<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"><channel rdf:about="http://onlinelibrary.wiley.com/rss/journal/10.1111/(ISSN)1748-6653" xmlns="http://purl.org/rss/1.0/"><title>Journal of Neuropsychology</title><description> Wiley Online Library : Journal of Neuropsychology</description><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2F%28ISSN%291748-6653</link><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc</dc:publisher><dc:language xmlns:dc="http://purl.org/dc/elements/1.1/">en</dc:language><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/">© The British Psychological Society</dc:rights><prism:issn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1748-6645</prism:issn><prism:eIssn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1748-6653</prism:eIssn><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-01T00:00:00-05:00</dc:date><prism:coverDisplayDate xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">March 2013</prism:coverDisplayDate><prism:volume xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">7</prism:volume><prism:number xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1</prism:number><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">147</prism:endingPage><image rdf:resource="http://onlinelibrary.wiley.com/store/10.1111/jnp.2013.7.issue-1/asset/cover.gif?v=1&amp;s=8138f9e76294d867038eb95c722d88d2bea965bb"/><items><rdf:Seq><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12021"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12020"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12019"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12013"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12017"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12018"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12015"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12014"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12016"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12010"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12011"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12009"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12007"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12008"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12005"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12006"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12004"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12003"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12002"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12000"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12001"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02027.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02031.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02032.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02033.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02034.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02035.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02036.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02037.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02038.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02040.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02030.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02039.x"/><rdf:li rdf:resource="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12012"/></rdf:Seq></items></channel><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12021" xmlns="http://purl.org/rss/1.0/"><title>A UK pilot study: The specificity of the Word Memory Test effort sub-tests in acute minimal to mild head injury</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12021</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A UK pilot study: The specificity of the Word Memory Test effort sub-tests in acute minimal to mild head injury</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Vicki L. Hall, Andrew Worthington, Katie Venables</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-16T05:33:19.218351-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12021</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12021</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</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 specificity of the Word Memory Test (WMT) effort indices was examined in 48 individuals with minimal to mild head injury (MHI) in the acute stages post-injury. None of the individuals was involved in litigation or disability claims. At the established cut-offs, the WMT had an unacceptable false-positive rate (18%). <em>T</em> test analysis was also carried out for WMT passers and failures on a battery of neuropsychometric measures and across a range of demographic variables. The WMT was performed at a significantly lower level on the Wechsler Memory Scale – III word list sub-tests and verbal fluency tests (<em>p</em> &lt; .05). This suggests that WMT failure may be indicative of a specific deficit in verbal processing in the acute phase of MHI.</p></div>
]]></content:encoded><description>
The specificity of the Word Memory Test (WMT) effort indices was examined in 48 individuals with minimal to mild head injury (MHI) in the acute stages post-injury. None of the individuals was involved in litigation or disability claims. At the established cut-offs, the WMT had an unacceptable false-positive rate (18%). T test analysis was also carried out for WMT passers and failures on a battery of neuropsychometric measures and across a range of demographic variables. The WMT was performed at a significantly lower level on the Wechsler Memory Scale – III word list sub-tests and verbal fluency tests (p &lt; .05). This suggests that WMT failure may be indicative of a specific deficit in verbal processing in the acute phase of MHI.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12020" xmlns="http://purl.org/rss/1.0/"><title>Motor imagery in spinal cord injury patients: Moving makes the difference</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12020</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Motor imagery in spinal cord injury patients: Moving makes the difference</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Federico Fiori, Anna Sedda, Elisa Raffaella Ferrè, Alessio Toraldo, Matteo Querzola, Fabrizio Pasotti, Daniela Ovadia, Chiara Piroddi, Roberta Dell'Aquila, Tiziana Redaelli, Gabriella Bottini</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-15T00:36:34.966511-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.12020</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/jnp.12020</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12020</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</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>Both real action control and execution and motor imagery abilities require knowledge of the spatial location of body parts, in other words efference copy information and feedbacks from the sensory system (Frith <em>et al</em>., 2000, Philos. Trans. R. Soc. Lond. B. Biol. Sci., <em>355</em>, 1771). Spinal cord injuries induce severe motor disability, due to a damage of the descending motor pathways (Cramer <em>et al</em>., 2007, Exp. Brain. Res., <em>177</em>, 233). Patients' motor imagery competences are variably reported as either normal or defective (Decety &amp; Boisson, 1990, Eur. Arch. Psychiatry Clin. Neurosci., <em>240</em>, 39; Lacourse <em>et al</em>., 1999, Behav. Brain Sci., <em>104</em>, 73). We explored biomechanical constraint effects in Spinal Cord Injury (SCI) patients, as they are considered the most reliable indexes of motor imagery abilities (Parsons, 1987b, Cogn. Psychol., <em>19</em>, 178). Sixteen spinal cord injuries patients and 16 neurologically unimpaired subjects have been administered with (1) the Hand Laterality Task (HLT), in which subjects were asked to judge the laterality of a rotated hand; and (2) the Mirror Letter Discrimination Task (MLD), in which subjects were asked to judge if a rotated character was in its correct upright position or mirror-reversed form. Our patients did not present the effect of stimulus orientation, neither did they show any effect related to biomechanical constraints. Based on these data, the hypothesis is that SCI patients' performance may be ascribed to the use of a different strategy to solve the tasks, based on memory rather than on mental rotation.</p></div>
]]></content:encoded><description>
Both real action control and execution and motor imagery abilities require knowledge of the spatial location of body parts, in other words efference copy information and feedbacks from the sensory system (Frith et al., 2000, Philos. Trans. R. Soc. Lond. B. Biol. Sci., 355, 1771). Spinal cord injuries induce severe motor disability, due to a damage of the descending motor pathways (Cramer et al., 2007, Exp. Brain. Res., 177, 233). Patients' motor imagery competences are variably reported as either normal or defective (Decety &amp; Boisson, 1990, Eur. Arch. Psychiatry Clin. Neurosci., 240, 39; Lacourse et al., 1999, Behav. Brain Sci., 104, 73). We explored biomechanical constraint effects in Spinal Cord Injury (SCI) patients, as they are considered the most reliable indexes of motor imagery abilities (Parsons, 1987b, Cogn. Psychol., 19, 178). Sixteen spinal cord injuries patients and 16 neurologically unimpaired subjects have been administered with (1) the Hand Laterality Task (HLT), in which subjects were asked to judge the laterality of a rotated hand; and (2) the Mirror Letter Discrimination Task (MLD), in which subjects were asked to judge if a rotated character was in its correct upright position or mirror-reversed form. Our patients did not present the effect of stimulus orientation, neither did they show any effect related to biomechanical constraints. Based on these data, the hypothesis is that SCI patients' performance may be ascribed to the use of a different strategy to solve the tasks, based on memory rather than on mental rotation.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12019" xmlns="http://purl.org/rss/1.0/"><title>Modified Taylor Complex Figure: Normative data from 290 adults</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12019</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Modified Taylor Complex Figure: Normative data from 290 adults</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Alessandra Casarotti, Costanza Papagno, Barbara Zarino</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-05-06T00:28:32.591113-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12019</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12019</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</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>Data for copying and delayed recall (after a 15-min delay) of the Modified Taylor Complex Figure (MTCF), an alternative form of the Rey-Osterrieth Complex Figure (ROCF), were collected from 290 healthy participants. Normative data are provided. Age and education were significantly correlated with MTCF scores and must be corrected for to interpret results accurately. More specifically, increasing age adversely affected performance, whereas a higher education resulted in a better performance. Twenty-five participants were tested with both complex figures (MTCF and ROCF) in two separate sessions to assess correlation, which proved to be high. The collected data allow using the MTCF as a valid alternative material for testing visual long-term memory avoiding implicit learning that can occur when the same version of the ROCF is used for repeated testing sessions.</p></div>
]]></content:encoded><description>
Data for copying and delayed recall (after a 15-min delay) of the Modified Taylor Complex Figure (MTCF), an alternative form of the Rey-Osterrieth Complex Figure (ROCF), were collected from 290 healthy participants. Normative data are provided. Age and education were significantly correlated with MTCF scores and must be corrected for to interpret results accurately. More specifically, increasing age adversely affected performance, whereas a higher education resulted in a better performance. Twenty-five participants were tested with both complex figures (MTCF and ROCF) in two separate sessions to assess correlation, which proved to be high. The collected data allow using the MTCF as a valid alternative material for testing visual long-term memory avoiding implicit learning that can occur when the same version of the ROCF is used for repeated testing sessions.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12013" xmlns="http://purl.org/rss/1.0/"><title>Impulsivity and apathy in Parkinson's disease</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12013</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Impulsivity and apathy in Parkinson's disease</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Nihal Sinha, Sanjay Manohar, Masud Husain</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-29T05:02:39.010657-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12013</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12013</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Issue Paper</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>Impulse control disorders (ICDs) and apathy are recognized as two important neuropsychiatric syndromes associated with Parkinson's disease (PD), but as yet we understand very little about the cognitive mechanisms underlying them. Here, we review emerging findings, from both human and animal studies, that suggest that impulsivity and apathy are opposite extremes of a dopamine-dependent spectrum of motivated decision making. We first argue that there is strong support for a hypodopaminergic state in PD patients with apathy, as well as for an association between dopamine therapy and development of ICDs. However, there is little evidence for a clear dose<b>-</b>response relationship, and great heterogeneity of findings. We argue that dopaminergic state on its own is an insufficient explanation, and suggest instead that there is now substantial evidence that both apathy and impulsivity are in fact multi-dimensional syndromes, with separate, dissociable mechanisms underlying their ‘surface’ manifestations. Some of these mechanisms might be dopamine-dependent. According to this view, individuals diagnosed as impulsive or apathetic may have very different mechanisms underlying their clinical states. We propose that impulsivity and apathy can arise from dissociable deficits in option generation, option selection, action initiation or inhibition and learning. Review of the behavioural and neurobiological evidence leads us to a new conceptual framework that might help understand the variety of functional deficits seen in PD.</p></div>
]]></content:encoded><description>
