Neuropsychological changes related to unilateral lenticulostriate infarcts.

According to previous studies, focal capsulostriatal lesions may produce aphasia, hemineglect, gestural apraxia, frontal lobe dysfunction, and memory impairment. A few reports of capsulostriate infarcts secondary to involvement of lenticulostriate arteries have confirmed that aphasia and hemineglect may occur whereas gestural apraxia, anosognosia and frontal-lobe symptoms are rare. Most studies used CT scan assessment and did not exclude possible associated lesions. Neuropsychological changes in 11 patients with lenticulostriate infarcts diagnosed by CT scan were prospectively investigated. MRI in five of the 11 patients showed an associated cortical lesion not seen on CT scan. Patients with pure lenticulostriate infarcts on MRI may exhibit aphasia of mild severity whereas Broca's aphasia, hemineglect, gestural apraxia, and anosognosia were only seen in the subgroup with associated cortical lesions. Aphasia in patients with pure lenticulostriate infarcts was characterised by prominent expressive and lexicosemantic task impairments. The results strongly suggest that cortical involvement is critical to the extent and severity of neuropsychological changes in patients with lenticulostriate infarcts.     

Should computed tomography appearance of lacunar stroke influence patient management?

Patients with a lacunar stroke syndrome may have cortical infarcts on brain imaging rather than lacunar infarcts, and patients with the clinical features of a small cortical stroke (partial anterior circulation syndrome, PACS) may have lacunar infarcts on imaging. The aim was to compare risk factors and outcome in lacunar syndrome (LACS) with cortical infarct, LACS with lacunar infarct, PACS with cortical infarct, and PACS with lacunar infarct to determine whether the clinical syndrome should be modified according to brain imaging. As part of a hospital stroke registry, patients with first ever stroke from 1990 to 1998 were assessed by a stroke physician who assigned a clinical classification using clinical features only. A neuroradiologist classified recent clinically relevant infarcts on brain imaging as cortical, posterior cerebral artery territory or lacunar. Of 1772 first ever strokes, there were 637 patients with PACS and 377 patients with LACS who had CT or MRI. Recent infarcts were seen in 395 PACS and 180 LACS. Atrial fibrillation was more common in PACS with cortical than lacunar infarcts (OR 2.3, 95% confidence interval (95% CI) 0.9-5.5), and in LACS with cortical than lacunar infarcts (OR 3.9, 1.2-12). Severe ipsilateral carotid stenosis or occlusion was more common in PACS with cortical than lacunar infarcts (OR 3.5, 1.3-9.5); and in LACS with cortical than lacunar infarcts (OR 3.7, 1.1-12). In conclusion, patients with cortical infarcts are more likely to have severe ipsilateral carotid stenosis or atrial fibrillation than those with lacunar infarcts irrespective of the presenting clinical syndrome. Brain imaging should modify the clinical classification and influence patient investigation.     

Effects of cerebral cortical lesions on the ipsilateral thalamus

An injury to the central nervous system causes a focal logical disturbance, and further may affect the blood flow, metabolism, and function of other brain regions. Recent studies using PET or SPECT have demonstrated that impairment of regional hemodynamics or metabolism in cerebrovascular disease involves not only the site of the lesion itself but also more remote areas. Although depression of the metabolism of the ipsilateral thalamus in patients with cerebral cortical lesions has been shown by PET study, the pathophysiological implications of this remain unclear. The functional and morphological effects of cortical infarcts on the ipsilateral thalamus were studied by assessment of cerebral blood flow using 123I-IMP SPECT and by determining atrophic changes on CT or MRI. Nine out of 17 patients with cortical infarcts showed hypoperfusion of the ipsilateral thalamus, especially patients with larger infarcts involving the frontal or parietal cortex. Thalamic hypoperfusion persisted from early after the insult to several months or even years later. In addition, atrophy of the ipsilateral thalamus was not uncommon following larger cortical infarcts. This tended to be evident about 1 year after the infarct and progressed over several years. Furthermore, atrophic changes in the thalamus was often demonstrated in such patients as hypoperfusion in the later stages. Thus, cortical lesions had functional and morphological effects on the ipsilateral thalamus ranging from early hypoperfusion to later irreversible atrophic changes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sensorimotor stroke; clinical features, MRI findings, and cardiac and vascular concomitants in 32 patients

