Decreased corpus callosum size in sickle cell disease: relationship with cerebral infarcts and cognitive functioning.

We assessed midsagittal corpus callosum size in sickle cell disease (SCD) and its relationship to lesion volume, lesion location, and cognitive functioning. Twenty-eight children with SCD and 16 demographic controls completed magnetic resonance imaging (MRI) and neuropsychological testing. Corpus callosum (CC) size was smaller for children with silent infarcts (n = 8) or overt stroke (n = 8) than for those without visible infarcts (n = 12) or control participants. Lesion volume was a robust predictor of IQ and other cognitive scores; total CC size did not typically add explanatory power for these measures. The size of the rostral body of the CC, however, independently predicted measures of distractibility, speeded production, and working memory. Posterior CC size was also decreased among many of the children with SCD, even in the absence of visible infarcts in this region. Brain morphology appears to provide additional information about SCD-related effects on the brain above and beyond visible infarcts.     

Detecting white matter injury in sickle cell disease using voxel-based morphometry

OBJECTIVE: Sickle cell disease (SCD) is associated with cerebrovascular disease, cerebral infarction, and cognitive dysfunction. This study aimed to detect the presence and extent of white matter abnormalities in individuals with SCD using voxel-based morphometry (VBM). METHODS: Thirty-six children and adolescents with SCD (age range, 9-24 years) and 31 controls (8-25 years) underwent magnetic resonance investigations using T1- and T2-weighted protocols. White and gray matter density maps were obtained from three-dimensional magnetic resonance imaging (MRI) data sets. Using VBM, we compared the maps between controls and SCD individuals with silent white matter infarct lesions (SCD+L; n = 16), and those without visible abnormality (SCD-L; n = 20). RESULTS: In comparison with controls, intelligence quotients (IQs) were lower in both SCD groups irrespective of presence of visible lesions. VBM showed widespread bilateral white matter abnormalities in the SCD+L group, extending beyond the regions of focal infarction in the deep anterior and posterior white matter borderzones. Bilateral white matter abnormalities were also observed in the SCD-L group, in locations similar to those in the SCD+L group. INTERPRETATION: VBM is sensitive to detection of widespread white matter injury in SCD patients in borderzones between arterial territories even in the absence of evidence of infarction. Those changes may contribute to cognitive deficits in this population.     

How to identify stroke mimics in patients eligible for intravenous thrombolysis?

Since decision-making for thrombolysis in acute stroke settings is restricted to a limited time window and based on clinical assessment and CT findings only, thrombolysis is sometimes applied to patients with a final diagnosis other than a stroke. From a prospectively collected stroke/MRI data bank (2004-2010) with 648 suspected ischemic stroke patients treated with rtPA, we identified patients without evidence of acute infarction on follow-up MRI and a final diagnosis other than a stroke or acute cerebrovascular event. We compared demographics, symptoms, complications, and outcome of patients with stroke mimics (SM) to those with acute infarction. In 42 patients, an SM was diagnosed: seizures in 20, conversion disorder in seven, dementia in six, migraine in three, brain tumor in two, and others in four patients. Patients with SM less often had typical stroke symptoms like dysarthria (p < 0.01), facial palsy (p < 0.001), hemiparesis (p < 0.001), horizontal gaze palsy (p < 0.001), and visuospatial neglect (p = 0.03), while aphasia (p = 0.004) and accompanying convulsions (p = 0.01) occurred more often. Independent predictors of SM were known cognitive impairment, aphasia, and accompanying convulsions. Thrombolysis-related complications (orolingual angioedema) occurred in one SM patient and none of the SM patients deteriorated clinically. Stroke mimics comprise neurological/psychiatric disorders and differ from ischemic stroke patients with regard to the clinical presentation at onset. This might be helpful in deciding which patients should undergo acute stroke MRI to rule out SM, facilitate treatment decisions, and reduce the risk of unnecessary therapy.     