Impulse control disorders (ICDs) and apathy are recognized as two important neuropsychiatric syndromes associated with Parkinson's disease (PD), but as yet we understand very little about the cognitive mechanisms underlying them. Here, we review emerging findings, from both human and animal studies, that suggest that impulsivity and apathy are opposite extremes of a dopamine-dependent spectrum of motivated decision making. We first argue that there is strong support for a hypodopaminergic state in PD patients with apathy, as well as for an association between dopamine therapy and development of ICDs. However, there is little evidence for a clear dose-response relationship, and great heterogeneity of findings. We argue that dopaminergic state on its own is an insufficient explanation, and suggest instead that there is now substantial evidence that both apathy and impulsivity are in fact multi-dimensional syndromes, with separate, dissociable mechanisms underlying their ‘surface’ manifestations. Some of these mechanisms might be dopamine-dependent. According to this view, individuals diagnosed as impulsive or apathetic may have very different mechanisms underlying their clinical states. We propose that impulsivity and apathy can arise from dissociable deficits in option generation, option selection, action initiation or inhibition and learning. Review of the behavioural and neurobiological evidence leads us to a new conceptual framework that might help understand the variety of functional deficits seen in PD.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12017" xmlns="http://purl.org/rss/1.0/"><title>Neuropsychological function and memory suppression in conversion disorder</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12017</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Neuropsychological function and memory suppression in conversion disorder</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Laura B. Brown, Timothy R. Nicholson, Selma Aybek, Richard A. Kanaan, Anthony S. David</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-15T03:35:49.50622-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12017</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12017</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</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>Conversion disorder (CD) is a condition where neurological symptoms, such as weakness or sensory disturbance, are unexplained by neurological disease and are presumed to be of psychological origin. Contemporary theories of the disorder generally propose dysfunctional frontal control of the motor or sensory systems. Classical (Freudian) psychodynamic theory holds that the memory of stressful life events is repressed. Little is known about the frontal (executive) function of these patients, or indeed their general neuropsychological profile, and psychodynamic theories have been largely untested. This study aimed to investigate neuropsychological functioning in patients with CD, focusing on executive and memory function. A directed forgetting task (DFT) using words with variable emotional valence was also used to investigate memory suppression. 21 patients and 36 healthy controls completed a battery of neuropsychological tests and patients had deficits in executive function and auditory-verbal (but not autobiographical) memory. The executive deficits were largely driven by differences in IQ, anxiety and mood between the groups. A subgroup of 11 patients and 28 controls completed the DFT and whilst patients recalled fewer words overall than controls, there were no significant effects of directed forgetting or valence. This study provides some limited support for deficits in executive, and to a lesser degree, memory function in patients with CD, but did not find evidence of altered memory suppression to support the psychodynamic theory of repression.</p></div>
]]></content:encoded><description>
Conversion disorder (CD) is a condition where neurological symptoms, such as weakness or sensory disturbance, are unexplained by neurological disease and are presumed to be of psychological origin. Contemporary theories of the disorder generally propose dysfunctional frontal control of the motor or sensory systems. Classical (Freudian) psychodynamic theory holds that the memory of stressful life events is repressed. Little is known about the frontal (executive) function of these patients, or indeed their general neuropsychological profile, and psychodynamic theories have been largely untested. This study aimed to investigate neuropsychological functioning in patients with CD, focusing on executive and memory function. A directed forgetting task (DFT) using words with variable emotional valence was also used to investigate memory suppression. 21 patients and 36 healthy controls completed a battery of neuropsychological tests and patients had deficits in executive function and auditory-verbal (but not autobiographical) memory. The executive deficits were largely driven by differences in IQ, anxiety and mood between the groups. A subgroup of 11 patients and 28 controls completed the DFT and whilst patients recalled fewer words overall than controls, there were no significant effects of directed forgetting or valence. This study provides some limited support for deficits in executive, and to a lesser degree, memory function in patients with CD, but did not find evidence of altered memory suppression to support the psychodynamic theory of repression.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12018" xmlns="http://purl.org/rss/1.0/"><title>Source memory in normal aging and Parkinson's disease</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12018</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Source memory in normal aging and Parkinson's disease</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Patrick S. R. Davidson, Shaun P. Cook, Leslie McGhan, Thomas Bouchard, Richard Camicioli</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-06T00:28:10.182974-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12018</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12018</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Issue Paper</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>Several theorists have described memory in Parkinson's disease (PD) as involving an amplification of the deficits seen in normal aging, and drawn parallels between PD and frontal lesion patients. Both normal aging and frontal lobe damage impair memory for the context in which one has encountered information (i.e., source memory). We thus sought to determine whether PD patients would show especially poor source memory. We assessed memory for perceptual (voice), spatial (location of loudspeaker), and temporal (list) source memory in 18 PD patients, 23 healthy older adults, and 35 young people. Although both the healthy aged and PD groups performed more poorly than the young on most of the memory tests, the PD patients failed to show significantly greater impairments than the healthy older adults. The PD patients did perform more poorly, however, on a measure of executive function (the Wisconsin Card Sorting Test [WCST]). We discuss potential reasons why PD had a surprisingly minimal effect on source memory in our study, and relate our data to broader theories of memory impairment in Parkinson's disease.</p></div>
]]></content:encoded><description>
Several theorists have described memory in Parkinson's disease (PD) as involving an amplification of the deficits seen in normal aging, and drawn parallels between PD and frontal lesion patients. Both normal aging and frontal lobe damage impair memory for the context in which one has encountered information (i.e., source memory). We thus sought to determine whether PD patients would show especially poor source memory. We assessed memory for perceptual (voice), spatial (location of loudspeaker), and temporal (list) source memory in 18 PD patients, 23 healthy older adults, and 35 young people. Although both the healthy aged and PD groups performed more poorly than the young on most of the memory tests, the PD patients failed to show significantly greater impairments than the healthy older adults. The PD patients did perform more poorly, however, on a measure of executive function (the Wisconsin Card Sorting Test [WCST]). We discuss potential reasons why PD had a surprisingly minimal effect on source memory in our study, and relate our data to broader theories of memory impairment in Parkinson's disease.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12015" xmlns="http://purl.org/rss/1.0/"><title>Neuroimaging of brain changes associated with cognitive impairment in Parkinson's disease</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12015</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Neuroimaging of brain changes associated with cognitive impairment in Parkinson's disease</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Leigh Christopher, Antonio P. Strafella</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-04-01T00:32:58.91748-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.12015</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/jnp.12015</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12015</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Issue Paper</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>Cognitive impairment occurs frequently in Parkinson's disease (PD) and the concept of Mild Cognitive Impairment in PD (PD-MCI) has recently emerged. Patients with mild impairment are at risk of developing dementia, and thus it is a topic of growing interest. Many previous studies have investigated the neural correlates of cognitive impairment, in particular executive dysfunction, in PD patients without dementia using neuroimaging techniques including structural MRI, functional MRI and PET imaging. These studies, which have provided a foundation for understanding which brain regions and neurotransmitter systems may be involved in executive dysfunction in PD, will be reviewed. Recent neuroimaging studies that have used specific criteria to classify patients as PD-MCI, in the hopes of gaining further insight into the underlying neural mechanisms will also be discussed. In particular, this review will cover key findings involving structural MRI investigating grey and white matter changes, functional MRI to examine changes in neural activation and PET imaging to investigate metabolic and neurochemical changes that have led to an improved understanding of pathology associated with executive dysfunction in PD without dementia and PD-MCI.</p></div>
]]></content:encoded><description>
Cognitive impairment occurs frequently in Parkinson's disease (PD) and the concept of Mild Cognitive Impairment in PD (PD-MCI) has recently emerged. Patients with mild impairment are at risk of developing dementia, and thus it is a topic of growing interest. Many previous studies have investigated the neural correlates of cognitive impairment, in particular executive dysfunction, in PD patients without dementia using neuroimaging techniques including structural MRI, functional MRI and PET imaging. These studies, which have provided a foundation for understanding which brain regions and neurotransmitter systems may be involved in executive dysfunction in PD, will be reviewed. Recent neuroimaging studies that have used specific criteria to classify patients as PD-MCI, in the hopes of gaining further insight into the underlying neural mechanisms will also be discussed. In particular, this review will cover key findings involving structural MRI investigating grey and white matter changes, functional MRI to examine changes in neural activation and PET imaging to investigate metabolic and neurochemical changes that have led to an improved understanding of pathology associated with executive dysfunction in PD without dementia and PD-MCI.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12014" xmlns="http://purl.org/rss/1.0/"><title>Autobiographical memory in Parkinson's disease: A retrieval deficit</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12014</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Autobiographical memory in Parkinson's disease: A retrieval deficit</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Celine Souchay, Sarah Jane Smith</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-21T11:40:13.891295-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12014</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12014</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special Issue Paper</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>This study examined the effects of providing cues to facilitate autobiographical memory retrieval in Parkinson's disease. Previous findings have shown that individuals with Parkinson's disease retrieve fewer specific autobiographical memories than older adult controls. These findings are clinically significant since the quality of autobiographical memory is linked to identity and sense of self. In the current study, 16 older adults with Parkinson's disease without dementia and 16 matched older adult controls were given 3 min in which to recall autobiographical memories associated with five different time periods and to give each memory a short title. Participants were later asked to retrieve the memories in three phases: firstly in a free recall phase; secondly in response to general cues (time periods) and finally in response to specific cues (the short titles previously given). The number of memories and the quality of the memory (general or specific) was recorded in each condition. Compared with matched older adult controls, the Parkinson's disease group was impaired in retrieving the memories that they had previously given in the free recall phase and in response to general cues. The performance of the group with Parkinson's disease was only equivalent to the older adults when they retrieved memories in response to self-generated cues. The findings are discussed in relation to theories of autobiographical memory and the neuropsychology of Parkinson's disease.</p></div>
]]></content:encoded><description>
This study examined the effects of providing cues to facilitate autobiographical memory retrieval in Parkinson's disease. Previous findings have shown that individuals with Parkinson's disease retrieve fewer specific autobiographical memories than older adult controls. These findings are clinically significant since the quality of autobiographical memory is linked to identity and sense of self. In the current study, 16 older adults with Parkinson's disease without dementia and 16 matched older adult controls were given 3 min in which to recall autobiographical memories associated with five different time periods and to give each memory a short title. Participants were later asked to retrieve the memories in three phases: firstly in a free recall phase; secondly in response to general cues (time periods) and finally in response to specific cues (the short titles previously given). The number of memories and the quality of the memory (general or specific) was recorded in each condition. Compared with matched older adult controls, the Parkinson's disease group was impaired in retrieving the memories that they had previously given in the free recall phase and in response to general cues. The performance of the group with Parkinson's disease was only equivalent to the older adults when they retrieved memories in response to self-generated cues. The findings are discussed in relation to theories of autobiographical memory and the neuropsychology of Parkinson's disease.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12016" xmlns="http://purl.org/rss/1.0/"><title>Behavioural coping patterns in Parkinson's patients with visual hallucinations</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12016</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Behavioural coping patterns in Parkinson's patients with visual hallucinations</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jim Barnes, Vince Connelly, Laura Boubert, Ksenija Maravic</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-21T11:35:24.276192-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12016</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12016</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special issue paper</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>Visual Hallucinations are considered to affect about 20%–40% of patients with Parkinson's disease. They are generally seen as a side effect of this long-term illness and can severely affect the daily quality of life of patients. The aim of this study was to determine the coping patterns or strategies used by patients and establish whether the phenomenology and behaviours used by patients enabled control of the phenomenon. Demographic and clinical variables were recorded, including motor measures, cognitive status, and depressive symptoms. Patient with hallucinations were at a more advance stage of the disease and displayed more depressive symptoms than their non-hallucinating counterparts. Most patients used more than one constructive coping strategy, the most common were simple behavioural strategies based around motor action or cognitive approaches resulting in visual modification. In addition, humour was a common technique used by the patients to deal with the phenomenon. Emotional responses varied between patients, but it was found that the actual content of the hallucination was not directly associated with whether it caused trouble to the patient, but perceived stress was strongly correlated with the subjective disturbing nature of visual hallucinations (VHs). This study gives insight into the role of cognitive-behavioural approaches when dealing with VHs and opens up avenues for future studies in helping patient to deal with hallucinations.</p></div>
