首发缺血性卒中患者无症状性腔隙性梗死严重程度的相关因素分析

目的 分析与无症状性腔隙性梗死严重程度相关的危险因素,并评价无症状性腔隙性梗死与缺血 性卒中病因亚型的相关性。 方法 连续选取791例7天以内首次发病的非心源性缺血性卒中患者。收集患者的人口学信息和血管 病的危险因素,评价患者的头颅磁共振成像包括无症状性腔隙性梗死的数量、脑白质疏松的严重程 度、缺血性卒中的病因亚型以及急性梗死灶的分布特征,并通过多元Logistic回归分析其与无症状性 腔隙性梗死相关的危险因素。 结果 296例患者（37.4%）伴无症状性腔隙性梗死。单因素分析发现：高龄、高血压、入院时血压 较高、糖尿病、脑出血病史、Fazekas评分≥3分、小动脉闭塞性卒中、单发梗死灶、无小的皮层梗死灶、 无分水岭梗死和流域性梗死与无症状性腔隙性梗死患病相关。多元Logistic回归发现：男性、高血压、 较高的舒张压、糖尿病、脑出血病史、Fazekas评分≥3分、小动脉闭塞性卒中是无症状性腔隙性梗死 患病的危险因素。 结论 首发非心源性缺血性卒中患者无症状性腔隙性梗死的患病率较高。伴无症状性腔隙性梗死 的首发非心源性缺血性卒中患者常有较重的脑白质疏松,并且所患缺血性卒中以小动脉闭塞性卒中 常见。     

急性腔隙性脑梗死患者脑白质疏松磁共振影像分层研究

目的 通过分析腔隙性脑梗死患者脑白质疏松磁共振成像（magnetic resonance imaging,MRI）特点并结合脑白质血液供应,探讨影像学分层的临床价值。 方法 连续选取北京天坛医院住院的合并脑白质疏松的急性腔隙性脑梗死患者61例,按其脑白质疏松部位不同分为3组（皮层下组、室旁组和混合组）,按其脑白质疏松的严重程度分为3级,分析各组患者临床一般资料的特点及各组、各级脑白质疏松MRI特点。 结果 皮层下组患者年龄较室旁组及混合组小,其差异具有统计学意义（P<0.05）。腔隙性脑梗死患者中,深部、室旁白质疏松及深部合并室旁白质疏松共占88.50%,而皮层下白质疏松占11.50%。深部/室旁白质疏松以2级常见,皮层下白质疏松以1级最常见。 结论 腔隙性脑梗死患者脑白质疏松随年龄增加而加重,而且其脑白质疏松多发生在深部和或室旁白质。     

脑小血管病患者认知状态与神经影像学特征的相关性分析

目的:本研究旨在探讨脑小血管病患者认知状态与皮质下腔隙性梗死部位及病灶数、白质病变和内侧颞叶萎缩之间的关系。方法:本研究纳入59例在上海交通大学医学院附属仁济医院神经内科脑血管病二级预防门诊登记的最近一次症状性缺血性卒中病史3个月的脑小血管病患者。根据详细的神经心理学评估结果,将59例患者分入无认知障碍组(24例)、轻度认知障碍组(22例)和血管性痴呆组(13例),采用头颅磁共振成像多重序列检查及斜冠状面重建,依据所得图像进行皮质下腔隙性梗死病灶计数、白质病变评分和内侧颞叶萎缩评分。结果:脑小血管病患者认知障碍的发生与皮质下腔隙性梗死病灶总数有关(P=0.004),其中皮质下白质部位腔隙性梗死病灶数在3组之间的差异有统计学意义(P=0.001);轻度认知障碍组和血管性痴呆组患者丘脑部位腔隙性梗死病灶数多于无认知障碍组的患者,但差异无统计学意义(P=0.058)。大部分的白质病变病灶位于额叶和顶枕叶,颞叶和基底节的白质病变较少。3组之间双侧额叶(P=0.033)和双侧基底节(P=0.009)的白质病变评分差异有统计学意义。59例患者中,43例完成磁共振成像斜冠状面重建。左右内侧颞叶萎缩一般呈同步发展;3组之间左或右内侧颞叶萎缩评分的差异均有统计学意义(P值均0.001)。在13例左内侧颞叶萎缩评分≥2分的患者中,11例为无认知障碍组和轻度认知障碍组患者;血管性痴呆组患者均有内侧颞叶萎缩,其中6例患者的左右侧平均内侧颞叶萎缩评分≥2分。多因素分析结果显示,皮质下白质腔隙性梗死病灶数[比值比:2.39(95%可信区间:1.19~5.80),P=0.005]和左内侧颞叶萎缩评分[比值比:10.21(95%可信区间:2.02~51.75),P=0.003]是脑小血管病认知功能的独立危险因素。结论:脑小血管病患者的认知损害程度与皮质下白质腔隙性梗死病灶数和左内侧颞叶萎缩评分相关。     