Background and purpose – Sensorimotor stroke (SMS) is often included among the lacunar syndromes, although the underlying cause of this stroke-subtype is less well documented. To this end we analysed 32 patients presenting with a sensorimotor syndrome. Methods – The study protocol included vascular risk factors, echocardiography, Doppler sonography of carotid arteries, CT scan and MRI of the brain. Results – There were 23 men and 9 women, mean age 65.7 years. Hypertension was present in 28% and diabetes in 19%. In all, 63% had sensorimotor deficit of faciobrachiocrural areas and 37% had faciobrachial or brachiocrural deficits. MRI disclosed a presumably relevant infarct in 26 patients (81 YO); 20 patients (62%) localized to the territory of small perforating arteries, 3 patients (9.5%) in the internal borderzone, and 3 patients (9.5%) in cortical territories. Eight of 20 deep infarcts were larger than 15 mm. No hemorrhage or non-vascular lesion was found. A potential cardioembolic source was present in 5 patients (l6%), whereas 2 patients (6%) had an ipsilateral carotid stenosis >50%. Conclusions – Small vessel disease was the most likely cause in 69% of our patients with SMS, whereas 31% had a potential cardioembolic source, large artery disease or infarcts not compatible with perforating artery disease.     

DWI对MCA狭窄患者卒中亚型的诊断

目的:评价弥散加权MRI(Diffusion-weighted imaging,DWl)对MCA狭窄患者急性梗死的诊断价值。方法:经TCD／MRA诊断的症状性大脑中动脉粥样硬化性狭窄(以下简称MCA闭塞性病变:middle cerebral artery occlesive disease MCAOD)患者,分别于病后1周内行头颅水抑制MRI成像(Fluid-attenuated inversion recovery,FLAIR)及DWI检查,比较FLAIR、DWI所示梗死灶的类型和数量。结果:238例症状性MCAOD患者的FLAIR结果表明,单发腑梗死137例(57.6％),多发性脑梗死101例(42.4％)。其中皮层区域内梗死82例(34.5％),深部小梗死120例(50.4％),变界区梗死143例(60.1％)。而内交界区梗死、半卵园中心梗死以及伴随的皮层小梗死的发生率分别为52.9％、22.7％、13.0％,84例MCAOD患者的DWl结果表明,73.8％患者呈多发性脑梗死表现,皮层区域内梗死、交界区梗死、深部小梗死的发生率分别为46.4％、56％和44.0％,而皮层播散性小梗死(22.6％)、半卵园中心梗死(29.1％)的诊断率高于FLAIR结果。结论:DWI对于微小梗死以及多发梗死的诊断明显优于FIAIR成像,尤其对于皮层播散性小梗死灶以及半卵园中心梗死的诊断更敏感,利于卒中亚型的诊断及卒中机制的判断。     

Mechanisms of single and multiple borderzone infarct: transcranial Doppler ultrasound/magnetic resonance imaging correlates

