58例进展性卒中影响因素分析

目的分析进展性卒中的影响因素。方法回顾性分析58例进展性卒中的影响因素，与同期住院病情无进展的58例脑梗死患者比较。结果58例进展性卒中组并发感染、高血压、高血糖、神经功能缺损评分均明显高于对照组。其影像学显示病灶较早，DSA检查提示其更多为大血管狭窄或闭塞。结论进展性卒中是多种因素多种机制共同作用的结果，早期预测和采取积极治疗措施，可以提高疗效。     

垂体瘤卒中3例误诊临床分析

垂体瘤卒中３例误诊临床分析杨力辉程永杰我们曾遇３例垂体瘤误诊，今报告如下。１临床资料例１，男，５８岁，１９９５年１０月５日入院。３天前夜间突然头顶部钻痛伴呕吐数次，次日左眼失明，门诊以“痛性眼肌麻痹”收入院。有高血压和冠心病史１５年。多饮多食１个月。...     

偏头痛性中风

偏头痛性中风病人３例均为女性，年龄为３５～４２岁，其中枕叶梗塞２例，大脑中动脉分布区梗塞１例。并结合文献，对偏头痛性中风的定义、中风类型、病灶分布与大小、预后、预防与治疗及发病机制进行了阐述     

自发性脑脊液鼻漏6例报告

我院１９９０年以来收治的自发性脑脊液鼻漏６例,现报告如下。ｌ 资料１．１ 一般资料：男３例,女３例。年龄１２－５８岁,平均年龄３９．７岁。所有病例均无外伤史。入院前脑脊液鼻漏持续１周至２个月。头痛者３例,视力视野改变者３例,嗅觉丧失者２例。１．２ 影像学检查：Ｘ线颅骨平片检查４例,３例存在鞍区骨质改变。ＣＴ检查６例,发现鞍区占位２例,空蝶鞍１例,颅内积气３例。ＭＲ检查４例,发现鞍区占位２例,空蝶鞍２例,颅内积气２例。ＣＴ脑池造影检查４例,３例明确漏口部位,其中１例可见造影剂通过漏口;另１例未能明确…     

偏头痛性中风（附3例报告及文献复习）

偏头痛性中风病人３例均为女性，年龄为３５～４２岁，其中枕叶梗塞２例，大脑中动脉分布区梗塞１例，并结合文献，对偏头痛性中风的定义，中风类型，病灶分布与大小，预后，预防与治疗及发病机制进行了阐述。     

腔隙性脑梗塞的MRI与临床

观察２２１例经头颅ＭＲＩ确诊为脑梗塞资料，１５７例为腔隙性梗塞，〈６０岁者发病率为２３．６％，≥６０岁者为７６．４％，其中８６．６％的患者伴有明确的中枢神经系统症状，１３．４％神经系统检查无异常，腔隙梗塞以基底节区最多见的６１．８％，脑叶１５．９％，侧脑室体旁放射冠，半卵圆中心１１．５％，丘脑５．１％，脑干及小脑分别为２．５％和３．２％，病灶部位分布及临床体征，对腔隙性脑梗塞的早期诊断，治疗及预后     