]]></content:encoded><description>
Visual Hallucinations are considered to affect about 20%–40% of patients with Parkinson's disease. They are generally seen as a side effect of this long-term illness and can severely affect the daily quality of life of patients. The aim of this study was to determine the coping patterns or strategies used by patients and establish whether the phenomenology and behaviours used by patients enabled control of the phenomenon. Demographic and clinical variables were recorded, including motor measures, cognitive status, and depressive symptoms. Patient with hallucinations were at a more advance stage of the disease and displayed more depressive symptoms than their non-hallucinating counterparts. Most patients used more than one constructive coping strategy, the most common were simple behavioural strategies based around motor action or cognitive approaches resulting in visual modification. In addition, humour was a common technique used by the patients to deal with the phenomenon. Emotional responses varied between patients, but it was found that the actual content of the hallucination was not directly associated with whether it caused trouble to the patient, but perceived stress was strongly correlated with the subjective disturbing nature of visual hallucinations (VHs). This study gives insight into the role of cognitive-behavioural approaches when dealing with VHs and opens up avenues for future studies in helping patient to deal with hallucinations.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12010" xmlns="http://purl.org/rss/1.0/"><title>Time to get rid of the ‘Modular’ in neuropsychology: A unified theory of anosognosia as aberrant predictive coding</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12010</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Time to get rid of the ‘Modular’ in neuropsychology: A unified theory of anosognosia as aberrant predictive coding</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Aikaterini Fotopoulou*</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-07T13:36:14.495309-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.12010</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/jnp.12010</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12010</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Elizabeth Warrington Prize Lecture</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>Cognitive neuroscience, being more inclusive and ambitious in scope than cognitive neuropsychology, seems to have taken the place of the latter within the modern neurosciences. Nevertheless, recent advances in the neurosciences afford neuropsychology with epistemic possibilities that simply did not exist even 15 years ago. Human lesion studies still have an important role to play in shaping such possibilities, particularly when combined with other methods of enquiry. I first outline theoretical and methodological advances within the neurosciences that can inform and shape the rebirth of a dynamic, non-modular neuropsychology. I then use an influential computational theory of brain function, the free energy principle, to suggest an unified account of anosognosia for hemiplegia as a research example of the potential for transition from a modular, cognitive neuropsychology to a dynamic, computational and even restorative neuropsychology. These and many other adjectives that can flexibly, take the place of ‘cognitive’ next to ‘neuropsychology’ will hopefully designate the much needed rebirth and demarcation of a field, neuropsychology itself, that has somehow lost its place within the modern neurosciences and yet seems to have a unique and important role to play in the future understanding of the brain.</p></div>
]]></content:encoded><description>
Cognitive neuroscience, being more inclusive and ambitious in scope than cognitive neuropsychology, seems to have taken the place of the latter within the modern neurosciences. Nevertheless, recent advances in the neurosciences afford neuropsychology with epistemic possibilities that simply did not exist even 15 years ago. Human lesion studies still have an important role to play in shaping such possibilities, particularly when combined with other methods of enquiry. I first outline theoretical and methodological advances within the neurosciences that can inform and shape the rebirth of a dynamic, non-modular neuropsychology. I then use an influential computational theory of brain function, the free energy principle, to suggest an unified account of anosognosia for hemiplegia as a research example of the potential for transition from a modular, cognitive neuropsychology to a dynamic, computational and even restorative neuropsychology. These and many other adjectives that can flexibly, take the place of ‘cognitive’ next to ‘neuropsychology’ will hopefully designate the much needed rebirth and demarcation of a field, neuropsychology itself, that has somehow lost its place within the modern neurosciences and yet seems to have a unique and important role to play in the future understanding of the brain.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12011" xmlns="http://purl.org/rss/1.0/"><title>Seeing why they cannot see: Understanding the syndrome and causes of posterior cortical atrophy</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12011</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Seeing why they cannot see: Understanding the syndrome and causes of posterior cortical atrophy</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sebastian J. Crutch</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-04T12:58:29.600418-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12011</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12011</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Elizabeth Warrington Prize Lecture</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>Posterior cortical atrophy (PCA) is a syndrome defined by focal neurodegeneration of the parietal, occipital, and occipito-temporal cortices and associated with progressive dysfunction of visual processing, praxis, numeracy and reading. The condition is most commonly caused by (and viewed as an atypical presentation of) Alzheimer's disease, although can also be caused by other degenerative diseases. The current paper examines the relationship of PCA to other degenerative syndromes, and considers what comparisons of these syndromes and disease phenotypes can tell us about underlying disease mechanisms. The focus then turns to neuropsychological investigations of the cognitive basis of symptoms which, although unusual in the broader context of a dementia clinic, are particularly characteristic of the PCA syndrome, before exploring implications for clinical management and patient and carer support.</p></div>
]]></content:encoded><description>
Posterior cortical atrophy (PCA) is a syndrome defined by focal neurodegeneration of the parietal, occipital, and occipito-temporal cortices and associated with progressive dysfunction of visual processing, praxis, numeracy and reading. The condition is most commonly caused by (and viewed as an atypical presentation of) Alzheimer's disease, although can also be caused by other degenerative diseases. The current paper examines the relationship of PCA to other degenerative syndromes, and considers what comparisons of these syndromes and disease phenotypes can tell us about underlying disease mechanisms. The focus then turns to neuropsychological investigations of the cognitive basis of symptoms which, although unusual in the broader context of a dementia clinic, are particularly characteristic of the PCA syndrome, before exploring implications for clinical management and patient and carer support.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12009" xmlns="http://purl.org/rss/1.0/"><title>Assessment of perception of morphed facial expressions using the Emotion Recognition Task: Normative data from healthy participants aged 8–75</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12009</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Assessment of perception of morphed facial expressions using the Emotion Recognition Task: Normative data from healthy participants aged 8–75</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Roy P.C. Kessels, Barbara Montagne, Angelique W. Hendriks, David I. Perrett, Edward H.F. Haan</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-02-14T07:49:44.870911-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.12009</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/jnp.12009</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12009</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</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 ability to recognize and label emotional facial expressions is an important aspect of social cognition. However, existing paradigms to examine this ability present only static facial expressions, suffer from ceiling effects or have limited or no norms. A computerized test, the Emotion Recognition Task (ERT), was developed to overcome these difficulties. In this study, we examined the effects of age, sex, and intellectual ability on emotion perception using the ERT. In this test, emotional facial expressions are presented as morphs gradually expressing one of the six basic emotions from neutral to four levels of intensity (40%, 60%, 80%, and 100%). The task was administered in 373 healthy participants aged 8–75. In children aged 8–17, only small developmental effects were found for the emotions anger and happiness, in contrast to adults who showed age-related decline on anger, fear, happiness, and sadness. Sex differences were present predominantly in the adult participants. IQ only minimally affected the perception of disgust in the children, while years of education were correlated with all emotions but surprise and disgust in the adult participants. A regression-based approach was adopted to present age- and education- or IQ-adjusted normative data for use in clinical practice. Previous studies using the ERT have demonstrated selective impairments on specific emotions in a variety of psychiatric, neurologic, or neurodegenerative patient groups, making the ERT a valuable addition to existing paradigms for the assessment of emotion perception.</p></div>
]]></content:encoded><description>
The ability to recognize and label emotional facial expressions is an important aspect of social cognition. However, existing paradigms to examine this ability present only static facial expressions, suffer from ceiling effects or have limited or no norms. A computerized test, the Emotion Recognition Task (ERT), was developed to overcome these difficulties. In this study, we examined the effects of age, sex, and intellectual ability on emotion perception using the ERT. In this test, emotional facial expressions are presented as morphs gradually expressing one of the six basic emotions from neutral to four levels of intensity (40%, 60%, 80%, and 100%). The task was administered in 373 healthy participants aged 8–75. In children aged 8–17, only small developmental effects were found for the emotions anger and happiness, in contrast to adults who showed age-related decline on anger, fear, happiness, and sadness. Sex differences were present predominantly in the adult participants. IQ only minimally affected the perception of disgust in the children, while years of education were correlated with all emotions but surprise and disgust in the adult participants. A regression-based approach was adopted to present age- and education- or IQ-adjusted normative data for use in clinical practice. Previous studies using the ERT have demonstrated selective impairments on specific emotions in a variety of psychiatric, neurologic, or neurodegenerative patient groups, making the ERT a valuable addition to existing paradigms for the assessment of emotion perception.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12007" xmlns="http://purl.org/rss/1.0/"><title>Where Am I? A new case of developmental topographical disorientation</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12007</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Where Am I? A new case of developmental topographical disorientation</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Filippo Bianchini, Liana Palermo, Laura Piccardi, Chiara Incoccia, Federico Nemmi, Umberto Sabatini, Cecilia Guariglia</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-21T11:07:45.502447-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12007</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12007</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research paper</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>Recently, developmental topographical disorientation (DTD) was described (Bianchini <em>et al</em>., 2010, <em>J Clin Exp Neuropsychol, 20,</em> 807–27; Iaria &amp; Barton, 2010, <em>Exp Brain Res</em>,<em> 206</em>, 189–96; Iaria, Bogod, Fox, &amp; Barton, 2009, <em>Neuropsychologia, 47</em>, 30–40) as a navigational deficit in the absence of neurological or psychiatric disorders. Here, we reported the case of a healthy subject who presented this disorder. Dr. WAI was a 29-year-old right-handed man with normal development and no clinical history of neurological or psychiatric diseases who was affected by a very pervasive topographical orientation and navigational disorder. A neuroradiological exam confirmed the absence of structural and anatomical alterations of the brain. Dr. WAI was submitted to an extensive neuropsychological examination and to a battery of tests specifically developed to assess developmental topographical disorder. Using this battery, we analysed Dr. WAI's acquisition of navigational information and re-orientation processes. He showed severe DTD accompanied by deficits of different cognitive processes directly or indirectly involved in navigational skills. Dr. WAI showed a deficit in developing cognitive maps, already found in previous cases, plus difficulties in evaluating distances and computing metric environmental features. He represents a further confirmation of the existence of DTD suggesting dissociations within the disorder related to the level of development of the ability to build cognitive maps and the association of different imagery deficits. Dr. WAI can help in shedding some light on the mechanisms underlying lack of development of navigational skills.</p></div>
