急性颅内大动脉粥样硬化与栓塞性缺血脑卒中机械取栓治疗的对比研究

目的 对比分析血管内机械取栓治疗颅内大动脉粥样硬化性(ICAS)和栓塞性(embolic)急性缺血性脑卒中的临床效果和安全性。方法 回顾性分析2019-01—2021-12采用血管内机械取栓治疗的118例急性大血管闭塞的缺血性脑卒中患者的临床资料,其中ICAS组27例(22.9%),Embolic组91例(77.1%)。结果 与Embolic组比较,ICAS组更高的后循环闭塞比例(37.0%vs 14.3%,P=0.009)、更高的球囊扩张(66.7%vs 7.7%,P<0.001)及支架置入比例(59.3%vs 6.6%,P<0.001),手术时间明显延长[110.00(80.00～130.00)min vs 85.00(55.00～120.00)min,P=0.021)],年龄更小[(63.67±11.48)岁vs(68.25±10.13)岁,P=0.047],合并冠心病比例(14.8%vs 41.8%,P=0.010)、心房颤动比例(7.4%vs 52.7%,P<0.001)及术后出血发生率(3.7%vs 23.1%,P=0.023)明显降低,2组血管成功再通率...     

颈内动脉急性闭塞致大面积脑梗死侧支循环建立及影响因素

目的评估颈内动脉急性闭塞致大面积脑梗死侧枝循环建立情况及影响因素。方法纳入29例经诊断为颈内动脉急性闭塞致大面积脑梗死的患者,所有患者均行颈动脉超声、经颅多普勒超声(TCD)、头颅CT、头颅磁共振血管造影(MRA)、心电图检查,同时收集患者基本信息。结果一级侧枝循环建立与糖尿病显著相关(P 0. 05),与房颤、高血压、吸烟、NIHSS评分无关(P 0. 05)。二级侧枝循环建立与房颤、高血压、糖尿病、吸烟、NIHSS评分均无关(P 0. 05)。心源性脑栓塞导致的急性大面积脑梗死与脑疝显著相关(P 0. 05)。TCD评估一级侧枝循环的建立与MRA具有高度一致性(Kappa值=0. 656,P 0. 05)。结论糖尿病可促进颈内动脉急性闭塞导致的大面积脑梗死一级侧枝开放。心源性脑栓塞导致的大面积脑梗死易发生脑疝。TCD可以较好评估颈内动脉急性闭塞导致的大面积脑梗死的一级侧枝循环建立。     

老年急性脑梗死患者并发心房颤动的危险因素分析

目的 探讨老年急性脑梗死患者并发心房颤动(AF)的危险因素.方法 回顾性分析224例老年急性脑梗死患者的临床资料,采用单因素及多因素Logistic回归法对老年急性脑梗死患者并发心房颤动的危险因素进行统计学分析.结果 224例患者中,42例并发房颤,发病率18.6％,经过单因素及多因素Logistic回归分析,最终筛选出年龄(OR=2.421)、家族性房颤史(OR=1.814)、糖尿病(OR=1.243)、高血压(OR=3.184)、大面积梗死(OR=2.793)、LAD(OR=1.733)、心功能分级(OR=1.113)是老年急性脑梗死患者并发房颤的高危因素,而发病前日常服用ACEI或ARB药物(OR=0.837)为保护因素.结论 老年急性脑梗死患者并发心房颤动的发病率较高,其发病与高龄、家族性房颤史、高血压及糖尿病病史、梗死面积、心功能分级及左房内径、是否服用ACEI或ARB药物密切相关,应当根据这些危险因素制定针对性的防治措施.     

大面积脑梗塞的预后

报告48例大面积脑梗塞,占同期住院464例脑梗塞的10.4%,其中男25例,女23例,年龄36—86岁;55岁以上38例占79.2%。既往史:高血压17例,动脉硬化32例,冠心病16例,风心病5例,房颤10例,慢性肾炎和糖尿病各1例,脑血栓8例,脑栓塞6例,本文侧重讨论大面积脑梗塞预后。诊断标准:45例经头部 CT 扫描,3例经尸检证实。45例 CT 扫描时间,发病后48小时以内25例;3～12天20例,发现额颞顶叶大面积梗塞41例,额顶叶大面积梗塞4例。梗塞范围最大9×4.5×4.0cm,最小6×3.5     

