, Amol S. Dahale, Rajendra Jha, Ranjan Das</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-07T03:28:22.658995-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00842.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00842.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00842.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs842-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Introduction</h4><div class="para"><p>Studies suggest that ethnicity and racial factors has an important role in the variation in epidemiology of stroke. The present study was conducted to assess the subtypes, risk factors, and outcome of stroke in the tribal community of Jharkhand state and to compare it with that in the non-tribals from the same geographical location.</p></div></div>
<div class="section" id="ijs842-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We carried out a hospital-based prospective observational study at Rajendra Institute of Medical Sciences-Ranchi. Patients of acute stroke, reporting to the medical outpatient department and emergency department from January 1, 2006 to December 31, 2010 were studied. Computed tomography scan was done immediately and again after 24 h to confirm the diagnosis of stroke. To compare the findings between tribal and non-tribal patients, we used chi-square test/Fisher exact test as appropriate.</p></div></div>
<div class="section" id="ijs842-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Of the total 1156 patients included in the study, 536 were tribals, while 620 were non-tribals. Significant differences were found in tribal stroke patients as compared with non-tribals: mean age of tribal subjects was 53·8 years (60·8 years in non-tribals); stroke in young individual was present in 25% of tribal subjects (17% in non-tribals, <em>P</em> = 0·01); primary intracerebral hemorrhage variety was present in 31% of tribals (18% in non-tribals, <em>P</em>-value &lt; 0·001); the 28th day case fatality rate was 43% among tribal subjects (35% among non-tribals, <em>P</em> = 0·02). Hypertension and alcohol abuse was found to be associated with intracerebral hemorrhage in tribal subjects, although no such association was found in non-tribals.</p></div></div>
<div class="section" id="ijs842-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Tribals have early onset, poor outcomes and higher proportion of ICH compared to non-tribals. [Correction added after online publication 7 Aug 2012: The sentence "Tribals have early with non-tribals." in the Conclusion section of the abstract was deleted.]</p></div></div>
]]></content:encoded><description>

Introduction
Studies suggest that ethnicity and racial factors has an important role in the variation in epidemiology of stroke. The present study was conducted to assess the subtypes, risk factors, and outcome of stroke in the tribal community of Jharkhand state and to compare it with that in the non-tribals from the same geographical location.


Methods
We carried out a hospital-based prospective observational study at Rajendra Institute of Medical Sciences-Ranchi. Patients of acute stroke, reporting to the medical outpatient department and emergency department from January 1, 2006 to December 31, 2010 were studied. Computed tomography scan was done immediately and again after 24 h to confirm the diagnosis of stroke. To compare the findings between tribal and non-tribal patients, we used chi-square test/Fisher exact test as appropriate.


Results
Of the total 1156 patients included in the study, 536 were tribals, while 620 were non-tribals. Significant differences were found in tribal stroke patients as compared with non-tribals: mean age of tribal subjects was 53·8 years (60·8 years in non-tribals); stroke in young individual was present in 25% of tribal subjects (17% in non-tribals, P = 0·01); primary intracerebral hemorrhage variety was present in 31% of tribals (18% in non-tribals, P-value &lt; 0·001); the 28th day case fatality rate was 43% among tribal subjects (35% among non-tribals, P = 0·02). Hypertension and alcohol abuse was found to be associated with intracerebral hemorrhage in tribal subjects, although no such association was found in non-tribals.


Conclusion
Tribals have early onset, poor outcomes and higher proportion of ICH compared to non-tribals. [Correction added after online publication 7 Aug 2012: The sentence "Tribals have early with non-tribals." in the Conclusion section of the abstract was deleted.]

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00849.x" xmlns="http://purl.org/rss/1.0/"><title>Pre- and post-treatment with cyclosporine A in a rat model of transient focal cerebral ischaemia with multimodal MRI screening</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00849.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Pre- and post-treatment with cyclosporine A in a rat model of transient focal cerebral ischaemia with multimodal MRI screening</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Tae-Hee Cho, Pierre Aguettaz, Oscar Campuzano, Christiane Charriaut-Marlangue, Adrien Riou, Yves Berthezène, Norbert Nighoghossian, Michel Ovize, Marlène Wiart, Fabien Chauveau</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-07T03:28:20.754836-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00849.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00849.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00849.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs849-sec-0101" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Irreversible damage may occur at reperfusion after sustained cerebral ischaemia.</p></div></div>
<div class="section" id="ijs849-sec-0102" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>We investigated the value of cyclosporine A for reducing the infarct size in a model of transient middle cerebral artery occlusion.</p></div></div>
<div class="section" id="ijs844-sec-0103" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Twenty-seven Sprague-Dawley rats sustained a middle cerebral artery occlusion of one-hour. Acute multimodal Magnetic Resonance Imaging (MRI) was used during occlusion to confirm the success of surgery and measure baseline lesion size. Animals were randomly treated by: (i) intracarotid cyclosporine A (10 mg/kg) 20 mins before middle cerebral artery occlusion (pretreatment group); (ii) intracarotid cyclosporine A (10 mg/kg) immediately after reperfusion (post-treatment group); and (iii) intracarotid saline immediately after reperfusion.</p></div></div>
<div class="section" id="ijs844-sec-0104" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Histopathological measurements on day 1 showed a significant reduction of infarct size in the pretreatment group compared to the post-treatment (percentage values of ipsilateral hemispheres: 16 ± 5% vs. 29 ± 11%, <em>P</em> = 0·004) and saline groups (16 ± 5% vs. 42 ± 12%, <em>P</em> = 0·015). No significant difference was observed between the post-treatment and saline groups (<em>P</em> = 0·065). Behavioural examinations on day 1 showed no significant difference between groups. Immunohistochemistry showed a statistically significant reduction of microglial cell count in the pretreatment group compared to either saline or cyclosporine A post-treatment groups.</p></div></div>
<div class="section" id="ijs844-sec-0105" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>We conclude that intracarotid cyclosporine A is effective in reducing infarct size when given prior to ischaemia, but not when administered at reperfusion.</p></div></div>
]]></content:encoded><description>

Background
Irreversible damage may occur at reperfusion after sustained cerebral ischaemia.


Aims
We investigated the value of cyclosporine A for reducing the infarct size in a model of transient middle cerebral artery occlusion.


Methods
Twenty-seven Sprague-Dawley rats sustained a middle cerebral artery occlusion of one-hour. Acute multimodal Magnetic Resonance Imaging (MRI) was used during occlusion to confirm the success of surgery and measure baseline lesion size. Animals were randomly treated by: (i) intracarotid cyclosporine A (10 mg/kg) 20 mins before middle cerebral artery occlusion (pretreatment group); (ii) intracarotid cyclosporine A (10 mg/kg) immediately after reperfusion (post-treatment group); and (iii) intracarotid saline immediately after reperfusion.


Results
Histopathological measurements on day 1 showed a significant reduction of infarct size in the pretreatment group compared to the post-treatment (percentage values of ipsilateral hemispheres: 16 ± 5% vs. 29 ± 11%, P = 0·004) and saline groups (16 ± 5% vs. 42 ± 12%, P = 0·015). No significant difference was observed between the post-treatment and saline groups (P = 0·065). Behavioural examinations on day 1 showed no significant difference between groups. Immunohistochemistry showed a statistically significant reduction of microglial cell count in the pretreatment group compared to either saline or cyclosporine A post-treatment groups.

 Conclusions
We conclude that intracarotid cyclosporine A is effective in reducing infarct size when given prior to ischaemia, but not when administered at reperfusion.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00828.x" xmlns="http://purl.org/rss/1.0/"><title>The effectiveness of dual antiplatelet treatment in acute ischemic stroke patients with intracranial arterial stenosis: a subgroup analysis of CLAIR study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00828.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The effectiveness of dual antiplatelet treatment in acute ischemic stroke patients with intracranial arterial stenosis: a subgroup analysis of CLAIR study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-07T03:28:18.387697-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00828.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00828.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00828.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs828-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Dual antiplatelet therapy with clopidogrel and aspirin reduces the presence and number of microembolic signals in patients with large artery disease. However, whether it is effective in patients with intracranial disease alone remains uncertain. We performed a subgroup analysis of the The CLopidogrel plus Aspirin for Infarction Reduction (CLAIR in acute stroke or transient ischemic attack patients with large artery stenosis and microembolic signals) study of only patients with intracranial occlusive disease, excluding those with extra cranial disease.</p></div></div>
<div class="section" id="ijs828-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>CLAIR was a randomized-controlled, open-label, multicenter clinical trial with blinded outcome evaluation, which recruited patients with symptoms of ischemic stroke or transient ischemic attack within seven-days of onset, with large artery stenosis verified by transcranial Doppler and carotid ultrasound, and with microembolic signals detected by transcranial Doppler recording. All patients were randomized to receive clopidogrel plus aspirin daily for seven-days (dual treatment), or aspirin alone for seven-days (monotherapy). Repeated transcranial Doppler recordings for microembolic signals were made on day one, two, and seven. This subgroup study only analyzed the patients with purely intracranial large artery disease and excluded those with extra cranial stenosis.</p></div></div>
<div class="section" id="ijs828-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>There were 70 patients recruited with purely intracranial stenosis, 34 in the dual treatment group and 36 in the monotherapy group. The proportion of the patients with positive emboli at day seven in the dual treatment group was significantly lower than that in the monotherapy group (relative risk reduction 56·5%, 95% confidence interval 2·5–80·6; <em>P</em> = 0·029). The number of emboli in the dual treatment group decreased significantly at day two (<em>P</em> = 0·043) and day seven (<em>P</em> = 0·018) compared with the monotherapy group. After adjustment for the number of emboli at day one, the effect of dual treatment was still significant for the reduction of presence (relative risk reduction 56·0%; 95% confidence interval 5·4−79·6; <em>P</em> = 0·036) and number (adjusted mean difference −0·9; 95% confidence interval −1·5 to −0·3; <em>P</em> = 0·004) of positive emboli at day seven.</p></div></div>
<div class="section" id="ijs828-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Dual treatment with clopidogrel and aspirin for seven-days is more effective than aspirin alone to reduce microembolic signals in patients with intracranial arterial stenosis.</p></div></div>
]]></content:encoded><description>

Background
Dual antiplatelet therapy with clopidogrel and aspirin reduces the presence and number of microembolic signals in patients with large artery disease. However, whether it is effective in patients with intracranial disease alone remains uncertain. We performed a subgroup analysis of the The CLopidogrel plus Aspirin for Infarction Reduction (CLAIR in acute stroke or transient ischemic attack patients with large artery stenosis and microembolic signals) study of only patients with intracranial occlusive disease, excluding those with extra cranial disease.


Methods
CLAIR was a randomized-controlled, open-label, multicenter clinical trial with blinded outcome evaluation, which recruited patients with symptoms of ischemic stroke or transient ischemic attack within seven-days of onset, with large artery stenosis verified by transcranial Doppler and carotid ultrasound, and with microembolic signals detected by transcranial Doppler recording. All patients were randomized to receive clopidogrel plus aspirin daily for seven-days (dual treatment), or aspirin alone for seven-days (monotherapy). Repeated transcranial Doppler recordings for microembolic signals were made on day one, two, and seven. This subgroup study only analyzed the patients with purely intracranial large artery disease and excluded those with extra cranial stenosis.


Results
There were 70 patients recruited with purely intracranial stenosis, 34 in the dual treatment group and 36 in the monotherapy group. The proportion of the patients with positive emboli at day seven in the dual treatment group was significantly lower than that in the monotherapy group (relative risk reduction 56·5%, 95% confidence interval 2·5–80·6; P = 0·029). The number of emboli in the dual treatment group decreased significantly at day two (P = 0·043) and day seven (P = 0·018) compared with the monotherapy group. After adjustment for the number of emboli at day one, the effect of dual treatment was still significant for the reduction of presence (relative risk reduction 56·0%; 95% confidence interval 5·4−79·6; P = 0·036) and number (adjusted mean difference −0·9; 95% confidence interval −1·5 to −0·3; P = 0·004) of positive emboli at day seven.