]]></content:encoded><description>
Recently, developmental topographical disorientation (DTD) was described (Bianchini et al., 2010, J Clin Exp Neuropsychol, 20, 807–27; Iaria &amp; Barton, 2010, Exp Brain Res, 206, 189–96; Iaria, Bogod, Fox, &amp; Barton, 2009, Neuropsychologia, 47, 30–40) as a navigational deficit in the absence of neurological or psychiatric disorders. Here, we reported the case of a healthy subject who presented this disorder. Dr. WAI was a 29-year-old right-handed man with normal development and no clinical history of neurological or psychiatric diseases who was affected by a very pervasive topographical orientation and navigational disorder. A neuroradiological exam confirmed the absence of structural and anatomical alterations of the brain. Dr. WAI was submitted to an extensive neuropsychological examination and to a battery of tests specifically developed to assess developmental topographical disorder. Using this battery, we analysed Dr. WAI's acquisition of navigational information and re-orientation processes. He showed severe DTD accompanied by deficits of different cognitive processes directly or indirectly involved in navigational skills. Dr. WAI showed a deficit in developing cognitive maps, already found in previous cases, plus difficulties in evaluating distances and computing metric environmental features. He represents a further confirmation of the existence of DTD suggesting dissociations within the disorder related to the level of development of the ability to build cognitive maps and the association of different imagery deficits. Dr. WAI can help in shedding some light on the mechanisms underlying lack of development of navigational skills.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12008" xmlns="http://purl.org/rss/1.0/"><title>Attentional control in patients with temporal lobe epilepsy</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12008</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Attentional control in patients with temporal lobe epilepsy</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">John M. Hudson, Kenneth A. Flowers, Kerri L. Walster</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-16T12:16:23.485388-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.12008</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/jnp.12008</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12008</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Brief communication</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>Across different studies, patients with temporal lobe epilepsy (TLE) demonstrate impairments on numerous measures of attentional control that are classically associated with frontal lobe functioning. One aspect of attentional control that has not been examined in TLE is the ability to execute two modality-specific tasks concurrently. We sought to examine the status of dual-task coordination in TLE. We further examined the cohorts' performance on a range of traditional measures of attentional control. Eighteen TLE patients and 22 healthy controls participated in the study. Dual-task performance involved comparing the capacity to execute a tracking and a digit recall task simultaneously with the capacity to execute the tasks separately. We also administered measures of: set shifting (odd-man-out test), sustained attention (elevator counting), selective attention (elevator counting with distraction), and divided attention (trail making test). We found that the proportional decrement in dual-task performance relative to single-task performance did not vary between the groups (TLE = 92.48%; controls = 93.70%), nor was there a significant difference in sustained attention (<em>p</em> &gt; .10). Patients with TLE did demonstrate marked deficits in selective attention (<em>p</em> &lt; .0001), divided attention (<em>p</em> &lt; .01), and set shifting (<em>p</em> &lt; .01). These findings add to the knowledge about cognitive dysfunction in TLE, indicating that impairments in attentional control in TLE tend to be selective. The greatest deficits appear to be on tasks that invoke a high level of processing resources. In contrast, sustained attention is less compromised and the capacity to allocate cognitive resources appears to be normal in patients with TLE.</p></div>
]]></content:encoded><description>
Across different studies, patients with temporal lobe epilepsy (TLE) demonstrate impairments on numerous measures of attentional control that are classically associated with frontal lobe functioning. One aspect of attentional control that has not been examined in TLE is the ability to execute two modality-specific tasks concurrently. We sought to examine the status of dual-task coordination in TLE. We further examined the cohorts' performance on a range of traditional measures of attentional control. Eighteen TLE patients and 22 healthy controls participated in the study. Dual-task performance involved comparing the capacity to execute a tracking and a digit recall task simultaneously with the capacity to execute the tasks separately. We also administered measures of: set shifting (odd-man-out test), sustained attention (elevator counting), selective attention (elevator counting with distraction), and divided attention (trail making test). We found that the proportional decrement in dual-task performance relative to single-task performance did not vary between the groups (TLE = 92.48%; controls = 93.70%), nor was there a significant difference in sustained attention (p &gt; .10). Patients with TLE did demonstrate marked deficits in selective attention (p &lt; .0001), divided attention (p &lt; .01), and set shifting (p &lt; .01). These findings add to the knowledge about cognitive dysfunction in TLE, indicating that impairments in attentional control in TLE tend to be selective. The greatest deficits appear to be on tasks that invoke a high level of processing resources. In contrast, sustained attention is less compromised and the capacity to allocate cognitive resources appears to be normal in patients with TLE.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12005" xmlns="http://purl.org/rss/1.0/"><title>Representation of action in Parkinson's disease: Imagining, observing, and naming actions</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12005</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Representation of action in Parkinson's disease: Imagining, observing, and naming actions</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ellen Poliakoff</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-01-15T07:53:54.354007-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12005</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12005</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Special issue</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>People with Parkinson's disease (PD) exhibit slowed movements and difficulty in initiating movements. This review addresses the issue of whether or not cognitive representations of actions in PD are affected, alongside these motor problems. In healthy people, the motor system can be involved in tasks such as observing a graspable object or another person's action, or imagining and naming actions, in the absence of overt movement. As described in this review, the fact that the slowed real movements exhibited by PD patients are coupled with slower motor imagery and verb processing provides additional evidence for the involvement of the motor system in these processes. On the other hand, PD patients can still engage in motor imagery and action observation to some extent, which is encouraging for the use of these processes in rehabilitation. Findings across the different domains of action-representation reveal several important factors. First, the nature of action is critical: patients' performance in observation and naming tasks is influenced by whether or not the action is in their repertoire and by the extent of motion required to execute the action. Second, people with PD may use alternative or compensatory mechanisms to represent actions, such as relying more on a third-person perspective or a visual strategy. Third, people with PD show a lack of specificity, responding as strongly to stimuli related and unrelated to actions. Investigating action-representation in PD has implications for our understanding of both the symptoms of PD and the cognitive representation of actions in the healthy system.</p></div>
]]></content:encoded><description>
People with Parkinson's disease (PD) exhibit slowed movements and difficulty in initiating movements. This review addresses the issue of whether or not cognitive representations of actions in PD are affected, alongside these motor problems. In healthy people, the motor system can be involved in tasks such as observing a graspable object or another person's action, or imagining and naming actions, in the absence of overt movement. As described in this review, the fact that the slowed real movements exhibited by PD patients are coupled with slower motor imagery and verb processing provides additional evidence for the involvement of the motor system in these processes. On the other hand, PD patients can still engage in motor imagery and action observation to some extent, which is encouraging for the use of these processes in rehabilitation. Findings across the different domains of action-representation reveal several important factors. First, the nature of action is critical: patients' performance in observation and naming tasks is influenced by whether or not the action is in their repertoire and by the extent of motion required to execute the action. Second, people with PD may use alternative or compensatory mechanisms to represent actions, such as relying more on a third-person perspective or a visual strategy. Third, people with PD show a lack of specificity, responding as strongly to stimuli related and unrelated to actions. Investigating action-representation in PD has implications for our understanding of both the symptoms of PD and the cognitive representation of actions in the healthy system.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12006" xmlns="http://purl.org/rss/1.0/"><title>Reduced audiovisual integration in synesthesia – evidence from bimodal speech perception</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12006</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Reduced audiovisual integration in synesthesia – evidence from bimodal speech perception</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Christopher Sinke, Janina Neufeld, Markus Zedler, Hinderk M. Emrich, Stefan Bleich, Thomas F. Münte, Gregor R. Szycik</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-20T10:28:02.304365-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12006</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12006</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</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 research suggests synesthesia as a result of a hypersensitive multimodal binding mechanism. To address the question whether multimodal integration is altered in synesthetes in general, grapheme-colour and auditory-visual synesthetes were investigated using speech-related stimulation in two behavioural experiments. First, we used the McGurk illusion to test the strength and number of illusory perceptions in synesthesia. In a second step, we analysed the gain in speech perception coming from seen articulatory movements under acoustically noisy conditions. We used disyllabic nouns as stimulation and varied signal-to-noise ratio of the auditory stream presented concurrently to a matching video of the speaker. We hypothesized that if synesthesia is due to a general hyperbinding mechanism this group of subjects should be more susceptible to McGurk illusions and profit more from the visual information during audiovisual speech perception. The results indicate that there are differences between synesthetes and controls concerning multisensory integration – but in the opposite direction as hypothesized. Synesthetes showed a reduced number of illusions and had a reduced gain in comprehension by viewing matching articulatory movements in comparison to control subjects. Our results indicate that rather than having a hypersensitive binding mechanism, synesthetes show weaker integration of vision and audition.</p></div>
]]></content:encoded><description>