进展性卒中的相关因素研究

目的 :寻找引起进展性卒中的危险因素。方法 :回顾性分析了 5 8例进展性卒中患者 ,对其血压、血糖、血脂水平、病情严重程度以及有无血管狭窄等情况进行了相关分析研究。结果 :15 8例进展性卒中患者伴高血压(Hypertension,HT)者 46例 ,其中 18例收缩压低于 15 0 mm Hg,13例脉压差小于 30 mm Hg,明显高于对照组 (P <0 .0 0 1)。 2 31例合并有糖尿病 (Diabetes Millium,DM) ,对照组仅仅 18例 ,两组比较差异显著 (P <0 .0 0 0 1)。 32 1例 SIP患者行 TCD或 /和 MRA检查者 14例显示有不同程度的颅内外血管狭窄 ,这部分患者脉压差下降以及由此导致的低灌流与进展性卒中有关。其中 12例 MD患者行 MRA或 TCD检查 ,均发现有小血管显影不良或狭窄 ,6例有大血管病变。 4影像学检查显示分水岭梗塞或顶深部侧脑室体旁梗塞多提示大血管病变 ,尤其是 MCA起始部或主干支狭窄 ,常预示进展性卒中的可能。结论 :进展性卒中的危险因素多与高血压 ,糖尿病以及是否并发颅内外大血管狭窄或闭塞有关。而患者的收缩压下降、脉压差小也易引起 SIP。SIP患者影像学上的特殊表现常提示此类患者侧枝循环建立不完善 ,故在抗凝治疗的同时 ,一定要保证充足的脑灌注压 ,切记不要过分降低血压 ,尤其疑为大血管病变者。     

卒中后癫痫的临床与机理探讨（附148例报告）

对１４８例卒中后癫痫的临床及发病机理与卒中类型进行分析研究，结果为卒中后癫痫的发生率为６．４％，早期癫痫发作４．３％，迟发性癫痫２．１％。卒中后癫痫的发生率与病灶部位（皮质／皮质下）有明显的相关性（Ｐ＜０．０１），与卒中类型无明显差异（Ｐ＞０．０５）。脑水肿是早期癫痫发作的重要致痫因素，迟发性癫痫可因胶质疤痕形成癫痫灶所致。     

脑桥被盖腔隙梗塞的临床与MRI

报道２０例脑桥被盖腔隙性梗塞患者的临床和ＭＲＩ改变。临床表现为感觉性卒中（ＳＳ）６例、共济失调轻偏瘫（ＡＨ）５例、纳吃－手笨拙综合征（ＤＡ－Ｃｈ）６例和无定位体征的脑桥被盖腔梗１例。ＭＲＩ发现ＳＳ患者的病灶均位于脑桥被盖外侧，ＤＡ－Ｃｈ和ＡＨ患者的病灶则位于脑桥近中线区，ＡＨ的病灶多位于下部脑桥。无定位体征的病灶均见于背内侧区。认为ＭＲＩ是确诊脑桥腔梗病灶的良好手段     

特发性甲状旁腺机能减退与癫痫发作

报道６例以癫痫为主人表现的特发性甲状旁腺机能减退患者，男４例，女２例，年龄２３－３７岁，平均２８．３岁。６例均为强直一阵挛发作，其中１例合并失神发作。合并手足搐搦２例，智能减退４例，小脑症状１例，锥体外系症状１例。血钙１．１３－１．５８ｍｍｏｌ／Ｌ，血磷１．０９－２．０８ｍｍｏｌ／Ｌ。头颅ＣＴ６例均有对称性基底节，小脑齿状核钙化。     

Cerebrovascular reactivity and subcortical infarctions

OBJECTIVES: To investigate the association between different kinds of ischemic lesions and cerebrovascular reactivity (CR) and to evaluate their relationships with the major risk factors for stroke. SUBJECTS AND METHODS: We evaluated CR using the breath-holding index technique during bilateral transcranial Doppler monitoring of flow velocity in the middle cerebral arteries of 41 consecutive patients attending our clinic for a recent, first-ever, ischemic stroke and in 15 control subjects. Based on the location of the lesion determined by computed tomography, the following 3 types of infarctions were identified: cortical (or territorial), single subcortical, and subcortical with multiple silent subcortical infarctions. Patients with a condition of severe carotid artery stenosis or occlusion, which in itself could account for altered CR, were excluded from this study. All physiological and pathologic conditions that could possibly cause an impairment in CR were recorded. RESULTS: The breath-holding index was significantly lower in the multiple subcortical infarctions group than in the control subjects (P < .001), single subcortical infarctions group (P < .01), and cortical infarctions group (P < .01). In all of the groups male sex (P < .05) and a history of hypertension (P < .05), regardless of whether hypertension was treated, correlated with low CR. The multiple regression analysis indicated that the only significant factor able to influence the breath-holding index was the type of lesion. CONCLUSIONS: Nonstenotic patients with first-ever stroke who had a recent symptomatic subcortical infarction associated with multiple silent infarctions seem to have an impaired cerebrovascular reserve capacity. The strong association of subcortical infarctions with multiple silent infarctions with low CR indicates the role of small vessel vasculopathy and hypoperfusion as possible pathogenetic mechanisms of subcortical infarctions with multiple silent infarctions.     