BACKGROUND AND PURPOSE: Hemodynamic patterns after borderzone (BZ) infarction are variable and dynamic. However, stroke mechanisms in different types of BZ infarctions have not been systematically studied by magnetic resonance angiography (MRA) and transcranial Doppler ultrasonography (TCD). METHODS: Forty-nine patients who experienced a stroke limited to the territory of either the superficial or internal borderzone proved on MRI included in our registry, corresponding to 4% of 1,200 patients with ischemic stroke, were studied. All these patients underwent MRA, extracranial Doppler ultrasonography, TCD and other investigations from the standard protocol of our registry. Twenty of them (41%) had a posterior BZ infarct, 14 (29%) an anterior BZ infarct, 10 (20%) a subcortical BZ infarct and 5 (10%) bilateral BZ infarcts. RESULTS: Unilateral internal carotid artery (ICA) tight stenosis or occlusion ipsilateral to the lesion was present in 14 patients (70%) with a posterior BZ infarct, in 72% of those with an anterior BZ infarct, in 80% of those with a subcortical BZ infarct and in 80% of those with bilateral BZ infarcts. TCD showed cross-filling of the middle cerebral artery via the anterior communicating artery in 5 patients (25%) with a posterior BZ infarct and 10% had an increased mean flow velocity (MFV) in the ipsilateral P1 posterior cerebral artery (PCA). In patients with an anterior BZ infarct, 3 (23%) had an MFV increase in the contralateral A1 anterior cerebral artery (ACA), and 2 (15%) had a higher MFV in the ipsilateral PCA. An elevated velocity at midline depths with reversed A1 ACA flow direction was seen in 2 patients (20%) with a subcortical infarct, and 1 patient (10%) had an MFV increase in the ipsilateral P1 PCA. Left ventricular systolic dysfunction (ejection fraction <40%) was present in 50% of patients with a posterior BZ infarct, in 36% of those with an anterior BZ infarct, in 20% of those with a subcortical BZ infarct and bilateral BZ infarcts each. CONCLUSION: The association of severe ICA stenosis or occlusion with cardiopathies and left ventricular dysfunction may play a critical role in those with BZ infarcts having inadequate collateral supply, while a cardioembolism or acute ICA dissection may also cause BZ infarction due to the rapidity of the occlusive process and the inability of the cerebral vasculature to recruit collateral pathways quickly enough.     

Carotid artery stenosis in ischemic stroke patients with nonvalvular atrial fibrillation.

PURPOSE: To study the prevalence, severity and clinical relevance of carotid atherosclerosis in ischemic stroke patients with nonvalvular atrial fibrillation (NVAF). MATERIAL AND METHODS: We reviewed carotid duplex sonography, computed tomography (CT) and clinical features in 103 consecutive ischemic stroke patients with NVAF. Both sonography and CT were performed within 3-7 days after stroke. There were 64 men and 39 women with a mean age at stroke onset of 69 years. RESULTS: High-grade (> or =50%) stenosis of the extracranial carotid artery was detected in 25 patients (24.3%), including 11 patients (10.6%) with internal carotid artery (ICA) occlusion. In 15 (66.7%) of the patients who had high-grade carotid stenosis, the lesion was ipsilateral to the infarct, including 8 ICA occlusions. Patients with high-grade stenosis smoked more cigarettes (p < 0.05) and had more peripheral vascular diseases (p < 0.05). Besides NVAF, all patients had more than one vascular risk factor. The clinical presentations (transient ischemic attacks, minor or major strokes) showed no significant difference between the groups of <50% and > or =50% stenosis. Clinical outcome was worse (dead and totally dependent in daily activities) in the group of high-grade stenosis (p < 0.05). Patients with high-grade carotid stenosis showed more cortical infarcts on cerebral CT (p < 0.01). Six out of 7 patients with a hemorrhagic transformation on the initial cerebral CT were in the low-grade carotid stenosis group, though this was statistically insignificant. CONCLUSIONS: Ischemic stroke with NVAF is not always cardiogenic. High-grade stenosis of the extracranial carotid artery is found in one fourth of ischemic stroke patients with NVAF and is related to more cortical infarction and worse clinical outcome. We speculate that ischemic stroke patients with NVAF who have high-grade carotid stenosis are less likely to develop hemorrhagic infarct. The pathogenesis of cerebral infarction and the therapeutic strategy in this clinical condition are complicated by the coexistence of carotid arterial lesions and cardiac disease.     