Perfusion magnetic resonance abnormalities in patients with sickle cell disease

Neurological complications are common in sickle cell disease (SCD). However, it is often difficult to relate the clinical presentation to conventional neuroimaging, because subclinical infarction is common and stroke has been described in the absence of large-vessel disease. We studied 48 patients with SCD aged 4-34 (median 13) years with T2-weighted, diffusion and perfusion magnetic resonance imaging (MRI) and with MR angiography. Forty-four underwent transcranial Doppler (TCD). Abnormalities on perfusion imaging were seen in 25 cases, 24 of whom had been symptomatic. The remaining patient had evidence of executive dysfunction and reduced perfusion in the frontal lobes. The perfusion abnormality was larger than the area of infarction in 9 patients and was seen in an arterial distribution with no infarction in a further 9. In 3 patients with transient ischemic attacks, perfusion abnormalities were demonstrated in the absence of any other neuroimaging abnormalities, and perfusion changes were seen in 3 others despite normal MR angiography and TCD. Perfusion abnormalities are associated with neurological symptoms in patients with SCD, whether or not MRI, MR angiography, and TCD are abnormal. It is likely that this technique will guide management in individual patients.     

Stroke prevention and treatment in sickle cell disease

While the problem of stroke in the patients with sickle cell disease (SCD) has been known for more than 75 years, adequate preventive and treatment strategies are just now being tested. Recent data on prevalence and incidence have been obtained from the Cooperative Study of Sickle Cell Disease of more than 4000 patients with SCD observed in 23 US clinical centers over a 10-year period.1 The overall age-specific incidence of first stroke in SCD (homozygous sickle cell anemia) is low (0.13%) at ages younger than 24 months, increasing to just over 1% at ages 2 to 5 years, with only a slight decrement to 0.79% at ages 6 to 9 years. The risk of brain infarction declines until a second peak is seen at ages older than 50 years, when the incidence again increases to nearly 1.3%. Although intracranial hemorrhage does occur in young children with SCD, the risk is low compared with older children and adults. The Cooperative Study of Sickle Cell Disease reported risk factors for infarction to be prior transient ischemic attack, low steady-state hemoglobin values, and rate and recency of episodes of acute chest syndrome, as well as elevated systolic blood pressure. Risk factors for intracranial hemorrhage included low steady-state hemoglobin values and a high leukocyte count. The burden of cerebrovascular disease is even higher if subclinical magnetic resonance imaging (MRI) lesions, presumed to be ischemic, are included. The prevalence of such lesions is more than 22% in patients with SCD, and most of these patients have not reported symptoms, although specialized neuropsychological testing shows lower scores in children with silent lesions on MRI scans. Patients with a history of clinical stroke typically have infarcts in the cortex and deep white matter, whereas silent infarcts tend to be more limited to deep white matter. Common infarction patterns are characterized by wedge-shaped lesions of large-vessel territories; border zone infarctions, particularly of the middle and cerebral artery watershed region; and small punctate lesions of the deep white matter. Fat embolism to the brain and venous thromboses are encountered rarely.     

Preliminary Study of Working Memory in Children with Stroke Related to Sickle Cell Disease

The verbal working memory abilities of children with stroke related to sickle cell disease (SCD) (n = 20) were compared to those of control children with SCD who had no history of stroke (n = 11). Memory span for one-, two-, and three-syllable words was assessed. For children with anterior infarcts, overall span was comparable to that of controls, but the typical effect of word length on span was reduced. For children with diffuse infarcts, overall span was reduced in comparison to that of controls, but the typical effect of word length on span was observed. For children with posterior infarcts, overall span was comparable to that of controls and the typical effect of word length on span was observed. These results provide preliminary evidence that patterns of working memory performance may vary across children with infarcts affecting different regions of the brain.     

Anatomy of sensory findings in patients with posterior cerebral artery territory infarction.

BACKGROUND: Posterior cerebral arteries (PCAs) supply the ventrolateral thalamic sensory nuclei and white matter sensory tracts to the somatosensory parietal cortex. Patients with PCA territory strokes often have visual, memory, cognitive, and sensory signs. Clinicoanatomic correlation of visual, cognitive, and memory functions are well defined but, to our knowledge, no systematic study has analyzed the anatomy of sensory abnormalities. OBJECTIVE: To assess the frequency and anatomic correlation of sensory symptoms and signs in patients with PCA territory infarction. PATIENTS AND METHODS: Sixty patients with hemispheral and hemispheral and deep PCA territory infarcts apparent on computed tomographic and magnetic resonance imaging scans were studied for the presence of sensory findings and location of infarcts. RESULTS: Sensory symptoms or signs were present in 15 (25%) of 60 patients. Among patients with sensory findings, 11 of 15 had infarcts in the ventrolateral thalamus in the territory of the thalamogeniculate or lateral posterior choroidal arteries. The other 4 patients had no ventrolateral thalamic or white matter infarction but had severe proximal vascular occlusive lesions that could have caused temporary thalamic ischemia. One of these 4 patients had a medial thalamic infarct and transient hemisensory symptoms. Twelve patients had thalamic infarcts and no recorded sensory findings. Seven patients with thalamic infarcts (6 medial and 1 ventrolateral) had no sensory findings, and sensory findings could not be accurately assessed in 4 patients with ventrolateral and 1 patient with medial thalamic infarcts. CONCLUSIONS: All patients with PCA territory infarcts and sensory findings either had thalamic infarcts in thalamogeniculate or lateral posterior choroidal artery territory or had thalamic ischemia. Sensory findings in PCA territory infarction indicate ventrolateral thalamic ischemia.     