心房颤动与急性缺血性卒中静脉溶栓致出血转化的相关性及危险因素分析

目的探讨心房颤动与急性缺血性卒中重组组织型纤溶酶原激活剂(rt-PA)静脉溶栓致出血转化的相关性,分析房颤患者溶栓后出血转化的危险因素。方法回顾性分析接受rt-PA静脉溶栓治疗的147例急性缺血性卒中患者,将入选病例分为非房颤组与房颤组,比较两组患者溶栓后出血转化(HT)的差异,采用单因素和logistic回归分析房颤患者溶栓后出血转化的危险因素。结果 147例入组患者中房颤患者66例,非房颤患者81例,房颤组HT与非房颤组比较差异有统计学意义[27.27%(18/66)与14.81%(12/81),χ2=3.071,P=0.028],房颤组症状性HT与非房颤组比较差异亦有统计学意义[12.12%(8/66)与3.70%(3/81),χ2=3.798,P=0.015],logistic回归分析表明伴发房颤的患者基线收缩压高(OR=11.285,95%CI 1.576-68.377,P=0.035)、基线NIHSS评分较高(OR=2.608,95%CI 1.072-4.380,P=0.013)、早期头部CT有缺血改变(OR=1.595,95%CI 1.164-3.258,P=0.023)、起病-溶栓时间(OTT)较长(OR=93.114,95%CI 7.385-177.972,P=0.006)、溶栓24h内血压变异性大(收缩压变异性OR=18.638,95%CI 1.433-65.634,P=0.004;舒张压变异性OR=21.449,95%CI 1.528-56.420,P=0.003)与溶栓后发生HT显著相关。结论房颤与静脉溶栓后HT具有相关性。基线收缩压高、基线NIHSS评分较高、早期头部CT有缺血改变、OTT较长、溶栓24h内血压变异性大是房颤患者静脉溶栓后发生HT的危险因素。     

心房颤动相关性脑梗死超早期rt-PA静脉溶栓治疗临床研究

目的观察急性脑梗死合并房颤患者超早期rt-PA静脉溶栓的疗效及安全性。方法选择神经内科急性脑梗死进行溶栓患者104例,根据有无房颤分为房颤组和非房颤组,其中房颤组42例,非房颤组62例,比较2组患者溶栓前后NIHSS评分、日常生活活动能力(ADL量表评分),以及颅内出血、死亡等不良结局情况。结果房颤组和非房颤组患者在入院时NIHSS评分、入院时的ADL评分、溶栓时间(发病至开始溶栓的时间)、糖尿病患者占比等差异均无统计学意义(均P0.05),但平均年龄、高血压占比差异均有统计学意义(均P0.05)。非房颤组溶栓前、溶栓后24h及7d时NIHSS评分比较差异有统计学意义(P=0.000),ADL评分差异有统计学意义(P=0.000)。房颤组溶栓前、溶栓后24h、7d时NIHSS评分比较差异有统计学意义(P=0.003),ADL评分比较差异有统计学意义(P=0.000)。房颤组溶栓后患者颅内出血转化11例,症状性颅内出血2例,不良结局6例,而非房颤组颅内出血转化为3例,无症状性颅内出血,不良结局2例,2组颅内出血转化差异有统计学意义(P=0.001),症状性颅内出血(P=0.076)及不良结局(P=0.078)差异无统计学意义(P0.05)。多因素回归分析提示房颤患者是颅内出血转化的独立危险因素(P=0.009)。结论房颤相关性卒中患者溶栓后虽明显增加颅内出血转化风险,但不增加症状性颅内出血及不良结局的风险。     

大面积皮质下梗塞的发病机制及临床表现

CT显示在基底节、内囊或皮质下白质大于1.5cm的脑梗塞同较小的皮质下梗塞相比,可能更多见于脑栓塞。较小的皮质下梗塞传统将其归类于腔隙性梗塞,通常为高血压性小血管闭塞所致。深部大而积脑梗塞产生的临床综合征同腔隙性梗塞相似,但前者可能同时伴有皮质受累症状。本文研究了51例病灶累及内囊、基底节或皮质下白质的大面积脑梗塞,以评价潜在的颈动脉、心脏栓子源以及梗塞后失语症、偏侧忽略和注视麻痹的发生率。     