Conclusions
Dual treatment with clopidogrel and aspirin for seven-days is more effective than aspirin alone to reduce microembolic signals in patients with intracranial arterial stenosis.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00851.x" xmlns="http://purl.org/rss/1.0/"><title>Silent brain infarction – a review of recent observations</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00851.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Silent brain infarction – a review of recent observations</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Katalin Réka Kovács, Dániel Czuriga, Dániel Bereczki, Natan M. Bornstein, László Csiba</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-01T20:09:06.460819-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00851.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00851.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00851.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Silent brain infarction is a cerebral ischaemic event evident on brain imaging without any clinical symptom. Silent brain infarction is often detected in apparently healthy, elderly people and in different selected patient groups as well. Lately, several studies were carried out in order to identify the clinical conditions leading to silent brain infarction. A large number of clinical and paraclinical parameters were found to increase silent brain infarction prevalence, and the continuously growing list of risk factors revealed that the majority of them are similar to those related to stroke. Accordingly, some consider silent brain infarction the preclinical stage of clinically overt stroke. This point of view emphasizes the early recognition and management of silent brain infarction-related risk factors, and a great need for comparative studies, which could elicit the most sensitive indicators of the increased silent brain infarction risk, especially the ones that could be cost-effectively screened in the large populations as well.</p></div>]]></content:encoded><description>Silent brain infarction is a cerebral ischaemic event evident on brain imaging without any clinical symptom. Silent brain infarction is often detected in apparently healthy, elderly people and in different selected patient groups as well. Lately, several studies were carried out in order to identify the clinical conditions leading to silent brain infarction. A large number of clinical and paraclinical parameters were found to increase silent brain infarction prevalence, and the continuously growing list of risk factors revealed that the majority of them are similar to those related to stroke. Accordingly, some consider silent brain infarction the preclinical stage of clinically overt stroke. This point of view emphasizes the early recognition and management of silent brain infarction-related risk factors, and a great need for comparative studies, which could elicit the most sensitive indicators of the increased silent brain infarction risk, especially the ones that could be cost-effectively screened in the large populations as well.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00826.x" xmlns="http://purl.org/rss/1.0/"><title>Thrombolysis in ischemic strokes with no arterial occlusion</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00826.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Thrombolysis in ischemic strokes with no arterial occlusion</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sourabh A. Lahoti, Louis R. Caplan, Gustavo Saposnik, David S. Liebeskind, Sankalp Gokhale, Shirish M. Hastak</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-01T20:09:01.113334-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00826.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00826.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00826.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs826-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Twelve million people develop ischemic stroke each year world over and 30–40% of them do not have arterial occlusions at presentation. Trials conducted to study the efficacy of thrombolytic drug reported better outcome with use of thrombolytic drug but none studied the subtypes of ischemic strokes specifically and adequately. The subgroups of patients with no arterial occlusion at presentation continue to receive thrombolytic therapy without proven benefit and with some risk.</p></div></div><div class="section" id="ijs826-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>The aim of this article is to study whether intravenous thrombolysis with alteplase improves clinical outcome in ischemic stroke patients who do not have arterial occlusion at presentation.</p></div></div><div class="section" id="ijs826-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>A retrospective medical record-based observational multicenter, multinational study.</p></div></div><div class="section" id="ijs826-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Outcomes</h4><div class="para"><p>Primary outcome measure would be clinical outcome at three-months from stroke onset measured by modified Rankin Scale and National Institute of Health Stroke Scale. Secondary outcome measure will be frequency of intracerebral hemorrhage causing worsening of clinical deficit defined as increase in National Institute of Health Stroke Scale by &gt;4.</p></div></div>]]></content:encoded><description>RationaleTwelve million people develop ischemic stroke each year world over and 30–40% of them do not have arterial occlusions at presentation. Trials conducted to study the efficacy of thrombolytic drug reported better outcome with use of thrombolytic drug but none studied the subtypes of ischemic strokes specifically and adequately. The subgroups of patients with no arterial occlusion at presentation continue to receive thrombolytic therapy without proven benefit and with some risk.AimThe aim of this article is to study whether intravenous thrombolysis with alteplase improves clinical outcome in ischemic stroke patients who do not have arterial occlusion at presentation.DesignA retrospective medical record-based observational multicenter, multinational study.OutcomesPrimary outcome measure would be clinical outcome at three-months from stroke onset measured by modified Rankin Scale and National Institute of Health Stroke Scale. Secondary outcome measure will be frequency of intracerebral hemorrhage causing worsening of clinical deficit defined as increase in National Institute of Health Stroke Scale by &gt;4.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00846.x" xmlns="http://purl.org/rss/1.0/"><title>Association between the amount of right-to-left shunt and infarct patterns in patients with cryptogenic embolic stroke: a transcranial Doppler study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00846.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Association between the amount of right-to-left shunt and infarct patterns in patients with cryptogenic embolic stroke: a transcranial Doppler study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ji Won Kim, Suk Jae Kim, Cindy W Yoon, Chang-Hyun Park, Kun Woo Kang, Soo Kyoung Kim, Yun-Hee Kim, Oh Young Bang</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-07-19T10:55:47.142313-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00846.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00846.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00846.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs846-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Paradoxical embolism has been documented as a mechanism of cryptogenic embolic stroke. We investigated the frequency of right-to-left shunt in patients with cryptogenic embolic stroke and evaluated the factors associated with diffusion-weighted imaging (DWI) lesion pattern.</p></div></div><div class="section" id="ijs846-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We analyzed data on 157 consecutive patients with acute ischemic stroke because of presumed cryptogenic embolism. Agitated saline transcranial Doppler study was conducted in all patients to detect right-to-left shunt. We evaluated the association of the amount (microemboli &lt;20 vs. ≥20) and activity (spontaneous vs. after Valsalva maneuver only) of right-to-left shunt with diffusion-weighted imaging lesion patterns.</p></div></div><div class="section" id="ijs846-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Right-to-left shunt was observed in 96 (61·1%) patients. The multiplicity and distribution of diffusion-weighted imaging lesions did not differ depending on the amount and activity of right-to-left shunt. However, the size of diffusion-weighted imaging lesions differed depending on the amount of right-to-left shunt (<em>P</em> = 0·019). Right-to-left shunt was more frequently observed in patients with small (&lt;1 cm) infarcts than in those with a large infarct (66·7% vs. 45·9%), and most patients with a larger amount of right-to-left shunt were found to have small infarcts on diffusion-weighted imaging (80%). The clinical characteristics, including Framingham stroke risk strategy, did not differ between the groups.</p></div></div><div class="section" id="ijs846-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Our results indicate that the amount of right-to-left shunt determines the Diffusion-weighted imaging lesion patterns and suggest that mechanisms of stroke other than paradoxical mechanism may play an important role in patients with large cryptogenic embolic stroke.</p></div></div>]]></content:encoded><description>BackgroundParadoxical embolism has been documented as a mechanism of cryptogenic embolic stroke. We investigated the frequency of right-to-left shunt in patients with cryptogenic embolic stroke and evaluated the factors associated with diffusion-weighted imaging (DWI) lesion pattern.MethodsWe analyzed data on 157 consecutive patients with acute ischemic stroke because of presumed cryptogenic embolism. Agitated saline transcranial Doppler study was conducted in all patients to detect right-to-left shunt. We evaluated the association of the amount (microemboli &lt;20 vs. ≥20) and activity (spontaneous vs. after Valsalva maneuver only) of right-to-left shunt with diffusion-weighted imaging lesion patterns.ResultsRight-to-left shunt was observed in 96 (61·1%) patients. The multiplicity and distribution of diffusion-weighted imaging lesions did not differ depending on the amount and activity of right-to-left shunt. However, the size of diffusion-weighted imaging lesions differed depending on the amount of right-to-left shunt (P = 0·019). Right-to-left shunt was more frequently observed in patients with small (&lt;1 cm) infarcts than in those with a large infarct (66·7% vs. 45·9%), and most patients with a larger amount of right-to-left shunt were found to have small infarcts on diffusion-weighted imaging (80%). The clinical characteristics, including Framingham stroke risk strategy, did not differ between the groups.ConclusionsOur results indicate that the amount of right-to-left shunt determines the Diffusion-weighted imaging lesion patterns and suggest that mechanisms of stroke other than paradoxical mechanism may play an important role in patients with large cryptogenic embolic stroke.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00848.x" xmlns="http://purl.org/rss/1.0/"><title>Does the cognitive measure Cog-4 show improvement among patients treated with thrombolysis after acute stroke?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00848.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Does the cognitive measure Cog-4 show improvement among patients treated with thrombolysis after acute stroke?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Karim Hajjar, Rachael L. Fulton, Hans-Christoph Diener, Kennedy R. Lees, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-07-19T10:39:48.247108-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00848.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00848.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00848.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs848-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Although the established measure of disability post stroke, the modified Rankin Scale emphasizes motor function and may underestimate the importance of cognitive impairment in more disabled patients. A subset of four items from the National Institutes of Health Stroke Scale has been proposed to assess cognitive function after stroke (Cog-4), and to correlate with modified Rankin Scale. Items correspond to orientation, executive function, language, and inattention. We investigated responsiveness of Cog-4 to treatment with thrombolysis and whether it offers information that supplements modified Rankin Scale.</p></div></div><div class="section" id="ijs848-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We included 6268 patients from the Virtual International Stroke Trials Archive: 2734 received intravenous thrombolysis and 3534 were treated conservatively. We compared day 90 outcomes between treated and untreated groups, by modified Rankin Scale (illustrative) and by Cog-4 (primary measure) adjusting for age, baseline National Institutes of Health stroke scale, hemispheric lateralisation as well as baseline Cog-4 and baseline National Institutes of Health Stroke Scale excluding baseline Cog-4 separately. Analysis of Cog-4 was repeated within strata of 90 day modified Rankin Scale. Statistical analyses included proportional odds logistic regression and Cochran–Mantel–Haenszel test.</p></div></div><div class="section" id="ijs848-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Modified Rankin Scale showed a difference between treatment groups of expected magnitude (odds ratio 1·56; 95%<b> confidence interval</b> 1·43–1·72; <em>P</em> &lt; 0·001). After adjustment for imbalance in baseline prognostic factors, the distribution of Cog-4 scores at 90 days was better in thrombolysed patients compared with nonthrombolysed patients (<b>odds ratio</b> 1·31; 95%<b> confidence interval</b> 1·18–1·47; <em>P</em> = 0·006). However, Cog-4 analysis stratified by 90-day modified Rankin Scale was neutral between treatment groups (OR 1·01; 95% CI 0·90–1·14), and Cog-4 was not responsive to treatment group even within modified Rankin Scale categories 4 and 5 despite substantial cognitive deficits in these patients.</p></div></div><div class="section" id="ijs848-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Although Cog-4 may be responsive to treatment effects, it does not provide additional information beyond modified Rankin Scale assessment.</p></div></div>]]></content:encoded><description>BackgroundAlthough the established measure of disability post stroke, the modified Rankin Scale emphasizes motor function and may underestimate the importance of cognitive impairment in more disabled patients. A subset of four items from the National Institutes of Health Stroke Scale has been proposed to assess cognitive function after stroke (Cog-4), and to correlate with modified Rankin Scale. Items correspond to orientation, executive function, language, and inattention. We investigated responsiveness of Cog-4 to treatment with thrombolysis and whether it offers information that supplements modified Rankin Scale.MethodsWe included 6268 patients from the Virtual International Stroke Trials Archive: 2734 received intravenous thrombolysis and 3534 were treated conservatively. We compared day 90 outcomes between treated and untreated groups, by modified Rankin Scale (illustrative) and by Cog-4 (primary measure) adjusting for age, baseline National Institutes of Health stroke scale, hemispheric lateralisation as well as baseline Cog-4 and baseline National Institutes of Health Stroke Scale excluding baseline Cog-4 separately. Analysis of Cog-4 was repeated within strata of 90 day modified Rankin Scale. Statistical analyses included proportional odds logistic regression and Cochran–Mantel–Haenszel test.ResultsModified Rankin Scale showed a difference between treatment groups of expected magnitude (odds ratio 1·56; 95% confidence interval 1·43–1·72; P &lt; 0·001). After adjustment for imbalance in baseline prognostic factors, the distribution of Cog-4 scores at 90 days was better in thrombolysed patients compared with nonthrombolysed patients (odds ratio 1·31; 95% confidence interval 1·18–1·47; P = 0·006). However, Cog-4 analysis stratified by 90-day modified Rankin Scale was neutral between treatment groups (OR 1·01; 95% CI 0·90–1·14), and Cog-4 was not responsive to treatment group even within modified Rankin Scale categories 4 and 5 despite substantial cognitive deficits in these patients.ConclusionAlthough Cog-4 may be responsive to treatment effects, it does not provide additional information beyond modified Rankin Scale assessment.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00829.x" xmlns="http://purl.org/rss/1.0/"><title>Comprehensive assessment for autonomic dysfunction in different phases after ischemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00829.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Comprehensive assessment for autonomic dysfunction in different phases after ischemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Li Xiong, Howan H. W. Leung, Xiang Yan Chen, Jing Hao Han, Thomas W. H. Leung, Yannie O. Y. Soo, Anne Y. Y. Chan, Alexander Y. L. Lau, Lawrence K. S. Wong</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-07-03T08:53:45.025606-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00829.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00829.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00829.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs829-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and purpose</h4><div class="para"><p>Studies mostly use the analysis of heart rate variability to measure cardiovascular autonomic regulation in ischemic stroke. Besides power spectral analysis of heart rate variability, this study sought to determine whether autonomic function was impaired during different phases in ischemic stroke by Ewing's battery of autonomic function tests.</p></div></div><div class="section" id="ijs829-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Ninety-four patients with ischemic stroke (34 patients in acute phase and 60 patients in chronic phase, average six-months after stroke onset) and thirty-seven elderly controls were recruited. Ewing's battery autonomic function tests and power spectral analysis of heart rate variability were performed in all the subjects.</p></div></div><div class="section" id="ijs829-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>From power spectral analysis of heart rate variability, stroke patients of both acute and chronic phases had significantly lower low frequency power spectral density than controls. From Ewing's battery of autonomic function tests, patients in acute phase showed impairment in two parasympathetic tests (Valsalva ratio: <em>P</em> = 0·002; heart rate response to deep breathing: <em>P</em> &lt; 0·001) and those in chronic phase showed impairment in all parasympathetic tests (all <em>P</em> &lt; 0·05) in comparison with controls.</p></div></div><div class="section" id="ijs829-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The comprehensive assessment indicates that autonomic dysfunction occurs in acute phase of ischemic stroke and may persist up to six-months after stroke. Parasympathetic dysfunction rather than sympathetic dysfunction is predominant after ischemic stroke.</p></div></div>]]></content:encoded><description>Background and purposeStudies mostly use the analysis of heart rate variability to measure cardiovascular autonomic regulation in ischemic stroke. Besides power spectral analysis of heart rate variability, this study sought to determine whether autonomic function was impaired during different phases in ischemic stroke by Ewing's battery of autonomic function tests.MethodsNinety-four patients with ischemic stroke (34 patients in acute phase and 60 patients in chronic phase, average six-months after stroke onset) and thirty-seven elderly controls were recruited. Ewing's battery autonomic function tests and power spectral analysis of heart rate variability were performed in all the subjects.ResultsFrom power spectral analysis of heart rate variability, stroke patients of both acute and chronic phases had significantly lower low frequency power spectral density than controls. From Ewing's battery of autonomic function tests, patients in acute phase showed impairment in two parasympathetic tests (Valsalva ratio: P = 0·002; heart rate response to deep breathing: P &lt; 0·001) and those in chronic phase showed impairment in all parasympathetic tests (all P &lt; 0·05) in comparison with controls.ConclusionsThe comprehensive assessment indicates that autonomic dysfunction occurs in acute phase of ischemic stroke and may persist up to six-months after stroke. Parasympathetic dysfunction rather than sympathetic dysfunction is predominant after ischemic stroke.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00827.x" xmlns="http://purl.org/rss/1.0/"><title>Growing burden of stroke in Pakistan: a review of progress and limitations</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00827.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Growing burden of stroke in Pakistan: a review of progress and limitations</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Mubashirah Hashmi, Maria Khan, Mohammad Wasay</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-07-03T08:27:18.001995-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00827.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00827.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00827.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Panorama</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Stroke rates in middle-aged people are five to ten times higher in Pakistan, India, Russia, China, and Brazil, compared with the United Kingdom or United States. South Asia is home to 20% of the world's population and has one of the highest burdens of cardiovascular disease in the world. With an aging population, there is an expected increase in the number of stroke cases and a corresponding increase in the burden of stroke in developing countries including South Asian countries like Pakistan. Limited data from prior studies in developing countries indicate that stroke epidemiology differs between these and Western countries. These differences include a higher incidence of stroke at younger ages, a higher prevalence of hemorrhagic stroke, and higher age-specific prevalence rates of stroke in women. The reasons for these differences in stroke epidemiology in developing countries are not clear. This may be explained by higher prevalence of established stroke risk factors, or potential nontraditional risk factors such as water pipe smoking, use of daldaghee or naswaar, and paan chewing; hepatitis and rheumatic heart disease may also contribute to these differences. Acute and long-term stroke treatment has shown limited progress in Pakistan like other developing countries because of poor awareness of patients and general physician on stroke symptomatology, management of stroke risk factors, lack of specialized stroke units in the country, very low utilization of thrombolytic therapy because of financial constraints and, above all, poor knowledge of physicians on the role of rehabilitation and its different aspects in the management of post stroke disability.</p></div>]]></content:encoded><description>Stroke rates in middle-aged people are five to ten times higher in Pakistan, India, Russia, China, and Brazil, compared with the United Kingdom or United States. South Asia is home to 20% of the world's population and has one of the highest burdens of cardiovascular disease in the world. With an aging population, there is an expected increase in the number of stroke cases and a corresponding increase in the burden of stroke in developing countries including South Asian countries like Pakistan. Limited data from prior studies in developing countries indicate that stroke epidemiology differs between these and Western countries. These differences include a higher incidence of stroke at younger ages, a higher prevalence of hemorrhagic stroke, and higher age-specific prevalence rates of stroke in women. The reasons for these differences in stroke epidemiology in developing countries are not clear. This may be explained by higher prevalence of established stroke risk factors, or potential nontraditional risk factors such as water pipe smoking, use of daldaghee or naswaar, and paan chewing; hepatitis and rheumatic heart disease may also contribute to these differences. Acute and long-term stroke treatment has shown limited progress in Pakistan like other developing countries because of poor awareness of patients and general physician on stroke symptomatology, management of stroke risk factors, lack of specialized stroke units in the country, very low utilization of thrombolytic therapy because of financial constraints and, above all, poor knowledge of physicians on the role of rehabilitation and its different aspects in the management of post stroke disability.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00822.x" xmlns="http://purl.org/rss/1.0/"><title>Poststroke infections are an independent risk factor for poor functional outcome after three-months in thrombolysed stroke patients</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00822.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Poststroke infections are an independent risk factor for poor functional outcome after three-months in thrombolysed stroke patients</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Andrea Rocco, Geraldine Fam, Marek Sykora, Jennifer Diedler, Simon Nagel, Peter Ringleb</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-05-28T04:40:34.099445-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00822.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00822.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00822.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs822-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Infections are common complications in patients with acute ischemic stroke; however, the pathophysiology of the stroke-induced immunodepression is still under debate. Although it has been shown that increased mortality and longer hospital stay are associated with the presence of poststroke infections, it remains unclear if early poststroke infections occurring in the first seven-days have an effect on the overall functional outcome.</p></div></div><div class="section" id="ijs822-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>Aim of our study was to identify the frequency of poststroke infections in thrombolysed stroke patients and to analyze their effect on the outcome after three-months.</p></div></div><div class="section" id="ijs822-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>From 1998 to 2011, all patients in our institution undergoing thrombolysis for acute ischemic stroke were included into a prospective database. Baseline variables, clinical, radiographic, and laboratory data were collected prospectively. Outcome measures included symptomatic intracerebral hemorrhage per European-Australasian Acute Stroke Study II criteria, mortality, and modified Rankin Scale at three-months. Logistic regression models were used to identify independent predictors for poor outcome where appropriate.</p></div></div><div class="section" id="ijs822-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>One thousand sixteen patients were included; of them, 36·3% had an infection during the first week. Pneumonia (9·6%) and urinary tract infections (5·4%) were most frequent. Severity of stroke (<em>P</em> &lt; 0·0001), infarct size (<em>P</em> &lt; 0·0001), atrial fibrillation (<em>P</em> = 0·005), and cardio embolic cause of stroke (<em>P</em> &lt; 0·0001) were associated with infections. Age (odds ratio 1·089, 95% confidence interval 1·064–1·115, <em>P</em> &lt; 0·0001), severity of stroke (odds ratio 1·111, 95% confidence interval 1·073–1·149; <em>P</em> &lt; 0·0001) history of diabetes (odds ratio 0·555. 95% confidence interval 0·357–0·864; <em>P</em> = 0·009), infarct size (odds ratio 4·256 95% confidence interval 2·697–6·745; <em>P</em> &lt; 0·0001), infections (odds ratio 1·548, 95% confidence interval 1·008–2·376; <em>P</em> = 0·046), and symptomatic intracerebral hemorrhage were independent predictors for poor outcome after three-months.</p></div></div><div class="section" id="ijs822-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>In our cohort of thrombolysed stroke patients, poststroke infections were frequent in patients with severe cardio embolic stroke, a large infarct, and a longer hospital stay; those patients have a higher risk of infection and a poorer functional outcome after three-months. This risk increases after occurrence of symptomatic intracerebral hemorrhage. Prevention of infection with antibiotic therapy or other prophylactic treatment could potentially lead to a better functional outcome and further randomized studies on this aspect are needed.</p></div></div>]]></content:encoded><description>BackgroundInfections are common complications in patients with acute ischemic stroke; however, the pathophysiology of the stroke-induced immunodepression is still under debate. Although it has been shown that increased mortality and longer hospital stay are associated with the presence of poststroke infections, it remains unclear if early poststroke infections occurring in the first seven-days have an effect on the overall functional outcome.AimsAim of our study was to identify the frequency of poststroke infections in thrombolysed stroke patients and to analyze their effect on the outcome after three-months.MethodsFrom 1998 to 2011, all patients in our institution undergoing thrombolysis for acute ischemic stroke were included into a prospective database. Baseline variables, clinical, radiographic, and laboratory data were collected prospectively. Outcome measures included symptomatic intracerebral hemorrhage per European-Australasian Acute Stroke Study II criteria, mortality, and modified Rankin Scale at three-months. Logistic regression models were used to identify independent predictors for poor outcome where appropriate.ResultsOne thousand sixteen patients were included; of them, 36·3% had an infection during the first week. Pneumonia (9·6%) and urinary tract infections (5·4%) were most frequent. Severity of stroke (P &lt; 0·0001), infarct size (P &lt; 0·0001), atrial fibrillation (P = 0·005), and cardio embolic cause of stroke (P &lt; 0·0001) were associated with infections. Age (odds ratio 1·089, 95% confidence interval 1·064–1·115, P &lt; 0·0001), severity of stroke (odds ratio 1·111, 95% confidence interval 1·073–1·149; P &lt; 0·0001) history of diabetes (odds ratio 0·555. 95% confidence interval 0·357–0·864; P = 0·009), infarct size (odds ratio 4·256 95% confidence interval 2·697–6·745; P &lt; 0·0001), infections (odds ratio 1·548, 95% confidence interval 1·008–2·376; P = 0·046), and symptomatic intracerebral hemorrhage were independent predictors for poor outcome after three-months.ConclusionsIn our cohort of thrombolysed stroke patients, poststroke infections were frequent in patients with severe cardio embolic stroke, a large infarct, and a longer hospital stay; those patients have a higher risk of infection and a poorer functional outcome after three-months. This risk increases after occurrence of symptomatic intracerebral hemorrhage. Prevention of infection with antibiotic therapy or other prophylactic treatment could potentially lead to a better functional outcome and further randomized studies on this aspect are needed.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00825.x" xmlns="http://purl.org/rss/1.0/"><title>Early supported discharge after stroke in Bergen (ESD Stroke Bergen): a randomized controlled trial comparing rehabilitation in a day unit or in the patients’ homes with conventional treatment</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00825.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Early supported discharge after stroke in Bergen (ESD Stroke Bergen): a randomized controlled trial comparing rehabilitation in a day unit or in the patients’ homes with conventional treatment</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Håkon Hofstad, Halvor Naess, Rolf Moe-Nilssen, Jan Sture Skouen</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-05-18T00:25:23.857178-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00825.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00825.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00825.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocol</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs825-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>As a result of demographic changes with a presumed rapidly increasing number of older people during the coming decades, a strong increase in the incidence and prevalence of stroke should be expected. Early supported discharge implies that the patients are discharged to their homes as soon as feasible and that rehabilitative treatment is offered after the discharge, with the patients being home-dwelling. This has proved beneficial in previous studies.</p></div></div><div class="section" id="ijs825-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The main objective of this study is to further characterize the important components of early supported discharge and to confirm superiority of early supported discharge over conventional treatment. The secondary aim will be to compare two different early supported discharge schemes. These early supported discharge schemes are composed of intensive rehabilitation treatment given by a multidisciplinary team in a day unit and, alternatively, the same treatment given in the patients’ homes.</p></div></div><div class="section" id="ijs825-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>The study is conducted as a randomized controlled trial with three arms: two different forms of early supported discharge and a control arm with conventional treatment. Patients with acute stroke admitted to our hospital's stroke unit and living in the Municipality of Bergen are considered for inclusion. A total of 350 stroke patients are expected.</p></div></div><div class="section" id="ijs825-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study outcomes</h4><div class="para"><p>Primary outcome is modified Rankin Scale six-months after inclusion. Secondary outcomes include Barthel Index and National Institute of Health Stroke Scale at several points in time after inclusion, as well as many other schemes, questionnaires and physical tests. The study is registered in <em>ClinicalTrials.gov</em> registration number NCT00771771.</p></div></div>]]></content:encoded><description>RationaleAs a result of demographic changes with a presumed rapidly increasing number of older people during the coming decades, a strong increase in the incidence and prevalence of stroke should be expected. Early supported discharge implies that the patients are discharged to their homes as soon as feasible and that rehabilitative treatment is offered after the discharge, with the patients being home-dwelling. This has proved beneficial in previous studies.AimsThe main objective of this study is to further characterize the important components of early supported discharge and to confirm superiority of early supported discharge over conventional treatment. The secondary aim will be to compare two different early supported discharge schemes. These early supported discharge schemes are composed of intensive rehabilitation treatment given by a multidisciplinary team in a day unit and, alternatively, the same treatment given in the patients’ homes.DesignThe study is conducted as a randomized controlled trial with three arms: two different forms of early supported discharge and a control arm with conventional treatment. Patients with acute stroke admitted to our hospital's stroke unit and living in the Municipality of Bergen are considered for inclusion. A total of 350 stroke patients are expected.Study outcomesPrimary outcome is modified Rankin Scale six-months after inclusion. Secondary outcomes include Barthel Index and National Institute of Health Stroke Scale at several points in time after inclusion, as well as many other schemes, questionnaires and physical tests. The study is registered in ClinicalTrials.gov registration number NCT00771771.