Balint's syndrome in a man with border-zone infarcts caused by atrial fibrillation

A 70-year-old man showed Balint's syndrome and other signs of bilateral posterior-hemisphere dysfunction of acute onset without initial unconsciousness. A computerized tomographic scan showed bilateral infarcts in the posterior arterial border-zone areas. Clinical evidence suggests that hypotension at the onset of atrial fibrillation caused these infarcts. There was a marked difference in the time course of recovery between the left and the right infarct which demonstrated that the elements of Balint's syndrome disappeared together with the left-hemisphere symptoms while the right-hemisphere symptoms were still present.     

内囊后肢梗死的临床特征及危险因素

目的探讨内囊后肢梗死患者的临床特征及危险因素。方法选择局限于内囊后肢的梗死患者94例,以同期年龄相近、性别相同94例未分类脑梗死患者为对照,比较两组危险因素分布的差异。并进一步对内囊后肢梗死患者亚组的危险因素进行比较,即进展性运动障碍组与非进展性组以及白质疏松与无白质疏松组、有多发腔隙性脑梗死(LI)组与无多发LI组的危险因素分布。结果内囊后肢梗死组患者的高血压患病率、吸烟率、高同型半胱氨酸血症(Hhcy)率较未分类脑梗死组高(P0.05)。进展性运动障碍组与非进展组的危险因素比较,无显著差异(P0.05)。结论内囊后肢梗死大多数为穿支动脉病变所致,高血压、吸烟、Hhcy是内囊后肢梗死的主要危险因素。内囊后肢梗死容易发生进展性运动功能障碍及预警综合征,其病理机制与内囊后肢固有的穿支动脉病变以及运动纤维分布特征有关。     

多灶性后循环缺血患者的病灶分布与血管形态异常及近期预后分析

目的 观察多灶性后循环缺血患者的病灶分布和血管形态异常的特点,评估患者出院时的近期预后及其与病灶分布和血管形态的关系.方法 对34例经过MR/所证实的多灶性后循环缺血患者行主动脉弓及全脑血管DSA,全面分析病灶分布及血管形态异常的特点;同时对患者出院时的近期预后用改良Rankin分级(MRS)评分表进行评估,分析病灶分布及血管形态异常与近期预后的关系.结果 多灶性后循环缺血患者最常被累及的部位是脑桥(22例),最常被累及的区段是中段+远段(12例);34例患者中有26例(76.5%)DSA显示出血管形态异常,最常被累及的动脉是椎动脉起始段(14例)和颅内段(13例)及基底动脉(7例);出院时7例患者(20.6%)存在预后不良,其中6例(17.6%)为重度残疾,1例(2.9%)死亡.近中远段同时受累和基底动脉受累的患者表现出预后不良.结论 血管形态异常是多灶性后循环缺血的重要病理基础和致病因素,病灶区段的分布和数目及血管受累部位是决定预后的关键因素.     

Spectrum of superficial posterior cerebral artery territory infarcts

Posterior cerebral artery (PCA) territory infarction is not uncommon. Published series were concentrated either on isolated deep PCA territory infarcts or on incomplete calcarine artery territory infarcts. Although, correlations between clinical symptoms, causes of stroke and outcome at 6-months in patients with superficial PCA territory stroke are less well known. We sought prospectively stroke causes, infarct topography, and clinical findings of 137 patients with superficial PCA territory infarcts with or without mesencephalic/thalamic involvement, representing 11% of patients with posterior circulation ischemic stroke in our Stroke Registry. We analyzed patients by subdividing into three subgroups; (1). cortical infarct (CI) group; (2). cortical and deep infarcts (CDI) (thalamic and/or mesencephalic involvement) group; (3). bilateral infarcts (BI) group. We studied the outcomes of patients at 6-month regarding clinical findings, risk factors and vascular mechanisms by means of comprehensive vascular and cardiac studies. Seventy-one patients (52%) had cortical (CI) PCA infarct, 52 patients (38%) had CDI, and 14 patients (10%) had bilateral PCA infarct (BI). In the CDI group, unilateral thalamus was involved in 38 patients (73%) and unilateral mesencephalic involvement was present in 27% of patients. The presumed causes of infarction were intrinsic PCA disease in 33 patients (26%), proximal large-artery disease (PLAD) in 33 (24%), cardioembolism in 23 (17%), co-existence of PLAD and cardioembolism in 7 (5%), vertebral or basilar artery dissection in 8 (6%), and coagulopathy in 2. The death rate was 7% in our series and stroke recurrence was 16% during 6-month follow-up period. Features of the stroke that was associated with significant increased risk of poor outcome included, consciousness disturbances at stroke onset (RR, 66.6; 95% CI, 8.6-515.5), mesencephalic and/or thalamic involvement (RR, 3.79; 95% CI, 1.49-9.65), PLAD (RR, 2.71; 95% CI, 1.09-6.73), and basilar artery disease (RR, 5.94; 95% CI, 1.73-20.47). The infarct mechanisms in three different types of superficial PCA territory stroke were quite similar, but cardioembolism was found more frequent in those with cortical PCA territory infarction. Although, the cause of stroke could not reliably dictate the infarct topography and clinical features. Visual field defect was the main clinical symptom in all groups, but sensorial, motor and neuropsychological deficits occurred mostly in those with CDI. Outcome is good in general, although patients having PLAD and basilar artery disease had more risk of stroke recurrence and poor outcome rather than those with intrinsic PCA disease.     