Recent research suggests synesthesia as a result of a hypersensitive multimodal binding mechanism. To address the question whether multimodal integration is altered in synesthetes in general, grapheme-colour and auditory-visual synesthetes were investigated using speech-related stimulation in two behavioural experiments. First, we used the McGurk illusion to test the strength and number of illusory perceptions in synesthesia. In a second step, we analysed the gain in speech perception coming from seen articulatory movements under acoustically noisy conditions. We used disyllabic nouns as stimulation and varied signal-to-noise ratio of the auditory stream presented concurrently to a matching video of the speaker. We hypothesized that if synesthesia is due to a general hyperbinding mechanism this group of subjects should be more susceptible to McGurk illusions and profit more from the visual information during audiovisual speech perception. The results indicate that there are differences between synesthetes and controls concerning multisensory integration – but in the opposite direction as hypothesized. Synesthetes showed a reduced number of illusions and had a reduced gain in comprehension by viewing matching articulatory movements in comparison to control subjects. Our results indicate that rather than having a hypersensitive binding mechanism, synesthetes show weaker integration of vision and audition.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12004" xmlns="http://purl.org/rss/1.0/"><title>Revisiting the effects of Parkinson's disease and frontal lobe lesions on task switching: The role of rule reconfiguration</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12004</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Revisiting the effects of Parkinson's disease and frontal lobe lesions on task switching: The role of rule reconfiguration</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Angie A. Kehagia, Roger A. Barker, Trevor W. Robbins</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-20T05:14:40.976164-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12004</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12004</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</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>This study investigated the hypothesis that rule reconfiguration in task switching can isolate aspects of intact and impaired control at different stages of Parkinson's disease (PD) by comparing switches between concrete naming rules pertaining to stimulus selection, to switches between abstract rules which allocate categorization responses to these stimuli. Based on previous findings, it was hypothesized that attentional switches, where task set competition emerges at the stimulus but not response set level, highlights striatal dopaminergic function. Conversely, increasing the degree of task set competition to encompass reconfiguration of response set when switching between abstract rules, represents a condition which engages the prefrontal cortex (PFC) and renders this manipulation sensitive to frontal damage. To this end, we investigated task switching with concrete and abstract rules in unilaterally (Hoehn &amp; Yahr stage I) and bilaterally (Hoehn &amp; Yahr stage II) affected PD patients, as well as striatally intact frontal lesion patients. As predicted, frontal lesion patients demonstrated switching deficits only with abstract categorization rules, where switching engendered complete task set reconfiguration and a new response, as did stage II PD patients with presumed frontal cortical pathology. Replicating previous findings, stage I PD patients with relatively circumscribed striatal pathology demonstrated no such impairment. Disease severity also impacted on attentional switching indexed by naming rules, since medicated stage II but not stage I patients demonstrated switching deficits emerging from stimulus set reconfiguration, suggesting that the ameliorative efficacy of dopaminergic medication is inversely related to the severity of the striatal deficit. These findings illustrate that the nature of the rules that are switched, and its implication in terms of reconfiguring different task set elements, highlights different neural characters of cognitive flexibility. These manipulations may help decipher the differential effects of progressive neurodegeneration on parkinsonian cognition, and provide a framework in which to conceptualize the contributions of cortical and subcortical regions to cognitive control.</p></div>
]]></content:encoded><description>
This study investigated the hypothesis that rule reconfiguration in task switching can isolate aspects of intact and impaired control at different stages of Parkinson's disease (PD) by comparing switches between concrete naming rules pertaining to stimulus selection, to switches between abstract rules which allocate categorization responses to these stimuli. Based on previous findings, it was hypothesized that attentional switches, where task set competition emerges at the stimulus but not response set level, highlights striatal dopaminergic function. Conversely, increasing the degree of task set competition to encompass reconfiguration of response set when switching between abstract rules, represents a condition which engages the prefrontal cortex (PFC) and renders this manipulation sensitive to frontal damage. To this end, we investigated task switching with concrete and abstract rules in unilaterally (Hoehn &amp; Yahr stage I) and bilaterally (Hoehn &amp; Yahr stage II) affected PD patients, as well as striatally intact frontal lesion patients. As predicted, frontal lesion patients demonstrated switching deficits only with abstract categorization rules, where switching engendered complete task set reconfiguration and a new response, as did stage II PD patients with presumed frontal cortical pathology. Replicating previous findings, stage I PD patients with relatively circumscribed striatal pathology demonstrated no such impairment. Disease severity also impacted on attentional switching indexed by naming rules, since medicated stage II but not stage I patients demonstrated switching deficits emerging from stimulus set reconfiguration, suggesting that the ameliorative efficacy of dopaminergic medication is inversely related to the severity of the striatal deficit. These findings illustrate that the nature of the rules that are switched, and its implication in terms of reconfiguring different task set elements, highlights different neural characters of cognitive flexibility. These manipulations may help decipher the differential effects of progressive neurodegeneration on parkinsonian cognition, and provide a framework in which to conceptualize the contributions of cortical and subcortical regions to cognitive control.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12003" xmlns="http://purl.org/rss/1.0/"><title>Autobiographical memory and episodic future thinking after moderate to severe traumatic brain injury</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12003</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Autobiographical memory and episodic future thinking after moderate to severe traumatic brain injury</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Katrine W. Rasmussen, Dorthe Berntsen</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-17T06:40:27.13595-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12003</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12003</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</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>Converging evidence suggests that autobiographical memory and episodic future thinking share a common neurocognitive basis. Although previous research has shown that traumatic brain injury (TBI) can impair the ability to remember the personal past, episodic future thinking has not previously been systematically examined within this population. In this study, we examined the ability to remember events in the personal past and the ability to imagine possible events in the personal future in a sample of moderate-to-severe TBI patients. We present data on nine patients and nine healthy controls, who were asked to report a series of events that had happened to them in the past and a series of events that might happen to them in the future. Transcriptions were scored according to a reliable system for categorizing internal (episodic) and external (semantic) information. For each event described, participants also completed two modified Autobiographical Memory Questionnaire items to assess self-reported phenomenal qualities associated with remembering and imagining. In addition, TBI patients underwent neuropsychological assessment. Results revealed that TBI patients recalled/imagined proportionally fewer episodic event-specific details for both past and future events compared to healthy controls (η<sup>2</sup><sub>p</sub> = 0.78). In contrast, there were no group differences in ratings of phenomenal characteristics. These results are discussed in relation to theories suggesting that remembering and imagining the future are the expression of the same underlying neurocognitive system.</p></div>
]]></content:encoded><description>
Converging evidence suggests that autobiographical memory and episodic future thinking share a common neurocognitive basis. Although previous research has shown that traumatic brain injury (TBI) can impair the ability to remember the personal past, episodic future thinking has not previously been systematically examined within this population. In this study, we examined the ability to remember events in the personal past and the ability to imagine possible events in the personal future in a sample of moderate-to-severe TBI patients. We present data on nine patients and nine healthy controls, who were asked to report a series of events that had happened to them in the past and a series of events that might happen to them in the future. Transcriptions were scored according to a reliable system for categorizing internal (episodic) and external (semantic) information. For each event described, participants also completed two modified Autobiographical Memory Questionnaire items to assess self-reported phenomenal qualities associated with remembering and imagining. In addition, TBI patients underwent neuropsychological assessment. Results revealed that TBI patients recalled/imagined proportionally fewer episodic event-specific details for both past and future events compared to healthy controls (η2p = 0.78). In contrast, there were no group differences in ratings of phenomenal characteristics. These results are discussed in relation to theories suggesting that remembering and imagining the future are the expression of the same underlying neurocognitive system.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12002" xmlns="http://purl.org/rss/1.0/"><title>Assessment of performance validity in the Stroop Color and Word Test in mild traumatic brain injury patients: a criterion-groups validation design</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12002</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Assessment of performance validity in the Stroop Color and Word Test in mild traumatic brain injury patients: a criterion-groups validation design</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Brian J. Guise, Matthew D. Thompson, Kevin W. Greve, Kevin J. Bianchini, Laura West</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-12-17T06:39:43.411233-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.12002</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/jnp.12002</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12002</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</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 current study assessed performance validity on the Stroop Color and Word Test (Stroop) in mild traumatic brain injury (TBI) using criterion-groups validation. The sample consisted of 77 patients with a reported history of mild TBI. Data from 42 moderate–severe TBI and 75 non-head-injured patients with other clinical diagnoses were also examined. TBI patients were categorized on the basis of Slick, Sherman, and Iverson (1999) criteria for malingered neurocognitive dysfunction (MND). Classification accuracy is reported for three indicators (Word, Color, and Color–Word residual raw scores) from the Stroop across a range of injury severities. With false-positive rates set at approximately 5%, sensitivity was as high as 29%. The clinical implications of these findings are discussed.</p></div>
]]></content:encoded><description>
The current study assessed performance validity on the Stroop Color and Word Test (Stroop) in mild traumatic brain injury (TBI) using criterion-groups validation. The sample consisted of 77 patients with a reported history of mild TBI. Data from 42 moderate–severe TBI and 75 non-head-injured patients with other clinical diagnoses were also examined. TBI patients were categorized on the basis of Slick, Sherman, and Iverson (1999) criteria for malingered neurocognitive dysfunction (MND). Classification accuracy is reported for three indicators (Word, Color, and Color–Word residual raw scores) from the Stroop across a range of injury severities. With false-positive rates set at approximately 5%, sensitivity was as high as 29%. The clinical implications of these findings are discussed.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12000" xmlns="http://purl.org/rss/1.0/"><title>Limited predictive power of hospitalization variables for long-term cognitive prognosis in adult patients with severe traumatic brain injury</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12000</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Limited predictive power of hospitalization variables for long-term cognitive prognosis in adult patients with severe traumatic brain injury</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Maria Emília Rodrigues Oliveira Thais, Gisele Cavallazzi, Douglas Afonso Formolo, Lucas D'Ávila Castro, Roseli Schmoeller, Ricardo Guarnieri, Marcelo Liborio Schwarzbold, Alexandre Paim Diaz, Alexandre Hohl, Rui D. S. Prediger, Maria Joana Mader, Marcelo Neves Linhares, Angelica Staniloiu, Hans J. Markowitsch, Roger Walz</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-11-20T16:16:27.834287-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12000</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12000</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Research Paper</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="jnp12000-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>Traumatic brain injury (TBI) is a main cause of mortality and morbidity. Association studies between hospitalization variables and cognitive impairment after TBI are frequently retrospective, including non-consecutive patients showing variable degrees of TBI severity, and poor management of missing (drop out) cases.</p></div></div>
<div class="section" id="jnp12000-sec-0002" xmlns="http://www.w3.org/1999/xhtml"><h4>Methods</h4><div class="para"><p>We assessed prospectively the demographic and hospitalization variables of 234 consecutive patients with severe TBI (admission Glasgow Coma Scale [GCS] ≤8) and determined their independent association with cognitive performance in a representative sample (<em>n</em> = 46) of surviving patients (<em>n</em> = 172) evaluated 3 (±1.8) years after hospitalization.</p></div></div>
<div class="section" id="jnp12000-sec-0003" xmlns="http://www.w3.org/1999/xhtml"><h4>Results</h4><div class="para"><p>In all, 85% of patients were male and the mean age was 34 (<em>SD</em> ±13) years. The education level was 9 (±4.7) years. As expected, education and age showed a moderately to strong linear relationship with the cognitive performance in 14 of 15 neuropsychological tests (<em>R</em> coefficient = 0.6–0.8). The cognitive test scores were not independently associated with gender, admission GCS, associated trauma, and Marshal CT classification. Admission-elevated blood glucose levels and the presence of sub-arachnoid haemorrhage were independently associated with lower scores on Rey Auditory Verbal Learning retention and Logical Memory-I tests, respectively.</p></div></div>
<div class="section" id="jnp12000-sec-0004" xmlns="http://www.w3.org/1999/xhtml"><h4>Conclusions</h4><div class="para"><p>After correction for education and age distribution, the variables that are commonly associated with mortality or Glasgow Outcome Scale including admission pupils' examination, Marshal CT Classification, GCS, and serum glucose showed a limited predictive power for long-term cognitive prognosis. Identification of clinical, radiological, and laboratory variables as well as new biomarkers independently associated with cognitive outcome remains an important challenge for further work involving severe TBI patients.</p></div></div>
]]></content:encoded><description>

Objectives
Traumatic brain injury (TBI) is a main cause of mortality and morbidity. Association studies between hospitalization variables and cognitive impairment after TBI are frequently retrospective, including non-consecutive patients showing variable degrees of TBI severity, and poor management of missing (drop out) cases.


Methods
We assessed prospectively the demographic and hospitalization variables of 234 consecutive patients with severe TBI (admission Glasgow Coma Scale [GCS] ≤8) and determined their independent association with cognitive performance in a representative sample (n = 46) of surviving patients (n = 172) evaluated 3 (±1.8) years after hospitalization.