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00823.x" xmlns="http://purl.org/rss/1.0/"><title>Cerebral vasospasm after sub-arachnoid hemorrhage as a clinical predictor and phenotype for genetic association study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00823.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Cerebral vasospasm after sub-arachnoid hemorrhage as a clinical predictor and phenotype for genetic association study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hyungsuk Kim, Elizabeth Crago, Mirim Kim, Paula Sherwood, Yvette Conley, Samuel Poloyac, Mary Kerr</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-05-09T04:10:37.007639-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00823.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00823.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00823.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs823-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>A typology of cerebral vasospasm has been proposed based on distinct clinical manifestations: delayed cerebral ischemia, symptomatic ‘vasospasm’, angiographic vasospasm, and transcranial Doppler vasospasm. We examined each distinct clinical manifestation in a nonparametric genetic association study.</p></div></div><div class="section" id="ijs823-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The purpose of this study was to examine and compare each four distinct acute clinical manifestations and test its perspectives in genetic association studies.</p></div></div><div class="section" id="ijs823-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Two hundred forty-five Caucasian patients with sub-arachnoid hemorrhage were evaluated for these four distinct clinical manifestations along with 906 600 single-nucleotide polymorphisms across the human genome.</p></div></div><div class="section" id="ijs823-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The four clinical manifestations were significantly associated with each other as <em>P</em>-values ranged from 3·31 × 10<sup>−4</sup> to 8·10 × 10<sup>−15</sup>. Transcranial Doppler vasospasm showed significant genetic association with single nucleotide polymorphism (SNP) (rs999662, <em>P</em> = 3·39 × 10<sup>−8</sup>). Statistical <em>P</em>-value of rs999662 in association with delayed cerebral ischemia, symptomatic ‘vasospasm’, and angiographic vasospasm was 0·0017, 0·0017, and 0·19, respectively.</p></div></div><div class="section" id="ijs823-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Despite different criteria for each of the four clinical manifestations, they are significantly associated with each other. Our results suggest transcranial Doppler vasospasm may be an appropriate intermediate but still clinically relevant phenotype for genetic association studies. Association with SNP rs999662 indicates a potential role for the region containing the solute carrier family 12 member 3 (SLC12A3) gene in transcranial Doppler vasospasm following sub-arachnoid hemorrhage.</p></div></div>]]></content:encoded><description>BackgroundA typology of cerebral vasospasm has been proposed based on distinct clinical manifestations: delayed cerebral ischemia, symptomatic ‘vasospasm’, angiographic vasospasm, and transcranial Doppler vasospasm. We examined each distinct clinical manifestation in a nonparametric genetic association study.AimsThe purpose of this study was to examine and compare each four distinct acute clinical manifestations and test its perspectives in genetic association studies.MethodsTwo hundred forty-five Caucasian patients with sub-arachnoid hemorrhage were evaluated for these four distinct clinical manifestations along with 906 600 single-nucleotide polymorphisms across the human genome.ResultsThe four clinical manifestations were significantly associated with each other as P-values ranged from 3·31 × 10−4 to 8·10 × 10−15. Transcranial Doppler vasospasm showed significant genetic association with single nucleotide polymorphism (SNP) (rs999662, P = 3·39 × 10−8). Statistical P-value of rs999662 in association with delayed cerebral ischemia, symptomatic ‘vasospasm’, and angiographic vasospasm was 0·0017, 0·0017, and 0·19, respectively.ConclusionsDespite different criteria for each of the four clinical manifestations, they are significantly associated with each other. Our results suggest transcranial Doppler vasospasm may be an appropriate intermediate but still clinically relevant phenotype for genetic association studies. Association with SNP rs999662 indicates a potential role for the region containing the solute carrier family 12 member 3 (SLC12A3) gene in transcranial Doppler vasospasm following sub-arachnoid hemorrhage.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00812.x" xmlns="http://purl.org/rss/1.0/"><title>Population-based study of acute- and long-term care costs after stroke in patients with AF</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00812.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Population-based study of acute- and long-term care costs after stroke in patients with AF</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ramon Luengo-Fernandez, Gabriel S.C. Yiin, Alastair M. Gray, Peter M. Rothwell</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-05-09T04:09:51.073315-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00812.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00812.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00812.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs812-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>New treatments for atrial fibrillation patients have been shown to be effective at reducing subsequent vascular event recurrence. However, there are few data on stroke costs in atrial fibrillation patients to allow the cost-effectiveness of these treatments to be assessed.</p></div></div><div class="section" id="ijs812-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>Using data from a population-based study, we assessed the acute and long-term costs of stroke in atrial fibrillation patients.</p></div></div><div class="section" id="ijs812-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Health-care costs one-year before and five-years after stroke were obtained from a large population-based study (Oxford Vascular study). Costs were assessed for the three-months poststroke (acute period) and annually thereafter (postacute period). Annual postacute costs were compared with annual baseline costs. Based on patients' living arrangements, costs of institutionalization after the event were included.</p></div></div><div class="section" id="ijs812-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>A total of 191 strokes occurred in 153 patients with known prior atrial fibrillation. Mean health-care costs after stroke were £10 413 (standard deviation 15 105) in the acute phase, with annual postacute health-care costs nonsignificantly smaller than those incurred before the event (£2400 vs. £3356, respectively; <em>P</em> = 0·198). However, for the 136 strokes surviving past the 90-day acute period, costs were nonsignificantly higher than those incurred in the year before the event (£3370 vs. £2566, respectively; <em>P</em> = 0·333). After stroke, 25 (13%) patients were newly admitted into long-term warden, nursing, or residential care, resulting in annual costs of £6880 (standard deviation 15 600) averaged across the 136 stroke cases surviving past the acute period.</p></div></div><div class="section" id="ijs812-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Although annual post acute phase hospital and primary health-care costs in stroke patients with prior atrial fibrillation were not significantly different to those incurred before the stroke, long-term nursing/residential care costs were substantial.</p></div></div>]]></content:encoded><description>BackgroundNew treatments for atrial fibrillation patients have been shown to be effective at reducing subsequent vascular event recurrence. However, there are few data on stroke costs in atrial fibrillation patients to allow the cost-effectiveness of these treatments to be assessed.AimsUsing data from a population-based study, we assessed the acute and long-term costs of stroke in atrial fibrillation patients.MethodsHealth-care costs one-year before and five-years after stroke were obtained from a large population-based study (Oxford Vascular study). Costs were assessed for the three-months poststroke (acute period) and annually thereafter (postacute period). Annual postacute costs were compared with annual baseline costs. Based on patients' living arrangements, costs of institutionalization after the event were included.ResultsA total of 191 strokes occurred in 153 patients with known prior atrial fibrillation. Mean health-care costs after stroke were £10 413 (standard deviation 15 105) in the acute phase, with annual postacute health-care costs nonsignificantly smaller than those incurred before the event (£2400 vs. £3356, respectively; P = 0·198). However, for the 136 strokes surviving past the 90-day acute period, costs were nonsignificantly higher than those incurred in the year before the event (£3370 vs. £2566, respectively; P = 0·333). After stroke, 25 (13%) patients were newly admitted into long-term warden, nursing, or residential care, resulting in annual costs of £6880 (standard deviation 15 600) averaged across the 136 stroke cases surviving past the acute period.ConclusionsAlthough annual post acute phase hospital and primary health-care costs in stroke patients with prior atrial fibrillation were not significantly different to those incurred before the stroke, long-term nursing/residential care costs were substantial.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00810.x" xmlns="http://purl.org/rss/1.0/"><title>Stressful life events as triggers of ischemic stroke: a case-crossover study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00810.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Stressful life events as triggers of ischemic stroke: a case-crossover study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Vincent Guiraud, Emmanuel Touzé, Frédéric Rouillon, Olivier Godefroy, Jean-Louis Mas</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-05-09T04:09:47.218577-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00810.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00810.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00810.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs810-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Acute stressors, such as stressful life events, might trigger ischemic stroke.</p></div></div><div class="section" id="ijs810-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>Our objective was to investigate the association between life events exposure and ischemic stroke onset.</p></div></div><div class="section" id="ijs810-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Consecutive patients were interviewed about life events exposure (e.g. bereavement) using the Interview for Recent Life Events. Using a case-crossover approach, life events exposure within one month of stroke onset (hazard period) was compared with exposure during five control periods of one month preceding the hazard period. Similarly, life events exposure within one week of stroke onset was compared with exposure during three control periods of one week. Odds ratios and 95% confidence intervals were calculated using conditional logistic regression.</p></div></div><div class="section" id="ijs810-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Two hundred forty-seven patients were interviewed within a median time of five days (interquartile range 3–7). Life events belonging to <em>bereavement</em>, <em>health</em>, and <em>other</em> categories accounted for half of life events. Over the six-month period, 187 patients were exposed to ≥1 life events. Patients were exposed to ≥1 life events more often during the first month preceding stroke onset than during the five control periods (odds ratio = 2·96; 95% confidence interval, 2·19–4·00). Over the four-week period, 97 patients were exposed to ≥1 life events. Patients were exposed to ≥1 life events more often during the first week preceding stroke onset than during the three control periods (odds ratio = 2·10; 1·40–3·17).</p></div></div><div class="section" id="ijs810-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Recent life events exposure is associated with an increased risk of ischemic stroke.</p></div></div>]]></content:encoded><description>BackgroundAcute stressors, such as stressful life events, might trigger ischemic stroke.AimsOur objective was to investigate the association between life events exposure and ischemic stroke onset.MethodsConsecutive patients were interviewed about life events exposure (e.g. bereavement) using the Interview for Recent Life Events. Using a case-crossover approach, life events exposure within one month of stroke onset (hazard period) was compared with exposure during five control periods of one month preceding the hazard period. Similarly, life events exposure within one week of stroke onset was compared with exposure during three control periods of one week. Odds ratios and 95% confidence intervals were calculated using conditional logistic regression.ResultsTwo hundred forty-seven patients were interviewed within a median time of five days (interquartile range 3–7). Life events belonging to bereavement, health, and other categories accounted for half of life events. Over the six-month period, 187 patients were exposed to ≥1 life events. Patients were exposed to ≥1 life events more often during the first month preceding stroke onset than during the five control periods (odds ratio = 2·96; 95% confidence interval, 2·19–4·00). Over the four-week period, 97 patients were exposed to ≥1 life events. Patients were exposed to ≥1 life events more often during the first week preceding stroke onset than during the three control periods (odds ratio = 2·10; 1·40–3·17).ConclusionsRecent life events exposure is associated with an increased risk of ischemic stroke.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00809.x" xmlns="http://purl.org/rss/1.0/"><title>Educational campaign on stroke in an urban population in Northern Germany: influence on public stroke awareness and knowledge</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00809.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Educational campaign on stroke in an urban population in Northern Germany: influence on public stroke awareness and knowledge</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hans Worthmann, Andreas Schwartz, Fedor Heidenreich, Eckhart Sindern, Reinhard Lorenz, Hans-Anton Adams, Andreas Flemming, Klaus Luettje, Ulla Walter, Birgit Haertle, Reinhard Dengler</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-05-09T04:05:55.707164-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00809.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00809.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00809.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs809-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Public stroke awareness and knowledge may be supportive for stroke prevention and emergency care-seeking behavior after the acute event, which is highly important for early treatment onset.</p></div></div><div class="section" id="ijs809-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>In an urban population in Northern Germany (Hannover), a six-month stroke educational campaign was conducted. We expected an increase in stroke knowledge and awareness thereafter.</p></div></div><div class="section" id="ijs809-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Computer-assisted telephone interviews were randomly conducted among 1004 representative participants before and 1010 immediately after the educational multimedia campaign. The computer-assisted telephone interviews focused on questions about stroke knowledge and interventions remembered.</p></div></div><div class="section" id="ijs809-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Knowledge of stroke risk factors increased during the campaign for overweight, physical inactivity, old age, and stroke in family (<em>P</em> &lt; 0·05). The knowledge of stroke warning signs was low, although it significantly increased during the campaign (<em>P</em> &lt; 0·001) as paresis/weakness (46%) and speech problems (31%) were most frequently named. The majority of respondents indicated that the first action after suffering from stroke should be calling emergency care (74% before vs. 84% after campaign, <em>P</em> &lt; 0·001).</p></div></div><div class="section" id="ijs809-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Our data indicate that stroke knowledge and awareness, which could provide earlier presentation to the emergency unit for timely treatment onset, are still low in urban Northern Germany but may decisively be increased by educational campaigns.</p></div></div>]]></content:encoded><description>BackgroundPublic stroke awareness and knowledge may be supportive for stroke prevention and emergency care-seeking behavior after the acute event, which is highly important for early treatment onset.AimsIn an urban population in Northern Germany (Hannover), a six-month stroke educational campaign was conducted. We expected an increase in stroke knowledge and awareness thereafter.MethodsComputer-assisted telephone interviews were randomly conducted among 1004 representative participants before and 1010 immediately after the educational multimedia campaign. The computer-assisted telephone interviews focused on questions about stroke knowledge and interventions remembered.ResultsKnowledge of stroke risk factors increased during the campaign for overweight, physical inactivity, old age, and stroke in family (P &lt; 0·05). The knowledge of stroke warning signs was low, although it significantly increased during the campaign (P &lt; 0·001) as paresis/weakness (46%) and speech problems (31%) were most frequently named. The majority of respondents indicated that the first action after suffering from stroke should be calling emergency care (74% before vs. 84% after campaign, P &lt; 0·001).ConclusionsOur data indicate that stroke knowledge and awareness, which could provide earlier presentation to the emergency unit for timely treatment onset, are still low in urban Northern Germany but may decisively be increased by educational campaigns.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00808.x" xmlns="http://purl.org/rss/1.0/"><title>Intravenous thrombolysis for acute ischemic stroke patients presenting with mild symptoms</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00808.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Intravenous thrombolysis for acute ischemic stroke patients presenting with mild symptoms</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-05-09T04:05:37.836769-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00808.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00808.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00808.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs808-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Thrombolysis of ischemic stroke patients presenting with mild symptoms is controversial.</p></div></div><div class="section" id="ijs808-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>We aimed to describe the clinical outcome and frequency of infarcts and symptomatic intracerebral hemorrhages on follow-up imaging of such thrombolysis-treated patients.</p></div></div><div class="section" id="ijs808-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Our cohort included 1398 consecutive ischemic stroke patients treated with intravenous thrombolysis at the Helsinki University Central Hospital, years 1995–2010. We analyzed the patients according to baseline National Institutes of Health Stroke Scale: ≤2, 3–4, 5–6, and &gt;6. In our institution, visualization of an artery occlusion or perfusion deficit is required for thrombolysis with National Institutes of Health Stroke Scale ≤ 2. We used univariate and multivariable methods to describe the cohort and study associations between the variables. Excellent three-month outcome was defined as modified Rankin Scale 0–1.</p></div></div><div class="section" id="ijs808-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Fifty-eight (4·1%) patients were treated with National Institutes of Health Stroke Scale ≤ 2, another 194 (13·6%) with 3–4 points, and 236 (16·5%) with 5–6 points. With National Institutes of Health Stroke Scale ≤ 2, 45 (78%) of the patients had excellent three-month outcome, achieved in 116 (59%) patients with National Institutes of Health Stroke Scale 3–4, in 130 (55%) with National Institutes of Health Stroke Scale 5–6, and in 241 (26%) with National Institutes of Health Stroke Scale &gt; 6. Frequencies of symptomatic intracerebral hemorrhage (European Cooperative Acute Stroke Study-2) were 0%, 2·6%, 2·1%, and 8·1%, and visible infarcts on follow-up imaging 48%, 43%, 48%, and 74%, respectively. In patients with baseline National Institutes of Health Stroke Scale ≤ 6, poor outcome was associated with previous stroke, diabetes, elevated admission blood glucose, and development of intracerebral hemorrhage.</p></div></div><div class="section" id="ijs808-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Half of patients presenting with National Institutes of Health Stroke Scale 0–6 developed an infarction despite thrombolysis, and 40% had poor outcome, which was associated with glucose metabolism and hemorrhagic complications. Managing thrombolysis candidates with mild symptoms warrants individual consideration often supported by multimodal imaging.</p></div></div>]]></content:encoded><description>BackgroundThrombolysis of ischemic stroke patients presenting with mild symptoms is controversial.AimWe aimed to describe the clinical outcome and frequency of infarcts and symptomatic intracerebral hemorrhages on follow-up imaging of such thrombolysis-treated patients.MethodsOur cohort included 1398 consecutive ischemic stroke patients treated with intravenous thrombolysis at the Helsinki University Central Hospital, years 1995–2010. We analyzed the patients according to baseline National Institutes of Health Stroke Scale: ≤2, 3–4, 5–6, and &gt;6. In our institution, visualization of an artery occlusion or perfusion deficit is required for thrombolysis with National Institutes of Health Stroke Scale ≤ 2. We used univariate and multivariable methods to describe the cohort and study associations between the variables. Excellent three-month outcome was defined as modified Rankin Scale 0–1.ResultsFifty-eight (4·1%) patients were treated with National Institutes of Health Stroke Scale ≤ 2, another 194 (13·6%) with 3–4 points, and 236 (16·5%) with 5–6 points. With National Institutes of Health Stroke Scale ≤ 2, 45 (78%) of the patients had excellent three-month outcome, achieved in 116 (59%) patients with National Institutes of Health Stroke Scale 3–4, in 130 (55%) with National Institutes of Health Stroke Scale 5–6, and in 241 (26%) with National Institutes of Health Stroke Scale &gt; 6. Frequencies of symptomatic intracerebral hemorrhage (European Cooperative Acute Stroke Study-2) were 0%, 2·6%, 2·1%, and 8·1%, and visible infarcts on follow-up imaging 48%, 43%, 48%, and 74%, respectively. In patients with baseline National Institutes of Health Stroke Scale ≤ 6, poor outcome was associated with previous stroke, diabetes, elevated admission blood glucose, and development of intracerebral hemorrhage.ConclusionsHalf of patients presenting with National Institutes of Health Stroke Scale 0–6 developed an infarction despite thrombolysis, and 40% had poor outcome, which was associated with glucose metabolism and hemorrhagic complications. Managing thrombolysis candidates with mild symptoms warrants individual consideration often supported by multimodal imaging.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00780.x" xmlns="http://purl.org/rss/1.0/"><title>Stroke subtyping for genetic association studies? A comparison of the CCS and TOAST classifications</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00780.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Stroke subtyping for genetic association studies? A comparison of the CCS and TOAST classifications</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Silvia Lanfranconi, Hugh S. Markus</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-04-22T21:52:04.507407-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00780.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00780.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00780.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs780-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>A reliable and reproducible classification system of stroke subtype is essential for epidemiological and genetic studies. The Causative Classification of Stroke system is an evidence-based computerized algorithm with excellent inter-rater reliability. It has been suggested that, compared to the Trial of ORG 10172 in Acute Stroke Treatment classification, it increases the proportion of cases with defined subtype that may increase power in genetic association studies. We compared Trial of ORG 10172 in Acute Stroke Treatment and Causative Classification of Stroke system classifications in a large cohort of well-phenotyped stroke patients.</p></div></div><div class="section" id="ijs780-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Six hundred ninety consecutively recruited patients with first-ever ischemic stroke were classified, using review of clinical data and original imaging, according to the Trial of ORG 10172 in Acute Stroke Treatment and Causative Classification of Stroke system classifications.</p></div></div><div class="section" id="ijs780-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>There was excellent agreement subtype assigned by between Trial of ORG 10172 in Acute Stroke Treatment and Causative Classification of Stroke system (kappa = 0·85). The agreement was excellent for the major individual subtypes: large artery atherosclerosis kappa = 0·888, small-artery occlusion kappa = 0·869, cardiac embolism kappa = 0·89, and undetermined category kappa = 0·884. There was only moderate agreement (kappa = 0·41) for the subjects with at least two competing underlying mechanism. Thirty-five (5·8%) patients classified as undetermined by Trial of ORG 10172 in Acute Stroke Treatment were assigned to a definite subtype by Causative Classification of Stroke system. Thirty-two subjects assigned to a definite subtype by Trial of ORG 10172 in Acute Stroke Treatment were classified as undetermined by Causative Classification of Stroke system.</p></div></div><div class="section" id="ijs780-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>There is excellent agreement between classification using Trial of ORG 10172 in Acute Stroke Treatment and Causative Classification of Stroke systems but no evidence that Causative Classification of Stroke system reduced the proportion of patients classified to undetermined subtypes. The excellent inter-rater reproducibility and web-based semiautomated nature make Causative Classification of Stroke system suitable for multicenter studies, but the benefit of reclassifying cases already classified using the Trial of ORG 10172 in Acute Stroke Treatment system on existing databases is likely to be small.</p></div></div>]]></content:encoded><description>BackgroundA reliable and reproducible classification system of stroke subtype is essential for epidemiological and genetic studies. The Causative Classification of Stroke system is an evidence-based computerized algorithm with excellent inter-rater reliability. It has been suggested that, compared to the Trial of ORG 10172 in Acute Stroke Treatment classification, it increases the proportion of cases with defined subtype that may increase power in genetic association studies. We compared Trial of ORG 10172 in Acute Stroke Treatment and Causative Classification of Stroke system classifications in a large cohort of well-phenotyped stroke patients.MethodsSix hundred ninety consecutively recruited patients with first-ever ischemic stroke were classified, using review of clinical data and original imaging, according to the Trial of ORG 10172 in Acute Stroke Treatment and Causative Classification of Stroke system classifications.ResultsThere was excellent agreement subtype assigned by between Trial of ORG 10172 in Acute Stroke Treatment and Causative Classification of Stroke system (kappa = 0·85). The agreement was excellent for the major individual subtypes: large artery atherosclerosis kappa = 0·888, small-artery occlusion kappa = 0·869, cardiac embolism kappa = 0·89, and undetermined category kappa = 0·884. There was only moderate agreement (kappa = 0·41) for the subjects with at least two competing underlying mechanism. Thirty-five (5·8%) patients classified as undetermined by Trial of ORG 10172 in Acute Stroke Treatment were assigned to a definite subtype by Causative Classification of Stroke system. Thirty-two subjects assigned to a definite subtype by Trial of ORG 10172 in Acute Stroke Treatment were classified as undetermined by Causative Classification of Stroke system.ConclusionsThere is excellent agreement between classification using Trial of ORG 10172 in Acute Stroke Treatment and Causative Classification of Stroke systems but no evidence that Causative Classification of Stroke system reduced the proportion of patients classified to undetermined subtypes. The excellent inter-rater reproducibility and web-based semiautomated nature make Causative Classification of Stroke system suitable for multicenter studies, but the benefit of reclassifying cases already classified using the Trial of ORG 10172 in Acute Stroke Treatment system on existing databases is likely to be small.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00778.x" xmlns="http://purl.org/rss/1.0/"><title>The FeSTivaLS trial protocol: A randomized evaluation of the efficacy of functional strength training on enhancing walking and upper limb function later post stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00778.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The FeSTivaLS trial protocol: A randomized evaluation of the efficacy of functional strength training on enhancing walking and upper limb function later post stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kathryn Mares, Jane Cross, Allan Clark, Garry R. Barton, Fiona Poland, Marie-Luce O'Driscoll, Martin J. Watson, Kate McGlashan, Phyo K. Myint, Valerie M. Pomeroy</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-04-17T23:27:46.152972-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00778.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00778.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00778.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocol</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs778-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Functional Strength Training may enhance motor function of people who are more than six months post stroke.</p></div></div><div class="section" id="ijs778-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>to evaluate the clinical efficacy of enhancing upper and lower limb motor function with FST to explore participants' views (expectations and experiences) of FST, and to determine what cost-effectiveness data to collect in a subsequent Phase III trial.</p></div></div><div class="section" id="ijs778-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Design</h4><div class="para"><p>Randomized, observer-blind trial with embedded qualitative investigation of participants' views of FST (<em>n</em> = 6, purposive sampling).</p></div></div><div class="section" id="ijs778-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Study</h4><div class="para"><p>Participants (<em>n</em> = 58), six months to five years after stroke with difficulty using their paretic upper (UL) and lower limbs (LL) for everyday functional activity. All will be randomized to either FST-UL or FST-LL delivered in their own homes for fours days each week for six weeks. FST involves repetitive progressive resisted exercise during goal directed functional activities. The therapist's main input is to provide verbal prompting and feedback.</p></div></div><div class="section" id="ijs778-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Outcomes</h4><div class="para"><p>Measures will be undertaken before randomization (baseline), after the six-week intervention (outcome) and six weeks thereafter (follow-up). Primary outcomes for clinical efficacy will be the Functional Ambulation Categories (FAC) and the Action Research Arm Test (ARAT). Clinical efficacy analysis will use the proportional odds model for FAC and a Mann-Whitney test for ARAT. Participants' views of FST will be explored at baseline and outcome through audiotaped, semi-structured, narrative approach, interviews. The analytic process for interviews will sort transcribed data thematically and seek categories to inform conceptualization (theory-building). A purpose-designed cost questionnaire will identify what cost resource items are likely to be affected by FST.</p></div></div>]]></content:encoded><description>RationaleFunctional Strength Training may enhance motor function of people who are more than six months post stroke.Aimsto evaluate the clinical efficacy of enhancing upper and lower limb motor function with FST to explore participants' views (expectations and experiences) of FST, and to determine what cost-effectiveness data to collect in a subsequent Phase III trial.DesignRandomized, observer-blind trial with embedded qualitative investigation of participants' views of FST (n = 6, purposive sampling).StudyParticipants (n = 58), six months to five years after stroke with difficulty using their paretic upper (UL) and lower limbs (LL) for everyday functional activity. All will be randomized to either FST-UL or FST-LL delivered in their own homes for fours days each week for six weeks. FST involves repetitive progressive resisted exercise during goal directed functional activities. The therapist's main input is to provide verbal prompting and feedback.OutcomesMeasures will be undertaken before randomization (baseline), after the six-week intervention (outcome) and six weeks thereafter (follow-up). Primary outcomes for clinical efficacy will be the Functional Ambulation Categories (FAC) and the Action Research Arm Test (ARAT). Clinical efficacy analysis will use the proportional odds model for FAC and a Mann-Whitney test for ARAT. Participants' views of FST will be explored at baseline and outcome through audiotaped, semi-structured, narrative approach, interviews. The analytic process for interviews will sort transcribed data thematically and seek categories to inform conceptualization (theory-building). A purpose-designed cost questionnaire will identify what cost resource items are likely to be affected by FST.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00781.x" xmlns="http://purl.org/rss/1.0/"><title>Cerebral edema in acute ischemic stroke patients treated with intravenous thrombolysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00781.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Cerebral edema in acute ischemic stroke patients treated with intravenous thrombolysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-09T01:57:56.367899-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00781.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00781.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00781.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs781-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Cerebral edema (CED) deteriorates outcome of ischemic stroke patients, and there is no effective medical treatment. Limited data exist on cerebral edema after stroke thrombolysis.</p></div></div><div class="section" id="ijs781-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>We aimed to analyze impact of cerebral edema on the outcome of thrombolysis-treated patients.</p></div></div><div class="section" id="ijs781-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Our cohort included 943 thrombolysis-treated ischemic stroke patients at the Helsinki University Central Hospital (1995–2008). Cerebral edema represented focal brain swelling up to 1/3 (CED-1) or greater than 1/3 (CED-2) of the hemisphere, or midline shift (CED-3). We studied baseline parameters associated with development of cerebral edema and association of cerebral edema with three-month outcome (modified Rankin Scale, mRS).