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.     

Multiple acute infarcts in the posterior circulation.

OBJECTIVE--to evaluate clinical, radiological, and prognostic features of patients with multiple acute infarcts in remote arterial territories of the posterior circulation. DESIGN--Data analysis from a prospective acute stroke registry in a community based primary care centre using a standard protocol including MRI and MRA. RESULTS--In three and a half years, 27 of the 236 patients (11%) with posterior circulation stroke had multiple acute infarcts in the posterior circulation as shown by gadolinium enhancement on MRI. Eighteen patients had multiple infratentorial and supratentorial infarcts including the cerebellum and posterior cerebral artery territory, with coexisting brainstem involvement in seven patients. Fourteen patients had a rostral basilar artery syndrome and cerebellar signs; four patients had a visual field defect with cerebellar signs. Causes were vertebral (six) or basilar (four) artery atheromatosis, and cardioembolism (four). Seven patients had multiple acute infarcts in the posterior circulation of the cerebellum and lower brainstem. Brainstem and cerebellar signs were found in most patients (five); aetiologies were small vessel disease (four), cardioembolism (one), and vertebral artery dissection (one). Two patients with large artery atheromatosis had multiple acute infarcts in the posterior circulation in the brainstem and posterior cerebral artery territory. One month after stroke more than 25% of the patients were dependent or had died. There was no difference in the outcome between the three groups, and recovery was linked to the size of infarcts rather than to a high number of infarcts. CONCLUSIONS--multiple acute infarcts in the posterior circulation usually involve the cerebellum. Simultaneous brainstem and posterior cerebral artery territory infarcts sparing the cerebellum are uncommon. They can be suspected clinically before neuroimaging, mainly when supratentorial and infratentorial infarcts coexist. This may be important, because different patterns of infarction are associated with different causes of stroke.     

Large striatocapsular infarcts: Clinical features and risk factors

We defined large striatocapsular infarcts as subcortical softenings of more than 20 mm in diameter involving the territories of the lateral and medial groups of lenticulostriate arteries. The aim of this study of 56 patients was to compare the clinical features and risk factors of these infarcts with those of cortical and lacunar infarcts. On the whole, our data suggest that both the clinical features and risk factors of large striatocapsular infarcts are similar to those of cortical infarcts, but significantly different from those of lacunar infarcts. The clinical manifestations of large striatocapsular infarcts with a maximum diameter of less than 50 mm may sometimes resemble those of lacunar infarcts because neuropsychological disorders are less frequent; however, our study indicates that, even in these cases, cardioembolic sources and artery-to-arteiy embolism are significantly more frequent in large striatocapsular than in lacunar infarcts, thus suggesting a different pathogenesis.     