卵圆孔未闭相关缺血性卒中的临床和神经影像学特征分析

目的 探讨卵圆孔未闭（patent foramen ovale,PFO）相关缺血性卒中的临床和神经影像学特征,并 根据不同的PFO解剖特点,确定其缺血性病变类型是否存在差异。 方法 本研究为单中心回顾性研究,入选2015年5月-2019年9月在首都医科大学附属北京天坛医院 心血管内科连续住院接受PFO介入封堵治疗的缺血性卒中患者。所有患者均接受颅脑MRI检查,并通 过TCD确定右向左分流（right-to-left shunt,RLS）量,经食道超声检查确定PFO诊断及其解剖结构。总 结PFO相关缺血性卒中的影像学特征,并根据不同的PFO解剖特点,确定其缺血性病变类型是否存在 差异。 结果 共入组108例患者,平均年龄46±11岁,其中男性78例（72.2%）。PFO直径（静息状态）平 均1.5±1.1 mm,雨帘状RLS 75例（69.4%）,原发隔活瓣长度平均9.5±3.7 mm,长隧道型PFO 37例 （34.3%）,PFO伴过间隔血流76例（70.4%）。PFO相关缺血性卒中患者MRI显示梗死血管累及前循环42 例（38.9%）（单侧前循环29例+双侧前循环13例）,后循环39例（36.1%）,皮层梗死22例（20.4%）, 皮层下梗死7例（6.5%）,深部梗死 44例（40.7%）,皮层、皮层下梗死+深部梗死35例（32.4%）;单 一梗死31例（28.7%）,多发梗死77例（71.3%）。不同的RLS量、PFO大小之间比较,脑梗死分布、梗死 部位和梗死数量方面未发现影像学差异。长隧道组和非长隧道组的梗死部位（P =0.037）和梗死 数量（P =0.016）差异均有统计学意义,其中长隧道组更多见皮层梗死（35.1% vs 12.7%）和单一梗死 （43.2% vs 21.1%）。有过间隔血流组和无过间隔血流组在梗死分布上差异有统计学意义（P =0.014）, 有过间隔血流组后循环梗死发生率更高（43.4% vs 18.8%）。 结论 PFO相关缺血性卒中患者影像学上梗死血管累及前循环和后循环的比率相似,梗死部位以 深部梗死和多发梗死为主。长隧道型PFO与非长隧道型相比,皮层梗死和单一梗死更多见。伴有过 间隔血流的PFO多发生后循环梗死。     

The validity of a simple clinical classification of acute ischaemic stroke

The aim of the study reported here was to test the validity of a simple clinical classification of acute ischaemic stroke (Oxfordshire Community Stroke Project, OCSP) in predicting the site and size of cerebral infarction on computed tomography (CT). Consecutive patients admitted to hospital with acute ischaemic stroke were prospectively identified and classified into one of four clinical syndromes according to the OCSP classification, blind to the result of CT. The CT brain scans were classified blind to the clinical features into those demonstrating: small, medium or large cortical infarcts; small or large subcortical infarcts in the anterior circulation territory; and posterior cerebral circulation territory infarcts. A total of 108 patients were included. A recent infarct was seen. on the CT scan in 91 patients (84%), and the clinical classification correctly predicted the site and size of the cerebral infarct in 80 of these (88%; 95% confidence interval 77–92%). The positive predictive value was best for large cortical infarcts (0.94) and worst for small subcortical infarcts (0.63). The OCSP clinical classification is a reasonably valid way of predicting the site and size of cerebral infarction on CT and can, therefore, be used very early after stroke onset before the infarct appears on the scan.     