</p></div></div><div class="section" id="ijs781-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>On control imaging, CED-1 was present in 167 (17·7%), CED-2 in 40 (4·2%), and CED-3 in 53 (5·6%) patients. Compared with patients without edema (<em>n</em> = 683), patients with cerebral edema had higher baseline National Institutes of Health Stroke Scale scores, more often hyperdense cerebral artery sign or early infarct signs on admission computerized tomography, and received thrombolysis later. Cerebral edema was independently associated with poor outcome (mRS 3–6) and mortality, whereas favorable outcome (mRS 0–2) was observed in 77 (46%), 5 (13%), and 3 (6%) patients with CED 1, 2, and 3, respectively. Anti-edema treatment was considered necessary and administered to 49/260 (19%) patients; only five had favorable outcome.</p></div></div><div class="section" id="ijs781-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Cerebral edema is frequent (28%) among thrombolysis-treated ischemic stroke patients, occurring in severe forms in 10%. Higher baseline National Institutes of Health Stroke Scale, presence of hyperdense cerebral artery sign or early infarct signs, and longer treatment delays are associated with edema development. Edema is a strong independent predictor of three-month outcome. Effect of anti-edema treatment was modest.</p></div></div>]]></content:encoded><description>BackgroundCerebral edema (CED) deteriorates outcome of ischemic stroke patients, and there is no effective medical treatment. Limited data exist on cerebral edema after stroke thrombolysis.AimsWe aimed to analyze impact of cerebral edema on the outcome of thrombolysis-treated patients.MethodsOur cohort included 943 thrombolysis-treated ischemic stroke patients at the Helsinki University Central Hospital (1995–2008). Cerebral edema represented focal brain swelling up to 1/3 (CED-1) or greater than 1/3 (CED-2) of the hemisphere, or midline shift (CED-3). We studied baseline parameters associated with development of cerebral edema and association of cerebral edema with three-month outcome (modified Rankin Scale, mRS).ResultsOn control imaging, CED-1 was present in 167 (17·7%), CED-2 in 40 (4·2%), and CED-3 in 53 (5·6%) patients. Compared with patients without edema (n = 683), patients with cerebral edema had higher baseline National Institutes of Health Stroke Scale scores, more often hyperdense cerebral artery sign or early infarct signs on admission computerized tomography, and received thrombolysis later. Cerebral edema was independently associated with poor outcome (mRS 3–6) and mortality, whereas favorable outcome (mRS 0–2) was observed in 77 (46%), 5 (13%), and 3 (6%) patients with CED 1, 2, and 3, respectively. Anti-edema treatment was considered necessary and administered to 49/260 (19%) patients; only five had favorable outcome.ConclusionsCerebral edema is frequent (28%) among thrombolysis-treated ischemic stroke patients, occurring in severe forms in 10%. Higher baseline National Institutes of Health Stroke Scale, presence of hyperdense cerebral artery sign or early infarct signs, and longer treatment delays are associated with edema development. Edema is a strong independent predictor of three-month outcome. Effect of anti-edema treatment was modest.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00758.x" xmlns="http://purl.org/rss/1.0/"><title>Sex after stroke: a content analysis of printable educational materials available online</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00758.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Sex after stroke: a content analysis of printable educational materials available online</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Natalie Hamam, Annie McCluskey, Spring Cooper Robbins</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-26T22:23:38.735656-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2011.00758.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2011.00758.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00758.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs758-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Providing written educational materials to stroke survivors is a key recommendation in many international stroke guidelines. Yet, sexual concerns are generally overlooked in current stroke rehabilitation and the content of educational materials on sexual concerns has not been analyzed nor evaluated in published stroke research.</p></div></div><div class="section" id="ijs758-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>The aim of this study was to identify, describe, and analyze printable educational materials on sexual concerns that are available online and easily shared with stroke survivors.</p></div></div><div class="section" id="ijs758-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Method</h4><div class="para"><p>Google search engine was used to locate printable educational materials from the Internet using a search term strategy of 35 phrases that were piloted for accuracy. The content of eligible materials was analyzed using NVivo software to produce both enumerative and thematic data.</p></div></div><div class="section" id="ijs758-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Nine educational materials from reputable organizations were included with an average length of seven pages and 1445 words (total 61 pages, 13 000 words). The content of the materials was similar and covered three main content areas:</p><ul class="bullet"><li>problems experienced after stroke: 30% coverage</li><li>suggested solutions: 32% coverage, and</li><li>reassurance: 9% coverage.</li></ul><p>Content describing potential problems reflected published research, but solutions and reassurance were general, nonspecific, and often not supported by evidence.</p></div></div><div class="section" id="ijs758-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Educational materials on sex after stroke may be helpful for health professionals, stroke survivors, and their partners, yet some messages appear to discourage recovery. Educators, health professionals, and organizations can use this analysis to evaluate their own educational resources and create resources that better address the sexual concerns of stroke survivors and their partners.</p></div></div>]]></content:encoded><description>BackgroundProviding written educational materials to stroke survivors is a key recommendation in many international stroke guidelines. Yet, sexual concerns are generally overlooked in current stroke rehabilitation and the content of educational materials on sexual concerns has not been analyzed nor evaluated in published stroke research.AimThe aim of this study was to identify, describe, and analyze printable educational materials on sexual concerns that are available online and easily shared with stroke survivors.MethodGoogle search engine was used to locate printable educational materials from the Internet using a search term strategy of 35 phrases that were piloted for accuracy. The content of eligible materials was analyzed using NVivo software to produce both enumerative and thematic data.ResultsNine educational materials from reputable organizations were included with an average length of seven pages and 1445 words (total 61 pages, 13 000 words). The content of the materials was similar and covered three main content areas:problems experienced after stroke: 30% coveragesuggested solutions: 32% coverage, andreassurance: 9% coverage.Content describing potential problems reflected published research, but solutions and reassurance were general, nonspecific, and often not supported by evidence.ConclusionsEducational materials on sex after stroke may be helpful for health professionals, stroke survivors, and their partners, yet some messages appear to discourage recovery. Educators, health professionals, and organizations can use this analysis to evaluate their own educational resources and create resources that better address the sexual concerns of stroke survivors and their partners.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00763.x" xmlns="http://purl.org/rss/1.0/"><title>Depressive symptoms as a predictor of quality of life in cerebral small vessel disease, acting independently of disability; a study in both sporadic small vessel disease and CADASIL</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00763.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Depressive symptoms as a predictor of quality of life in cerebral small vessel disease, acting independently of disability; a study in both sporadic small vessel disease and CADASIL</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Rebecca L. Brookes, Thomas A. Willis, Bhavini Patel, Robin G. Morris, Hugh S. Markus</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-26T22:23:32.650499-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2011.00763.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2011.00763.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00763.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs763-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Cerebral small vessel disease causes lacunar stroke, and more recently has been implicated as a cause of depression. Factors causing reduced quality of life in small vessel disease, including the relative contributions of disability and depressive symptoms, remain uncertain.</p></div></div><div class="section" id="ijs763-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>One hundred patients with small vessel disease and 55 controls completed the Stroke-Specific Quality of Life scale. The protocol was repeated in 40 patients with the young-onset genetic form of small vessel disease, cerebral autosomal dominant arteriopathy with sub-cortical infarcts and leukoencephalopathy, and 35 controls. Disability, activities of daily living, cognition and depression were measured.</p></div></div><div class="section" id="ijs763-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Quality of life was significantly lower in small vessel disease versus controls: mean (standard deviation), 196⋅8 (35⋅2) vs. 226⋅8 (15⋅3), <em>P</em> &lt; ⋅0001. Depressive symptoms were the major predictor of quality of life, explaining 52⋅9% of variance. The only other independent predictor was disability, explaining an additional 18⋅4%. A similar pattern was found in the young-onset genetic group, with reduced quality of life 202⋅0 (29⋅7) vs. controls 228⋅6 (13⋅1) <em>P</em> &lt; ⋅0001, and depressive symptoms accounting for 42⋅2% of variance. Disability explained an additional 17⋅6%. Relationships between depression and quality of life, and disability and quality of life were independent of one another.</p></div></div><div class="section" id="ijs763-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Depressive symptoms, often unrecognized, are a major determinant of reduced quality of life in small vessel disease. They account for greater reduction than, and are independent of, disability. This relationship may reflect the proposed causal association between white matter disease and depression. Treatment of depressive symptoms might significantly improve quality of life in small vessel disease.</p></div></div>]]></content:encoded><description>BackgroundCerebral small vessel disease causes lacunar stroke, and more recently has been implicated as a cause of depression. Factors causing reduced quality of life in small vessel disease, including the relative contributions of disability and depressive symptoms, remain uncertain.MethodsOne hundred patients with small vessel disease and 55 controls completed the Stroke-Specific Quality of Life scale. The protocol was repeated in 40 patients with the young-onset genetic form of small vessel disease, cerebral autosomal dominant arteriopathy with sub-cortical infarcts and leukoencephalopathy, and 35 controls. Disability, activities of daily living, cognition and depression were measured.ResultsQuality of life was significantly lower in small vessel disease versus controls: mean (standard deviation), 196⋅8 (35⋅2) vs. 226⋅8 (15⋅3), P &lt; ⋅0001. Depressive symptoms were the major predictor of quality of life, explaining 52⋅9% of variance. The only other independent predictor was disability, explaining an additional 18⋅4%. A similar pattern was found in the young-onset genetic group, with reduced quality of life 202⋅0 (29⋅7) vs. controls 228⋅6 (13⋅1) P &lt; ⋅0001, and depressive symptoms accounting for 42⋅2% of variance. Disability explained an additional 17⋅6%. Relationships between depression and quality of life, and disability and quality of life were independent of one another.ConclusionsDepressive symptoms, often unrecognized, are a major determinant of reduced quality of life in small vessel disease. They account for greater reduction than, and are independent of, disability. This relationship may reflect the proposed causal association between white matter disease and depression. Treatment of depressive symptoms might significantly improve quality of life in small vessel disease.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00761.x" xmlns="http://purl.org/rss/1.0/"><title>Design of a prospective, dose-escalation study evaluating the Safety of Pioglitazone for Hematoma Resolution in Intracerebral Hemorrhage (SHRINC)</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00761.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Design of a prospective, dose-escalation study evaluating the Safety of Pioglitazone for Hematoma Resolution in Intracerebral Hemorrhage (SHRINC)</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Nicole R. Gonzales, Jharna Shah, Navdeep Sangha, Lenis Sosa, Rebecca Martinez, Loren Shen, Mallikarjunarao Kasam, Miriam M. Morales, M Monir Hossain, Andrew D. Barreto, Sean I. Savitz, George Lopez, Vivek Misra, Tzu-Ching Wu, Ramy El Khoury, Amrou Sarraj, Preeti Sahota, William Hicks, Indrani Acosta, M. Rick Sline, Mohammad H. Rahbar, Xiurong Zhao, Jaroslaw Aronowski, James C. Grotta</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-20T02:45:53.620491-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2011.00761.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2011.00761.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00761.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocols</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs761-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale </h4><div class="para"><p>Preclinical work demonstrates that the transcription factor peroxisome proliferator-activated receptor gamma plays an important role in augmenting phagocytosis while modulating oxidative stress and inflammation. We propose that targeted stimulation of phagocytosis to promote efficient removal of the hematoma without harming surrounding brain cells may be a therapeutic option for intracerebral hemorrhage.</p></div></div><div class="section" id="ijs761-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims </h4><div class="para"><p>The primary objective is to assess the safety of the peroxisome proliferator-activated receptor gamma agonist, pioglitazone, in increasing doses for three-days followed by a maintenance dose, when administered to patients with spontaneous intracerebral hemorrhage within 24 h of symptom onset compared with standard care. We will determine the maximum tolerated dose of pioglitazone.</p></div></div><div class="section" id="ijs761-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Study design </h4><div class="para"><p>This is a prospective, randomized, blinded, placebo-controlled, dose-escalation safety trial in which patients with spontaneous intracerebral hemorrhage are randomly allocated to placebo or treatment. The Continual Reassessment Method for dose finding is used to determine the maximum tolerated dose of pioglitazone. Hematoma and edema resolution is evaluated with serial magnetic resonance imaging (MRI) at specified time points. Functional outcome will be evaluated at three- and six-months.</p></div></div><div class="section" id="ijs761-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Outcomes </h4><div class="para"><p>The primary safety outcome is mortality at discharge. Secondary safety outcomes include mortality at three-months and six-months, symptomatic cerebral edema, clinically significant congestive heart failure, edema, hypoglycemia, anemia, and hepatotoxicity. Radiographic outcomes will explore the time frame for resolution of 25%, 50%, and 75% of the hematoma. Clinical outcomes are measured by the National Institutes of Health Stroke Scale (NIHSS), the Barthel Index, modified Rankin Scale, Stroke Impact Scale-16, and EuroQol at three- and six-months.</p></div></div>]]></content:encoded><description>Rationale Preclinical work demonstrates that the transcription factor peroxisome proliferator-activated receptor gamma plays an important role in augmenting phagocytosis while modulating oxidative stress and inflammation. We propose that targeted stimulation of phagocytosis to promote efficient removal of the hematoma without harming surrounding brain cells may be a therapeutic option for intracerebral hemorrhage.Aims The primary objective is to assess the safety of the peroxisome proliferator-activated receptor gamma agonist, pioglitazone, in increasing doses for three-days followed by a maintenance dose, when administered to patients with spontaneous intracerebral hemorrhage within 24 h of symptom onset compared with standard care. We will determine the maximum tolerated dose of pioglitazone.Study design This is a prospective, randomized, blinded, placebo-controlled, dose-escalation safety trial in which patients with spontaneous intracerebral hemorrhage are randomly allocated to placebo or treatment. The Continual Reassessment Method for dose finding is used to determine the maximum tolerated dose of pioglitazone. Hematoma and edema resolution is evaluated with serial magnetic resonance imaging (MRI) at specified time points. Functional outcome will be evaluated at three- and six-months.Outcomes The primary safety outcome is mortality at discharge. Secondary safety outcomes include mortality at three-months and six-months, symptomatic cerebral edema, clinically significant congestive heart failure, edema, hypoglycemia, anemia, and hepatotoxicity. Radiographic outcomes will explore the time frame for resolution of 25%, 50%, and 75% of the hematoma. Clinical outcomes are measured by the National Institutes of Health Stroke Scale (NIHSS), the Barthel Index, modified Rankin Scale, Stroke Impact Scale-16, and EuroQol at three- and six-months.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00752.x" xmlns="http://purl.org/rss/1.0/"><title>Vascular risk prediction in ischemic stroke patients undergoing in-patient rehabilitation – insights from the investigation of patients with ischemic stroke in neurologic rehabilitation (INSIGHT) registry</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00752.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Vascular risk prediction in ischemic stroke patients undergoing in-patient rehabilitation – insights from the investigation of patients with ischemic stroke in neurologic rehabilitation (INSIGHT) registry</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Christian Weimar, Mario Siebler, Tobias Brandt, Daniela Römer, Ludger Rosin, Peter Bramlage, Dirk Sander</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-20T02:44:55.680521-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2011.00752.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2011.00752.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00752.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs752-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>In-patient rehabilitation following ischemic stroke offers a unique opportunity for risk factor and lifestyle modification. Quantification of risk in this setting may help to tailor therapy, increase physician awareness and patient compliance and thus to reduce recurrent vascular events.</p></div></div><div class="section" id="ijs752-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>To validate the predictive value of established secondary stroke risk scores.</p></div></div><div class="section" id="ijs752-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>One thousand one hundred sixty-three patients undergoing in-patient rehabilitation following recent ischemic stroke in 15 German neurologic rehabilitation centers were included 0·9 ± 0·5 months after the index event. Outcome information was available for 846 participants (72·7%) after a mean follow-up of 13 ± 2·3 months.</p></div></div><div class="section" id="ijs752-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Patients' mean age was 66·3 ± 12·3 years and 42·5% were women. The National Institutes of Health Stroke Scale (mean 4·0 ± 3·9), modified Rankin scale (median 2, range 0–5), and Barthel Index (median 90, range 0–100) indicated good functional status. A recurrent fatal or nonfatal stroke during follow-up occurred in 6·7% and combined vascular events (stroke, myocardial infarction, vascular death) in 10·9%. The predictive accuracy for recurrent stroke was slightly higher on the Essen Stroke Risk Score than on the Stroke Prognostis Instrument II (area under the curve 0·62 vs. 0·56), while both scores had a similar predictive accuracy for combined vascular events.</p></div></div><div class="section" id="ijs752-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Risk stratification on the Essen Stroke Risk Score and Stroke Prognostis Instrument II provides a moderate accuracy for the prediction of recurrent stroke and vascular events in patients undergoing neurologic in-patient rehabilitation. Although individual risk prediction may remain imprecise, the use of these scores should be encouraged.</p></div></div>]]></content:encoded><description>BackgroundIn-patient rehabilitation following ischemic stroke offers a unique opportunity for risk factor and lifestyle modification. Quantification of risk in this setting may help to tailor therapy, increase physician awareness and patient compliance and thus to reduce recurrent vascular events.AimsTo validate the predictive value of established secondary stroke risk scores.MethodsOne thousand one hundred sixty-three patients undergoing in-patient rehabilitation following recent ischemic stroke in 15 German neurologic rehabilitation centers were included 0·9 ± 0·5 months after the index event. Outcome information was available for 846 participants (72·7%) after a mean follow-up of 13 ± 2·3 months.ResultsPatients' mean age was 66·3 ± 12·3 years and 42·5% were women. The National Institutes of Health Stroke Scale (mean 4·0 ± 3·9), modified Rankin scale (median 2, range 0–5), and Barthel Index (median 90, range 0–100) indicated good functional status. A recurrent fatal or nonfatal stroke during follow-up occurred in 6·7% and combined vascular events (stroke, myocardial infarction, vascular death) in 10·9%. The predictive accuracy for recurrent stroke was slightly higher on the Essen Stroke Risk Score than on the Stroke Prognostis Instrument II (area under the curve 0·62 vs. 0·56), while both scores had a similar predictive accuracy for combined vascular events.ConclusionsRisk stratification on the Essen Stroke Risk Score and Stroke Prognostis Instrument II provides a moderate accuracy for the prediction of recurrent stroke and vascular events in patients undergoing neurologic in-patient rehabilitation. Although individual risk prediction may remain imprecise, the use of these scores should be encouraged.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00750.x" xmlns="http://purl.org/rss/1.0/"><title>Treatment with tPA predicts better outcome even if MCA occlusion persists</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00750.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Treatment with tPA predicts better outcome even if MCA occlusion persists</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Micha Kablau, Angelika Alonso, Michael G. Hennerici, Marc Fatar</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-20T02:44:25.015865-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2011.00750.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2011.00750.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00750.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs750-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background and hypothesis</h4><div class="para"><p>Functional improvement after middle cerebral artery ischaemia seems to depend on recanalization of large-vessel occlusion as early as possible. The only approved medical treatment for acute stroke is early IV tissue plasminogen activator administration. However, while some patients do not benefit from quick recanalization, others recover despite persistent middle cerebral artery occlusion. We wondered whether there are different effects of tissue plasminogen activator treatment on large artery and small artery reopening.</p></div></div><div class="section" id="ijs750-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We enrolled 55 acute stroke patients who showed persisting middle cerebral artery occlusion evidenced by transcranial colour-coded duplex ultrasonography in follow-up examination within 48 h postonset of middle cerebral artery stroke syndromes (mean 30·8 ± 5·4 h after admission). Twenty-two of 55 had been treated with tissue plasminogen activator and 33/55 had been treated without tissue plasminogen activator. We compared neurological (National Institutes of Health Stroke Scale) and functional (modified Rankin Scale) scores at baseline, after seven-days, and then after two-months. Risk factors, previous stroke prophylaxis, as well as clinical baseline characteristics were analysed to exclude significant differences between both groups.</p></div></div><div class="section" id="ijs750-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Despite later admission to hospital (tissue plasminogen activator patients 1·6 ± 0·66 h vs. non-tissue plasminogen activator patients 7·4 ± 5·84 h; <em>P</em> &lt; 0·001), there was no significant difference between both groups concerning demographic data, severity of symptoms on admission, risk factors, stroke prophylaxis, as well as basic laboratory values (international normalized ratio, leucocyte count, C-reactive protein) blood pressure and body temperature on admission.</p></div><div class="para"><p>Irrespective of Doppler findings demonstrating persistent middle cerebral artery occlusion in all 55 patients, there was a significant neurological and functional improvement in tissue plasminogen activator patients compared to non-tissue plasminogen activator patients. Tissue plasminogen activator patients had a mean improvement on National Institutes of Health Stroke Scale within the first seven-days of 2·8 points, while non-tissue plasminogen activator patients deteriorated by 2·2 points (<em>P</em> &lt; 0·001). Concerning modified Rankin Scale tissue plasminogen activator-treated patients showed a mean improvement within the first seven-days of 0·5 points, while non-tissue plasminogen activator patients deteriorated by 0·3 points (<em>P</em> = 0·019). A favourable overall short-term clinical course (i.e. improvement on National Institutes of Health Stroke Scale &gt;3 points and/or modified Rankin Scale &gt;1 point) was found in 36·4% of tissue plasminogen activator patients and in 6·1% of non-tissue plasminogen activator patients (<em>P</em> = 0·0047). At two-months follow-up, patients still showed a median modified Rankin Scale of 4 points after tissue plasminogen activator treatment and 5 points after non-tissue plasminogen activator treatment (<em>P</em> = 0·023).</p></div></div><div class="section" id="ijs750-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Although the prognosis of patients with persisting middle cerebral artery occlusion after tissue plasminogen activator administration is known to be poor, patients do better if treated with tissue plasminogen activator vs. those who could not be treated – mainly for late presentation. This may be due to sufficient small vascular territory recanalization despite persistence of large artery occlusion after tissue plasminogen activator treatment.</p></div></div>]]></content:encoded><description>Background and hypothesisFunctional improvement after middle cerebral artery ischaemia seems to depend on recanalization of large-vessel occlusion as early as possible. The only approved medical treatment for acute stroke is early IV tissue plasminogen activator administration. However, while some patients do not benefit from quick recanalization, others recover despite persistent middle cerebral artery occlusion. We wondered whether there are different effects of tissue plasminogen activator treatment on large artery and small artery reopening.MethodsWe enrolled 55 acute stroke patients who showed persisting middle cerebral artery occlusion evidenced by transcranial colour-coded duplex ultrasonography in follow-up examination within 48 h postonset of middle cerebral artery stroke syndromes (mean 30·8 ± 5·4 h after admission). Twenty-two of 55 had been treated with tissue plasminogen activator and 33/55 had been treated without tissue plasminogen activator. We compared neurological (National Institutes of Health Stroke Scale) and functional (modified Rankin Scale) scores at baseline, after seven-days, and then after two-months. Risk factors, previous stroke prophylaxis, as well as clinical baseline characteristics were analysed to exclude significant differences between both groups.ResultsDespite later admission to hospital (tissue plasminogen activator patients 1·6 ± 0·66 h vs. non-tissue plasminogen activator patients 7·4 ± 5·84 h; P &lt; 0·001), there was no significant difference between both groups concerning demographic data, severity of symptoms on admission, risk factors, stroke prophylaxis, as well as basic laboratory values (international normalized ratio, leucocyte count, C-reactive protein) blood pressure and body temperature on admission.Irrespective of Doppler findings demonstrating persistent middle cerebral artery occlusion in all 55 patients, there was a significant neurological and functional improvement in tissue plasminogen activator patients compared to non-tissue plasminogen activator patients. Tissue plasminogen activator patients had a mean improvement on National Institutes of Health Stroke Scale within the first seven-days of 2·8 points, while non-tissue plasminogen activator patients deteriorated by 2·2 points (P &lt; 0·001). Concerning modified Rankin Scale tissue plasminogen activator-treated patients showed a mean improvement within the first seven-days of 0·5 points, while non-tissue plasminogen activator patients deteriorated by 0·3 points (P = 0·019). A favourable overall short-term clinical course (i.e. improvement on National Institutes of Health Stroke Scale &gt;3 points and/or modified Rankin Scale &gt;1 point) was found in 36·4% of tissue plasminogen activator patients and in 6·1% of non-tissue plasminogen activator patients (P = 0·0047). At two-months follow-up, patients still showed a median modified Rankin Scale of 4 points after tissue plasminogen activator treatment and 5 points after non-tissue plasminogen activator treatment (P = 0·023).ConclusionAlthough the prognosis of patients with persisting middle cerebral artery occlusion after tissue plasminogen activator administration is known to be poor, patients do better if treated with tissue plasminogen activator vs. those who could not be treated – mainly for late presentation. This may be due to sufficient small vascular territory recanalization despite persistence of large artery occlusion after tissue plasminogen activator treatment.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00759.x" xmlns="http://purl.org/rss/1.0/"><title>Properties of proxy-derived modified Rankin Scale assessment</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00759.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Properties of proxy-derived modified Rankin Scale assessment</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kate McArthur, Michael L. C. Beagan, Andrew Degnan, Rosanne C. Howarth, Kirsten A. Mitchell, Fiona B. McQuaige, Mary Ann C. Shannon, DJ Stott, Terence J. Quinn</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-15T05:35:49.468406-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2011.00759.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2011.00759.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00759.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs759-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Cognitive or communication issues may preclude direct modified Rankin Scale interview, necessitating interview with a suitable surrogate. The clinimetric properties of this proxy modified Rankin Scale assessment have not been described.</p></div></div><div class="section" id="ijs759-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>To describe reliability of proxy-derived modified Rankin Scale and compare with traditional direct patient interview.</p></div></div><div class="section" id="ijs759-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Researchers assessed consenting stroke inpatients and their proxies using a nonstructured modified Rankin Scale approach. Paired interviewers (trained in modified Rankin Scale) performed independent and blinded modified Rankin Scale assessment of patients and appropriate proxies. Interobserver variability and agreement between patient and proxy modified Rankin Scale were described using kappa statistics (<em>k</em>, 95% confidence interval) and percentage agreement.</p></div></div><div class="section" id="ijs759-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Ninety-seven stroke survivors were assessed. Proxies were family members (<em>n</em> = 29), nurses (<em>n</em> = 50), or physiotherapists (<em>n</em> = 25). Median modified Rankin Scale from both patient and proxies was 3 [interquartile range (IQR): 2-4]. Reliability for patient modified Rankin Scale interview was weighted kappa = 0·70 (95% confidence interval: 0·30–1·00). Reliability for proxy modified Rankin Scale weighted kappa = 0·62 (95% confidence interval: 0·34–0·90). Subgroup analysis of various proxy information sources were as follows: family weighted kappa = 0·61; nurse weighted kappa = 0·58; therapist weighted kappa = 0·58. There was disagreement between patient-derived modified Rankin Scale and corresponding proxy modified Rankin Scale weighted kappa = 0·64 (95% CI: 0·42–0·86).</p></div></div><div class="section" id="ijs759-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>There is potential for substantial interobserver variability in proxy modified Rankin Scale and validity of certain proxy assessments is questionable. Direct modified Rankin Scale interview is preferred.</p></div></div>]]></content:encoded><description>BackgroundCognitive or communication issues may preclude direct modified Rankin Scale interview, necessitating interview with a suitable surrogate. The clinimetric properties of this proxy modified Rankin Scale assessment have not been described.AimsTo describe reliability of proxy-derived modified Rankin Scale and compare with traditional direct patient interview.MethodsResearchers assessed consenting stroke inpatients and their proxies using a nonstructured modified Rankin Scale approach. Paired interviewers (trained in modified Rankin Scale) performed independent and blinded modified Rankin Scale assessment of patients and appropriate proxies. Interobserver variability and agreement between patient and proxy modified Rankin Scale were described using kappa statistics (k, 95% confidence interval) and percentage agreement.ResultsNinety-seven stroke survivors were assessed. Proxies were family members (n = 29), nurses (n = 50), or physiotherapists (n = 25). Median modified Rankin Scale from both patient and proxies was 3 [interquartile range (IQR): 2-4]. Reliability for patient modified Rankin Scale interview was weighted kappa = 0·70 (95% confidence interval: 0·30–1·00). Reliability for proxy modified Rankin Scale weighted kappa = 0·62 (95% confidence interval: 0·34–0·90). Subgroup analysis of various proxy information sources were as follows: family weighted kappa = 0·61; nurse weighted kappa = 0·58; therapist weighted kappa = 0·58. There was disagreement between patient-derived modified Rankin Scale and corresponding proxy modified Rankin Scale weighted kappa = 0·64 (95% CI: 0·42–0·86).ConclusionsThere is potential for substantial interobserver variability in proxy modified Rankin Scale and validity of certain proxy assessments is questionable. Direct modified Rankin Scale interview is preferred.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00755.x" xmlns="http://purl.org/rss/1.0/"><title>Cerebral and extracerebral vasoreactivity in symptomatic lacunar stroke patients: a case-control study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00755.