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Keywords:

  • Partial seizures;
  • SPECT in epilepsy;
  • Epilepsy semiology

Summary

  1. Top of page
  2. Summary
  3. Patients and Methods
  4. Results
  5. Discussion
  6. Acknowledgment
  7. Disclosure
  8. References
  9. Supporting Information

Purpose: Patients who have seizure onset from different brain regions can produce seizures that appear clinically indistinguishable from one another. These clinically stereotypic manifestations reflect epileptic activation of specific networks. Several studies have shown that ictal perfusion single photon emission computed tomography (SPECT) can reveal propagated ictal activity. We hypothesize that the pattern of hyperperfusion may reflect neuronal networks that generated specific ictal symptomatology.

Methods: All patients were identified who were injected with 99mTc-hexamethyl-propylene-amine-oxime (HMPAO) during versive seizures (n = 5), bilateral asymmetric tonic seizures (BATS; n = 5), and hypermotor seizures (n = 7) in the presurgical epilepsy evaluation between 2001 and 2005. The SPECT ictal–interictal difference image pairs of each subgroup were compared with image pairs of 14 controls using statistical parametric mapping (SPM 2) to identify regions of significant hyperperfusion. Hyperperfused regions with corrected cluster-level significance p < 0.05 were considered significant.

Results: We have identified a distinct ictal perfusion pattern in each subgroup. In versive seizure subgroup, prominent hyperperfusion was present in the frontal eye field opposite to the direction of head version. In addition, there was associated caudate and crossed cerebellar hyperperfusion. The BATS subgroup showed pronounced hyperperfusion supplementary sensorimotor area ipsilateral to the epileptogenic region, bilateral basal ganglia, and contralateral cerebellar hemisphere. The hypermotor seizure subgroup demonstrated two clusters of significant hyperperfusion: one involving bilateral frontomesial regions, cingulate gyri, and caudate nuclei, and another involving ipsilateral anteromesial temporal structures, frontoorbital region, insula, and basal ganglia.

Discussion: We have identified distinct hyperperfusion patterns for specific ictal symptomatology. Our findings provide further insight into understanding the anatomic basis of seizure semiology.

Epileptic seizures are often characterized based on careful analysis of the semiologic features during seizures (Luders et al., 1998; So, 2006; Noachtar & Peters, 2009). However, the anatomic basis underlying several clinical signs occurring during partial seizures remains unclear. Direct cortical electrical stimulation or electrocorticographic recording has been attempted previously to unravel the mechanisms of ictal symptomatology, but these methods are constrained by limited spatial sampling and current spread (Luders et al., 1987; Lim et al., 1994). Ictal radionuclide brain perfusion single photon emission computed tomography (SPECT) can provide a global appraisal of brain activity at one phase in the seizure. Although it is used primarily in the presurgical evaluation of refractory epilepsy to localize the ictal onset zone, ictal SPECT also shows hyperemic regions representing propagated ictal activity to the symptomatogenic zone because radiopharmaceutical is injected after noting seizure onset (Van Paesschen et al., 2007). Therefore, the topography of ictal hyperperfusion should reflect activated structures responsible for the evolution of symptomatology in the course of the seizure. In this study, we have examined ictal SPECT scans of patients with same seizure semiology to identify the neuronal networks generating specific ictal symptomatology.

Patients and Methods

  1. Top of page
  2. Summary
  3. Patients and Methods
  4. Results
  5. Discussion
  6. Acknowledgment
  7. Disclosure
  8. References
  9. Supporting Information

Patient selection

The study was approved by the ethics committee in Western Sydney Area Health Services. Between 2001 and 2005, 229 scalp video–electroencephalography (EEG) monitoring sessions were performed in 213 patients for presurgical evaluation of medically intractable partial epilepsy at Westmead Hospital. During video-EEG monitoring, 147 patients were injected with 99mTc-hexamethyl-propylene-amine-oxime (99mTc-HMPAO) during a seizure. For this study, we identified all patients who were injected with 99mTc-HMPAO immediately prior (<10 s) or during versive seizures (n = 7), bilateral asymmetric tonic seizures (BATS; n = 8), and hypermotor seizures (n = 7). From these groups, patients who developed secondarily generalized tonic–clonic seizures (n = 2) and patients with previous brain surgery were excluded (n = 3).