Transesophageal echocardiographic findings in patients with anterior and posterior circulation infarcts

Objectives - The aim of this study was to assess the role of transesophageal echocardiography in detecting the source of cerebral embolism in ischemic stroke patients and to evaluate the difference in occurrence of heart abnormalities in anterior and posterior circulation infarcts. Material and Methods - The study group included 104 patients, 51 males and 53 females with ischemic stroke without significant atherosclerosis in the carotid arteries. Age of the patients ranged from 14 to 82 years (mean 55). The clinical picture of stroke suggested the embolic etiology, 34 of them had atrial fibrillation. Transthoracic and transesophageal echocardiography were performed in all patients. All patients were separated as anterior or posterior circulation infarcts. The control group consisted of 100 patients aged from 14 to 73 years (mean 53) without stroke history. Results - Transesophageal echocardiography (TEE) examination revealed left atrial thrombus in 12%, left atrial spontaneous contrast in 16%, interatrial communication in 31%, mitral valve prolapse in 20%, atrial septal aneurysm in 14%, ventricular thrombus in 6% and aortic atheromas of 5 mm or more in size in 7% of stroke patients. In the control group left atrial spontaneous contrast was found in 10%, interatrial communication in 17%, mitral valve prolapse in 4%, atrial septal aneurysm in 8%, neither atrial nor ventricular thrombi were found. At least one abnormal TEE finding was present in 70 (67%) of stroke patients. Abnormal TEE findings were more often seen in patients with anterior circulation infarct than in those with posterior circulation infarcts, although the difference was not statistically significant. Left atrial thrombus and mitral valve prolapse occurred statistically significantly more often in stroke patients than in the control group. Conclusions - Echocardiographic examination is often abnormal in patients with ischemic stroke. The study did not reveal the statistically significant difference in the prevalence of abnormal transesophageal echocardiography findings between patients with anterior and posterior circulation infarcts.     

Large striatocapsular infarcts: clinical presentation and pathogenesis in comparison with lacunar and cortical infarcts

In a well-defined prospective series of 247 patients with a first-ever supratentorial brain infarct, 15 patients (6%; 95% confidence interval 3-9%) had a large striatocapsular infarct. Twelve (80%) had signs of cortical dysfunction, whereas risk factor profile, frequency of significant carotid stenosis, and frequency of potential cardioembolic sources did not differ between patients with striatocapsular and those with cortical infarction. However, patients with striatocapsular infarction more frequently had potential cardioembolic source and significant carotid stenosis than patients with lacunar infarction. Our findings show that large striatocapsular infarcts differ from lacunar infarcts with regard to both presenting signs and symptoms, and pathogenesis, whereas they resemble infarcts involving the cortex. Such patients should therefore be managed and treated as patients with cortical infarction.     

Mitochondrial myopathy and cardiomyopathy with neurodegenerative features and multiple brain infarcts

We report a case of ragged-red fiber myopathy with abnormal mitochondria also present in the heart. Neither diffuse spongiosis nor abnormal mitochondria could be found in the CNS, but there were multiple areas of infarction in the brain, without vascular pathology. These infarcts appeared to be due to the cardiomyopathy, either from cardiac failure or embolism. This case may be included in the group of Kearns-Sayre syndrome or represent a new variant among mitochondrial myopathies.     

Clinical features, topographic patterns on DWI and etiology of thalamic infarcts

Thalamic infarcts may lead to diverse neurological disturbances, which easily results in misdiagnosis. Diffusion-weighed magnetic resonance imaging (DWI) is sensitive for the early diagnosis of the infarct and identification of the territory involved. The aim of this study was to analyze the clinical features, topographic appearance on DWI and etiology of thalamic infarcts. We reviewed clinical data, vascular risk factors, topographic patterns and etiology of thalamic infarcts. The patients were divided into 2 groups according to DWI patterns: isolated thalamic infarcts (ISO-TH) and combined thalamic infarcts (COM-TH). The former were further subdivided into 2 subgroups: inferolateral isolated thalamic infarcts (INF-TH) and non-inferolateral isolated thalamic infarcts (NON-INF) according to the vascular territories. The Patients were also divided according to etiology based on TOAST classification. The association of clinical features, DWI patterns and etiology was analyzed. Twenty nine patients were included, among which, 23 (79.3%) were ISO-TH and 6 (20.7%) were COM-TH. The most common territory involved in the ISO-TH was inferolateral territory [n=17 (73.9%)], followed by tuberothalamic artery territory [n=3 (13.0%)], and posterior choroidal artery territory [n=2 (8.7%)]. In COM-TH, the most common territory also was the inferolateral territory (n=3), followed by posterior choroidal artery territory (n=1). In 2 patients, the lesions involved more than one vascular thalamic territory. Significant association between small-vessel occlusion (SVO) and ISO-TH (INF-TH+NON-IFN) infarcts were found. Our study suggested that SVO was more prevalent in ISO-TH, and COM-TH needed more etiological examination. DWI might provide meaningful clues about etiology of thalamic infarcts.