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Cerebral and extracerebral vasoreactivity in symptomatic lacunar stroke patients: a case-control study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-15T05:35:45.846683-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2011.00755.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2011.00755.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00755.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs755-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Whether cerebral artery endothelial dysfunction is a key factor of symptomatic lacunar stroke and cerebral small vessel disease remains unclear.</p></div></div><div class="section" id="ijs755-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Cerebral and extracerebral vasoreactivity were measured in 81 patients with recent symptomatic lacunar stroke and in 81 control subjects matched for main vascular risk factors. Cerebral vasoreactivity and carotid endothelial-dependent vasodilation were measured after five-minutes of carbon dioxide-induced hypercapnia. Brachial endothelial-dependent vasodilation was assessed after hyperemia induced by deflating a cuff around the forearm previously inflated to 200 mmHg for four-minutes. Carotid and brachial endothelial-independent vasodilation were measured five-minutes after administration of sublingual nitroglycerin 300 μg. Brain magnetic resonance imaging were analyzed in lacunar stroke patients.</p></div></div><div class="section" id="ijs755-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>One-month after stroke onset, patients had more severely impaired cerebral vasoreactivitys than matched controls (mean ± standard deviation, 14·4 ± 12·1% vs. 19·4 ± 17·4%; <em>P</em> = 0·049). Severe alterations of both carotid and brachial endothelial-dependent and at a lesser degree of carotid and brachial endothelial-independent vasodilation were observed in both groups. After adjustment for confounders, subjects with a cerebral vasoreactivity value in the two lower tertiles (≤19·6%) were more likely to have had a symptomatic lacunar stroke (adjusted odds ratio, 3·78; 95% confidence interval, 1·42 to 10·08; <em>P</em> = 0·008). Only alteration of brachial endothelial-independent vasodilation correlated with parenchymal abnormalities, namely microbleeds and leukoaraiosis.</p></div></div><div class="section" id="ijs755-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>While abnormalities in extracerebral vasoreactivity seem related to vascular risk factors, the severity of endothelial dysfunction in cerebral arteries may be determinant in the occurrence of symptomatic lacunar stroke in patients with small vessel disease.</p></div></div>]]></content:encoded><description>BackgroundWhether cerebral artery endothelial dysfunction is a key factor of symptomatic lacunar stroke and cerebral small vessel disease remains unclear.MethodsCerebral and extracerebral vasoreactivity were measured in 81 patients with recent symptomatic lacunar stroke and in 81 control subjects matched for main vascular risk factors. Cerebral vasoreactivity and carotid endothelial-dependent vasodilation were measured after five-minutes of carbon dioxide-induced hypercapnia. Brachial endothelial-dependent vasodilation was assessed after hyperemia induced by deflating a cuff around the forearm previously inflated to 200 mmHg for four-minutes. Carotid and brachial endothelial-independent vasodilation were measured five-minutes after administration of sublingual nitroglycerin 300 μg. Brain magnetic resonance imaging were analyzed in lacunar stroke patients.ResultsOne-month after stroke onset, patients had more severely impaired cerebral vasoreactivitys than matched controls (mean ± standard deviation, 14·4 ± 12·1% vs. 19·4 ± 17·4%; P = 0·049). Severe alterations of both carotid and brachial endothelial-dependent and at a lesser degree of carotid and brachial endothelial-independent vasodilation were observed in both groups. After adjustment for confounders, subjects with a cerebral vasoreactivity value in the two lower tertiles (≤19·6%) were more likely to have had a symptomatic lacunar stroke (adjusted odds ratio, 3·78; 95% confidence interval, 1·42 to 10·08; P = 0·008). Only alteration of brachial endothelial-independent vasodilation correlated with parenchymal abnormalities, namely microbleeds and leukoaraiosis.ConclusionsWhile abnormalities in extracerebral vasoreactivity seem related to vascular risk factors, the severity of endothelial dysfunction in cerebral arteries may be determinant in the occurrence of symptomatic lacunar stroke in patients with small vessel disease.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00751.x" xmlns="http://purl.org/rss/1.0/"><title>Intracranial vessel localization with power motion Doppler (PMD-TCD) compared with CT angiography in patients with acute ischaemic stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00751.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Intracranial vessel localization with power motion Doppler (PMD-TCD) compared with CT angiography in patients with acute ischaemic stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kristian Barlinn, Zeljko Zivanovic, Limin Zhao, Maruthi Kesani, Clotilde Balucani, Georgios Tsivgoulis, Andrei V. Alexandrov</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-15T05:35:40.634269-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2011.00751.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2011.00751.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00751.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs751-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Introduction</h4><div class="para"><p>With a view to develop an operator-independent monitoring system for sonothrombolysis, we aimed to evaluate the per cent agreement of power motion transcranial Doppler vessel tracks compared with computed tomography angiography in identification of the anterior and posterior circulation vessels in patients with acute ischaemic stroke.</p></div></div><div class="section" id="ijs751-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Consecutive acute ischaemic stroke patients who underwent emergent brain computed tomography angiography and bedside power motion transcranial Doppler were studied. Depth ranges for detecting anterior and posterior circulation vessels were derived from power motion transcranial Doppler flow tracks and computed tomography angiography images of the circle of Willis. We calculated percent agreement of power motion transcranial Doppler with computed tomography angiography for the anterior and posterior circulation vessel localization using computed tomography angiography as reference.</p></div></div><div class="section" id="ijs751-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Samples were obtained from 34 acute ischaemic stroke patients (mean age 61 ± 16 years, 62% men, median National Institutes of Health Stroke Scale (NIHSS) score 5, interquartile range 2–8). A total of 229 Power motion Doppler computed tomography angiography vessel pairs were analysed. Power motion transcranial Doppler tracks for M1 and proximal M2 middle cerebral artery (MCA) were located at 24–68 mm (M1 MCA: 36–68 mm; M2 MCA: 24–53 mm); anterior cerebral artery (ACA): 50–78 mm; P1 posterior cerebral artery (PCA): 50–74 mm; left vertebral artery: 30–74 mm; right vertebral artery: 30–78 mm; basilar artery: 76–106 mm. The per cent agreement of power motion Doppler-transcranial Doppler for identifying proximal intracranial arteries compared to computed tomography angiography was: M1 and M2 MCA: 100% (95% confidence interval: 96–100%); M1 MCA: 98% (95% confidence interval: 86–100%); M2 MCA: 94% (95% confidence interval: 79–99%); A1 ACA: 82% (95% confidence interval: 68–91%); P1 PCA: 70% (95% confidence interval: 53–83%); left vertebral artery: 96% (95% confidence interval: 80–100%); right vertebral artery: 96% (95% confidence interval: 79–100%); basilar artery: 100% (95% confidence interval: 89–100%).</p></div></div><div class="section" id="ijs751-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Power motion transcranial Doppler intercepts proximal vessels with good-to-excellent agreement with computed tomography angiography. Depth ranges (as opposed to average depths) can be used to target intracranial arterial segments for sonothrombolysis.</p></div></div>]]></content:encoded><description>IntroductionWith a view to develop an operator-independent monitoring system for sonothrombolysis, we aimed to evaluate the per cent agreement of power motion transcranial Doppler vessel tracks compared with computed tomography angiography in identification of the anterior and posterior circulation vessels in patients with acute ischaemic stroke.MethodsConsecutive acute ischaemic stroke patients who underwent emergent brain computed tomography angiography and bedside power motion transcranial Doppler were studied. Depth ranges for detecting anterior and posterior circulation vessels were derived from power motion transcranial Doppler flow tracks and computed tomography angiography images of the circle of Willis. We calculated percent agreement of power motion transcranial Doppler with computed tomography angiography for the anterior and posterior circulation vessel localization using computed tomography angiography as reference.ResultsSamples were obtained from 34 acute ischaemic stroke patients (mean age 61 ± 16 years, 62% men, median National Institutes of Health Stroke Scale (NIHSS) score 5, interquartile range 2–8). A total of 229 Power motion Doppler computed tomography angiography vessel pairs were analysed. Power motion transcranial Doppler tracks for M1 and proximal M2 middle cerebral artery (MCA) were located at 24–68 mm (M1 MCA: 36–68 mm; M2 MCA: 24–53 mm); anterior cerebral artery (ACA): 50–78 mm; P1 posterior cerebral artery (PCA): 50–74 mm; left vertebral artery: 30–74 mm; right vertebral artery: 30–78 mm; basilar artery: 76–106 mm. The per cent agreement of power motion Doppler-transcranial Doppler for identifying proximal intracranial arteries compared to computed tomography angiography was: M1 and M2 MCA: 100% (95% confidence interval: 96–100%); M1 MCA: 98% (95% confidence interval: 86–100%); M2 MCA: 94% (95% confidence interval: 79–99%); A1 ACA: 82% (95% confidence interval: 68–91%); P1 PCA: 70% (95% confidence interval: 53–83%); left vertebral artery: 96% (95% confidence interval: 80–100%); right vertebral artery: 96% (95% confidence interval: 79–100%); basilar artery: 100% (95% confidence interval: 89–100%).ConclusionsPower motion transcranial Doppler intercepts proximal vessels with good-to-excellent agreement with computed tomography angiography. Depth ranges (as opposed to average depths) can be used to target intracranial arterial segments for sonothrombolysis.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00749.x" xmlns="http://purl.org/rss/1.0/"><title>The identification of acute stroke: an analysis of emergency calls</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00749.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The identification of acute stroke: an analysis of emergency calls</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-15T05:35:35.239604-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2011.00749.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2011.00749.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00749.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs749-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Accurate dispatch of emergency medical services at the onset of acute stroke is vital in expediting assessment and treatment. We examined the relationship between callers’ description of potential stroke symptoms to the emergency medical dispatcher and the subsequent classification and prioritisation of emergency medical services response.</p></div></div><div class="section" id="ijs749-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>To identify key ‘indicator’ words used by people making emergency calls for suspected stroke, comparing these with the subsequent category of response given by the emergency medical dispatcher.</p></div></div><div class="section" id="ijs749-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Method</h4><div class="para"><p>A retrospective chart review (hospital and emergency medical services) in North West England (October 1, 2006 to September 30, 2007) identified digitally recorded emergency medical services calls, which related to patients who had a diagnosis of suspected stroke at some point on the stroke pathway (from the emergency medical services call taker through to final medical diagnosis). Using content analysis, words used to describe stroke by the caller were recorded. A second researcher independently followed the same procedure in order to produce a list of ‘indicator’ words. Description of stroke-specific and nonstroke-specific problems reported by the caller was compared with subsequent emergency medical services dispatch coding and demographic features.</p></div></div><div class="section" id="ijs749-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Six hundred forty-three calls were made to emergency medical services of which 592 (92%) had complete emergency medical services and hospital data. The majority of callers were female (67%) and family members (55%). The most frequently reported problems first said by callers to the emergency medical dispatcher were collapse or fall (26%) and stroke (25%). Callers who identified that the patient was having a stroke were correct in 89% of cases. Calls were dispatched as stroke in 45% of cases, of which 83% had confirmed stroke. Of the first reported problems, Face Arm Speech Test stroke symptoms were mentioned in less than 5% of calls, with speech problems being the most common symptom. No callers mentioned all three Face Arm Speech Test symptoms.</p></div></div><div class="section" id="ijs749-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusion</h4><div class="para"><p>Callers who contacted emergency medical services for suspected stroke and said stroke as the first reported problem were often correct. Calls categorised as stroke by the emergency medical dispatcher were commonly confirmed as stroke in the hospital. Speech problems were the most commonly reported element of the Face Arm Speech Test test to be reported by callers. Recognition of possible stroke diagnosis in fall and other presentations should be considered by emergency medical dispatchers. Further development and training are needed in the community to improve prehospital stroke recognition in order to expedite hyperacute stroke care.</p></div></div>]]></content:encoded><description>BackgroundAccurate dispatch of emergency medical services at the onset of acute stroke is vital in expediting assessment and treatment. We examined the relationship between callers’ description of potential stroke symptoms to the emergency medical dispatcher and the subsequent classification and prioritisation of emergency medical services response.AimTo identify key ‘indicator’ words used by people making emergency calls for suspected stroke, comparing these with the subsequent category of response given by the emergency medical dispatcher.MethodA retrospective chart review (hospital and emergency medical services) in North West England (October 1, 2006 to September 30, 2007) identified digitally recorded emergency medical services calls, which related to patients who had a diagnosis of suspected stroke at some point on the stroke pathway (from the emergency medical services call taker through to final medical diagnosis). Using content analysis, words used to describe stroke by the caller were recorded. A second researcher independently followed the same procedure in order to produce a list of ‘indicator’ words. Description of stroke-specific and nonstroke-specific problems reported by the caller was compared with subsequent emergency medical services dispatch coding and demographic features.ResultsSix hundred forty-three calls were made to emergency medical services of which 592 (92%) had complete emergency medical services and hospital data. The majority of callers were female (67%) and family members (55%). The most frequently reported problems first said by callers to the emergency medical dispatcher were collapse or fall (26%) and stroke (25%). Callers who identified that the patient was having a stroke were correct in 89% of cases. Calls were dispatched as stroke in 45% of cases, of which 83% had confirmed stroke. Of the first reported problems, Face Arm Speech Test stroke symptoms were mentioned in less than 5% of calls, with speech problems being the most common symptom. No callers mentioned all three Face Arm Speech Test symptoms.ConclusionCallers who contacted emergency medical services for suspected stroke and said stroke as the first reported problem were often correct. Calls categorised as stroke by the emergency medical dispatcher were commonly confirmed as stroke in the hospital. Speech problems were the most commonly reported element of the Face Arm Speech Test test to be reported by callers. Recognition of possible stroke diagnosis in fall and other presentations should be considered by emergency medical dispatchers. Further development and training are needed in the community to improve prehospital stroke recognition in order to expedite hyperacute stroke care.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00748.x" xmlns="http://purl.org/rss/1.0/"><title>Inpatient stroke rehabilitation in Ontario: are dedicated units better?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00748.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Inpatient stroke rehabilitation in Ontario: are dedicated units better?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Norine Foley, Matthew Meyer, Katherine Salter, Mark Bayley, Ruth Hall, Ying Liu, Deborah Willems, J. Andrew McClure, Robert Teasell</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-15T05:35:33.262533-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2011.00748.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2011.00748.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00748.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs748-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The superiority of dedicated stroke rehabilitation over generalized rehabilitation services has been suggested by the literature; however, these models of service delivery have not been evaluated in terms of their relative effectiveness <em>in situ</em>.</p></div></div><div class="section" id="ijs748-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>A comparison of the process indicators associated with these two models of service provision was undertaken within the Ontario healthcare system.</p></div></div><div class="section" id="ijs748-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>All adults admitted with a diagnosis of stroke for inpatient rehabilitation in Ontario, Canada during the years 2006–2008 were identified from the National Rehabilitation Reporting System database. Each of the admitting institutions was classified as providing rehabilitation services on either a stroke dedicated or nondedicated unit. A dedicated unit was identified by the presence of a collection of geographically distinct, stroke-dedicated beds and dedicated therapists. Selected process indicators from the National Rehabilitation Reporting System database were compared between the two facility types.</p></div></div><div class="section" id="ijs748-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Sixty-seven facilities provided stroke rehabilitation services to 6709 adult stroke patients during the years 2006–2008. Of the total number of patients who entered inpatient rehabilitation, 1725 (25·7%) received care in eight facilities that met basic criteria for a dedicated stroke rehabilitation unit. On average, these patients took significantly longer to arrive for inpatient rehabilitation (37·2 ± 155·5 vs. 22·8 ± 95·0 days, <em>P</em> &lt; 0·001), were admitted with higher Functional Independence Measure scores (77·5 ± 22·5 vs. 74·8 ± 24·5, <em>P</em> &lt; 0·001), had significantly longer lengths of stay (42·1 ± 25·9 vs. 35·4 ± 27·2 days, <em>P</em> &lt; 0·001), and demonstrated significantly lower Functional Independence Measure efficiency scores (0·62 ± 0·47 vs. 0·88 ± 1·03, <em>P</em> &gt; 0·001) compared with patients who were admitted to nondedicated units. The proportion of patients admitted to a dedicated unit and subsequently discharged home was similar to that of patients discharged from nondedicated units (70·5% vs. 68·8%, <em>P</em> = 0·206).</p></div></div><div class="section" id="ijs748-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>In Ontario, patients admitted to dedicated stroke rehabilitation units fared no better on commonly-used process metrics compared with patients admitted to nondedicated rehabilitation units.</p></div></div>]]></content:encoded><description>BackgroundThe superiority of dedicated stroke rehabilitation over generalized rehabilitation services has been suggested by the literature; however, these models of service delivery have not been evaluated in terms of their relative effectiveness in situ.AimsA comparison of the process indicators associated with these two models of service provision was undertaken within the Ontario healthcare system.MethodsAll adults admitted with a diagnosis of stroke for inpatient rehabilitation in Ontario, Canada during the years 2006–2008 were identified from the National Rehabilitation Reporting System database. Each of the admitting institutions was classified as providing rehabilitation services on either a stroke dedicated or nondedicated unit. A dedicated unit was identified by the presence of a collection of geographically distinct, stroke-dedicated beds and dedicated therapists. Selected process indicators from the National Rehabilitation Reporting System database were compared between the two facility types.ResultsSixty-seven facilities provided stroke rehabilitation services to 6709 adult stroke patients during the years 2006–2008. Of the total number of patients who entered inpatient rehabilitation, 1725 (25·7%) received care in eight facilities that met basic criteria for a dedicated stroke rehabilitation unit. On average, these patients took significantly longer to arrive for inpatient rehabilitation (37·2 ± 155·5 vs. 22·8 ± 95·0 days, P &lt; 0·001), were admitted with higher Functional Independence Measure scores (77·5 ± 22·5 vs. 74·8 ± 24·5, P &lt; 0·001), had significantly longer lengths of stay (42·1 ± 25·9 vs. 35·4 ± 27·2 days, P &lt; 0·001), and demonstrated significantly lower Functional Independence Measure efficiency scores (0·62 ± 0·47 vs. 0·88 ± 1·03, P &gt; 0·001) compared with patients who were admitted to nondedicated units. The proportion of patients admitted to a dedicated unit and subsequently discharged home was similar to that of patients discharged from nondedicated units (70·5% vs. 68·8%, P = 0·206).ConclusionsIn Ontario, patients admitted to dedicated stroke rehabilitation units fared no better on commonly-used process metrics compared with patients admitted to nondedicated rehabilitation units.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00754.x" xmlns="http://purl.org/rss/1.0/"><title>Transcranial laser therapy for acute ischemic stroke: a pooled analysis of NEST-1 and NEST-2</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00754.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Transcranial laser therapy for acute ischemic stroke: a pooled analysis of NEST-1 and NEST-2</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-02T22:53:21.698059-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2011.00754.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2011.00754.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00754.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">n/a</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="section" id="ijs754-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>NeuroThera Effectiveness and Safety Trials (NEST) 1 and 2 have demonstrated safety of transcranial laser therapy (TLT) for human treatment in acute ischemic stroke. NEST 1 study suggested efficacy of TLT but the following NEST 2, despite strong signals, missed reaching significance on its primary efficacy endpoint. In order to assess efficacy in a larger cohort, a pooled analysis was therefore performed.</p></div></div><div class="section" id="ijs754-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The two studies were first compared for heterogeneity, and then a pooled analysis was performed to assess overall safety and efficacy, and examined particular subgroups. The primary endpoint for the pooled analysis was dichotomized modified Rankin scale (mRS) 0–2 at 90 days.</p></div></div><div class="section" id="ijs754-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Efficacy analysis for the intention-to-treat population was based on a total of 778 patients. Baseline characteristics and prognostic factors were balanced between the two groups. The TLT group (<em>n</em> = 410) success rate measured by the dichotomized 90-day mRS was significantly higher compared with the sham group (<em>n</em> = 368) (<em>P</em> = 0·003, OR: 1·67, 95% CI: 1·19–2·35). The distribution of scores on the 90-day mRS was significantly different in TLT compared with sham (<em>P</em> = 0·0005 Cochran–Mantel–Haenszel). Subgroup analysis identified moderate strokes as a predictor of better treatment response.</p></div></div><div class="section" id="ijs754-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>This pooled analysis support the likelihood that transcranial laser therapy is effective for the treatment of acute ischemic stroke when initiated within 24 h of stroke onset. If ultimately confirmed, transcranial laser therapy will change management and improve outcomes of far more patients with acute ischemic stroke.</p></div></div>]]></content:encoded><description>BackgroundNeuroThera Effectiveness and Safety Trials (NEST) 1 and 2 have demonstrated safety of transcranial laser therapy (TLT) for human treatment in acute ischemic stroke. NEST 1 study suggested efficacy of TLT but the following NEST 2, despite strong signals, missed reaching significance on its primary efficacy endpoint. In order to assess efficacy in a larger cohort, a pooled analysis was therefore performed.MethodsThe two studies were first compared for heterogeneity, and then a pooled analysis was performed to assess overall safety and efficacy, and examined particular subgroups. The primary endpoint for the pooled analysis was dichotomized modified Rankin scale (mRS) 0–2 at 90 days.ResultsEfficacy analysis for the intention-to-treat population was based on a total of 778 patients. Baseline characteristics and prognostic factors were balanced between the two groups. The TLT group (n = 410) success rate measured by the dichotomized 90-day mRS was significantly higher compared with the sham group (n = 368) (P = 0·003, OR: 1·67, 95% CI: 1·19–2·35). The distribution of scores on the 90-day mRS was significantly different in TLT compared with sham (P = 0·0005 Cochran–Mantel–Haenszel). Subgroup analysis identified moderate strokes as a predictor of better treatment response.ConclusionsThis pooled analysis support the likelihood that transcranial laser therapy is effective for the treatment of acute ischemic stroke when initiated within 24 h of stroke onset. If ultimately confirmed, transcranial laser therapy will change management and improve outcomes of far more patients with acute ischemic stroke.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00640.x" xmlns="http://purl.org/rss/1.0/"><title>Ischemic involvement of the primary motor cortex is a prognostic factor in acute stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00640.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Ischemic involvement of the primary motor cortex is a prognostic factor in acute stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Dilaver Kaya, Alp Dincer, Fehim Arman, Nadi Bakirci, Canan Erzen, M. Necmettin Pamir</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2011-10-04T05:37:32.521865-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2011.00640.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2011.00640.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2011.00640.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p><b>Background
					</b> The location of the primary motor cortex can be detected in healthy adults using the findings of ‘T2 hypointensity’ and the ‘double layer sign’ on 3 T diffusion-weighted imaging. The aim of this study was to assess whether ischemic involvement of the primary motor cortex can be identified on 3 T diffusion-weighted imaging within six-hours after stroke onset and to evaluate whether this finding could predict clinical outcome three-months after ischemic stroke.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods
					</b> Sixty-five patients who had paralysis and ischemia of the anterior circulation underwent 3 T magnetic resonance imaging within six-hours of symptom onset. Follow-up MRI was obtained at 72 h. Anatomic localization and ischemic involvement of the primary motor cortex were evaluated on diffusion-weighted imaging by two investigators. Ischemic involvement on the primary motor cortex was classified into three grades. Ischemic lesion volumes were measured. We compared the favorable outcomes at three-months between subjects with and without ischemic involvement on the primary motor cortex using the NIHSS and modified Rankin Scale.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results
					</b> Ischemic involvement on the primary motor cortex was identified in 52% of patients. Interrater agreement coefficients were 0·93 for the identification of ischemic involvement of primary motor cortex. As defined by scores on the modified Rankin Scale, among the patients with ischemic involvement of the primary motor cortex were worse than the patients without ischemic involvement of the primary motor cortex (<em>P</em>=0·01). The mean ischemic lesion volume at baseline diffusion-weighted imaging was 38·7 ± 41·7 cm<sup>3</sup> and was 89·8 ± 93·6 cm<sup>3</sup> at follow-up T2-WI. Ischemic involvement on the primary motor cortex (odds ratio: 14·7) was a determinant for worse outcome.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusions
					</b> 3T diffusion-weighted imaging can identify ischemic involvement on the primary motor cortex and may provide useful information for predicting outcome during the hyperacute stage. Ischemic involvement on the primary motor cortex has a significant negative impact on recovery.</p></div>]]></content:encoded><description>Background
					 The location of the primary motor cortex can be detected in healthy adults using the findings of ‘T2 hypointensity’ and the ‘double layer sign’ on 3 T diffusion-weighted imaging. The aim of this study was to assess whether ischemic involvement of the primary motor cortex can be identified on 3 T diffusion-weighted imaging within six-hours after stroke onset and to evaluate whether this finding could predict clinical outcome three-months after ischemic stroke.Methods
					 Sixty-five patients who had paralysis and ischemia of the anterior circulation underwent 3 T magnetic resonance imaging within six-hours of symptom onset. Follow-up MRI was obtained at 72 h. Anatomic localization and ischemic involvement of the primary motor cortex were evaluated on diffusion-weighted imaging by two investigators. Ischemic involvement on the primary motor cortex was classified into three grades. Ischemic lesion volumes were measured. We compared the favorable outcomes at three-months between subjects with and without ischemic involvement on the primary motor cortex using the NIHSS and modified Rankin Scale.Results
					 Ischemic involvement on the primary motor cortex was identified in 52% of patients. Interrater agreement coefficients were 0·93 for the identification of ischemic involvement of primary motor cortex. As defined by scores on the modified Rankin Scale, among the patients with ischemic involvement of the primary motor cortex were worse than the patients without ischemic involvement of the primary motor cortex (P=0·01). The mean ischemic lesion volume at baseline diffusion-weighted imaging was 38·7 ± 41·7 cm3 and was 89·8 ± 93·6 cm3 at follow-up T2-WI. Ischemic involvement on the primary motor cortex (odds ratio: 14·7) was a determinant for worse outcome.Conclusions
					 3T diffusion-weighted imaging can identify ischemic involvement on the primary motor cortex and may provide useful information for predicting outcome during the hyperacute stage. Ischemic involvement on the primary motor cortex has a significant negative impact on recovery.</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12105" xmlns="http://purl.org/rss/1.0/"><title>The midyear overview 2013</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12105</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The midyear overview 2013</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Geoffrey A. Donnan</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12105</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12105</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12105</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Editorial</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">219</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">219</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00790.x" xmlns="http://purl.org/rss/1.0/"><title>Risk of recurrent stroke before carotid endarterectomy: The ANSYSCAP study</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00790.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Risk of recurrent stroke before carotid endarterectomy: The ANSYSCAP study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">E. P. Johansson, C. Arnerlöv, P. Wester</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-04-11T23:40:35.430401-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00790.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00790.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00790.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">220</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">227</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs790-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Carotid endarterectomy yields greater risk reduction for ipsilateral ischemic stroke when performed within two-weeks of the last cerebrovascular symptom than when performed two-weeks or more after the last symptom. However, additional benefit might be gained if carotid endarterectomy is performed earlier than within two-weeks.</p></div></div>
<div class="section" id="ijs790-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>To investigate the 90-day risk of ipsilateral ischemic stroke recurrence after amaurosis fugax, retinal artery occlusion, transient ischemic attack, or minor ischemic stroke in patients with 50–99% carotid stenosis before carotid endarterectomy, with emphasis on the first 14 days.</p></div></div>
<div class="section" id="ijs790-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Prospective cohort study. 230 consecutive patients with symptomatic 50–99% carotid stenosis (North American Symptomatic Carotid Endarterectomy Trial grading method) who underwent evaluation before carotid endarterectomy. Of these, 183 underwent carotid endarterectomy; the median delay to carotid endarterectomy was 29 days. Blood pressure lowering medication was used by 93% and lipid-lowering medication by 90%.</p></div></div>
<div class="section" id="ijs790-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The risk of ipsilateral ischemic stroke recurrence before carotid endarterectomy was 5·2% (<em>n</em> = 12) within two-days, 7·9% (<em>n</em> = 18) within seven-days, 11·2% (<em>n</em> = 25) within 14 days, and 18·6% (<em>n</em> = 33) within 90 days of the presenting event. The risk of ipsilateral ischemic stroke recurrence was higher if the presenting event was a stroke (adjusted hazard ratio 12·4, <em>P</em> = 0·015) or transient ischemic attack (adjusted hazard ratio 10·2, <em>P</em> = 0·026) compared with an amaurosis fugax.</p></div></div>
<div class="section" id="ijs790-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Discussion</h4><div class="para"><p>The risk of recurrent ipsilateral ischemic stroke was high within the first days of the presenting event. Many recurrences would likely have been avoided if carotid endarterectomy had been performed within the first days of the presenting event.</p></div></div>
]]></content:encoded><description>