高血压患者血压近日节律变化对腔隙性梗死的影响

目的 分析血压近日节律变化,了解高血压与腔隙性梗死的关系.方法 收集高血压合并腔隙性梗死患者共119例,腔隙性梗死患者121例,高血压105例,正常对照组109例.分别进行连续24 h血压监测.用余弦法分析4组血压的近日节律特征,采用t检验进行比较.结果 4组均存在近日节律,高血压患者的调整中值高于血压正常组,而振幅低于血压正常组;高血压合并腔隙性梗死组调整中值高于其他3组,而振幅低于其他3组;高血压组与腔隙性梗死组调整中值及振幅无统计学意义,但调整中值高于正常对照组,振幅低于正常对照组.结论 血压近日节律的振幅降低是高血压及腔隙性梗死患者有别于健康人的特征,并且可能参与了腔隙性梗死发病.     

脑梗死患者动脉粥样硬化与OCSP分型关系的研究

目的 探讨脑梗死患者动脉粥样硬化所致的颈动脉颅外段狭窄与OCSP分型各亚型的关系。方法 对161例急性脑梗死（ACI）患者进行OCSP分型,并对其中配合检查的156例以及54例单纯高血压患者和43例健康正常人进行颈动脉彩色多普勒超声检测颈动脉颅外段的狭窄程度,并探讨OCSP各亚型与颈动脉狭窄的关系。结果 脑梗死组颈动脉颅外段狭窄发生率为75％,较高血压组35．19％,和正常对照组27．91％明显升高（P〈0．01）。脑梗死组OCSP各亚型构成比为：腔隙性梗死49．1％,部分前循环梗死37．9％,和后循环梗死7．5％,完全性前循环梗死5．6％。OCSP各亚型急性脑梗死患者之间的颈动脉狭窄阳性率无显著性差异（P〉0．05）。前循环和后循环梗死中重度的血管狭窄明显高于腔隙性梗死。结论 脑梗死同颈动脉颅外段的狭窄明显相关,OCSP分型不能提示脑梗死患者动脉粥样硬化病因。     

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。     

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。     

代谢综合征在脑卒中患者中患病状况的分析

目的研究代谢综合征在脑卒中患者中的患病状况。方法研究对象为390例初发脑卒中患者,对照组为400例年龄、性别匹配者,研究总结代谢综合征及其危险因素的患病率,经Logistic回归分析其对脑卒中的危险性。结果代谢综合征的现患率在脑卒中组高于对照组。代谢综合征的现患率在脑卒中病例组为28.3%,对照组为9.8%,差异有显著意义。腔隙性脑梗死、脑梗死和脑出血的代谢综合征现患率分别为26.0%、29.5%和27.3%。Logistic回归分析显示代谢综合征是脑卒中的独立危险因素。结论代谢综合征在脑卒中患者中患病率较正常人群高,是脑卒中的独立危险因素。     

急性脑梗死患者临床分型及梗死面积与心电图改变的关系

目的 探讨急性脑梗死患者临床分型和梗死面积与心电图(ECG)改变的关系.方法 给216例急性脑梗死患者进行ECG检查,按牛津郡社区卒中项目(OCSP)分型和梗死面积分型,对各组患者的ECG检查结果进行分析比较.结果 OCSP分型完全前循环梗死(TACI)组、部分前循环梗死(PACI)组、后循环梗死(POCI)组和腔隙性梗死(LACI)组患者的ECG异常率分别是: 95. 5%、80.4%、62.5%和48.5%,TACI组和PACI组明显高于LACI组(P＜0.05～0.01);大中面积梗死组(83.7%)的ECG异常率明显高于小面积梗死组(60.4%)和腔隙性梗死组(53.2%)(P＜0.05～0.01);小面积梗死组的ECG异常率高于腔隙性梗死组(P＜0.05).OCSP和梗死面积分型各亚型组出现ST-T改变和心律失常的比率差异有统计学意义(P＜0.05～0.01).结论 急性脑梗死临床分型病情重和梗死面积大的患者ECG异常率高.     

皮层下缺血性血管性痴呆

皮层下缺血性血管性痴呆（subcortical ischemic vascular dementia, SIVD）是血管性认知障碍（Vascular cognitive impairment, VCI）的一个亚型,具有认知障碍和皮层下脑缺血病灶的证据。其包括腔隙状态、关键部位梗死性痴呆和Binswanger综合征等3个类型。认知障碍的特征是显著的执行功能障碍和相对轻微的工作记忆减退。对脑血管病危险因素的干预有助于皮层下缺血性血管性痴呆的防治。     

Prevalence of metabolic syndrome and serum marker levels in patients with four subtypes of cerebral infarction in Japan.