Klinisch stumme Hirninfarkte

Silent brain infarctions are frequently found by modern cerebral imaging. Up to 30% of persons without a clinical history of stroke were found to have silent brain infarction in epidemiological studies. "Silent" refers to ischemic brain lesions for which no matching clinical syndrome can be found based on history or clinical investigation. Age, education, and ethnic background have a strong impact on noticing and reporting stroke symptoms. The current clinical definition of stroke is insensitive for cognitive deficits which can also be caused by brain infarctions. The majority of silent brain infarctions are localized in the subcortical white matter of the brain; however, about 10% of silent brain infarctions are cortical. Silent brain infarctions are strongly associated with stroke risk factors and comorbidities that are known to cause clinically overt stroke. Silent brain infarctions are 5 to 10 times more frequent than clinically overt strokes. Silent brain infarctions as defined by DWI lesions on MRI imaging are a frequent finding during operative or interventional procedures and their monitoring may help improve the respective techniques in order to decrease the risk of periprocedural stroke.     

Silent stroke in the NINCDS Stroke Data Bank

Previous brain infarctions seen on CT are common in the absence of history of stroke. Eleven percent of patients (135/1,203) without stroke history had ischemic lesions on their first CT, unrelated to the presenting stroke. Stroke Data Bank files were reviewed to determine whether the occurrence, location, and CT characteristics of those lesions are associated with their undetected status. Two distinct patterns were seen: (1) Small lesions of 1 cm or less were left hemisphere predominant and involved the deep structures of the brain; the majority of these were clinically silent. (2) Lesions greater than 1 cm occurred more frequently in the right hemisphere and were mostly superficial; these infarcts produced signs unrecognized by the patient or family. Risk factors for silent stroke were similar to those for stroke in general. Frequencies of in-hospital complications and 30-day fatality rates from the presenting stroke were not influenced by the existence of a prior silent stroke.     

Cerebral infarction in patients with transient ischemic attacks

Summary Cranial computed tomography of 284 patients with transient ischemic attacks (TIAs) and without previous stroke was evaluated. The sample population included patients with carotid and/or vertebrobasilar TIAs. Computed tomography revealed cerebral infarction in 34 patients, including 5 with multiple infarctions. The lesion location was consistent with TIA symptoms in 16 patients. In another 16 patients, however, the lesion location did not correspond to the TIA symptoms; these lesions were attributed to previous silent infarctions. Two patients with multiple infarctions had both symptomatic and asymptomatic lesions. Age and carotid stenosis were each significantly related to an increased chance of detecting cerebral infarction (either symptomatic or asymptomatic). No significant relationship between race, gender, hypertension, diabetes, cardiac disease, or smoking and the incidence of infarction was found by either univariate or multivariate analyses.     

Impact of stroke type on survival and functional health.

In a cohort 760 consecutive stroke patients (23 hospitals in the Netherlands), we studied prognosis in relation to stroke type and focused on (a) short-term and long-term mortality, and (b) long-term functional health. Based on clinical and CT data, we distinguished infratentorial strokes from supratentorial strokes (lacunar infarctions, (sub)cortical infarctions and intracerebral hemorrhages). Cumulative mortality for all stroke patients was 34% at 6 months, 51% at 3 years, and 62% at 5 years. Short-term mortality could be explained by stroke type, whereas long-term mortality could not. Of all survivors, 55% were in poor functional health at 6 months, 49% at 3 years and 42% at 5 years. Long-term functional health outcomes were associated with stroke type. We conclude that the impact of stroke type on mortality is limited to the first 6 months, whereas the type of stroke influences the long-term functional health.     