Hyperglycemia and cognitive outcome after ischemic stroke

BACKGROUND: Post-stroke hyperglycemia (HG) is associated with poor physical recovery, in particular in patients with cortical stroke. We tested whether HG is also associated with cognitive impairment after ischemic stroke. METHODS: We recruited patients from a prospective consecutive cohort with a first-ever supratentorial infarct. Neuropsychological examination included abstract reasoning, verbal memory, visual memory, visual perception and construction, language, and executive functioning. We related HG (glucose >7.0 mmol/L) to cognition and functional outcome (modified Barthel Index) at baseline and after 6-10 months, and to neurological deficit (National Institutes of Health Stroke Scale) and infarct size at baseline. In additional analyses cortical and subcortical infarcts were considered separately. RESULTS: Of 113 patients, 43 had HG (38%) and 55 had cortical infarcts (49%). Follow-up was obtained from 76 patients (68%). In the acute phase, in patients with cortical infarcts HG was associated with impaired executive function (B=-0.65; 95% confidence limits (CL): -1.3-0.00; p<0.05), larger lesion size (p<0.01), and more severe neurological deficits (p<0.01). These associations were not observed in patients with subcortical infarcts and the association between HG and cognitive functioning at follow-up was not significant in either group. CONCLUSIONS: In first-ever ischemic stroke, HG was not associated with impaired cognition after 6-10 months. In the acute phase of stroke HG was associated with impaired executive function, but only in patients with cortical infarcts.     

磁共振对颈内动脉狭窄与闭塞患者卒中解剖模式诊断价值的初步探讨

摘要】 目的 研究单侧动脉粥样硬化性颈内动脉狭窄与闭塞的急性缺血性卒中患者在磁共振上的病灶模式,探讨颈内动脉病变引起卒中的发病机制。 方法 利用数字减影脑血管造影定位动脉粥样硬化性颈内动脉重度狭窄（≥70%）或闭塞而无同侧大脑中动脉闭塞性病变。利用常规磁共振成像（magnetic resonance imaging,MRI）和液体衰减翻转恢复（fluid-attenuated inversion recovery,FLAIR）序列研究颈内动脉闭塞性病变引起缺血性卒中的形态学表现。有潜在心源性栓子患者除外。 结果 94例患者中,颈内动脉重度狭窄（≥70%）45例,颈内动脉闭塞49例。磁共振上缺血病灶的局部解剖模式分为4种：区域梗死、皮质下梗死、边缘带梗死、弥散小梗死。颈内动脉闭塞组中区域梗死的发生率较颈内动脉狭窄组高（47% vs 22%;P<0.05）;颈内动脉狭窄组中边缘带梗死的发生率较颈内动脉闭塞组高（42% vs 22%;P<0.05)。 结论 动脉粥样硬化性颈内动脉闭塞患者多见于区域梗死,而颈内动脉重度狭窄（≥70%）患者多见于边缘带梗死。     

Magnetic resonance imaging and laterobulbar infarction

Six patients with a clinical diagnosis of lateral medullary infarction have been studied by CT scan and Magnetic Resonance Imaging (MRI). The MRI study was performed on a CGR Magniscan 5000 with a superconducting magnet of 5 Tesla. In all patients T2 weighted images (TR = 2000, TE 60, 120) in joined section of 9 or 6 mm thickness were obtained in the axial plane. Three patients were also studied in T1 weighted sequences (TR = 500, TE = 28). A lateral medullary infarct was shown in 5 patients. MRI findings were consistent with a hemorrhagic infarct in one case. Occlusion of a vertebral artery was suggested in 2 cases and was confirmed by angiography. In 3 cases, an associated ipsilateral cerebellar infarct was demonstrated. The CT scan had only shown bleeding in the medulla oblongata in the hemorrhagic infarction case, and a cerebellar infarction in another case. Some clinical manifestations are discussed with regard to the results of MRI. MRI appears as the best current method to improve clinico-topographic correlations in medullary infarcts.     

Mechanisms involved in large subcortical infarcts]