东菱精纯克栓酶(DF—521)治疗脑梗塞并发出血8例报告

我们统计了我院急诊科和神经科一年来应用东菱精纯克栓酶(DF—521)治疗急性脑梗塞60例,其中8例并发出血,7例脑内出血,1例脑外出血,(男5例,女3例,年龄24～90岁)。8例中5例为大面积脑梗塞;5例合并高血症;4例在发病6小时后用药;3例合并应用抗血小板凝集药物。提示在应用DF—521治疗急性脑梗塞时下列情况需慎重应用:①大面积脑梗塞;②伴脑出血危险因素如高血压;③高龄;④梗塞时间较长及合并应用其它抗血小板凝集药物。     

脑梗死静脉溶栓治疗后出血性转化临床分析

目的探讨急性脑梗死患者溶栓治疗后出血性转化(hemorrhagic transformation,HT)的危险因素以及继发HT患者的溶栓后并发症。方法回顾性分析62例经静脉溶栓治疗的急性脑梗死患者的临床资料,结合文献选择溶栓后继发HT的危险因素,包括年龄、性别、高血压、糖尿病、心功能不全史、脑卒中史、有无早期CT缺血改变、是否大面积脑梗死、是否心源性脑栓塞、发病至溶栓时间、溶栓药物、溶栓前NIHSS评分、溶栓前血糖水平、溶栓后3d内最低纤维蛋白原水平、血小板计数、肌酐水平等进行分析,对单因素分析法发现有统计学差异的危险因素进一步行Logistic回归分析。结果单因素分析发现,与无HT组相比,继发HT组年龄较大(P<0.01),溶栓前血糖水平(P<0.05)、溶栓后6h和12h的收缩压和舒张压较高(均P<0.05),大面积脑梗死发病至溶栓时间>3h、有早期CT缺血改变的患者比例高(均P<0.05)。Logistic多因素回归分析发现高龄(OR:1.129,P<0.05)、溶栓时间>3h(OR:2.592,P<0.05)、早期CT有缺血改变(OR:1.728,P<0.05)是继发HT的危险因素。继发HT组出现颅外出血并发症(52.2%vs 20.5%,χ2=6.637,P<0.05)、重度脑水肿(30.4%vs 5.1%,χ2=5.567,P<0.05)和脑疝形成(26.1%vs 2.6%,P<0.05)的比例更高。结论急性脑梗死患者静脉溶栓后HT的发生率高,高龄、发病至溶栓时间>3h和早期CT缺血改变是HT的危险因素。     

短暂性脑缺血发作后缺血性脑卒中的危险因素

目的探讨TIA后缺血性脑卒中的危险因素。方法收集184例TIA患者的临床资料,分析TIA后缺血性脑卒中的危险因素。结果与无缺血性脑梗死组比较,缺血性脑梗死组高龄(≥60岁)、高血压、糖尿病以及有吸烟、饮酒史的比率显著升高(P0.05~0.01),性别及高血脂比率差异无统计学意义(均P0.05)。与无缺血性脑梗死组比较,缺血性脑梗死组发作时间≥30 min、发作次数≥3次、病程≥24 h(P0.05~0.01),而TIA类型差异无统计学意义(均P0.05)。Logistic回归分析显示,高龄、高血压、糖尿病以及吸烟、饮酒史与TIA进展为缺血性脑卒中呈正相关(OR=29.799,95%CI:2.189~405.569,P=0.011;OR=0.649,95%CI:0.038~6.850,P=0.005;OR=8.569,95%CI:1.314~55.862,P=0.025;OR=0.158,95%CI:0.025~0.980,P=0.048)。结论高龄、高血压、糖尿病、有吸烟饮酒史是TIA发展为缺血性脑卒中的独立危险因素。     