Background
Carotid endarterectomy yields greater risk reduction for ipsilateral ischemic stroke when performed within two-weeks of the last cerebrovascular symptom than when performed two-weeks or more after the last symptom. However, additional benefit might be gained if carotid endarterectomy is performed earlier than within two-weeks.


Aims
To investigate the 90-day risk of ipsilateral ischemic stroke recurrence after amaurosis fugax, retinal artery occlusion, transient ischemic attack, or minor ischemic stroke in patients with 50–99% carotid stenosis before carotid endarterectomy, with emphasis on the first 14 days.


Methods
Prospective cohort study. 230 consecutive patients with symptomatic 50–99% carotid stenosis (North American Symptomatic Carotid Endarterectomy Trial grading method) who underwent evaluation before carotid endarterectomy. Of these, 183 underwent carotid endarterectomy; the median delay to carotid endarterectomy was 29 days. Blood pressure lowering medication was used by 93% and lipid-lowering medication by 90%.


Results
The risk of ipsilateral ischemic stroke recurrence before carotid endarterectomy was 5·2% (n = 12) within two-days, 7·9% (n = 18) within seven-days, 11·2% (n = 25) within 14 days, and 18·6% (n = 33) within 90 days of the presenting event. The risk of ipsilateral ischemic stroke recurrence was higher if the presenting event was a stroke (adjusted hazard ratio 12·4, P = 0·015) or transient ischemic attack (adjusted hazard ratio 10·2, P = 0·026) compared with an amaurosis fugax.