Preliminary study of working memory in children with stroke related to sickle cell disease

The verbal working memory abilities of children with stroke related to sickle cell disease (SCD) (n = 20) were compared to those of control children with SCD who had no history of stroke (n = 11). Memory span for one-, two-, and three-syllable words was assessed. For children with anterior infarcts, overall span was comparable to that of controls, but the typical effect of word length on span was reduced. For children with diffuse infarcts, overall span was reduced in comparison to that of controls, but the typical effect of word length on span was observed. For children with posterior infarcts, overall span was comparable to that of controls and the typical effect of word length on span was observed. These results provide preliminary evidence that patterns of working memory performance may vary across children with infarcts affecting different regions of the brain.     

Therapy insight: stroke risk and its management in patients with sickle cell disease

Children with sickle cell disease, a chronic hemolytic anemia, present with a wide variety of neurological syndromes, including ischemic and hemorrhagic stroke, transient ischemic attacks, 'soft neurological signs', seizures, headache, coma, visual loss, altered mental status, cognitive difficulties, and covert or 'silent' infarction. Those with ischemic stroke usually have stenosis or occlusion of the distal internal carotid and proximal middle cerebral arteries. Indefinite transfusion prevents recurrence in most patients who have had a stroke, and can prevent first stroke in those with high transcranial Doppler velocities. High white cell count, low hemoglobin and oxyhemoglobin desaturation predict neurological complications. Other risk factors for overt ischemic stroke include hypertension, previous transient ischemic attack, covert infarction and chest crisis. For hemorrhagic stroke, aneurysms are common in adults but not children, who often present with hypertension after transfusion or corticosteroids. Seizures are particularly common in patients with cerebrovascular disease and covert infarction; the latter is also associated with hyposplenism and infrequent pain. Factors associated with cognitive difficulties include thrombocytosis, infarction, large-vessel disease, and perfusion abnormality on neuroimaging. As well as investigating the role of genes and the possibility that hydroxyurea or blood pressure control reduce neurological complications, we should explore the modifiable effects of poor nutrition, chronic infection, hemolysis and oxyhemoglobin desaturation on stroke risk.     

Functional outcome in patients with pontine infarction after acute rehabilitation

We examined the clinical features of patients with pontine infarction in the acute stage and the factors affecting functional prognosis and outcome. Lesions, neurological manifestations at initial physical status examinations, cognitive function, swallowing function and outcome [activities of daily living (ADL), status of nutritional intake at discharge and destination after discharge] were evaluated in 68 patients (47 males and 21 females) who had pontine lesions with acute phase cerebral infarction. The mean length of stay was 24.4 days. The symptoms (number of patients) observed included paralysis (50), dysarthria (47), ataxia (18), diplopia (11), dysphagia (49) and poor cognitive performance (37). The types of lesions (number of patients) included lacunar infarcts in the ventral pontine area (15), lacunar infarcts in the dorsal pontine area (13) and large lacunar infarcts (LLIs) (41). After hospital discharge, 23 patients were discharged home, 44 were transferred to another hospital and 1 died. Twenty-three patients were on a regular diet, 22 were receiving a dysphagia diet and 22 were on enteral feeding at discharge. Patients with LLIs more frequently had poor cognitive performance, paralysis, dysphagia at discharge and a tendency for a longer length of stay compared with patients who had lacunar infarct. Most patients who returned home were those who were younger in age, had fewer neurological symptoms, had better cognitive function and ADL performance, and could ingest food. In an acute hospital, age, neurological symptoms, ADL, cognitive function, and dysphagia were considered important factors for determining the outcome in patients with pontine infarction.     