Seizure semiology and determination of 99mTc-HMPAO-SPECT injection timing

Seizures were defined according to the semiologic seizure classification (Luders et al., 1998). Versive seizures are seizures with sustained and extreme degree of head and eye deviation to one side (Wyllie et al., 1986). The versive movements are often accompanied by small clonic lateral movements of the head, and the chin moves not only laterally but also upwards (Luders et al., 1998). BATS are seizures characterized by tonic posturing involving the trunk and limbs that is bilateral but asymmetric (Bleasel & Luders, 2000). Hypermotor seizures consist of complex, organized movements affecting predominantly the proximal segments of the limbs and trunk, resulting in large movements that may appear “violent” when they occur at high speeds (Luders et al., 1998).

The timing of the 99mTc-HMPAO injection was determined on retrospective video and EEG review. Seizure onset was defined as the earliest EEG or clinical evidence of seizure activity (McNally et al., 2005) and seizure cessation when no EEG evidence of seizure activity was present.

99mTc-HMPAO-SPECT acquisition, image processing, and SPM analysis

Approximately 800 MBq of 99mTc-HMPAO was injected as a bolus into either a cephalic or an antecubital vein of the forearm after noting seizure onset. 99mTc-HMPAO–SPECT images were acquired within 4 h of injection. Patients with a seizure duration lasting <30 s were allocated a trained nurse to sit by the bedside for radiopharmaceutical injection, whereas those with a seizure of greater duration relied on a trained nurse responding to a seizure alarm for radiopharmaceutical injection. Interictal 99mTc-HMPAO–SPECT in the same patients was obtained after >24 h of no seizure activity. 99mTc-HMPAO–SPECT images of the brain were acquired using Siemens Orbiter (Siemens Healthcare, Hoffman Estates, IL, U.S.A.) single head gamma camera with neurofocal collimator and ADAC (Milpitas, CA, U.S.A.) Vertex and ADAC Forte dual head cameras with fanbeam collimators. Sixty-four projections were collected on a 128 × 128 matrix. The projection images were reconstructed with filtered back projection (Butterworth filter, 0.2–0.4 Nyquist cutoff frequency, 10th order) and corrected for attenuation using the Chang analytic method.

In the versive seizure subgroup, the direction of head turning can be defined clearly. We transposed horizontally the SPECT images of patients with right head deviation and combined them with the patients with left head deviation using IMAGEJ (Rasband, 1997–2009). Therefore, the direction of head turn was uniform assuming the homologous symptomatogenic network was represented on the contralateral side to the head deviation. In hypermotor seizures and BATS, it was not possible to normalize to a lateralized motor feature because motor manifestations were complex or consisted of bilateral tonic posturing. As such, we flipped the SPECT images so that all the ictal onsets were lateralized to the left, assuming seizures will propagate to involve a consistent network responsible for the semiology.

99mTc-HMPAO–SPECT was pre-processed as described by McNally et al. (2005) using Statistical Parametric Mapping (SPM 2, Wellcome Department of Cognitive Neurology, London, United Kingdom). Details of pre-processing, including downloads of 14 healthy normal SPECT image pairs from normal subjects, are available at http://spect.yale.edu/. In brief, SPECT images were realigned, spatially normalized, and smoothed by convolution with 16-mm Full-Width Half-Maximum (FWHM) Gaussian kernel. Global intensity normalization using proportional scaling with an analysis threshold of 0.8 was applied. For statistical analysis, SPECT ictal–interictal difference image pairs of each subgroup were compared voxel-by-voxel with image pairs of 14 healthy normal controls using multigroup condition and covariates model (McNally et al., 2005) to identify all clusters of voxels with significant hyperperfusion. Significant hyperperfusion was defined as clusters with corrected cluster-level significance p < 0.05 (voxel threshold p = 0.01, extent threshold ≥ 125).