Results
In all, 85% of patients were male and the mean age was 34 (SD ±13) years. The education level was 9 (±4.7) years. As expected, education and age showed a moderately to strong linear relationship with the cognitive performance in 14 of 15 neuropsychological tests (R coefficient = 0.6–0.8). The cognitive test scores were not independently associated with gender, admission GCS, associated trauma, and Marshal CT classification. Admission-elevated blood glucose levels and the presence of sub-arachnoid haemorrhage were independently associated with lower scores on Rey Auditory Verbal Learning retention and Logical Memory-I tests, respectively.


Conclusions
After correction for education and age distribution, the variables that are commonly associated with mortality or Glasgow Outcome Scale including admission pupils' examination, Marshal CT Classification, GCS, and serum glucose showed a limited predictive power for long-term cognitive prognosis. Identification of clinical, radiological, and laboratory variables as well as new biomarkers independently associated with cognitive outcome remains an important challenge for further work involving severe TBI patients.

</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12001" xmlns="http://purl.org/rss/1.0/"><title>Subtle cognitive deficits in severe alcohol addicts – Do they show a specific profile?</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12001</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Subtle cognitive deficits in severe alcohol addicts – Do they show a specific profile?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Frank A. Wollenweber, Sarah Halfter, Elisabeth Brügmann, Christina Weinberg, Edna C. Cieslik, Veronika I. Müller, Robert M. Hardwick, Simon B. Eickhoff</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-10-29T06:11:33.693608-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12001</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12001</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Brief communication</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>Although alcohol dependency is a burden to society, data on cognitive performance in therapy-resistant patients after multiple withdrawals are poor. In this study, 22 patients without reported cognitive deficits and 20 control subjects performed extensive cognitive testing and a motor task assessing short-term memory. Patients displayed subtle deficits (mainly in executive function), while memory functions were relatively unimpaired. Our results suggest that subtle frontal-executive deficits may contribute to a poor prognosis, but could be missed by routine clinical tests.</p></div>
]]></content:encoded><description>
Although alcohol dependency is a burden to society, data on cognitive performance in therapy-resistant patients after multiple withdrawals are poor. In this study, 22 patients without reported cognitive deficits and 20 control subjects performed extensive cognitive testing and a motor task assessing short-term memory. Patients displayed subtle deficits (mainly in executive function), while memory functions were relatively unimpaired. Our results suggest that subtle frontal-executive deficits may contribute to a poor prognosis, but could be missed by routine clinical tests.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02027.x" xmlns="http://purl.org/rss/1.0/"><title>Response inhibition in children with and without ADHD after traumatic brain injury</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02027.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Response inhibition in children with and without ADHD after traumatic brain injury</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Tisha J. Ornstein, Jeffrey E. Max, Russell Schachar, Maureen Dennis, Marcia Barnes, Linda Ewing-Cobbs, Harvey S. Levin</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-30T10:21:40.524953-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1748-6653.2012.02027.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.1748-6653.2012.02027.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02027.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">11</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>Children with attention-deficit hyperactivity disorder (ADHD) and traumatic brain injury (TBI) show deficient response inhibition. ADHD itself is a common consequence of TBI, known as secondary ADHD (S-ADHD). Similarity in inhibitory control in children with TBI, S-ADHD, and ADHD would implicate impaired frontal-striatal systems; however, it is first necessary to delineate similarities and differences in inhibitory control in these conditions. We compared performance of children with ADHD and those with TBI without pre-injury ADHD on a stop signal, response inhibition task. Participants were 274 children aged 6–14 years. There were 92 children with ADHD, 103 children with TBI, and 79 typically developing children who served as controls. Among the TBI participants, injury severity ranged from mild to severe. Children with ADHD and TBI showed deficient inhibition. The deficit in children with ADHD was as great as or greater than that in children with TBI, regardless of degree of TBI severity or the presence of S-ADHD. The finding indicates that TBI results in deficient inhibition regardless of the development of S-ADHD.</p></div>
]]></content:encoded><description>
Children with attention-deficit hyperactivity disorder (ADHD) and traumatic brain injury (TBI) show deficient response inhibition. ADHD itself is a common consequence of TBI, known as secondary ADHD (S-ADHD). Similarity in inhibitory control in children with TBI, S-ADHD, and ADHD would implicate impaired frontal-striatal systems; however, it is first necessary to delineate similarities and differences in inhibitory control in these conditions. We compared performance of children with ADHD and those with TBI without pre-injury ADHD on a stop signal, response inhibition task. Participants were 274 children aged 6–14 years. There were 92 children with ADHD, 103 children with TBI, and 79 typically developing children who served as controls. Among the TBI participants, injury severity ranged from mild to severe. Children with ADHD and TBI showed deficient inhibition. The deficit in children with ADHD was as great as or greater than that in children with TBI, regardless of degree of TBI severity or the presence of S-ADHD. The finding indicates that TBI results in deficient inhibition regardless of the development of S-ADHD.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02031.x" xmlns="http://purl.org/rss/1.0/"><title>Response interference between functional and structural object-related actions is increased in patients with ideomotor apraxia</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02031.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Response interference between functional and structural object-related actions is increased in patients with ideomotor apraxia</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Steven A. Jax, Laurel J. Buxbaum</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-04-20T04:18:44.934154-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1748-6653.2012.02031.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.1748-6653.2012.02031.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02031.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">12</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">18</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>We report data from two left hemisphere stroke patients with moderate-to-severe ideomotor apraxia who exhibited deficits in positioning their hands to use ‘conflict’ objects (objects grasped and used with different hand postures) relative to controls and patients with mild apraxia. These novel data support the claim that actions to common objects are subject to interference between multiple responses, and suggest that errors in apraxia may be attributed to deficient resolution of competition between appropriate and inappropriate actions.</p></div>
]]></content:encoded><description>
We report data from two left hemisphere stroke patients with moderate-to-severe ideomotor apraxia who exhibited deficits in positioning their hands to use ‘conflict’ objects (objects grasped and used with different hand postures) relative to controls and patients with mild apraxia. These novel data support the claim that actions to common objects are subject to interference between multiple responses, and suggest that errors in apraxia may be attributed to deficient resolution of competition between appropriate and inappropriate actions.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02032.x" xmlns="http://purl.org/rss/1.0/"><title>Lack of awareness of neuropsychological deficit in cerebral small vessel disease: The relationship with executive and episodic memory functions</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02032.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Lack of awareness of neuropsychological deficit in cerebral small vessel disease: The relationship with executive and episodic memory functions</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Rebecca L. Brookes, Kristin Hannesdottir, Hugh S. Markus, Robin G. Morris</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-06-14T06:45:35.064704-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1748-6653.2012.02032.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.1748-6653.2012.02032.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02032.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">19</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">28</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>A common cause of neuropsychological impairment in older adults is cerebral small vessel disease (SVD), but little is known as to whether lack of awareness of neuropsychological impairment is a feature of this clinical condition. In this study, we investigated awareness deficits in a well-phenotyped population of patients with SVD (<em>n</em>= 45; 21 with defined concomitant neuropsychological impairment) and made comparisons with 24 Alzheimer's disease (AD) patients and a further 80 control participants. Awareness of performance on a range of neuropsychological measures was examined based on the Brief Memory and Executive Test Battery (BMET) (Brookes, Hannesdottir, Lawrence, <a href="#b4" rel="references:#b4">Morris, &amp; Markus, 2012</a>), exploring the relationship between awareness and memory and executive function. The results revealed significant awareness deficits in both the SVD and AD groups. When splitting the SVD group into those with or without concomitant neuropsychological impairment, only those with neuropsychological impairment showed reduced awareness. For the SVD group, executive function was significantly correlated with awareness but memory was not. By comparison, memory was significantly correlated with awareness in the AD group, with executive function showing a trend but remaining non-significant. The results show that lack of awareness of deficit is a clinical feature of SVD and indicate that there are distinct neuropsychological associations with awareness deficit for SVD and AD.</p></div>
]]></content:encoded><description>
A common cause of neuropsychological impairment in older adults is cerebral small vessel disease (SVD), but little is known as to whether lack of awareness of neuropsychological impairment is a feature of this clinical condition. In this study, we investigated awareness deficits in a well-phenotyped population of patients with SVD (n= 45; 21 with defined concomitant neuropsychological impairment) and made comparisons with 24 Alzheimer's disease (AD) patients and a further 80 control participants. Awareness of performance on a range of neuropsychological measures was examined based on the Brief Memory and Executive Test Battery (BMET) (Brookes, Hannesdottir, Lawrence, Morris, &amp; Markus, 2012), exploring the relationship between awareness and memory and executive function. The results revealed significant awareness deficits in both the SVD and AD groups. When splitting the SVD group into those with or without concomitant neuropsychological impairment, only those with neuropsychological impairment showed reduced awareness. For the SVD group, executive function was significantly correlated with awareness but memory was not. By comparison, memory was significantly correlated with awareness in the AD group, with executive function showing a trend but remaining non-significant. The results show that lack of awareness of deficit is a clinical feature of SVD and indicate that there are distinct neuropsychological associations with awareness deficit for SVD and AD.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02033.x" xmlns="http://purl.org/rss/1.0/"><title>Motor excitability is reduced prior to voluntary movements in children and adolescents with Tourette syndrome</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02033.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Motor excitability is reduced prior to voluntary movements in children and adolescents with Tourette syndrome</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Stephen R. Jackson, Amy Parkinson, Valentina Manfredi, Guy Millon, Chris Hollis, Georgina M. Jackson</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-07-16T09:39:46.788526-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1748-6653.2012.02033.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.1748-6653.2012.02033.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02033.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">29</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">44</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>Tourette syndrome (TS) is a neuro-developmental disorder characterized by the occurrence of motor and vocal tics: involuntary, repetitive, stereotyped behaviours that occur with a limited duration, often typically many times in a single day. Previous studies suggest that children and adolescents with TS may undergo compensatory, neuroplastic changes in brain structure and function that help them gain control over their tics. In the current study we used single-pulse and dual-site paired-pulse transcranial magnetic stimulation (TMS), in conjunction with a manual choice reaction time task that induces high levels of inter-manual conflict, to investigate this conjecture in a group of children and adolescents with TS, but without co-morbid Attention Deficit Hyperactivity Disorder (ADHD). We found that performance on the behavioural response-conflict task did not differ between the adolescents with TS and a group of age-matched typically developing individuals. By contrast, our study demonstrated that cortical excitability, as measured by TMS-induced motor-evoked potentials (MEPs), was significantly reduced in the TS group in the period immediately preceding a finger movement. This effect is interpreted as consistent with previous suggestions that the cortical hyper-excitability that may give rise to tics in TS is actively suppressed by cognitive control mechanisms. Finally, we found no reliable evidence for altered patterns of functional inter-hemispheric connectivity in TS. These results provide evidence for compensatory brain reorganization that may underlie the increased self-regulation mechanisms that have been hypothesized to bring about the control of tics during adolescence.</p></div>