Large subcortical infarcts(maximum diameter of infarct > or = 20 mm) result from various stroke patterns, including striatocapsular infarcts (SCI), corona radiata infarcts, centrum semiovale infarcts, and internal borderzone infarcts. A systematic investigation of stroke pathogenesis involved in large subcortical infarcts, however, has not been performed. This study attempted to clarify the stroke mechanisms involved in large subcortical infarcts, by examining 50 patients with large subcortical infarcts out of 430 ischemic stroke patients consecutively registered in our department. The subjects were divided into two groups according to the vascular territories involved on the MRI: 1) the lenticulostriate arteries group for 39 patients whose infarcts were restricted to within the vicinity of the lenticulostriate arteries; 2) the internal borderzone group for 11 patients whose infarcts mainly involved the internal borderzone (the upper part of the corona radiata and the centrum semiovale) between the territories of the deep perforating branches from the basal cerebral arteries and the medullary branches from the superficial pial arteries. Stroke pathogenesis were classified into the following 6 categories: A) cardiogenic embolism, 9 patients; B) artery-to-artery embolism, 6 patients; C) cryptogenic embolism, 2 patients; D) thrombotic MCA (M1) occlusion, 9 patients; E) thrombotic ICA occlusion, 10 patients; F) undetermined cause, 14 patients. The lenticulostriate arteries group consisted of 9 patients with cardiogenic embolism, 6 with artery-to-artery embolism, 2 with cryptogenic embolism, 8 with thrombotic M1 occlusion, and 14 with undetermined cause. The internal borderzone group consisted of 10 patients with thrombotic ICA occlusion and 1 patient with thrombotic M1 occlusion. The stroke pathogenesis of the undetermined cause is considered to be thrombotic occlusion at the orifice of the lateral lenticulostriate artery, a so-called "branch atheromatous disease (BAD)". The patients in this group experienced a gradual onset, and did not have a cardiac source of the embolism or proximal large artery disease. Among the patients reported as having SCI, BAD may play a role in some cases, especially in those whose the cause was classified as "undetermined". In conclusion, the lenticulostriate arteries group exhibited a higher frequency of cerebral embolisms (cardiogenic embolism, artery-to-artery embolism, and cryptogenic embolism) and thrombotic M1 occlusion, whereas the internal borderzone group had a higher frequency of thrombotic ICA occlusion.     

Transient ischemic attacks with and without a relevant infarct on computed tomographic scans cannot be distinguished clinically. Dutch Transient Ischemic Attack Study Group

We prospectively studied clinical and computed tomographic (CT) scan findings in 79 patients with a transient ischemic attack (TIA) and a relevant cerebral infarction on CT, also known as cerebral infarction with transient signs (CITS). We compared the results with those of 527 concurrent patients with TIA and without cerebral infarction and also with 646 patients with persistent neurological symptoms and a relevant infarct on CT. All patients were participating in a multicenter trial. In both groups, most infarcts were of the lacunar type. Compared with TIAs without cerebral infarction, patients with CITS slightly more often had a history of hypertension (52% vs 33%), the attacks lasted longer (greater than 1 hour, 52% vs 34%) and disappeared more slowly (over the course of hours, 39% vs 24%), and the symptoms more frequently involved speech (61% vs 41%). Despite these small differences, the reverse--the prediction of evidence on CT of infarction on the basis of the nature or time course of symptoms--proved impossible, since in each category the majority of patients had a normal CT scan. In comparison with patients with stroke and visible infarction, patients with CITS slightly more often had abnormal speech (61% vs 45%) and had a larger number of attacks (multiple attacks, 46% vs 18%). In conclusion, we found only minor clinical differences between patients with TIA with or without a relevant infarct on CT and equally small differences between patients with CITS and patients with stroke and cerebral infarction. These clinical similarities do not exclude a difference in prognosis.     

Computed tomographic changes of the brain and clinical outcome of patients with seizures and epilepsy after an ischaemic hemispheric stroke.