Results

  1. Top of page
  2. Summary
  3. Patients and Methods
  4. Results
  5. Discussion
  6. Acknowledgment
  7. Disclosure
  8. References
  9. Supporting Information

The results of patient demographics are summarized in Table 1. Five patients with versive seizure, five with BATS, and seven with hypermotor seizure were studied. The median age was 24 years [interquartile range (IQR) 25–75%: 21–34; range 11–43]. Fifteen patients underwent resective surgery. In the nine surgical patients with normal magnetic resonance imaging (MRI), invasive subdural electrode evaluation and electrocorticography were carried out to determine the region of ictal onset, the areas involved in early propagation, and the proximity to eloquent cortex prior to resection. Postoperatively, 12 patients achieved Engel class I seizure freedom (Table 2).

Table 1.   Patient demographics
 Versive seizureBilateral asymmetric tonic seizureHypermotor seizure
  1. F, frontal lobe; T, temporal lobe; O, occipital lobe.

Gender (female/male)2:33:23:4
Age (years, median; range)23; 11–2730; 18–4224; 16–43
Age of onset (years, median; range)7; 4–1110; 8–1713; 2–21
MRI visible lesionF = 1, T = 2, O = 20T = 1
Surgical outcome [Engel class 1 (total patient operated)]5 (5)3 (4)4 (6)
Seizure duration (seconds, median; range)115; 27–32334; 11–6447; 9–157
Radiopharmaceutical injection in relation to seizure onset (seconds, median; range)88; 7–1137; 3–3714; 5–54
Table 2.   Summary of clinical features, investigation results, and surgical outcome
Patient, (age/gender), age onset, MRISemiologyCompletion of injection to the onset of semiologySeizure duration; completion of injection (s)Lobe of ictal onsetaType of surgerySeizure outcome (follow-up duration)/pathology
  1. M, male; F, female; Rt, right; Lt, left; FL, frontal lobe; TL, temporal lobe; OL, occipital lobe.

  2. aLobe of ictal onset was determined based on clinical history, scalp, and intracranial video-EEG monitoring, MRI, fluorodeoxyglucose (FDG) –PET, HMPAO–SPECT, and neuropsychological studies.