]]></content:encoded><description>
Tourette syndrome (TS) is a neuro-developmental disorder characterized by the occurrence of motor and vocal tics: involuntary, repetitive, stereotyped behaviours that occur with a limited duration, often typically many times in a single day. Previous studies suggest that children and adolescents with TS may undergo compensatory, neuroplastic changes in brain structure and function that help them gain control over their tics. In the current study we used single-pulse and dual-site paired-pulse transcranial magnetic stimulation (TMS), in conjunction with a manual choice reaction time task that induces high levels of inter-manual conflict, to investigate this conjecture in a group of children and adolescents with TS, but without co-morbid Attention Deficit Hyperactivity Disorder (ADHD). We found that performance on the behavioural response-conflict task did not differ between the adolescents with TS and a group of age-matched typically developing individuals. By contrast, our study demonstrated that cortical excitability, as measured by TMS-induced motor-evoked potentials (MEPs), was significantly reduced in the TS group in the period immediately preceding a finger movement. This effect is interpreted as consistent with previous suggestions that the cortical hyper-excitability that may give rise to tics in TS is actively suppressed by cognitive control mechanisms. Finally, we found no reliable evidence for altered patterns of functional inter-hemispheric connectivity in TS. These results provide evidence for compensatory brain reorganization that may underlie the increased self-regulation mechanisms that have been hypothesized to bring about the control of tics during adolescence.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02034.x" xmlns="http://purl.org/rss/1.0/"><title>Drawing perseveration in neglect: Effects of target density</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02034.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Drawing perseveration in neglect: Effects of target density</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lorenzo Pia, Raffaella Ricci, Patrizia Gindri, Giuseppe Vallar</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-05-30T08:53:36.865906-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1748-6653.2012.02034.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.1748-6653.2012.02034.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02034.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">45</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">57</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 cancellation tasks, patients with unilateral spatial neglect typically fail to mark targets within the side of the sheet contralateral to the side of the lesion (contralesional). Moreover, they can show a perseverative behaviour, which consists in repeatedly cancelling stimuli, mainly in the side of the display ipsilateral to the side of the lesion (ipsilesional). We investigated in 13 right-brain-damaged patients with left spatial neglect and perseverative behaviour whether and how different densities of horizontal targets modulated omission and perseverative errors. We found that the density of targets modulated the patients’ distribution of neglect (area of omission), but not its extent, as indexed by the percentage of omissions. Specifically, the area of omissions tightened when target density increased leftwards. On the other hand, target density did not affect the distribution of perseverative behaviour (area of perseveration), as well as its extent, as indexed by the percentage of perseverations. Correlation analyses showed that both the extent and the distribution of omissions were positively correlated to clinical measures of spatial neglect. Conversely, perseverations did not show such a correlation. These findings support the view that two different pathological mechanisms might be involved in left spatial neglect and in ipsilesional perseverative behaviour.</p></div>
]]></content:encoded><description>
In cancellation tasks, patients with unilateral spatial neglect typically fail to mark targets within the side of the sheet contralateral to the side of the lesion (contralesional). Moreover, they can show a perseverative behaviour, which consists in repeatedly cancelling stimuli, mainly in the side of the display ipsilateral to the side of the lesion (ipsilesional). We investigated in 13 right-brain-damaged patients with left spatial neglect and perseverative behaviour whether and how different densities of horizontal targets modulated omission and perseverative errors. We found that the density of targets modulated the patients’ distribution of neglect (area of omission), but not its extent, as indexed by the percentage of omissions. Specifically, the area of omissions tightened when target density increased leftwards. On the other hand, target density did not affect the distribution of perseverative behaviour (area of perseveration), as well as its extent, as indexed by the percentage of perseverations. Correlation analyses showed that both the extent and the distribution of omissions were positively correlated to clinical measures of spatial neglect. Conversely, perseverations did not show such a correlation. These findings support the view that two different pathological mechanisms might be involved in left spatial neglect and in ipsilesional perseverative behaviour.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02035.x" xmlns="http://purl.org/rss/1.0/"><title>Impaired body but not face perception in patients with obsessive–compulsive disorder</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02035.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Impaired body but not face perception in patients with obsessive–compulsive disorder</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Na Young Shin, Joon Hwan Jang, Hee Sun Kim, Geumsook Shim, Jae Yeon Hwang, Sung Nyun Kim, Jun Soo Kwon</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-06-14T08:16:51.902033-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1748-6653.2012.02035.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.1748-6653.2012.02035.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02035.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">58</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">71</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> Empirical evidence involving the processing of social information by patients with obsessive–compulsive disorder (OCD) has been relatively scarce. Our study investigated the perceptual abilities of patients with OCD to recognize human faces and bodies.</p></div>
<div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Method.</b> Fifty-four drug-free or drug-naïve patients with OCD and 42 healthy controls performed discrimination tasks consisting of four types of stimuli: two sets of faces that were manipulated with regard to configuration and features, human bodies, and chairs. The stimuli were presented in upright and upside-down orientations.</p></div>
<div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results.</b> Patients with OCD were significantly less accurate in discriminating pairs of bodily postures implying actions. However, we found no significant differences between patient and control groups in the ability to recognize faces and chairs. The inversion effects for bodies and faces were also comparable between the two groups.</p></div>
<div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusions.</b> The current findings suggest that patients with OCD experience difficulty in perceiving static forms of bodily postures, but are able to adequately recognize human faces. Our data indicate a selective deficit in the perception of bodily postures in those with OCD and suggest that this deficit is probably not related to the abnormal configurational processing of social objects.</p></div>
]]></content:encoded><description>
Background. Empirical evidence involving the processing of social information by patients with obsessive–compulsive disorder (OCD) has been relatively scarce. Our study investigated the perceptual abilities of patients with OCD to recognize human faces and bodies.
Method. Fifty-four drug-free or drug-naïve patients with OCD and 42 healthy controls performed discrimination tasks consisting of four types of stimuli: two sets of faces that were manipulated with regard to configuration and features, human bodies, and chairs. The stimuli were presented in upright and upside-down orientations.
Results. Patients with OCD were significantly less accurate in discriminating pairs of bodily postures implying actions. However, we found no significant differences between patient and control groups in the ability to recognize faces and chairs. The inversion effects for bodies and faces were also comparable between the two groups.
Conclusions. The current findings suggest that patients with OCD experience difficulty in perceiving static forms of bodily postures, but are able to adequately recognize human faces. Our data indicate a selective deficit in the perception of bodily postures in those with OCD and suggest that this deficit is probably not related to the abnormal configurational processing of social objects.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02036.x" xmlns="http://purl.org/rss/1.0/"><title>Visuospatial asymmetry in dual-task performance after subacute stroke</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02036.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Visuospatial asymmetry in dual-task performance after subacute stroke</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Marlies E. Kessel, Ilse J. W. Nes, Alexander C. H. Geurts, Wiebo H. Brouwer, Luciano Fasotti</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-11-05T12:43:17.681204-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1748-6653.2012.02036.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.1748-6653.2012.02036.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02036.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">72</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">90</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>Various authors have referred to an association between neglect and non-spatial components of attention. It has been suggested that an increase in attentional load could exacerbate neglect symptoms and reveal subtle, well-compensated neglect. In the present study, 21 RH and 22 LH subacute stroke patients and 20 controls performed a computerized single-detection task (CVRT) and a dual task (CVRT-D) combining the detection task with a driving simulation task. Omissions, reaction times (RTs) and RT asymmetries were analysed to investigate the influence of increasing attentional load on neglect symptoms. RT asymmetries were most pronounced in RH patients. Although a clear increase in RT asymmetries between CVRT and CVRT-D was observed, the amount of increase did not differ between both patient groups. Within both patient groups, correlations between RT asymmetries and ipsilesional RTs as a measure of general attention were significant in the single task but not in the dual task, indicating that increased attentional load may result in different degrees of lateralized and general attentional problems. Half of the patients with neglect on the BIT (Behavioural Inattention Test) showed increased RT asymmetries from CVRT to CVRT-D. Moreover, two LH and RH patients without neglect symptoms on the BIT and CVRT showed distinctively increased asymmetries in the CVRT-D, fostering the idea of an emergence of subtle neglect under increased attentional load. Dual-task performance may draw attention towards patients who, without obvious signs of neglect, may show visuospatial attention deficits in complex situations.</p></div>
]]></content:encoded><description>
Various authors have referred to an association between neglect and non-spatial components of attention. It has been suggested that an increase in attentional load could exacerbate neglect symptoms and reveal subtle, well-compensated neglect. In the present study, 21 RH and 22 LH subacute stroke patients and 20 controls performed a computerized single-detection task (CVRT) and a dual task (CVRT-D) combining the detection task with a driving simulation task. Omissions, reaction times (RTs) and RT asymmetries were analysed to investigate the influence of increasing attentional load on neglect symptoms. RT asymmetries were most pronounced in RH patients. Although a clear increase in RT asymmetries between CVRT and CVRT-D was observed, the amount of increase did not differ between both patient groups. Within both patient groups, correlations between RT asymmetries and ipsilesional RTs as a measure of general attention were significant in the single task but not in the dual task, indicating that increased attentional load may result in different degrees of lateralized and general attentional problems. Half of the patients with neglect on the BIT (Behavioural Inattention Test) showed increased RT asymmetries from CVRT to CVRT-D. Moreover, two LH and RH patients without neglect symptoms on the BIT and CVRT showed distinctively increased asymmetries in the CVRT-D, fostering the idea of an emergence of subtle neglect under increased attentional load. Dual-task performance may draw attention towards patients who, without obvious signs of neglect, may show visuospatial attention deficits in complex situations.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02037.x" xmlns="http://purl.org/rss/1.0/"><title>Perception of affective prosody in patients at an early stage of relapsing–remitting multiple sclerosis</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02037.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Perception of affective prosody in patients at an early stage of relapsing–remitting multiple sclerosis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Markus Kraemer, Michele Herold, Jennifer Uekermann, Bernhard Kis, Irene Daum, Jens Wiltfang, Peter Berlit, Rolf R. Diehl, Mona Abdel-Hamid</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-11-05T12:41:10.366148-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1748-6653.2012.02037.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.1748-6653.2012.02037.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02037.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">91</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">106</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>Cognitive dysfunction is well known in patients suffering from multiple sclerosis (MS) and has been described for many years. Cognitive impairment, memory, and attention deficits seem to be features of advanced MS stages, whereas depression and emotional instability already occur in early stages of the disease. However, little is known about processing of affective prosody in patients in early stages of relapsing–remitting MS (RRMS). In this study, tests assessing attention, memory, and processing of affective prosody were administered to 25 adult patients with a diagnosis of RRMS at an early stage and to 25 healthy controls (HC). Early stages of the disease were defined as being diagnosed with RRMS in the last 2 years and having an Expanded Disability Status Scale (EDSS) of 2 or lower. Patients and HC were comparable in intelligence quotient (IQ), educational level, age, handedness, and gender. Patients with early stages of RRMS performed below the control group with respect to the subtests ‘discrimination of affective prosody’ and ‘matching of affective prosody to facial expression’ for the emotion ‘angry’ of the ‘Tübingen Affect Battery’. These deficits were not related to executive performance. Our findings suggest that emotional prosody comprehension is deficient in young patients with early stages of RRMS. Deficits in discriminating affective prosody early in the disease may make misunderstandings and poor communication more likely. This might negatively influence interpersonal relationships and quality of life in patients with RRMS.</p></div>