Lacunar infarcts in patients aged 85 years and older

OBJECTIVES: To compare the occurrence of lacunar infarcts in the very elderly ( > or = 85 years of age) and in patients below 85. MATERIAL AND METHODS: Data of 374 consecutive patients with lacunar infarcts were collected from a prospective hospital-based stroke registry in which 2000 patients are included. Distinctive clinical features of lacunar infarct in the very elderly were assessed by multiple logistic regression analysis. RESULTS: Lacunar infarcts were diagnosed in 39 (15%) of the 262 very elderly patients of our stroke registry. Lacunar infarcts in the very elderly accounted for 10.5% of all lacunes. There was no statistical difference in the occurrence of different lacunar syndromes between the very elderly patients and patients below 85. However, the very old group with lacunar infarct showed a significantly higher proportion of the female sex (56.4% vs 37.3%) and history of atrial fibrillation (28.2% vs 8.7%), chronic renal disease and pathologic condition and a significantly lower proportion of hypertension (61.5% vs 77.3%), diabetes (7.7%) vs 28.4%), ischemic heart disease, hypercholesterolemia, and absence of neurologic deficit at discharge from the hospital than patients below 85. After multivariate analysis only atrial fibrillation (OR = 3.77), female gender (OR =2.52), hypertension (OR = 0.35), and diabetes (OR = 0.16) were independent clinical factors for developing lacunar infarction in the very elderly. CONCLUSION: In the very elderly the higher occurrence of atrial fibrillation, the lower prevalence of hypertension and diabetes, and the greater focal neurological impairment suggest that the cardioembolic pathogenetic mechanisms may be more frequent than generally established for lacunar infarcts in stroke patients.     

Clinical study of lacunar infarcts in non-hypertensive patients

Lacunar infarcts in non-hypertensive patients have been scantly assessed. The objective of this study was to determine clinical features of lacunar infarct in patients without hypertension (n = 91) in comparison with characteristics of lacunar infarcts occurring in patients with hypertension (n = 283) collected from a prospective hospital-based stroke registry in which 2000 patients with acute stroke are included. Predictors of lacunar infarct in patients without hypertension were assessed by multiple logistic regression analysis. The group of non-hypertensive patients with lacunar infarction showed a significantly higher frequency of male gender, age 85 years or older, history of atrial fibrillation, chronic obstructive pulmonary disease and diabetes mellitus, and a significantly lower frequency of female gender and absence of limitation at hospital discharge than hypertensive patients with lacunar infarct. Differences between hypertensive and non-hypertensive patients in relation to frequency of the different lacunar syndromes were not observed. After multivariate analysis, age 85 years or older (odds ratio 3.13), diabetes (odds ratio 2.57), and male gender (odds ratio 1.99) seemed to be independent factors associated with lacunar infarct in patients without hypertension. Lacunar infarct in non-hypertensive patients showed some differential clinical features compared to the remaining lacunar infarctions because it occurred more frequently in male patients aged 85 years or older. In this group, diabetes was the most important modificable risk factor. These results suggest an ealier effect of arteriopathy caused by hypertension favoring lacunar brain ischemia, whereas in non-hypertensive patients, arteropathy responsible for small vessel disease would take a more prolonged time in causing lacunar infarction.     

Clinical study of 222 patients with pure motor stroke

The objective was to assess the frequency of pure motor stroke caused by different stroke subtypes and to compare demographic, clinical, neuroimaging, and outcome data of pure motor stroke with those of patients with other lacunar stroke as well as with those of patients with non-lacunar stroke. Data from 2000 patients with acute stroke (n=1761) or transient ischaemic attack (n=239) admitted consecutively to the department of neurology of an acute care 350 bed teaching hospital were prospectively collected in the Sagrat Cor Hospital of Barcelona stroke registry over a 10 year period. For the purpose of the study 222 (12.7%) patients with pure motor stroke were selected. The other study groups included 218 (12.3%) patients with other lacunar strokes and 1321 (75%) patients with non-lacunar stroke. In relation to stroke subtype, lacunar infarcts were found in 189 (85%) patients, whereas ischaemic lacunar syndromes not due to lacunar infarcts occurred in 23 (10.4%) patients (atherothrombotic stroke in 12, cardioembolic stroke in seven, infarction of undetermined origin in three, and infarction of unusual aetiology in one) and haemorrhagic lacunar syndromes in 10 (4.5%). Patients with pure motor stroke showed a better outcome than patients with non-lacunar stroke with a significantly lower number of complications and in hospital mortality rate, shorter duration of hospital stay, and a higher number of symptom free patients at hospital discharge. After multivariate analysis, hypertension, diabetes, obesity, hyperlipidaemia, non-sudden stroke onset, internal capsule involvement, and pons topography seemed to be independent factors of pure motor stroke in patients with acute stroke. In conclusion, about one of every 10 patients with acute stroke had a pure motor stroke. Pure motor stroke was caused by a lacunar infarct in 85% of patients and by other stroke subtypes in 15%. Several clinical features are more frequent in patients with pure motor stroke than in patients with non-lacunar stroke.     