Discussion
The risk of recurrent ipsilateral ischemic stroke was high within the first days of the presenting event. Many recurrences would likely have been avoided if carotid endarterectomy had been performed within the first days of the presenting event.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00801.x" xmlns="http://purl.org/rss/1.0/"><title>The influence of anterior cerebral artery flow diversion measured by transcranial Doppler on acute infarct volume and clinical outcome in anterior circulation stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00801.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The influence of anterior cerebral artery flow diversion measured by transcranial Doppler on acute infarct volume and clinical outcome in anterior circulation stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hossein Zareie, Debbie A. Quain, Mark Parsons, Kerry J. Inder, Patrick McElduff, Ferdinand Miteff, Neil J. Spratt, Christopher Levi</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-05-09T04:09:29.660839-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00801.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00801.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00801.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">228</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">234</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs801-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Introduction</h4><div class="para"><p>Anterior cerebral artery flow diversion, measured by transcranial Doppler ultrasound, is correlated with leptomeningeal collateral flow on digital subtraction angiography in the setting of middle cerebral artery occlusion. We aimed to assess the influence of flow diversion as a marker of leptomeningeal collateralization on infarct size and penumbral volume.</p></div></div>
<div class="section" id="ijs801-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We assessed consecutive patients presenting within six-hours of ischaemic stroke. Anterior cerebral artery flow diversion, defined as ipsilateral mean velocity of at least 30% greater than the contralateral artery, was used as the Doppler index of leptomeningeal collateralization. Multivariable regression analysis was performed to assess the impact of anterior cerebral artery flow diversion, controlling for other important clinical variables. Leptomeningeal collateralization was also graded on computed tomography angiography. Infarct core and penumbral volumes were defined using computed tomography perfusion thresholds of cerebral blood volume and mean transit time. Infarct volume, reperfusion, and vessel status were measured at 24 h using magnetic resonance techniques.</p></div></div>
<div class="section" id="ijs801-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Fifty-three patients qualified for analysis. Anterior cerebral artery flow diversion was associated with good collateral flow on computed tomography angiography (<em>P</em> &lt; 0·001) and was an independent predictor of admission infarct core volume (<em>P</em> &lt; 0·001), and 24 h infarct volume (<em>P</em> &lt; 0·001). The likelihood of a favourable outcome (modified Rankin Score 0–2) was higher (odds ratio = 27·5, <em>P</em> &lt; 0·001) in those with flow diversion.</p></div></div>
<div class="section" id="ijs801-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Anterior cerebral artery flow diversion indicates effective leptomeningeal collateralization as measured by computed tomography angiography, and independently predicts acute infarct size and 90-day clinical outcome. Flow diversion appears to provide penumbral perfusion, offering some protection against infarct expansion. Acute bedside transcranial Doppler assessment of flow diversion aids prognostication and therapeutic decision making in anterior circulation stroke.</p></div></div>
]]></content:encoded><description>

Introduction
Anterior cerebral artery flow diversion, measured by transcranial Doppler ultrasound, is correlated with leptomeningeal collateral flow on digital subtraction angiography in the setting of middle cerebral artery occlusion. We aimed to assess the influence of flow diversion as a marker of leptomeningeal collateralization on infarct size and penumbral volume.


Methods
We assessed consecutive patients presenting within six-hours of ischaemic stroke. Anterior cerebral artery flow diversion, defined as ipsilateral mean velocity of at least 30% greater than the contralateral artery, was used as the Doppler index of leptomeningeal collateralization. Multivariable regression analysis was performed to assess the impact of anterior cerebral artery flow diversion, controlling for other important clinical variables. Leptomeningeal collateralization was also graded on computed tomography angiography. Infarct core and penumbral volumes were defined using computed tomography perfusion thresholds of cerebral blood volume and mean transit time. Infarct volume, reperfusion, and vessel status were measured at 24 h using magnetic resonance techniques.


Results
Fifty-three patients qualified for analysis. Anterior cerebral artery flow diversion was associated with good collateral flow on computed tomography angiography (P &lt; 0·001) and was an independent predictor of admission infarct core volume (P &lt; 0·001), and 24 h infarct volume (P &lt; 0·001). The likelihood of a favourable outcome (modified Rankin Score 0–2) was higher (odds ratio = 27·5, P &lt; 0·001) in those with flow diversion.


Conclusions
Anterior cerebral artery flow diversion indicates effective leptomeningeal collateralization as measured by computed tomography angiography, and independently predicts acute infarct size and 90-day clinical outcome. Flow diversion appears to provide penumbral perfusion, offering some protection against infarct expansion. Acute bedside transcranial Doppler assessment of flow diversion aids prognostication and therapeutic decision making in anterior circulation stroke.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00804.x" xmlns="http://purl.org/rss/1.0/"><title>Stroke complicating transcatheter aortic valve implantation: incidence, risk factors and outcome</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00804.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Stroke complicating transcatheter aortic valve implantation: incidence, risk factors and outcome</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ronen R. Leker, Roni Eichel, Ami Verber, Jose. E. Cohen, Chaim Lotan, Haim D. Danenberg</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-04-17T23:29:01.745567-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00804.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00804.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00804.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">235</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">239</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs804-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Transcatheter aortic valve implantation is a novel therapeutic option for patients at high risk for surgical heart valve replacement that carries a risk for periprocedural stroke.</p></div></div>
<div class="section" id="ijs804-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Patients and methods</h4><div class="para"><p>Consecutive patients undergoing transcatheter aortic valve implantation with the self-expandable Medtronic-Corevalve Revalving system were included in a single-centre prospective database. Strokes complicating transcatheter aortic valve implantation in the first five-days following the procedure were documented, and the differences between patients with and without stroke were studied.</p></div></div>
<div class="section" id="ijs804-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Seventy-two patients (32 men, mean age 80·5 ± 6·2) underwent transcatheter aortic valve implantation from September 2008 to April 2011. Of these, eight (11%) had focal neurological deficits in the periprocedural period (three transient ischaemic attacks, five strokes of which three were minor, one moderate, and one major). Patients with stroke/transient ischaemic attacks did not differ from those without cerebral ischaemia in baseline criteria or procedural variables. Six of the events were believed to be embolic resulting from dislodgement of calcific material from the aortic valve, and one transient ischaemic attack was secondary to hypoperfusion during severe bradycardia. One patient with basilar occlusion died, but the remaining six patients survived and all had a modified Rankin score ≤2 at 90 days. None of the patients had a recurrent stroke during follow-up.</p></div></div>
<div class="section" id="ijs804-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Discussion</h4><div class="para"><p>Periprocedural cerebral ischaemia following transcatheter aortic valve implantation is not uncommon, but most patients have good outcomes. There was no particular pre-transcatheter aortic valve implantation or procedural risk factor profile that increased the risk for periprocedural stroke. Further studies are warranted to examine whether patients that are at higher risk for developing stroke after transcatheter aortic valve implantation can be identified.</p></div></div>
]]></content:encoded><description>

Background
Transcatheter aortic valve implantation is a novel therapeutic option for patients at high risk for surgical heart valve replacement that carries a risk for periprocedural stroke.


Patients and methods
Consecutive patients undergoing transcatheter aortic valve implantation with the self-expandable Medtronic-Corevalve Revalving system were included in a single-centre prospective database. Strokes complicating transcatheter aortic valve implantation in the first five-days following the procedure were documented, and the differences between patients with and without stroke were studied.


Results
Seventy-two patients (32 men, mean age 80·5 ± 6·2) underwent transcatheter aortic valve implantation from September 2008 to April 2011. Of these, eight (11%) had focal neurological deficits in the periprocedural period (three transient ischaemic attacks, five strokes of which three were minor, one moderate, and one major). Patients with stroke/transient ischaemic attacks did not differ from those without cerebral ischaemia in baseline criteria or procedural variables. Six of the events were believed to be embolic resulting from dislodgement of calcific material from the aortic valve, and one transient ischaemic attack was secondary to hypoperfusion during severe bradycardia. One patient with basilar occlusion died, but the remaining six patients survived and all had a modified Rankin score ≤2 at 90 days. None of the patients had a recurrent stroke during follow-up.


Discussion
Periprocedural cerebral ischaemia following transcatheter aortic valve implantation is not uncommon, but most patients have good outcomes. There was no particular pre-transcatheter aortic valve implantation or procedural risk factor profile that increased the risk for periprocedural stroke. Further studies are warranted to examine whether patients that are at higher risk for developing stroke after transcatheter aortic valve implantation can be identified.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00835.x" xmlns="http://purl.org/rss/1.0/"><title>Predictors of poststroke driving or riding in Indian stroke patients (POINT Study)</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00835.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Predictors of poststroke driving or riding in Indian stroke patients (POINT Study)</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Shiti Bose, Paramdeep Kaur, Sudeepa Dhillon, Rinu Susan Raju, Jeyaraj D. Pandian</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-05-28T04:40:45.982932-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00835.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00835.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00835.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">240</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">244</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs835-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>There is no information regarding the proportion of stroke patients who drive or ride after a stroke from developing countries.</p></div></div>
<div class="section" id="ijs835-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>We aimed to study the predictors of poststroke driving or riding and its impact on social life in Indian patients.</p></div></div>
<div class="section" id="ijs835-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>This study was done in the stroke and neurology clinics of Christian Medical College, Ludhiana, from May 1, 2008 to May 31, 2010. Patients were recruited if they had completed ≥1-year follow-up. Subjects were interviewed using a structured questionnaire. Stroke outcome was assessed by using the modified Rankin scale. Outcome was classified as good (modified Rankin scale ≤2) and poor (modified Rankin scale &gt;2).</p></div></div>
<div class="section" id="ijs835-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Two hundred and one patients were interviewed. Mean age was 58·0 ± 13·4 years (median 59 years, range 17–85 years), 139 (69·2%) were men. The mean duration of follow-up was 37·4 ± 29·2 months (range 19–210 months). Out of 201 patients, 132 (65·7%) drove or rode before stroke and among them only 54 (40·9%) returned to driving or riding after stroke [men 53 (98·1%)]. Among the 78 who did not return to driving or riding, 51 (65·4%) had an impact on social life. In the multivariate logistic regression analysis, the predictors of inability to drive were lower education (odds ratio 0·32, confidence interval 0·12–0·89, <em>P</em> = 0·03), unemployment (odds ratio 4·59, confidence interval 1·67–12·6, <em>P</em> = 0·003), and poor outcome (odds ratio 3·97, confidence interval 1·06–14·8, <em>P</em> = 0·04).</p></div></div>
<div class="section" id="ijs835-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Only 40·9% of the patients returned to driving or riding. Lower education, unemployment, and poor recovery were the predictors of inability to drive or ride. Inability to drive had a major impact in their social life.</p></div></div>
]]></content:encoded><description>

Background
There is no information regarding the proportion of stroke patients who drive or ride after a stroke from developing countries.


Aim
We aimed to study the predictors of poststroke driving or riding and its impact on social life in Indian patients.


Methods
This study was done in the stroke and neurology clinics of Christian Medical College, Ludhiana, from May 1, 2008 to May 31, 2010. Patients were recruited if they had completed ≥1-year follow-up. Subjects were interviewed using a structured questionnaire. Stroke outcome was assessed by using the modified Rankin scale. Outcome was classified as good (modified Rankin scale ≤2) and poor (modified Rankin scale &gt;2).


Results
Two hundred and one patients were interviewed. Mean age was 58·0 ± 13·4 years (median 59 years, range 17–85 years), 139 (69·2%) were men. The mean duration of follow-up was 37·4 ± 29·2 months (range 19–210 months). Out of 201 patients, 132 (65·7%) drove or rode before stroke and among them only 54 (40·9%) returned to driving or riding after stroke [men 53 (98·1%)]. Among the 78 who did not return to driving or riding, 51 (65·4%) had an impact on social life. In the multivariate logistic regression analysis, the predictors of inability to drive were lower education (odds ratio 0·32, confidence interval 0·12–0·89, P = 0·03), unemployment (odds ratio 4·59, confidence interval 1·67–12·6, P = 0·003), and poor outcome (odds ratio 3·97, confidence interval 1·06–14·8, P = 0·04).


Conclusions
Only 40·9% of the patients returned to driving or riding. Lower education, unemployment, and poor recovery were the predictors of inability to drive or ride. Inability to drive had a major impact in their social life.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00830.x" xmlns="http://purl.org/rss/1.0/"><title>Body mass index and risk of total and type-specific stroke in Chinese adults: results from a longitudinal study in China</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00830.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Body mass index and risk of total and type-specific stroke in Chinese adults: results from a longitudinal study in China</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Chunxiu Wang, Yunhai Liu, Qidong Yang, Xiuying Dai, Shengping Wu, Wenzhi Wang, Xunming Ji, Lin Li, Xianghua Fang</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-10-08T05:16:24.423734-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00830.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00830.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00830.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">245</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">250</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs830-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The prevalence rate of overweight and obese has been escalating over the past two decades in China. Even so, the association between obesity and stroke still remains unclear to some extent.</p></div></div>
<div class="section" id="ijs830-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims</h4><div class="para"><p>The aim of this study was to elucidate the association between body mass index and stroke in a large Chinese population cohort.</p></div></div>
<div class="section" id="ijs830-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>A cohort of 26 607 Chinese people, aged over 35 years, was investigated in 1987. Baseline information of body weight and height was used to calculate BMI (weight in kilograms divided by height in meters squared, kg/m<sup>2</sup>). Cox proportional hazards model was fitted to estimate hazard ratios of stroke adjusted for age, educational level, smoking and alcohol consumption.</p></div></div>
<div class="section" id="ijs830-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>The 11-year follow-up revealed (241 149 person-years) a total of 1108 stroke events (614 ischemic, 451 hemorrhagic, and 44 undefined stroke). Body mass index ≥ 30·0 was an independent risk factor for stroke both in men and women. Compared with normal weight, hazard ratios for total stroke were 0·74 in men underweight (95% confidence interval: 0·53∼1·03), 1·63 overweight (95% confidence interval: 1·35∼1·96), and 2·20 with obesity (95% confidence interval: 1·47∼3·30); and with ischemic stroke, hazard ratios were 0·52 in those underweight (95% confidence interval: 0·30∼0·89), 2·08 overweight (95% confidence interval: 1·65∼2·62), and 3·80 with obesity (95% confidence interval: 2·47∼5·86). In women, the corresponding hazard ratios for total stroke were 0·79 underweight (95% confidence interval: 0·58∼1·07), 1·42 overweight (95% confidence interval: 1·16∼1·73), and 1·57 with obesity (95% confidence interval: 1·06∼2·31); and for those with ischemic stroke, 0·92 underweight (95% confidence interval: 0·59∼1·43), 1·90 overweight (95% confidence interval: 1·44∼2·50), and 2·42 with obesity (95% confidence interval: 1·50∼3·93). There appeared an evident dose-response relationship between body mass index and the risk of developing stroke, which still appeared, however, adjusted low for hypertension, diabetes, and heart disease. Decreased risk for stroke in the leanest group was confined to men only. No association was found between body mass index and hemorrhagic stroke in both genders.</p></div></div>
<div class="section" id="ijs830-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Our data suggest that body mass index was an independent risk factor for total and ischemic stroke but not for hemorrhagic stroke in both genders. Association between body mass index and stroke was extremely mediated by hypertension, diabetes, and heart disease. Decreased risk for the leanest group was confined to men.</p></div></div>
]]></content:encoded><description>

Background
The prevalence rate of overweight and obese has been escalating over the past two decades in China. Even so, the association between obesity and stroke still remains unclear to some extent.


Aims
The aim of this study was to elucidate the association between body mass index and stroke in a large Chinese population cohort.


Methods
A cohort of 26 607 Chinese people, aged over 35 years, was investigated in 1987. Baseline information of body weight and height was used to calculate BMI (weight in kilograms divided by height in meters squared, kg/m2). Cox proportional hazards model was fitted to estimate hazard ratios of stroke adjusted for age, educational level, smoking and alcohol consumption.


Results
The 11-year follow-up revealed (241 149 person-years) a total of 1108 stroke events (614 ischemic, 451 hemorrhagic, and 44 undefined stroke). Body mass index ≥ 30·0 was an independent risk factor for stroke both in men and women. Compared with normal weight, hazard ratios for total stroke were 0·74 in men underweight (95% confidence interval: 0·53∼1·03), 1·63 overweight (95% confidence interval: 1·35∼1·96), and 2·20 with obesity (95% confidence interval: 1·47∼3·30); and with ischemic stroke, hazard ratios were 0·52 in those underweight (95% confidence interval: 0·30∼0·89), 2·08 overweight (95% confidence interval: 1·65∼2·62), and 3·80 with obesity (95% confidence interval: 2·47∼5·86). In women, the corresponding hazard ratios for total stroke were 0·79 underweight (95% confidence interval: 0·58∼1·07), 1·42 overweight (95% confidence interval: 1·16∼1·73), and 1·57 with obesity (95% confidence interval: 1·06∼2·31); and for those with ischemic stroke, 0·92 underweight (95% confidence interval: 0·59∼1·43), 1·90 overweight (95% confidence interval: 1·44∼2·50), and 2·42 with obesity (95% confidence interval: 1·50∼3·93). There appeared an evident dose-response relationship between body mass index and the risk of developing stroke, which still appeared, however, adjusted low for hypertension, diabetes, and heart disease. Decreased risk for stroke in the leanest group was confined to men only. No association was found between body mass index and hemorrhagic stroke in both genders.


Conclusions
Our data suggest that body mass index was an independent risk factor for total and ischemic stroke but not for hemorrhagic stroke in both genders. Association between body mass index and stroke was extremely mediated by hypertension, diabetes, and heart disease. Decreased risk for the leanest group was confined to men.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00841.x" xmlns="http://purl.org/rss/1.0/"><title>A modified Essen stroke risk score for predicting recurrent cardiovascular events: development and validation</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00841.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A modified Essen stroke risk score for predicting recurrent cardiovascular events: development and validation</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Shigeki Sumi, Hideki Origasa, Kiyohiro Houkin, Yasuo Terayama, Shinichiro Uchiyama, Hiroyuki Daida, Hiroshi Shigematsu, Shinya Goto, Kortaro Tanaka, Susumu Miyamoto, Kazuo Minematsu, Masayasu Matsumoto, Yasushi Okada, Motoki Sato, Norihiro Suzuki</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-07-03T08:53:49.900413-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00841.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00841.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00841.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">251</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">257</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs841-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>The Essen stroke risk score is widely applied to predict the risk of recurrent ischemic stroke. We developed a modified Essen stroke risk score and validated it using a large prospective Effective Vascular Event REduction after STroke (EVEREST) registry including 3588 patients with ischemic stroke in Japan. Patients with cardioembolic stroke were excluded, and follow-up was one-year.</p></div></div>
<div class="section" id="ijs841-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>The modified Essen stroke risk score was calculated from scores for waist circumference, stroke subtype by etiology, and gender in addition to age, hypertension, diabetes mellitus, previous myocardial infarction, other cardiovascular diseases except myocardial infarction and atrial fibrillation, peripheral artery disease, smoking, and previous stroke or transient ischemic attack. A multiple logistic regression model identified the predictors (each assigned one or two points) and provided c-statistics for the modified Essen stroke risk score. We considered two outcomes, recurrent ischemic stroke and cardiovascular events (defined as the combined outcomes of fatal or nonfatal stroke, myocardial infarction, nonfatal unstable angina, and cardiac death).</p></div></div> <div class="section" id="ijs841-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>Recurrent ischemic stroke occurred in 121 patients (3·7%) and cardiovascular events occurred in 133 (4·0%) within a year. The c-statistic (used for discrimination) was 0·632 for recurrent stroke and 0·640 for cardiovascular events. Patients scoring 6 or greater were classified as high risk, otherwise were classified as low risk. Kaplan–Meier analysis revealed that the modified risk score was more predictive than the Essen stroke risk score in both men and women.</p></div></div>
<div class="section" id="ijs841-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>The modified Essen stroke risk score increased the ability of the Essen stroke risk score to predict recurrent cardiovascular events. Patients with a high modified Essen stroke risk score should be candidates for intensified secondary prevention strategies.</p></div></div>
]]></content:encoded><description>

Background
The Essen stroke risk score is widely applied to predict the risk of recurrent ischemic stroke. We developed a modified Essen stroke risk score and validated it using a large prospective Effective Vascular Event REduction after STroke (EVEREST) registry including 3588 patients with ischemic stroke in Japan. Patients with cardioembolic stroke were excluded, and follow-up was one-year.


Methods
The modified Essen stroke risk score was calculated from scores for waist circumference, stroke subtype by etiology, and gender in addition to age, hypertension, diabetes mellitus, previous myocardial infarction, other cardiovascular diseases except myocardial infarction and atrial fibrillation, peripheral artery disease, smoking, and previous stroke or transient ischemic attack. A multiple logistic regression model identified the predictors (each assigned one or two points) and provided c-statistics for the modified Essen stroke risk score. We considered two outcomes, recurrent ischemic stroke and cardiovascular events (defined as the combined outcomes of fatal or nonfatal stroke, myocardial infarction, nonfatal unstable angina, and cardiac death).
 
Results
Recurrent ischemic stroke occurred in 121 patients (3·7%) and cardiovascular events occurred in 133 (4·0%) within a year. The c-statistic (used for discrimination) was 0·632 for recurrent stroke and 0·640 for cardiovascular events. Patients scoring 6 or greater were classified as high risk, otherwise were classified as low risk. Kaplan–Meier analysis revealed that the modified risk score was more predictive than the Essen stroke risk score in both men and women.