长期住院对精神分裂症患者认知功能的影响

目的：探讨长期住院对精神分裂症患者认知功能的影响。方法：对56例长期住院（≥5年）与49例住院时间较短（≤1年）的精神分裂症患者的精神症状和认知功能进行比较，采用阳性与阴性症状量表（PANSS）、韦氏成人智力量表（WAIS-R）、威斯康星卡片分类试验（WCST）等评定患者的认知功能。结果：长期住院（≥5年）组在智商、注意、记忆，以及信息整合与执行功能等均显著较差。结论：长期住院对精神分裂症患者认知功能有负面影响。     

Epidemiological characteristics of lacunar infarcts in a population

BACKGROUND AND PURPOSE: This study evaluated the characteristics and natural history of patients with lacunar (small, deep) cerebral infarcts in a defined population for comparison of these characteristics to those in patients with nonlacunar infarcts. METHODS: This is a population-based study in Rochester, Minnesota, from 1960 to 1984, that used the medical record-linkage system to identify and characterize patients with cerebral infarction. RESULTS: The age- and sex-adjusted average annual incidence rate of lacunar cerebral infarction was 13.4/100,000 persons, accounting for 12% of all first cerebral infarcts. Temporal trends in incidence rates, stroke recurrence rates, prevalence of diabetes mellitus, and causes of death (given survival for 30 days) for cases of lacunar infarction were not significantly different from those for cases of nonlacunar infarction. Hypertension was found in 81% of patients who had a lacunar infarct and in 70% of patients who had a nonlacunar infarct (p = 0.05). A potential cardiac source of embolism was found in 12% of patients who had a lacunar infarct and in 28% of patients who had a nonlacunar infarct (p = 0.002). Survival was significantly better after a lacunar infarct than after a nonlacunar infarct. CONCLUSIONS: Small, deep cerebral infarcts had many of the epidemiological characteristics of other cerebral infarcts but there was a slightly higher frequency of hypertension, significantly lower frequency of a cardiac embolic source, and significantly better survival in patients with lacunar infarction than in those with nonlacunar infarction.     

Silent MRI infarcts and the risk of future stroke: the cardiovascular health study

BACKGROUND: Silent infarcts are commonly discovered on cranial MRI in the elderly. OBJECTIVE: To examine the association between risk of stroke and presence of silent infarcts, alone and in combination with other stroke risk factors. METHODS: Participants (3,324) in the Cardiovascular Health Study (CHS) without a history of stroke underwent cranial MRI scans between 1992 and 1994. Silent infarcts were defined as focal lesions greater than 3 mm that were hyperintense on T2 images and, if subcortical, hypointense on T1 images. Incident strokes were identified and classified over an average follow-up of 4 years. The authors evaluated the risk of subsequent symptomatic stroke and how it was modified by other potential stroke risk factors among those with silent infarcts. RESULTS: Approximately 28% of CHS participants had evidence of silent infarcts (n = 923). The incidence of stroke was 18.7 per 1,000 person-years in those with silent infarcts (n = 67) compared with 9.5 per 1,000 person-years in the absence of silent infarcts. The adjusted relative risk of incident stroke increased with multiple (more than one) silent infarcts (hazard ratio 1.9 [1.2 to 2.8]). Higher values of diastolic and systolic blood pressure, common and internal carotid wall thickness, and the presence of atrial fibrillation were associated with an increased risk of strokes in those with silent infarcts (n = 53 strokes). CONCLUSION: The presence of silent cerebral infarcts on MRI is an independent predictor of the risk of symptomatic stroke over a 4-year follow- up in older individuals without a clinical history of stroke.     

Wisconsin card sorting test as a measure of frontal pathology: A review

We reviewed studies of the Wisconsin Card Sorting Test (WCST) in which the test was administered to subjects with and without evidence of focal frontal-lobe dysfunction. This review indicated that few studies had investigated the differential performance of normals and those with frontal dysfunction. The evidence that frontal patients perform more poorly than nonfrontal patients is weak. There is insubstantial evidence to conclude that the WCST is a measure of dorsolateral-frontal dysfunction. The clinical utility of the test as a measure of frontal-lobe dysfunction is not supported nor is the use of the test as a marker of frontal dysfunction for research purposes.     