V1. (20 years/F), onset: 7 years MRI: Rt inferior-mesial occipital lobe lesionVisual aura (visual disturbances, flashing lights) [RIGHTWARDS ARROW]Versive seizure (Forced sustained eye and head version to the left) [RIGHTWARDS ARROW]Dialeptic seizure (Behavioral pause, stare, not responding to questions, occasional subtle lip movements)6 s prior to onset of eye version323; 113Rt OLRt inferior mesial occipital corticectomyEngel class 1 (8 years) Non–balloon cell cortical dysplasia
V2. (24 years/M), onset: 8 years MRI: Rt inferior-mesial occipital lobe lesionVisual aura (strain behind both eyes, flashing lights) [RIGHTWARDS ARROW]Versive seizure (Forced sustained eye and head version to the left)1 s prior to onset of eye version27; 7Rt OLRt inferior mesial occipital corticectomyEngel class 1 (3 years) Microdysgenesis
V3. (11 years/F), onset: 4 years MRI: Rt lateral temporal lesionAura (lightheadedness, vagueness) [RIGHTWARDS ARROW]Versive seizure (Forced sustained eye and head version to the left)7 s prior to onset of eye version141; 88Rt TLRt lateral temporal corticectomyEngel class 1 (8 years) Dysembryoplastic neuroepithelial tumor
V4. (27 years/M), onset: 11 years MRI: Rt frontopolar lesionAura (rising epigastric feeling) [RIGHTWARDS ARROW]Versive seizure (Forced sustained eye and head version to the left)13 s after onset of eye version115, 110Rt FLRt frontal pole corticectomyEngel class 1 (8 years) Balloon cell cortical dysplasia
V5. (23 years/M), onset: 6 years MRI: Lt hippocampal sclerosisAura (fearful feeling, epigastric discomfort) [RIGHTWARDS ARROW]Automotor seizure (Lip smacking, chewing, rubbing hands on legs, looks around) [RIGHTWARDS ARROW]Versive seizure (Forced sustained eye and head version to the right)8 s after onset of eye version60, 45Lt TLLt temporal lobectomyEngel class 1 (4 years) Hippocampal sclerosis
S1. (30 years/F), onset: 8 years MRI: normalBilateral asymmetric tonic seizure7 s after onset of bilateral asymmetric tonic seizure30; 7Lt FLLt mesial frontal corticectomyEngel class 1 (7 years) Non-balloon cell cortical dysplasia
S2. (32 years/F); onset: 17 years MRI: normalBilateral asymmetric tonic seizure37 s after onset of bilateral asymmetric tonic seizure43; 37Lt FLNot operated 
S3. (18 years/F), onset: 10 years MRI: normalBilateral asymmetric tonic seizure28 s after onset of bilateral asymmetric tonic seizure64; 28Rt FLRt mesial frontal corticectomyEngel class 1 (8 years) Neuronal heterotopia
S4. (23 years/M), onset: 14 years MRI: normalAura (unusual feeling in left leg) [RIGHTWARDS ARROW]Bilateral asymmetric tonic seizure1 s prior to onset of bilateral asymmetric tonic seizure11; 3Rt FLRt mesial frontoparietal corticectomyEngel class 1 (2 years) Balloon cell cortical dysplasia
S5. (42 years/M); onset: 10 years MRI: normalBilateral asymmetric tonic seizure4 s after onset of bilateral asymmetric tonic seizure34; 4Rt FLRt mesial frontal corticectomyEngel class II (6 years) Non–balloon cell cortical dysplasia
H1. (36 years/F), onset: 13 years MRI: Rt hippocampal sclerosisAura (sounds become distant; sense of impending doom) [RIGHTWARDS ARROW]Hypermotor seizure: (Covers face with left hand; turning vigorously in bed; whimpering vocalization)3 s after onset of hypermotor seizure97; 19Rt TLRt temporal lobectomyEngel class 1 (3 years) Hippocampal sclerosis
H2. (16 years/M), onset: 13 years MRI: normalAura (fearful feeling) [RIGHTWARDS ARROW]Hypermotor seizure: (Looks around in a restless manner; rocking of body back and forth; shuffling from side to side; sniff heavily; fumbling with clothing)6 s after onset of hypermotor seizure26; 10Rt FL Rt frontomesial corticectomyEngel class 1 (3 years) Neuronal heterotopia
H3. (43 years/M), onset: 21 years MRI: normalAura (fearful feeling) [RIGHTWARDS ARROW]Hypermotor seizure: (Looks around in a restless manner; rocking of body back and forth; shuffling from side to side; chews, lip smacking; fumbling with clothing).At onset of hypermotor seizure39; 14Rt TLRt temporal lobectomyEngel class 1 (5 years) Neuronal heterotopia
H4. (24 years/F), onset: 16 years MRI: normalAura (feels hot in the head and going to blackout) [RIGHTWARDS ARROW]Hypermotor seizure: (Rocking of body back and forth with facial grimacing; grabbing pillows; turning vigorously in bed; whimpering vocalization)43 s after onset of hypermotor seizure65; 54Rt FL or TLNot operated 
H5. (23 years/F), onset: 2 years MRI: normalNo Aura [RIGHTWARDS ARROW]Hypermotor seizure: (Moving both arms in a restless manner; rocking of body back and forth; shuffling from side to side; whimpering vocalization)41 s after onset of hypermotor seizure157; 41Lt FLLt dorsolateral frontal corticectomyEngel class 1 (4 years) Neuronal heterotopia
H6. (22 years/M), onset: 11 years MRI: normalAura (feels dizzy or a sense of leg weakness) [RIGHTWARDS ARROW]Hypermotor seizure: (Rocking of body back and forth; shuffling from side to side; scissoring of legs; jumping in and out of bed; frenetic and large amplitude peddling movements of lower limbs; writhing trunk)10 s after onset of hypermotor seizure47; 13Lt FLLt frontomesial corticectomyEngel class III (6 years) Neuronal heterotopia
H7. (37 years /M), onset: 12 years MRI: normalAura (feels his face is being pulled forward) [RIGHTWARDS ARROW]Hypermotor seizure: (Screams; complex arm movements; legs kicking violently; rocking of body back and forth; shuffling from side to side, turning vigorously in bed; back arching)2 s after onset of hypermotor seizure9; 5Lt FLLt fronto-orbital corticectomyEngel class II (5 years) Microdysgenesis