Conclusions
The modified Essen stroke risk score increased the ability of the Essen stroke risk score to predict recurrent cardiovascular events. Patients with a high modified Essen stroke risk score should be candidates for intensified secondary prevention strategies.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12090" xmlns="http://purl.org/rss/1.0/"><title>Trials of endovascular therapies or collaterals?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12090</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Trials of endovascular therapies or collaterals?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">David S. Liebeskind</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12090</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12090</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12090</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Leading opinion</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">258</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">259</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Several landmark clinical trials of endovascular therapy for acute ischemic stroke have recently jolted the concerted multidisciplinary efforts to develop effective revascularization strategies. Further consideration of these four endovascular stroke trials published in the last year suggests a more fundamental question: are these trials of specific treatments or have the results simply reflected the importance of underlying pathophysiology? Data from IMS III, MR RESCUE, SWIFT and TREVO2 consistently demonstrate the dramatic impact of collateral perfusion in acute ischemic stroke. Such collateral, or parallel, trials of the underlying pathophysiology in stroke reveal that diagnosis or selection of optimal candidates may be paramount to the specific drug or device therapy. Future trials of endovascular therapies may harness the influential role of collaterals as critical selection criteria for intervention, with triage based on imaging rather than time alone. Treating the optimal patient may be more important than chasing an elusive magical therapy.</p></div>
]]></content:encoded><description>
Several landmark clinical trials of endovascular therapy for acute ischemic stroke have recently jolted the concerted multidisciplinary efforts to develop effective revascularization strategies. Further consideration of these four endovascular stroke trials published in the last year suggests a more fundamental question: are these trials of specific treatments or have the results simply reflected the importance of underlying pathophysiology? Data from IMS III, MR RESCUE, SWIFT and TREVO2 consistently demonstrate the dramatic impact of collateral perfusion in acute ischemic stroke. Such collateral, or parallel, trials of the underlying pathophysiology in stroke reveal that diagnosis or selection of optimal candidates may be paramount to the specific drug or device therapy. Future trials of endovascular therapies may harness the influential role of collaterals as critical selection criteria for intervention, with triage based on imaging rather than time alone. Treating the optimal patient may be more important than chasing an elusive magical therapy.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00850.x" xmlns="http://purl.org/rss/1.0/"><title>Comprehensive stroke units: a review of comparative evidence and experience</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00850.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Comprehensive stroke units: a review of comparative evidence and experience</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Daniel K. Y. Chan, Dennis Cordato, Fintan O'Rourke, Daniel L Chan, Michael Pollack, Sandy Middleton, Chris Levi</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-07-19T10:39:52.090166-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00850.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00850.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00850.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">260</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">264</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs850-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Background</h4><div class="para"><p>Stroke unit care offers significant benefits in survival and dependency when compared to general medical ward. Most stroke units are either acute or rehabilitation, but comprehensive (combined acute and rehabilitation) model (comprehensive stroke unit) is less common.</p></div></div>
<div class="section" id="ijs850-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aim</h4><div class="para"><p>To examine different levels of evidence of comprehensive stroke unit compared to other organized inpatient stroke care and share local experience of comprehensive stroke units.</p></div></div>
<div class="section" id="ijs850-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>Cochrane Library and Medline (1980 to December 2010) review of English language articles comparing stroke units to alternative forms of stroke care delivery, different types of stroke unit models, and differences in processes of care within different stroke unit models. Different levels of comparative evidence of comprehensive stroke units to other models of stroke units are collected.</p></div></div>
<div class="section" id="ijs850-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>There are no randomized controlled trials directly comparing comprehensive stroke units to other stroke unit models (either acute or rehabilitation). Comprehensive stroke units are associated with reduced length of stay and greatest reduction in combined death and dependency in a meta-analysis study when compared to other stroke unit models. Comprehensive stroke units also have better length of stay and functional outcome when compared to acute or rehabilitation stroke unit models in a cross-sectional study, and better length of stay in a ‘before-and-after’ comparative study. Components of stroke unit care that improve outcome are multifactorial and most probably include early mobilization. A comprehensive stroke unit model has been successfully implemented in metropolitan and rural hospital settings.</p></div></div>
<div class="section" id="ijs850-sec-0005" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>Comprehensive stroke units are associated with reductions in length of stay and combined death and dependency and improved functional outcomes compared to other stroke unit models. A comprehensive stroke unit model is worth considering as the preferred model of stroke unit care in the planning and delivery of metropolitan and rural stroke services.</p></div></div>
]]></content:encoded><description>

Background
Stroke unit care offers significant benefits in survival and dependency when compared to general medical ward. Most stroke units are either acute or rehabilitation, but comprehensive (combined acute and rehabilitation) model (comprehensive stroke unit) is less common.


Aim
To examine different levels of evidence of comprehensive stroke unit compared to other organized inpatient stroke care and share local experience of comprehensive stroke units.


Methods
Cochrane Library and Medline (1980 to December 2010) review of English language articles comparing stroke units to alternative forms of stroke care delivery, different types of stroke unit models, and differences in processes of care within different stroke unit models. Different levels of comparative evidence of comprehensive stroke units to other models of stroke units are collected.


Results
There are no randomized controlled trials directly comparing comprehensive stroke units to other stroke unit models (either acute or rehabilitation). Comprehensive stroke units are associated with reduced length of stay and greatest reduction in combined death and dependency in a meta-analysis study when compared to other stroke unit models. Comprehensive stroke units also have better length of stay and functional outcome when compared to acute or rehabilitation stroke unit models in a cross-sectional study, and better length of stay in a ‘before-and-after’ comparative study. Components of stroke unit care that improve outcome are multifactorial and most probably include early mobilization. A comprehensive stroke unit model has been successfully implemented in metropolitan and rural hospital settings.


Conclusions
Comprehensive stroke units are associated with reductions in length of stay and combined death and dependency and improved functional outcomes compared to other stroke unit models. A comprehensive stroke unit model is worth considering as the preferred model of stroke unit care in the planning and delivery of metropolitan and rural stroke services.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00853.x" xmlns="http://purl.org/rss/1.0/"><title>Haemorrhagic strokes in pregnancy and puerperium</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00853.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Haemorrhagic strokes in pregnancy and puerperium</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Maria Khan, Mohammad Wasay</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-08-01T20:09:09.124585-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00853.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00853.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00853.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Review</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">265</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">272</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>There is an increased risk of strokes in pregnancy and puerperium. Intracranial haemorrhage is the rarer of the two stroke subtypes but carries a greater morbidity and mortality for both the mother and the child. This review highlights the causes of pregnancy-related intracranial haemorrhage and its management. The incidence varies from region to region with the highest being reported from China and Taiwan. Majority of these haemorrhages are secondary to hypertensive disorders of pregnancy with smaller proportions related to aneurysm and arteriovenous malformation rupture. A small but important contributor is cortical venous thrombosis which, although predominantly gives rise to ischaemic lesions, may lead to parenchymal haemorrhages as well. Presentation is usually with headaches or seizures, with or without focal deficits. Diagnosis requires brain imaging with computerized tomography or magnetic resonance imaging, and the necessity of investigation when this diagnosis is suspected supersedes the small risk of fetal malformation. Management follows the general management principles for intracranial haemorrhage management. Blood pressures need to be strictly monitored and medicines used for controlling them may differ slightly due to teratogenic effects. For preeclampsia, early but safe delivery is the best treatment. For cortical venous thrombosis, low-molecular-weight heparin is the preferred agent. Aneurysms and vascular malformations need to be definitively treated to prevent re-bleed and this can be achieved through surgical or endovascular procedures. The timing of surgery depends on neurosurgical considerations. However, the timing and mode of delivery are governed by obstetric factors. Risk of future haemorrhage depends on whether the underlying aetiology can be and has been definitively treated.</p></div>
]]></content:encoded><description>
There is an increased risk of strokes in pregnancy and puerperium. Intracranial haemorrhage is the rarer of the two stroke subtypes but carries a greater morbidity and mortality for both the mother and the child. This review highlights the causes of pregnancy-related intracranial haemorrhage and its management. The incidence varies from region to region with the highest being reported from China and Taiwan. Majority of these haemorrhages are secondary to hypertensive disorders of pregnancy with smaller proportions related to aneurysm and arteriovenous malformation rupture. A small but important contributor is cortical venous thrombosis which, although predominantly gives rise to ischaemic lesions, may lead to parenchymal haemorrhages as well. Presentation is usually with headaches or seizures, with or without focal deficits. Diagnosis requires brain imaging with computerized tomography or magnetic resonance imaging, and the necessity of investigation when this diagnosis is suspected supersedes the small risk of fetal malformation. Management follows the general management principles for intracranial haemorrhage management. Blood pressures need to be strictly monitored and medicines used for controlling them may differ slightly due to teratogenic effects. For preeclampsia, early but safe delivery is the best treatment. For cortical venous thrombosis, low-molecular-weight heparin is the preferred agent. Aneurysms and vascular malformations need to be definitively treated to prevent re-bleed and this can be achieved through surgical or endovascular procedures. The timing of surgery depends on neurosurgical considerations. However, the timing and mode of delivery are governed by obstetric factors. Risk of future haemorrhage depends on whether the underlying aetiology can be and has been definitively treated.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00884.x" xmlns="http://purl.org/rss/1.0/"><title>The burden of stroke in the Lao People's Democratic Republic</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00884.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The burden of stroke in the Lao People's Democratic Republic</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Keat Wei Loo, Siew Hua Gan</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-09-13T19:50:32.368332-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00884.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00884.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00884.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Panorama</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">273</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">275</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>In the Lao People's Democratic Republic (Laos), stroke is ranked as the third leading cause of death, with a 9·01% mortality rate. To date, neither the prevalence nor the incidence of stroke has been recorded in Laos. This omission may be attributed to a lack of awareness among Laotians of the signs and symptoms of stroke, incomplete data, or insufficient database recording. The only risk factor for stroke that has been studied extensively is cigarette smoking; studies have found that smokers have twice the risk of stroke. Unfortunately, smoking is increasing among youths, adults, and even healthcare professionals. The Southeast Asia Tobacco Control Alliance stated that 42% of hospitalized stroke patients are smokers. Laos is one of the least developed countries in the world, and the country has only one fully trained neurologist for the growing number of stroke cases. The Laos government should seek help from international bodies, such as the World Health Organization, to monitor and rehabilitate stroke patients and prevent stroke occurrence and recurrence.</p></div>
]]></content:encoded><description>
In the Lao People's Democratic Republic (Laos), stroke is ranked as the third leading cause of death, with a 9·01% mortality rate. To date, neither the prevalence nor the incidence of stroke has been recorded in Laos. This omission may be attributed to a lack of awareness among Laotians of the signs and symptoms of stroke, incomplete data, or insufficient database recording. The only risk factor for stroke that has been studied extensively is cigarette smoking; studies have found that smokers have twice the risk of stroke. Unfortunately, smoking is increasing among youths, adults, and even healthcare professionals. The Southeast Asia Tobacco Control Alliance stated that 42% of hospitalized stroke patients are smokers. Laos is one of the least developed countries in the world, and the country has only one fully trained neurologist for the growing number of stroke cases. The Laos government should seek help from international bodies, such as the World Health Organization, to monitor and rehabilitate stroke patients and prevent stroke occurrence and recurrence.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12058" xmlns="http://purl.org/rss/1.0/"><title>The Iberoamerican Cerebrovascular Diseases Society: 15 years moving forward</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12058</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The Iberoamerican Cerebrovascular Diseases Society: 15 years moving forward</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Oscar H. Del Brutto, Exuperio Diez-Tejedor, Claudio Sacks, Sebastián F. Ameriso, Juan Náder, María Alonso de Leciñana, Ayrton Massaro</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12058</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12058</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12058</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Panorama</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">276</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">277</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>The Iberoamerican Cerebrovascular Diseases Society was founded 15 years ago. Being aware of the increased burden of stroke in Latin America, its members have been working to enhance the knowledge on stroke among physicians in the region, to increase public awareness on stroke warning signs, and to motivate public health authorities to implement programs that speed the access of stroke patients to specialized units. Besides organizing annual meetings that have convened an increasing number of attendees, the Society has been actively involved in the elaboration of guidelines for stroke classification and therapy that will be practical for use at a regional level, as well as in the consolidation of links with other stroke societies to increase the diffusion of local stroke issues to the medical community at large. The Society is also involved in the Safe Implementation of Treatment in Stroke trial as well as in other studies that will increase the knowledge on stroke management and prognosis in the region.</p></div>
]]></content:encoded><description>
The Iberoamerican Cerebrovascular Diseases Society was founded 15 years ago. Being aware of the increased burden of stroke in Latin America, its members have been working to enhance the knowledge on stroke among physicians in the region, to increase public awareness on stroke warning signs, and to motivate public health authorities to implement programs that speed the access of stroke patients to specialized units. Besides organizing annual meetings that have convened an increasing number of attendees, the Society has been actively involved in the elaboration of guidelines for stroke classification and therapy that will be practical for use at a regional level, as well as in the consolidation of links with other stroke societies to increase the diffusion of local stroke issues to the medical community at large. The Society is also involved in the Safe Implementation of Treatment in Stroke trial as well as in other studies that will increase the knowledge on stroke management and prognosis in the region.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12040" xmlns="http://purl.org/rss/1.0/"><title>Details of a prospective protocol for a collaborative meta-analysis of individual participant data from all randomized trials of intravenous rt-PA vs. control: statistical analysis plan for the Stroke Thrombolysis Trialists’ Collaborative meta-analysis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12040</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Details of a prospective protocol for a collaborative meta-analysis of individual participant data from all randomized trials of intravenous rt-PA vs. control: statistical analysis plan for the Stroke Thrombolysis Trialists’ Collaborative meta-analysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-03T02:13:00.343102-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12040</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12040</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12040</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Protocol</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">278</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">283</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[
<div class="section" id="ijs12040-sec-0001" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><h4>Rationale</h4><div class="para"><p>Thrombolysis with intravenous alteplase is both effective and safe when administered to particular types of patient within 4·5 hours of having an ischemic stroke. However, the extent to which effects might vary in different types of patient is uncertain.</p></div></div>
<div class="section" id="ijs12040-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Aims and Design</h4><div class="para"><p>We describe the protocol for an updated individual patient data meta-analysis of trials of intravenous alteplase, including results from the recently reported third International Stroke Trial, in which a wide range of patients enrolled up to six-hours after stroke onset were randomized to alteplase vs. control.</p></div></div>
<div class="section" id="ijs12040-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Study Outcomes</h4><div class="para"><p>This protocol will specify the primary outcome for efficacy, specified prior to knowledge of the results from the third International Stroke Trial, as the proportion of patients having a ‘favorable’ stroke outcome, defined by modified Rankin Score 0–1 at final follow-up at three- to six-months. The primary analysis will be to estimate the extent to which the known benefit of alteplase on modified Rankin Score 0–1 diminishes with treatment delay, and the extent to which it is independently modified by age and stroke severity. Key secondary outcomes include effect of alteplase on death within 90 days; analyses of modified Rankin Score using ordinal, rather than dichotomous, methods; and effects of alteplase on symptomatic intracranial hemorrhage, fatal intracranial hemorrhage, symptomatic ischemic brain edema and early edema, effacement and/or midline shift.</p></div></div>
<div class="section" id="ijs12040-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Discussion</h4><div class="para"><p>This collaborative meta-analysis of individual participant data from all randomized trials of intravenous alteplase vs. control will demonstrate how the known benefits of alteplase on ischemic stroke outcome vary across different types of patient.</p></div></div>
]]></content:encoded><description>

Rationale
Thrombolysis with intravenous alteplase is both effective and safe when administered to particular types of patient within 4·5 hours of having an ischemic stroke. However, the extent to which effects might vary in different types of patient is uncertain.


Aims and Design
We describe the protocol for an updated individual patient data meta-analysis of trials of intravenous alteplase, including results from the recently reported third International Stroke Trial, in which a wide range of patients enrolled up to six-hours after stroke onset were randomized to alteplase vs. control.


Study Outcomes
This protocol will specify the primary outcome for efficacy, specified prior to knowledge of the results from the third International Stroke Trial, as the proportion of patients having a ‘favorable’ stroke outcome, defined by modified Rankin Score 0–1 at final follow-up at three- to six-months. The primary analysis will be to estimate the extent to which the known benefit of alteplase on modified Rankin Score 0–1 diminishes with treatment delay, and the extent to which it is independently modified by age and stroke severity. Key secondary outcomes include effect of alteplase on death within 90 days; analyses of modified Rankin Score using ordinal, rather than dichotomous, methods; and effects of alteplase on symptomatic intracranial hemorrhage, fatal intracranial hemorrhage, symptomatic ischemic brain edema and early edema, effacement and/or midline shift.


Discussion
This collaborative meta-analysis of individual participant data from all randomized trials of intravenous alteplase vs. control will demonstrate how the known benefits of alteplase on ischemic stroke outcome vary across different types of patient.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12093" xmlns="http://purl.org/rss/1.0/"><title>What are the most important barriers for thrombolytic therapy in ischemic stroke patients?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12093</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">What are the most important barriers for thrombolytic therapy in ischemic stroke patients?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hormoz Ayromlou, Hassan Soleimanpour, Mehdi Farhoudi, Elyar Sadeghi-Hokmabadi, Rouzbeh Rajaei Ghafouri, Ehsan Sharifipour, Somayeh Mostafaei, Mehdi Najafi Nashali</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12093</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12093</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12093</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E7</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E7</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00940.x" xmlns="http://purl.org/rss/1.0/"><title>Scorpion stings: focus on cerebrovascular complications of envenoming</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00940.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Scorpion stings: focus on cerebrovascular complications of envenoming</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Oscar H. Del Brutto, Victor J. Del Brutto</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00940.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00940.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00940.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E8</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E8</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00944.x" xmlns="http://purl.org/rss/1.0/"><title>NINDS stroke genetics network (SiGN) experience with the causative classification system</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00944.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">NINDS stroke genetics network (SiGN) experience with the causative classification system</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">James F. Meschia, Bradford B. Worrall, Robert D. Brown, Hakan Ay, Patrick F. McArdle, Tatjana Rundek, Steven J. Kittner</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00944.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00944.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00944.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E9</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E9</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00956.x" xmlns="http://purl.org/rss/1.0/"><title>The transference of a successful strategy to the care of stroke patients</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00956.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The transference of a successful strategy to the care of stroke patients</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">David R. McGowan, Helen M. Sims, Laura H. Stuttaford, Joseph M. Norris</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00956.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00956.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00956.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E10</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E10</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00965.x" xmlns="http://purl.org/rss/1.0/"><title>Reliability of NIHSS by telemedicine in non-neurologists</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00965.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Reliability of NIHSS by telemedicine in non-neurologists</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Eric Berthier, Pierre Decavel, Fabrice Vuillier, Clotilde Verlut, Thierry Moulin, Elisabeth Bustos Medeiros</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00965.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00965.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00965.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E11</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E11</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00964.x" xmlns="http://purl.org/rss/1.0/"><title>Mechanical endovascular therapy in ischaemic stroke: temporal trend of outcomes</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00964.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Mechanical endovascular therapy in ischaemic stroke: temporal trend of outcomes</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Valeria Fadda, Dario Maratea, Sabrina Trippoli, Andrea Messori</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00964.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00964.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00964.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E12</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E13</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00959.x" xmlns="http://purl.org/rss/1.0/"><title>Differences in neuropsychological profiles of long-term intracerebral hemorrhage and subarachnoid hemorrhage survivors</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00959.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Differences in neuropsychological profiles of long-term intracerebral hemorrhage and subarachnoid hemorrhage survivors</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Suzanne Barker-Collo, Valery Feigin, Rita Krishmnamurthi</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1747-4949.2012.00959.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1747-4949.2012.00959.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1747-4949.2012.00959.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E14</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E14</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12104" xmlns="http://purl.org/rss/1.0/"><title>Risk of cognitive impairment in acute phase of intracerebral haemorrhage</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12104</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Risk of cognitive impairment in acute phase of intracerebral haemorrhage</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Taizen Nakase, Masahiro Sasaki, Shotaroh Yoshioka, Yasuko Ikeda, Akifumi Suzuki</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12104</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12104</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12104</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E15</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E15</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12095" xmlns="http://purl.org/rss/1.0/"><title>Aspiration pneumonia in patients with stroke in Northeast Nigeria</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12095</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Aspiration pneumonia in patients with stroke in Northeast Nigeria</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Musa Mamman Watila, Yakub Wilberforce Nyandaiti, Salisu A. Balarabe, Bukar Bakki, Nura Hamidu Alkali, Abdullahi Ibrahim, Elijah Gargah Tonde, Ijiptil Chiroma</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12095</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12095</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12095</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E16</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E16</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12094" xmlns="http://purl.org/rss/1.0/"><title>Population attributable risks of stroke from intracranial atherosclerotic disease (ICAD) in South Asian Pakistanis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12094</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Population attributable risks of stroke from intracranial atherosclerotic disease (ICAD) in South Asian Pakistanis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ayeesha Kamran Kamal, Muhammad Faisal Wadiwala, Bilal Ahmed, Maria Khan, Farzin Majeed, Asif Rasheed, </dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-20T21:29:48.552636-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/ijs.12094</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/ijs.12094</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fijs.12094</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Letter to the editor</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E17</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">E17</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item></rdf:RDF>