Hyperhomocysteinemia is associated with volumetric white matter change in patients with small vessel disease

Background Hyperhomocysteinemia is associated with cerebral small vessel disease (SVD). We examined the relationship between homocysteine and 1) volumetric measure of white matter change (WMC), 2) silent brain infarcts, 3) cerebral atrophy on MRI and 4) cognition on a consecutive cohort of patients with stroke associated with SVD. Subjects and methods Fifty–seven patients consecutively admitted to the Acute Stroke Unit in a university hospital due to stroke associated with SVD were recruited and assessed three months after the stroke. Non–fasting homocysteine was obtained. Using MRI, the number of infarcts, volume of WMC and cerebral atrophy were measured. General cognitive functions were assessed using the Mini Mental State Examination and Alzheimer's disease Assessment Scale. Mattis Dementia Rating Scale – Initiation/Perseveration subset was used to assess executive cognitive functions. Results Hyperhomocysteinemia (≥ 14.88 μmol/L) significantly accounted for the volume of WMC on MRI in a multivariate stepwise regression model (adjusted R²=0.058, p <0.05) after adjustment for age and folate level. Patients in the highest quartile of WMC volume had significantly higher levels of homocysteine than those in lowest quartile (p <0.001). No significant relationship was found between homocysteine and silent brain infarcts, cerebral atrophy and performance on psychometric tests. Conclusion Hyperhomocysteinemia is associated with volumetric measure of WMC among patients with SVD. The role of homocysteine in the development of silent brain infarcts and cerebral atrophy as previously reported cannot be ascertained in this study. No direct relationship was found between homocysteine and cognitive functions. This study was supported by the Neurology research fund of Division of Neurology, Department of Medicine and Therapeutics, Chinese University of Hong Kong.     

Cognitive impairment and functional outcome after stroke associated with small vessel disease

OBJECTIVES: Although stroke associated with small vessel disease (SSVD) can induce both motor and cognitive impairment, the latter has received less attention. We aimed to evaluate the frequency of the varying severity levels of cognitive impairment, the determinants of severe cognitive impairment, and the association of cognitive impairment with functional outcome after SSVD. METHODS: Consecutive patients admitted to hospital because of SSVD were assessed at 3 months after stroke. We performed a semi-structured clinical interview to screen for cognitive symptoms. Severity of cognitive symptoms was graded according to the Clinical Dementia Rating Scale (CDR). Performance on psychometric tests (Mini-Mental State Examination, Alzheimer's Disease Assessment Scale (cognition subscale), Mattis Dementia Rating Scale (initiation/perseverence subscale; MDRS I/P)) of patients of different CDR gradings was compared with that of 42 healthy controls. Basic demographic data, vascular risk factors, stroke severity (National Institute of Health Stroke Scale; NIHSS), pre-stroke cognitive decline (Informant Questionnaire on Cognitive Decline in the Elderly; IQCODE), functional outcome (Barthel index; BI), Instrumental Activities Of Daily Living; IADL), and neuroimaging features (site of recent small infarcts, number of silent small infarcts, white matter changes) were also compared among the groups. Regression analyses were performed to find predictors of severe cognitive impairment and poor functional outcome. RESULTS: Among the 75 included patients, 39 (52%) complained of cognitive symptoms. The number of patients in each CDR grading was as follows: 39 (52%) had a CDR of 0, 26 (34.7%) had a CDR of 0.5, 10 (13.3%) had a CDR of > or =1. Pre-stroke IQCODE and previous stroke predicted CDR> or =1. The NIHSS was associated with more impaired BI. The NIHSS and MDRS I/P contributed most to impaired IADL. CONCLUSIONS: Half of the patients with SSVD complained of varying severity of cognitive problems 3 months after stroke. Pre-stroke cognitive decline and previous stroke predict severe cognitive impairment post stroke. Stroke severity and executive dysfunction contribute most to a poor functional outcome.     