SPM analysis revealed a distinctive pattern of significant ictal hyperperfusion in each subgroup (Fig. 1 and Supplemental Fig. S1–3) as follows:

image

Figure 1.   In versive seizure subgroup (top), significant hyperperfusion was identified in the middle frontal gyrus and the adjacent cortex opposite to the direction of the head turn. Ipsilateral caudate and contralateral cerebellum significant hyperperfusion was also present. In the bilateral asymmetric tonic seizure subgroup (middle), significantly hyperperfusion involved primarily the supplementary sensorimotor area ipsilateral to the hemisphere of ictal onset, bilateral basal ganglia, and contralateral cerebellum. In the hypermotor seizure subgroup (bottom), two clusters of significant hyperperfusion were found: One involved bilateral frontomesial cortex and cingulate gyrus, and the other involved the temporal lobe, frontoorbital cortex, insula, and basal ganglia ipsilateral to the hemisphere of ictal onset.

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  • 1. Versive seizure subgroup showed a prominent hyperperfusion anterior to the precentral sulcus in the frontal eye field opposite to the direction of the head turn. In addition, there was associated ipsilateral caudate and crossed cerebellar hyperperfusion.

  • 2. BATS subgroup showed pronounced hyperperfusion in the supplementary sensorimotor area (SSMA) ipsilateral to the hemisphere of ictal onset and bilateral basal ganglia. Crossed cerebellar hyperperfusion was also present.

  • 3. Hypermotor seizure subgroup demonstrated two clusters of significant hyperperfusion: one involving both frontomesial regions, cingulate gyri, and caudate nuclei, and another involving ipsilateral temporal pole, mesial temporal structures, frontoorbital region, insula, and basal ganglia.

Discussion

  1. Top of page
  2. Summary
  3. Patients and Methods
  4. Results
  5. Discussion
  6. Acknowledgment
  7. Disclosure
  8. References
  9. Supporting Information

The major finding of our work is that specific perfusion patterns are associated with different ictal semiology. Our study was based on the concept that the same ictal symptomatology resulted from activation of the same cortical network (Spencer, 2002), and by analyzing groups of patients injected in the same ictal semiology we hypothesized the brain regions most consistently involved could be identified by quantitative voxel-based analysis on 99mTc-HMPAO–SPECT.

Despite the varied location of seizure onset and histopathology, similar semiologic features during seizures can exist. This observation had been reported previously by several investigators (Wyllie et al., 1986; Bleasel et al., 1997; So, 2006). The network structures within the brain are connected functionally and structurally. It is not surprising that seizures arising from different sites can propagate in a variably extensive way to involve the same neural network (Spencer, 2002).

In our cohort of versive seizures, forced and sustained head and eye version was associated with pronounced hyperperfusion in the contralateral frontal eye field. In addition, there was associated contralateral with caudate and ipsilateral cerebellar hyperperfusion. In another SPECT study, head turning was also noted to be associated with increases in cortical blood flow on the hemisphere opposite to the direction of version (Newton et al., 1992). Wyllie et al. (1986) found versive head and eye movements reliably lateralizing the seizure onset to the contralateral hemisphere. These versive movements can be elicited by direct electrical stimulation of frontal eye field in the posterior part of the middle frontal gyrus and the immediate adjacent part of the superior frontal gyrus (Foerster, 1931; Godoy et al., 1990; Blanke et al., 2000).