A polymorphism of the aldehyde dehydrogenase 2 gene is a risk factor for multiple lacunar infarcts in Japanese men: the Takahata Study

The objective of the present study was to examine the association between a polymorphism of the aldehyde dehydrogenase 2 (ALDH2) gene and lacunar infarcts of the brain. We conducted a population-based, cross-sectional study on residents from two age groups (61- and 72-year olds). A total of 376 subjects participated in the study, which included brain magnetic resonance image and genetic analysis of the ALDH2 gene. Of the 61- and 72-year-old subjects, 46.4% and 64.3%, respectively, had one or more lacunar infarcts. The average number of infarcts also increased from 2.0 to 2.8 in men and from 2.3 to 3.5 in women. No significant association between the ALDH2 genotype and the presence of lacunar infarction (≥1) was found. However, in subjects with lacunar infarction, the genotype of ALDH2 *1/*1 was associated with a larger number of the lesion ['single' versus 'multiple' odds ratio (OR) 3.73, 95%CI: 1.43–9.74] in men. The OR was comparable even after adjusting for alcohol consumption, tobacco habits, age, hypertension, hypercholesterolemia, and diabetes mellitus (DM) (OR 3.88; 95% CI: 1.10–13.66). In women, there was no significant association between the ALDH2 genotypes and lacunar infarcts. The present study revealed that the ALDH2 *1/*1 genotype was significantly associated with the prevalence of multiple lacunar infarcts in Japanese men.     

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.     

Differences between hypertensive and non-hypertensive ischemic stroke

We compared risk factors, clinical features, neuroimaging data, and outcome between hypertensive and non-hypertensive ischemic stroke patients. Differential features of ischemic stroke patients with hypertension (n = 768) and without hypertension (n = 705) were assessed by bivariate analysis. Independent predictors of hypertensive ischemic stroke were determined by multivariate analysis. Atherothrombotic infarction and lacunar infarct were significantly more common in the hypertensive group, in which older age and a higher occurrence of previous cerebral infarction, hyperlipidemia, acute stroke onset, lacunar syndrome, and pons topography was also observed. Age of 85 years or older, valvular heart disease, and decreased consciousness were more common in non-hypertensive patients. After multivariate analysis, lacunar syndrome, female gender, and previous infarction were directly associated with hypertensive ischemic stroke. Age of 85 years or older and valvular heart disease were inversely associated with hypertensive ischemic stroke. Hypertension was the main cardiovascular risk factor only for lacunes and atherothrombotic infarction, that is, ischemic stroke associated with small- and large-artery disease.     

Patients with Acute Lacunar Infarction Have Benefit from Intravenous Thrombolysis

Introduction: Usefulness of intravenous thrombolysis in patients with acute lacunar cerebral infarction is questionable. The aim of this study was to evaluate the efficacy and safety of intravenous thrombolysis in patients with lacunar infarction in comparison with patients with nonlacunar infarction as well as with patients with lacunar infarction who were not treated with intravenous thrombolysis. Materials and methods: In the first part of the study, among patients with acute ischemic stroke treated with intravenous thrombolysis, characteristics and outcomes of 46 patients with lacunar and 221 patients with nonlacunar infarction were compared. In the second part, 46 patients with lacunar infarction treated with intravenous thrombolysis were compared with 45 lacunar infarction patients who were not treated with intravenous thrombolysis. Results: Patients with lacunar infarction had a lower National Institutes of Health Stroke Scale score (9.2 versus 13.9, P < .001), a greater Alberta Stroke Program Early computed tomography (CT) score (9.7 versus 9.2, P?=?.002), a lower prevalence of atrial fibrillation (6.5% versus 41.2%, P < .001), and significantly more frequently an excellent outcome after 3 months (76.1% versus 36.2%, P < .001) compared with patients with nonlacunar infarction. Among patients with lacunar infarction, an excellent outcome at discharge was significantly more frequent in the intravenous thrombolysis group (41.3% versus 15.6%, P?=?.01), and the length of hospitalization was significantly shorter (9.5 days versus 14.3 days, P?=?.002). There was no hemorrhagic transformation among patients with lacunar infarction treated with intravenous thrombolysis. Conclusion: Intravenous thrombolysis has proven to be effective and safe in patients with lacunar infarction and should always be applied if there are no absolute contraindications.     