Raised plasma oxidised LDL in acute cerebral infarction

BACKGROUND: The association between oxidised low density lipoprotein (OxLDL) and cerebral infarction is suspected but not established. OBJECTIVES: To determine whether plasma OxLDL is a useful marker for monitoring oxidative stress in stroke patients. METHODS: Plasma OxLDL concentrations were determined in 56 stroke patients with cerebral infarction (n = 45) or cerebral haemorrhage (n = 11), and in 19 age matched controls, using a novel sandwich enzyme linked immunosorbent assay. RESULTS: Compared with the controls (0.130 (0.007) ng/ micro g LDL, mean (SEM)), OxLDL was significantly raised in patients with cerebral infarction (0.245 (0.022); p < 0.0001) but not in those with haemorrhage (0.179 (0.023)). Patients with cortical ischaemic infarcts (n = 22) had higher OxLDL levels than either the controls (p < 0.0001) or the patients with non-cortical ischaemic infarcts (n = 23) (p < 0.001). Increased OxLDL concentrations in patients with cortical infarcts persisted until the third day after stroke onset. The National Institutes of Health stroke scales in patients with cortical infarction were higher than in those with non-cortical infarction (p < 0.01). CONCLUSIONS: There is a significant association between raised plasma OxLDL and acute cerebral infarction, especially cortical infarction. Plasma OxLDL may reflect oxidative stress in stroke patients.     

Neuropsychological abnormalities associated with lacunar infarction

The objective of this study was to assess neuropsychological abnormalities in 40 patients with lacunar infarction. Topography of infarction, presence of isolated or multiple silent infarcts and white matter hyperintensities were correlated with results of neuropsychological tests and subtypes of lacunar infarction. Patients were studied within 1 month after stroke. A total of 21 patients were males and the mean age was 70.7 years; 30% had a single infarction (mean number of infarctions was 3.4). Twelve patients had pure motor hemiparesis, 9 pure sensory stroke, 8 dysarthria-clumsy hand/ataxic hemiparesis, 8 atypical lacunar syndrome, and 3 sensorimotor stroke. The mean score of the Mini-Mental State Examination was 28.4. Mild cognitive impairment of subcortical vascular features occurred in 23 patients and isolated executive disturbances in 4. Neuropsychological results showed that patients with atypical lacunar syndrome followed by pure motor hemiparesis showed significantly more cognitive executive disturbances. Patients with dysarthria-clumsy hand/ataxic hemiparesis accounted for the best scores in some tests of visuoconstructive function and visual memory. In summary, mild neuropsychological disturbances (57.5%) are not infrequent in acute lacunar infarcts especially in patients with atypical lacunar syndrome and pure motor hemiparesis. Neuropsychological impairment should be considered as common clinical feature in acute lacunar infarction.     

The impact of magnetic resonance imaging on the management of acute ischemic stroke.

Despite rapid advances in imaging technology, the etiology of stroke remains unestablished in 40% of patients. MRI improves localization in acute stroke. However, it is not known whether "accurate localization" results in better management. We reviewed the hospital records of all patients admitted with a diagnosis of acute ischemic stroke and who had had cranial CTs and MRI within 10 days of admission. Between January 1987 and June 1990, 116 patients (69 men, 47 women; mean age, 66 years) were identified. Compared with CT localization, infarcts were better localized in nine of 39 patients with cerebral cortical lesions, in 20 of 22 patients with brainstem and cerebellar lesions, and in three of three patients with isolated cerebellar lesions. In 22 patients (18.9%), MRI showed multiple infarcts in two or more vascular territories, suggesting embolic disease and leading to anticoagulation. MRI also showed arterial occlusions in 11 patients (9.5%). Based on the information obtained with MRI, the clinical diagnosis was changed in 19 patients (16.3%), resulting in changes in the management of most of those patients. Thus, we confirm earlier reports that MRI improves localization after acute cerebral infarction and show that such information alters patient management.     

Neuropsychologic outcomes in a case series of twins discordant for perinatal stroke

Perinatal stroke may affect cognitive development, but few studies have addressed the details of cognitive function after perinatal stroke. The present study was designed to compare the neuropsychologic features of five sets of twins discordant for perinatal stroke. All of the affected children had unilateral middle cerebral artery infarction (two left, three right); four of the five infarcts were large-branch, affecting the entire M1 territory. Three of the five affected children had comorbid epilepsy. Measures of intelligence, memory, language, attention, executive function, visual-motor integration, and fine motor skills were administered to children at a median age of 5 years (range, 5-8 years). Relative to their unaffected co-twins, the twins with perinatal stroke exhibited lower levels of full scale (p=0.005), verbal (p=0.006), and nonverbal (p=0.005) intelligence. Children with perinatal stroke also showed significant deficits on tests of verbal memory (p=0.041), receptive language (p=0.011), verbal fluency (p=0.019), and visual attention (p=0.011), compared with their unaffected co-twins. Twin gestation may be a risk factor for poor cognitive outcome after perinatal stroke. Large infarct size and comorbid epilepsy may have contributed to some of the poor cognitive outcomes in this cohort.