The basal ganglia is a complex structure implicated in a variety of regulatory controls of movement and posture. Hyperperfusion of this structure is often associated with dystonic posturing of limbs during seizures. However, none of our patients in the versive seizure subgroup had ictal dystonia. Several investigators have shown that the frontal eye field sends large direct projections to the caudate nucleus (Leichnetz & Gonzalo-Ruiz, 1996; Cui et al., 2003). We suggest that the caudate is part of the neuronal circuitry activated in a versive seizure.

Crossed cerebellar hyperperfusion is frequently observed in focal seizures (Bohnen et al., 1998). This phenomenon, like that of crossed cerebellar diaschisis (Baron et al., 1981; Won et al., 1996), reflects perfusion alterations of structures functionally connected through the corticopontocerebellar pathway during seizures. The frontal lobes have extensive efferent projections to the contralateral cerebellar hemisphere (Brodal, 1972). Our finding of crossed cerebellar hyperperfusion accords with this neuronal connection.

Several investigators recognized that electrical stimulation of the SSMA could elicit sustained tonic truncal and bilateral asymmetric limb posturing (Penfield & Welch, 1951; Woolsey et al., 1952). This characteristic posture is also accepted by The International League Against Epilepsy (ILAE) to be one of the distinctive ictal semiologies characteristic of SSMA seizures (Commission, 1989). The mechanism underlying bilateral motor activities is debated. Chauvel et al. (1992) found epileptic discharge spread from ipsilateral SSMA into the contralateral SSMA during BATS and postulated that this was the mechanism of bilateral motor manifestations. However, it is also known that unilateral SSMA damage can produce bilateral motor impairment (Laplane et al., 1977; Zentner et al., 1996).

Our SPM analysis suggested that ictal activation confined to one SSMA produces BATS. In our BATS subgroup, the subcortical activation pattern involved bilaterally basal ganglia and contralateral cerebellum. This subcortical pattern is consistent with known projections from SSMA to bilateral basal ganglia and contralateral cerebellum (Wiesendanger, 1986). Laich et al. (1997) examined SSMA propagation pathways using ictal SPECT and found similar subcortical hyperperfusion pattern involving bilateral basal ganglia and contralateral cerebellum. However, only two of their six patients with bilateral asymmetric tonic posturing had ipsilateral SSMA hyperperfusion, whereas the rest showed bilateral but asymmetric frontomesial hyperperfusion with predominance ipsilateral to the ictal onset. It is possible that the stringent criteria of our SPM analysis did not show bilateral SSMA hyperperfusion because involvement of contralateral SSMA is not sufficiently consistent to produce a sufficiently large perfusion increase in the group analysis. Further investigation will be needed to determine the mechanism, but in any case, not all patients with bilateral asymmetric tonic posturing had bilateral frontomesial hyperperfusion.

In patients with hypermotor seizure, two clusters of significant hyperperfusion were present. One cluster involved bilateral frontomesial regions, cingulate gyrus, and caudate, and the other involving ipsilateral temporal pole, mesial temporal structures, frontoorbital region, insula, and basal ganglia. The precise symptomatogenic zone for hypermotor seizures remains largely unknown, although there is increasing evidence that it involves the orbitofrontal cortex and anterior cingulate cortex (Schlaug et al., 1997; Rheims et al., 2008). Rheims et al. (2008) reported the hypermotor seizures consisting mainly of body rocking, limb hyperkinetic movements, and facial expression of fear showed stereoelectroencephalography (SEEG) ictal changes centered mainly on the ventromesial frontal cortex, whereas hypermotor seizures consisting of truncal movements or rotation with frequent tonic/dystonic posturing showed changes localized within the mesial premotor cortex and dorsal anterior cingulate. These reported electrical changes overlap with our regions of hyperperfusion. However, this study had technical limitations of SEEG spatial sampling and did not include all patients with hypermotor seizure.