It is not well established whether seizures and epilepsy after an ischaemic stroke increase the disability of patients. Seventy-two patients with delayed seizures after a hemispheric infarct (37 with a single seizure and 35 with epilepsy) were included in the study. The modified Rankin scale was used to compare disability of the patients at 1 month after stroke and at 2 weeks after single or the last seizure, in case of epilepsy. The size of the X-ray hypoattenuation zone was compared on computed tomographic (CT) scans, performed in the weeks after the stroke and 1 week after single or repeated seizures. Lesion size was determined by superimposing the CT slices on digital cerebral vascular maps, on which the contours of the infarct area were delineated. The extent of the infarcts was expressed as the percentage fraction of the total surface area of the cerebral hemisphere. Groups with a single seizure and with epilepsy were mutually compared. Infarcts predominated in the parieto-temporal cortical regions. In the overall group the median Rankin score worsened significantly after seizures. The average size of the X-ray hypoattenuation zone was also significantly increased on the CT scans after the seizures, compared with those after stroke, without clear evidence of recent infarction. Mutual comparison of patients with a single seizure episode and of those with epilepsy showed only a trend of more severe disability and of increase in lesion size in the post-stroke epilepsy group. Delayed seizures and epilepsy after ischaemic stroke are accompanied by an increase in lesion size on CT and by worsening of the disability of the patients. This study does not allow to determine whether this is due to stroke recurrence or due to additional damage as a result of the seizures themselves.     

Prior antiplatelet use and infarct volume in ischemic stroke

BACKGROUND: Conflicting data exist on the role of antiplatelet agents in reducing incident ischemic stroke magnitude, but most prior studies used clinically-assessed neurologic deficit as the index of stroke extent rather than more precise volumetric measurements of infarct size. We assessed the relation of premorbid antiplatelet use to initial diffusion-weighted MRI (DWI) lesion volumes among acute ischemic stroke patients. METHODS: Consecutive patients presenting within 24 h of ischemic stroke over an 18-month period were studied. DWI lesions were outlined using a semi-automated threshold technique. Subjects were categorized into two groups: antiplatelet (AP) or no antithrombotic (NA). The relationship between prestroke antithrombotic status and DWI infarct volumes was examined using multivariate quantile regression. RESULTS: One hundred sixty-six individuals met study criteria: 75 AP and 91 NA patients. Median DWI volume was lower in the AP group than in the NA group (1.5 cc vs. 5.4 cc, p=0.031). A multivariable model (adjusting for age, history of transient ischemic attack, admission temperature, admission blood pressure, admission serum glucose, stroke onset to imaging interval, stroke mechanism, premorbid statin and antihypertensive use) demonstrated smaller infarcts in the AP vs. NA group (adjusted volume difference: -1.3 cc, 95% CI=-0.09, -2.5, p=0.037). Prior statin use, no history of TIA, large vessel atherosclerosis and microvascular ischemic disease stroke mechanism were also independently associated with reduced infarct volume. CONCLUSIONS: Prior antiplatelet treatment is independently associated with reduced cerebral infarct volume among acute ischemic stroke patients. Premorbid statin use, TIA history and stroke mechanism also predict infarct volume in ischemic stroke.     

Frontal lobe dysfunction in unilateral lenticulostriate infarcts. Prominent role of cortical lesions.

Most studies on frontal lobe dysfunction (FLD) in patients with striatal lesions did not consider possible associated cortical lesions not seen on computed tomographic scans. To determine the possible role of such cortical lesions, we assessed FLD in 10 patients with unilateral lenticulostriate infarct on computed tomographic scans. Magnetic resonance imaging revealed an associated cortical infarct not seen on computed tomographic scans in four patients. Using a battery of neuropsychological tests sensitive to FLD, we found that (1) the crossed tapping test was the only FLD test significantly disturbed in patients with pure unilateral lenticulostriate infarcts, (2) FLD was only present in patients with associated cortical infarct, and (3) caudate lesions only account for the number of echopraxic errors in the crossed tapping test. We conclude that unilateral isolated lenticulostriate infarcts might not lead to FLD, even though they may disturb the development of strategies involved in motor procedural learning.     