Patterns of infarction in hemodynamic failure

BACKGROUND AND PURPOSE: The mechanism of stroke in patients with atherosclerotic occlusive disease and hemodynamic failure may be primarily hemodynamic or a combination of hemodynamic and embolic factors. The purpose of this study was to investigate the clinical and imaging features of stroke in these patients. METHODS: Eleven patients with complete atherosclerotic carotid artery occlusion and increased oxygen extraction fraction measured in the hemisphere distal to the occlusion developed an ischemic stroke during the observation phase of a prospective study of cerebral hemodynamics and stroke risk. The medical and study records related to the endpoint event for these 11 patients were reviewed. Records were reviewed for evidence of associated hypotension and for specific details of the neurological deficit. Infarct location was characterized, based on review of imaging and clinical features, as: (1) middle cerebral artery (MCA) core; (2) possible cortical border zone, or (3) internal border zone. RESULTS: One patient had a retinal infarction; the remaining 10 had MCA territory strokes. Six of the 10 infarctions occurred in the MCA core territory. Two of these 6 were fatal hemispheric events. One of the 10 infarctions occurred in the cortical border zone region. Two of the remaining 3 infarctions were localized to the internal border zone. One was indeterminate. CONCLUSIONS: The clinical features and radiological patterns of stroke in many patients with hemodynamic impairment failure and carotid occlusion are most consistent with large artery thromboembolic stroke. These data suggest a synergistic effect between embolic and hemodynamic mechanisms for large artery thromboembolic stroke.     

Stroke in pediatric acquired immunodeficiency syndrome

In a 4 1/2-year period, 4 of 68 children in a longitudinal study of neurological complications of human immunodeficiency virus (HIV) infection had clinical and/or neuroradiological evidence of stroke, yielding a clinical incidence of stroke in this population of 1.3% per year. During this period, 32 subjects died, and permission for autopsy was granted in 18 of the patients, including 3 of 4 who had clinical evidence of stroke. The prevalence of cerebrovascular pathological features in our consecutive autopsy series was higher than the clinical incidence. At autopsy cerebrovascular disease was documented in 6 (24%) of 25 children with HIV infection, including all 3 children who had clinical evidence of stroke. Four patients had intracerebral hemorrhages, 6 patients had nonhemorrhagic infarcts, and 3 had both. Hemorrhage was catastrophic in 1 child and clinically silent in 3 children, all of whom had immune thrombocytopenia. One child had an arteriopathy that affected meningocerebral arteries. In another child, the arteries of the circle of Willis were aneurysmally dilated. Two children had coexisting cardiomyopathy and subacute necrotizing encephalomyelopathy with vascular proliferation. These results suggest that stroke should be considered when children with HIV infection develop focal neurological signs.     