Nobili et al. (2004) recently reported three patients with hypermotor seizures, symptomatic of temporobasal cortical dysplasia, where SEEG showed temporal lobe ictal onset. In the study, they found that hypermotor manifestations appeared only when the ictal discharge in the temporal lobe involved extratemporal structures such as the cingulate and frontal regions. The orbitofrontal cortex and anterior cingulate cortex are reciprocally connected and they are linked extensively to the mesial frontal regions, amygdala, hippocampus, temporal pole, insula, and basal ganglia (Salloway et al., 2001). Our data support the hypothesis that the entire circuitry participates in the expression of hypermotor seizure.

Shin et al. (2002) examined the ictal SPECT in patients with seizures of mesial temporal lobe origin and showed that ictal hyperperfusion patterns were related to the semiologic progression of seizures. In our study, group analysis was performed to eliminate interindividual perfusion variability and identify consistent hyperperfusion pattern. However, SPECT injection was performed without depth electrode or subdural grid electroencephalographic recording, and several of our patients were injected during the expression of the specified semiology. Taking into account a 30 s transit time for 99mTc-HMPAO injection to reach the brain and that brain uptake reaches maximum within 1 min after injection (Andersen, 1989; Pastor et al., 2008), it is, therefore, possible that some of the perfusion changes may be postictal. Future study of patients with same semiology injected 30 s prior to manifestation of the semiologic features with seizure lasting a minute or more will be needed to confirm our findings. Another potential limitation of our study is our small sample size. Different SPECT gamma cameras used during the study duration can add also heterogeneity to 99mTc-HMPAO–SPECT data. To address this issue, we used a large Gaussian kernel filter to smooth images before beginning the statistical analysis.

SPECT has been used to study dystonic limb posturing during seizures and associated this ictal sign with contralateral basal ganglia hyperperfusion (Newton et al., 1992; Joo et al., 2004). With SPM group analysis, we have identified the most consistently involved regions for a specified ictal behavior in groups of patients. These cortical and subcortical changes are individual to each ictal symptomatology and provide us with further insight into the neuroanatomic network underlying some of the clinical signs observed during a seizure.

Acknowledgment

  1. Top of page
  2. Summary
  3. Patients and Methods
  4. Results
  5. Discussion
  6. Acknowledgment
  7. Disclosure
  8. References
  9. Supporting Information

This work was supported in part by University of Sydney Postgraduate Award, Millennium Institute Stipend, and Pfizer Neuroscience Research Grant to Dr Chong H Wong.

Disclosure

  1. Top of page
  2. Summary
  3. Patients and Methods
  4. Results
  5. Discussion
  6. Acknowledgment
  7. Disclosure
  8. References
  9. Supporting Information

Dr. Armin Mohamed, Dr. George Larcos, Ms. Rochelle McCredie, Dr. Ernest Somerville, and Dr. Andrew Bleasel report no disclosures. We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.

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  1. Top of page
  2. Summary
  3. Patients and Methods
  4. Results
  5. Discussion
  6. Acknowledgment
  7. Disclosure
  8. References
  9. Supporting Information
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Supporting Information

  1. Top of page
  2. Summary
  3. Patients and Methods
  4. Results
  5. Discussion
  6. Acknowledgment
  7. Disclosure
  8. References
  9. Supporting Information

Figure S1. SPM output for Versive seizure subgroup.

Figure S2. SPM output for Bilateral asymmetric tonic seizure subgroup.

Figure S3. SPM output for Hypermotor seizure subgroup.

FilenameFormatSizeDescription
EPI_2723_sm_fig1.tif337KSupporting info item
EPI_2723_sm_fig2.tif451KSupporting info item
EPI_2723_sm_fig3.tif961KSupporting info item

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