]]></content:encoded><description>
Cognitive dysfunction is well known in patients suffering from multiple sclerosis (MS) and has been described for many years. Cognitive impairment, memory, and attention deficits seem to be features of advanced MS stages, whereas depression and emotional instability already occur in early stages of the disease. However, little is known about processing of affective prosody in patients in early stages of relapsing–remitting MS (RRMS). In this study, tests assessing attention, memory, and processing of affective prosody were administered to 25 adult patients with a diagnosis of RRMS at an early stage and to 25 healthy controls (HC). Early stages of the disease were defined as being diagnosed with RRMS in the last 2 years and having an Expanded Disability Status Scale (EDSS) of 2 or lower. Patients and HC were comparable in intelligence quotient (IQ), educational level, age, handedness, and gender. Patients with early stages of RRMS performed below the control group with respect to the subtests ‘discrimination of affective prosody’ and ‘matching of affective prosody to facial expression’ for the emotion ‘angry’ of the ‘Tübingen Affect Battery’. These deficits were not related to executive performance. Our findings suggest that emotional prosody comprehension is deficient in young patients with early stages of RRMS. Deficits in discriminating affective prosody early in the disease may make misunderstandings and poor communication more likely. This might negatively influence interpersonal relationships and quality of life in patients with RRMS.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02038.x" xmlns="http://purl.org/rss/1.0/"><title>Cognitive and affective Theory of Mind in mild to moderate Alzheimer's disease</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02038.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Cognitive and affective Theory of Mind in mild to moderate Alzheimer's disease</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Mickaël Laisney, Laetitia Bon, Catherine Guiziou, Nathalie Daluzeau, Francis Eustache, Béatrice Desgranges</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-10-23T05:50:50.927305-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1748-6653.2012.02038.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.1748-6653.2012.02038.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02038.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">107</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">120</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>Theory of Mind (ToM) allows one's own and others' cognitive and emotional mental states to be inferred. Although many patients with Alzheimer's disease (AD) display impaired social functioning as their disease progresses, very few studies have investigated ToM in AD. Those that have done so suggest that patients' ToM deficits are the consequence of other cognitive impairments. The aim of this study was thus to investigate changes in both the cognitive and the affective dimensions of ToM in AD, using tasks designed to circumvent the patients' comprehension difficulties. Sixteen mild to moderate AD patients and 15 healthy controls matched on age, sex and education level underwent cognitive (preference judgment and first- and second-order false belief) and affective (Reading the Mind in the Eyes) ToM assessments. Comprehension of false belief stories was verified and an additional neuropsychological examination was undergone. We observed impaired performances by AD patients on all the ToM tasks. While working memory and executive functioning impairments contributed to the deterioration in the more complex aspects of cognitive ToM abilities as highlighted by a correlation analysis, we failed to observe any comprehension difficulties in patients who performed poorly on simple cognitive ToM tasks, which suggests that AD truly affects cognitive ToM.</p></div>
]]></content:encoded><description>
Theory of Mind (ToM) allows one's own and others' cognitive and emotional mental states to be inferred. Although many patients with Alzheimer's disease (AD) display impaired social functioning as their disease progresses, very few studies have investigated ToM in AD. Those that have done so suggest that patients' ToM deficits are the consequence of other cognitive impairments. The aim of this study was thus to investigate changes in both the cognitive and the affective dimensions of ToM in AD, using tasks designed to circumvent the patients' comprehension difficulties. Sixteen mild to moderate AD patients and 15 healthy controls matched on age, sex and education level underwent cognitive (preference judgment and first- and second-order false belief) and affective (Reading the Mind in the Eyes) ToM assessments. Comprehension of false belief stories was verified and an additional neuropsychological examination was undergone. We observed impaired performances by AD patients on all the ToM tasks. While working memory and executive functioning impairments contributed to the deterioration in the more complex aspects of cognitive ToM abilities as highlighted by a correlation analysis, we failed to observe any comprehension difficulties in patients who performed poorly on simple cognitive ToM tasks, which suggests that AD truly affects cognitive ToM.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02040.x" xmlns="http://purl.org/rss/1.0/"><title>Alteration of affective Theory of Mind in amnestic mild cognitive impairment</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02040.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Alteration of affective Theory of Mind in amnestic mild cognitive impairment</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Michele Poletti, Ubaldo Bonuccelli</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-11-05T12:43:14.827063-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1748-6653.2012.02040.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.1748-6653.2012.02040.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02040.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Original Article</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">121</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">131</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 concept of amnestic mild cognitive impairment (aMCI) concerns a population of older individuals at high risk of developing probable Alzheimer's disease (AD). Impairments of the cognitive component of Theory of Mind (ToM), that is the inference about other people's beliefs, have been well documented in AD; on the contrary, controversial findings have been reported on the affective component of ToM (inference about other's feelings), a process mainly based on medial portions of the prefrontal cortex. The current study aimed at evaluating the affective component of ToM in aMCI subjects. Twenty aMCI subjects and 20 age-matched healthy controls (HC) underwent a standard neuropsychological assessment and the assessment of affective ToM with the full 36-item version of reading the mind in the eyes (RME). Although aMCI subjects had formal impaired performances only in memory tasks, HC outperformed aMCI subjects in several cognitive tasks, including also the RME (mean RME scores 21.7 ± 3.0 vs. 17.0 ± 3.8%; 60.3% of correct answers vs. 47.2%). The lower RME performance of aMCI patients provides the first empirical evidence that aMCI may be associated with difficulties in tasks of affective ToM, in accordance with recent findings of early difficulties of aMCI patients in other processes that are mainly dependent on the medial prefrontal cortex, such as reversal learning and decision making under ambiguity. Findings of the current study need further empirical confirmation in larger samples of aMCI patients and also the investigation of other MCI subtypes is needed.</p></div>
]]></content:encoded><description>
The concept of amnestic mild cognitive impairment (aMCI) concerns a population of older individuals at high risk of developing probable Alzheimer's disease (AD). Impairments of the cognitive component of Theory of Mind (ToM), that is the inference about other people's beliefs, have been well documented in AD; on the contrary, controversial findings have been reported on the affective component of ToM (inference about other's feelings), a process mainly based on medial portions of the prefrontal cortex. The current study aimed at evaluating the affective component of ToM in aMCI subjects. Twenty aMCI subjects and 20 age-matched healthy controls (HC) underwent a standard neuropsychological assessment and the assessment of affective ToM with the full 36-item version of reading the mind in the eyes (RME). Although aMCI subjects had formal impaired performances only in memory tasks, HC outperformed aMCI subjects in several cognitive tasks, including also the RME (mean RME scores 21.7 ± 3.0 vs. 17.0 ± 3.8%; 60.3% of correct answers vs. 47.2%). The lower RME performance of aMCI patients provides the first empirical evidence that aMCI may be associated with difficulties in tasks of affective ToM, in accordance with recent findings of early difficulties of aMCI patients in other processes that are mainly dependent on the medial prefrontal cortex, such as reversal learning and decision making under ambiguity. Findings of the current study need further empirical confirmation in larger samples of aMCI patients and also the investigation of other MCI subtypes is needed.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02030.x" xmlns="http://purl.org/rss/1.0/"><title>Preservation of person-specific knowledge in semantic memory disorder: A longitudinal investigation in two cases of dementia</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02030.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Preservation of person-specific knowledge in semantic memory disorder: A longitudinal investigation in two cases of dementia</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Catherine Haslam, Mazen Sabah</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-30T10:22:41.133632-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1748-6653.2012.02030.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.1748-6653.2012.02030.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02030.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Brief communication</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">132</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">138</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 double dissociation involving person-specific and general semantic knowledge is supported by numerous patient studies, though cases with preservation of the former are few. In this paper, we report longitudinal data from two cases. Their knowledge in both domains was preserved at the start of the investigation, but progressive deterioration was primarily observed on tests of general semantics. These data strengthen the evidence-base for preservation of person-specific knowledge in semantic memory disorder, and support its separate representation from object knowledge.</p></div>
]]></content:encoded><description>
The double dissociation involving person-specific and general semantic knowledge is supported by numerous patient studies, though cases with preservation of the former are few. In this paper, we report longitudinal data from two cases. Their knowledge in both domains was preserved at the start of the investigation, but progressive deterioration was primarily observed on tests of general semantics. These data strengthen the evidence-base for preservation of person-specific knowledge in semantic memory disorder, and support its separate representation from object knowledge.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02039.x" xmlns="http://purl.org/rss/1.0/"><title>Decision making is affected in obstructive sleep apnoea syndrome</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02039.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Decision making is affected in obstructive sleep apnoea syndrome</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Agnès Daurat, Matthieu Ricarrère, Michel Tiberge</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-10-23T05:50:53.335691-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1748-6653.2012.02039.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.1748-6653.2012.02039.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fj.1748-6653.2012.02039.x</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Brief communication</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">139</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">144</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>We assessed decision making in 20 patients newly diagnosed with obstructive sleep apnoea (OSA) and 20 healthy controls with the Iowa Gambling Task (IGT), which evaluates the ability to learn to sacrifice immediate rewards in favour of long-term gains. A standard neuropsychological battery was administered. Switching scores tended to be lower in patients. Patients persisted in selecting risky decks throughout the IGT, whereas controls behaved normally. Performance was correlated with hypoxaemia. Brain regions underlying decision making may be affected by OSA-related hypoxaemia.</p></div>
]]></content:encoded><description>
We assessed decision making in 20 patients newly diagnosed with obstructive sleep apnoea (OSA) and 20 healthy controls with the Iowa Gambling Task (IGT), which evaluates the ability to learn to sacrifice immediate rewards in favour of long-term gains. A standard neuropsychological battery was administered. Switching scores tended to be lower in patients. Patients persisted in selecting risky decks throughout the IGT, whereas controls behaved normally. Performance was correlated with hypoxaemia. Brain regions underlying decision making may be affected by OSA-related hypoxaemia.
</description></item><item rdf:about="http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12012" xmlns="http://purl.org/rss/1.0/"><title>Editorial acknowledgement</title><link>http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12012</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Editorial acknowledgement</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2013-03-06T07:38:35.275174-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/jnp.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/jnp.12012</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fjnp.12012</prism:url><prism:section xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">Editorial acknowledgement</prism:section><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">145</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">147</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item></rdf:RDF>