Are hypertension or cardiac embolism likely causes of lacunar infarction?

We tested the hypothesis that hypertension is more common and cardiac embolism less common in patients with lacunar infarction than in patients with other types of cerebral infarction. We studied risk factor profiles in a series of 102 consecutive patients with a lacunar infarct and 202 consecutive patients with a carotid artery-distribution infarct involving the cortex registered in the Oxfordshire Community Stroke Project, a community-based study of first-ever stroke. The two groups did not differ in the prevalence of prestroke hypertension (defined in a number of ways) or in the prevalence of markers of sustained hypertension. The presence of atrial fibrillation and a history of myocardial infarction, particularly during the 6 weeks before the stroke, were significantly more common in the group with carotid-distribution infarcts involving the cortex. There was no significant difference in the prevalence of other accepted risk factors for ischemic stroke, including previous transient ischemic attack, cervical bruit, diabetes mellitus, peripheral vascular disease, or cigarette smoking. Our results suggest that hypertension is no more important in the development of lacunar infarction than it is in the development of other types of ischemic stroke that are presumed to be due to atherosclerotic thromboembolism in a major cerebral artery. Our data support the autopsy evidence that cardioembolic occlusion is an unusual cause of lacunar infarction.     

Clinical-computed tomographic correlations of lacunar infarction in the Stroke Data Bank

Lacunar stroke was diagnosed in 337 (26%) of the 1,273 patients with cerebral infarction among the 1,805 total in the Stroke Data Bank. We analyzed the 316 patients with classic lacunar syndromes. Among these, 181 (57%) had pure motor hemiparesis, 63 (20%) sensorimotor syndrome, 33 (10%) ataxic hemiparesis, 21 (7%) pure sensory syndrome, and 18 (6%) dysarthria-clumsy hand syndrome. No striking differences were found among the risk factors for the lacunar subtypes, but differences were found between lacunar stroke as a group and other types of infarcts. Compared to 113 patients with large-vessel atherosclerotic infarction, those with lacunar stroke had fewer previous transient ischemic attacks and strokes. Compared to 246 with cardioembolic infarction, patients with lacunar stroke more frequently had hypertension and diabetes and less frequently had cardiac disease. We found a lesion in 35% of the lacunar stroke patients' computed tomograms, with most lesions located in the internal capsule and corona radiata. The mean infarct volume was greater in patients with pure motor hemiparesis or sensorimotor syndrome than in those with the other lacunar stroke subtypes. In patients with pure motor hemiparesis and infarcts in the posterior limb of the internal capsule, there was a correlation between lesion volume and hemiparesis severity except for the few whose infarct involved the lowest portion of the internal capsule; in these patients severe deficits occurred regardless of lesion volume. Taken together, the computed tomographic correlations with the syndromes of hemiparesis showed only slight support for the classical view of a homunculus in the internal capsule.     

缺血性卒中患者脑内微出血特点及危险因素的研究

目的 探讨脑内微出血在缺血性卒中患者中的发生率及在脑内各区域的分布情况,观察缺血性卒中亚型之间微出血发生率的差异,初步分析其相关因素及其与腔隙性脑梗死、脑白质病变等微小血管病变程度之间的关系。方法 连续入选261例心源性栓塞型、大动脉粥样硬化型及小动脉闭塞型3个亚型的缺血性卒中患者。记录患者一般临床资料及实验室检查结果,应用头颅磁共振梯度回波T2*加权成像（gradient-echoT2*-weighted,GRE-T2*）观察脑内微出血的数目及部位,同时观察腔隙性脑梗死数目和部位以及脑白质病变程度。结果 80例患者（30.70%）存在脑内微出血,数目为1～109个。微出血最常见于皮质-皮质下区（46.09%）,其次位于基底节区（27.80%）。各亚型中小动脉闭塞型患者脑内微出血的发生率最高（53.30%）。高血压、腔隙性脑梗死数目及脑白质改变程度为缺血性卒中患者脑内微出血发生的独立危险因素,比值比（odds ratio,OR）分别为4.364、1.190和1.310;脑内微出血的分级与腔隙性梗死分级（r =0.519,P <0.001）及白质改变程度（r =0.437,P <0.001）显著相关。结论 微出血在缺血性卒中患者特别是小动脉闭塞患者中发生率较高,微出血与腔隙性脑梗死数目及脑白质改变明显相关。