Reduced severity of strokes in patients with silent brain infarctions

Background: Silent brain infarctions (SBIs), leukoaraiosis (LA), and microbleeds (MBs) are ischaemic silent radiologic abnormalities that act as predictors of subsequent strokes. This study investigated the independent effect of silent radiologic abnormalities on initial stroke severity and short‐term outcome. Methods: A consecutive series of patients who had their first ischaemic stroke within 72 h of symptom onset were included. Demographic and clinical characteristics were collected on admission, and magnetic resonance imaging was performed to evaluate the ischaemic lesion, SBI, LA, and MB. Factors potentially associated with lower initial stroke severity (admission NIH Stroke Scale 0–5) and good short‐term outcome (discharge NIH Stroke Scale 0–5, modified Rankin Scale 0–1) were validated by multivariate analysis. Results: Silent brain infarctions were noted in 82 (45%) of the 182 patients. Although there were no statistically significant differences in stroke subtypes and lesion location, univariate analysis revealed that patients with SBI had reduced stroke severity (P = 0.005) and infarction volume (P = 0.001). After adjusting for covariates, the presence of SBI was independently associated with lower stroke severity and good short‐term outcome when the NIH Stroke Scale was used as dependent variable (OR 3.368, 95% CI 1.361–8.332, P = 0.009; OR 3.459, 95% CI 1.227–9.755, P = 0.019, respectively). However, the presence of SBI lost significance when the discharge‐modified Rankin Scale was used as dependent variable (P = 0.058). Conclusion: Amongst silent radiologic abnormalities, SBI was the only predictor of reduced stroke severity and infarct volume. Silent brain infarction deserves more attention in evaluating stroke severity.     

Cerebral small vessel disease in pseudoxanthoma elasticum: three cases

BACKGROUND: Cerebral small vessel disease is rarely described in association with pseudoxanthoma elasticum (PXE), a hereditary connective tissue disorder with skin, eye and vascular manifestations. This autosomally inherited elastic tissue disease has been attributed to mutations in the ABCC6 gene located on chromosome 16p13.1. Different stroke mechanisms are suggested in PXE patients, arterial hypertension and accelerated atherosclerosis being the leading ones. CASE DESCRIPTIONS: Case 1: A 49-year-old man with history of mild hypertension presented with recurrent transient ischemic attacks. At the age of 42, evaluation for progressive visual loss and skin changes led to diagnosis of PXE. Brain magnetic resonance imaging (MRI) disclosed multiple lacunar infarctions and confluent periventricular white matter lesions (WML). Case 2: A 71-year-old woman with history of mild hypertension suffered right-sided stroke. Diagnosis of PXE was made at the age of 48 due to severe visual loss and skin changes. Brain MRI revealed multiple lacunar infarctions and subcortical ischemic leukoencephalopathy. Case 3: A 47-year-old woman with prominent skin changes and bilateral amblyopia developed right-sided weakness. Skin biopsy confirmed PXE. Several lacunar infarcts in deep white matter and pons were revealed on MRI. DISCUSSION: We present three patients with clinical and histopathological features of PXE who presented with multiple lacunar strokes, two with extensive confluent WML. These cases illustrate that PXE is a rare but significant risk factor for small vessel disease and stroke in patients of all age groups. Occlusive small vessel disease and subsequent lacunar infarcts and WML represent important PXE manifestations.     

Frequency and characteristics of early seizures in Chinese acute stroke

We retrospectively studied 1200 hospitalized acute strokes of all etiologies between July 1990 and August 1992. Ninety-six % of all strokes underwent computed tomography of the head. Fifty-eight percent of the 1200 strokes were brain infarction, 32% brain hemorrhage, 6% subarachnoid hemorrhage and 4% were other stroke subtypes. Thirty (2.5%) of all strokes suffered from early seizures. The incidences of early seizures were 2.8% in brain hemorrhage, 2.3% in brain infarction, 2.7% in subarachnoid hemorrhage and 2% in other stroke subtypes. Early seizures were documented in 6% of the patients with carotid territory cortical infarctions and 12% of the patients with lobar hemorrhage, whereas only 0.6% of the patients without carotid territory cortical infarctions and 0.6% of the patients without lobar hemorrhage were affected. Sixty- six percent of 30 early seizures were partial seizures, 24% generalized and status epilepticus were seen only in 10%. In conclusion, we found the early seizure incidence was 2.5% in Chinese patients hospitalized with acute strokes. There was no correlation between seizure occurrence and stroke subtypes. Early seizure developed significantly higher in acute stroke patients with lesions of the cortex than those patients without cortical involvement. The partial seizures were the most frequent type occurring in 66% of all acute stroke patients with early seizures.