Topographic Patterns of Small Subcortical Infarcts Associated with MCA Stenosis: A Diffusion-Weighted MRI Study

BACKGROUND AND PURPOSE: Small subcortical infarcts (SSI, maximum lesion diameter < or =2.0 cm) are usually considered as infarcts caused by small vessel disease. However, SSI can also be associated with large artery occlusive disease such as middle cerebral artery (MCA) stenosis. We performed a prospective study to investigate the relationship between MCA stenosis and SSI distribution and further to investigate the mechanism of SSI caused by MCA stenosis. METHODS: Magnetic resonance angiography (MRA) and diffusion-weighed MRI (DWI) of consecutive acute ischemic stroke patients with recent SSI were studied. The distribution of acute infarcts on DWI was categorized as cortical infarct (CI), border zone infarct (BI), or perforating artery infarct (PAI). RESULTS: Totally, 93 cases were recruited, among which 12 had single SSI with MCA stenosis (group 1) and 26 patients had multiple SSI with MCA stenosis (group 2), while 55 patients without MCA stenosis had single SSI (group 3). For patients with single SSI and MCA stenosis, 6 had BI and 6 had PAI; for patients with multiple SSI and MCA stenosis, 25 had BI, 4 had PAI and 9 had CI (compared with group 1: P= .001); for patients with single SSI but without MCA stenosis, 20 had BI and 35 had PAI (compared with group 1: P= .58). CONCLUSION: Multiple acute infarcts along the border zone are the commonest pattern in small infarcts with MCA stenosis, especially among those with multiple acute infarcts. Our data suggest that hemodynamic compromise and artery-to-artery embolism may be both important factors for infarcts in patients with MCA stenosis.     

Combined diffusion and perfusion MRI with correlation to single-photon emission CT in acute ischemic stroke. Ischemic penumbra predicts infarct growth.

BACKGROUND AND PURPOSE: More effective imaging methods are needed to overcome the limitations of CT in the investigation of treatments for acute ischemic stroke. Diffusion-weighted MRI (DWI) is sensitive in detecting infarcted brain tissue, whereas perfusion-weighted MRI (PWI) can detect brain perfusion in the same imaging session. Combining these methods may help in identifying the ischemic penumbra, which is an important concept in the hemodynamics of acute stroke. The purpose of this study was to determine whether combined DWI and PWI in acute (<24 hours) ischemic stroke can predict infarct growth and final size. METHODS: Forty-six patients with acute ischemic stroke underwent DWI and PWI on days 1, 2, and 8. No patient received thrombolysis. Twenty-three patients underwent single-photon emission CT in the acute phase. Lesion volumes were measured from DWI, SPECT, and maps of relative cerebral blood flow calculated from PWI. RESULTS: The mean volume of infarcted tissue detected by DWI increased from 46.1 to 75.6 cm(3) between days 1 and 2 (P<0.001; n=46) and to 78.5 cm(3) after 1 week (P<0.001; n=42). The perfusion-diffusion mismatch correlated with infarct growth (r=0. 699, P<0.001). The volume of hypoperfusion on the initial PWI correlated with final infarct size (r=0.827, P<0.001). The hypoperfusion volumes detected by PWI and SPECT correlated significantly (r=0.824, P<0.001). CONCLUSIONS: Combined DWI and PWI can predict infarct enlargement in acute stroke. PWI can detect hypoperfused brain tissue in good agreement with SPECT in acute stroke.     

Epilepsy associated with lupus anticoagulant.

INTRODUCTION: Lupus anticoagulant (LA) is commonly present in patients with systemic lupus erythematosus (SLE) who present with an ischemic cerebral stroke. Reports have noted the presence of LA in patients with epilepsy who do not have SLE. These patients are usually elderly, and it has been postulated that their epilepsy is due to subclinical ischemic infarcts. METHODS: Two cases are presented in young patients (age < 35 years) who developed epileptic seizures and were LA positive. These patients did not have SLE or have cerebral infarcts that could explain the presence of their seizures.RESULTS: A 28-year-old woman was admitted for aortic insufficiency and new onset seizures. The clinical history, physical examination and magnetic resonance imaging did not reveal an antecedent cortical ischemic event. Serological testing revealed the presence of LA. The second patient was a 33-year-old man with medically intractable epilepsy in whom serological testing revealed the presence of LA. The clinical history, physical examination, and MRI did not reveal any evidence of an antecedent ischemic event. Neither patient had SLE. CONCLUSIONS: In young patients without SLE and cerebral infarcts, LA may be associated with epileptic seizures.