In this hospital-based cross-sectional study we investigated differences in the levels of serum atherosclerotic and fibrinolytic markers and the prevalence of metabolic syndrome (MS) among patients with four subtypes of cerebral infarctions. Blood samples were taken from 171 cerebral infarction inpatients to determine the levels of high-sensitivity C-reactive protein, serum total homocysteine, serum plasminogen activator inhibitor 1 and lipoprotein a. Subjects were also screened for MS. Atherothrombotic infarction was most prevalent, followed by lacunar and embolic infarction. The median length of hospital stay was longest for embolic infarcts. There were no statistically significant differences in serum marker concentrations. The proportion of MS varied significantly among the subtypes, and was highest among patients with embolic infarctions with the lowest high density cholesterol levels. MS was most prevalent among patients having undergone embolic events that are reported to have the worst prognoses. Further epidemiologic studies are needed to better understand the characteristics and differences in the etiology of cerebral infarction subtypes.     

The significance of cerebral white matter lesions in vascular dementia--from psychiatric aspects

The significance of cerebral white matter lesions in vascular dementia was mentioned, based on the findings of 50 autopsied cases at Yokuhukai Geriatric Hospital. Neuropathology of vascular dementia is classified to 5 types, i.e. 1) lacunar type, 2) cortical type, 3) cortico-white matter type, 4) white matter type, and 5) Binswanger type. Our findings on 50 patients revealed no lacunar type, cortical type in 8 cases, cortico-white matter type in 19, white matter type in 9, and Binswanger type in 14. The fact that 42 patients out of 50 showed some lesions involving the cerebral white matter suggested the important role of the white matter lesions in the pathogenesis of dementia of vascular type. Our cases also indicated that Binswanger type be commonly observed, although dementia of this type has been thought to be very rare since Binswanger (1894) and Alzheimer (1902) had reported similar patients. The patients with cerebral white matter lesions develop more marked dementia, especially of frontal and parieto-occipital type, than ones with cortical lesions, but the characteristics of symptoms of white matter and Binswanger type remain to be fully clarified.     

Silent intracerebral lesions identified on magnetic resonance imaging in patients presenting with initial stroke--comparative studies of the affected hemisphere and the contralateral one]

Among patients who had undergone MRI examinations with a clinical suspicion of stroke, we selected 82 patients with initial cerebral infarction being located only in a unilateral cerebral hemisphere. Seventeen (21%) subjects had wedge-shaped lesions including cerebral cortex (the cortical type), 65 (79%) had them predominantly in white matter and/or territory of the deep perforators (the subcortical type). Fifty nine cases out of total 82 (72%:9 in the cortical type, 50 in the subcortical type) had the silent cerebral infarction in the contralateral hemisphere to the affected side found on the 1.5 tesla superconductive system T2 weighted magnetic resonance imaging. Among them, 57 had the contralateral small cortical and/or subcortical (white matter) infarction, the other 2 cases had the contralateral lacunar infarction in the basal ganglia-internal capsule area as the silent lesion. The incidence of the cortical type was high in cases without the silent cerebral infarction in the contralateral hemisphere. It might be suspected that the cortical type had tendency to present clinical symptoms caused by initial stroke without prior silent cerebral infarction. The author proposed that the cerebral embolism might play an important role in showing the sudden onset clinical symptoms of the cortical type. And the author also proposed that there might be a difference in the development of clinical symptoms between the silent cerebral infarction located in the basal ganglia-internal capsule area and the cortical-subcortical (white matter) area.     

缺血性卒中合并脑白质病变的危险因素研究

目的 探讨缺血性卒中合并脑白质病变的患病情况及相关危险因素,通过对其干预以降低脑白质病变的发生率。方法 本研究连续入选2007年8月至2008年10月在北京天坛医院神经内科住院的缺血性卒中患者共483例,依据有无脑白质病变分成伴脑白质病变组和无白质病变两组,得出我院住院的缺血性卒中患者合并脑白质病变的患病率,以有无脑白质病变作为因变量,各种血管病危险因素作为自变量进行Logistic回归多因素分析。结果 我院住院的缺血性卒中患者脑白质病变的患病率为53.8%,随年龄增长发生率和病变严重程度增加（P均<0.01）。Logistic回归显示高龄［比值比（odds ratio,OR）=1.03,95%可信区间（confidence interval,CI）1.00～1.05,P<0.05］、高血压病（OR=1.77,95%CI 1.07～2.91,P<0.05）、卒中病史（OR=1.71,95%CI 1.02～2.88,P<0.05）、高血糖（OR=1.07,95%CI 1.00～1.15,P<0.05）和腔隙性脑梗死（OR=1.89,95%CI 1.17～3.06,P<0.05）是脑梗死患者合并脑白质病变的独立危险因素。结论 随年龄增长,脑白质病变的患病率和严重程度增加;高龄、高血压病、卒中病史、高血糖和腔隙性脑梗死是缺血性卒中患者合并脑白质病变的独立危险因素。     

Lacunar infarcts. Pathogenesis and validity of the clinical syndromes.

BACKGROUND AND PURPOSE: In this study, we investigated the lacunar hypothesis to answer three questions: 1) Is the lacunar syndrome valid for diagnosing lacunar infarction? 2) What is the frequency of potential cardiac versus carotid sources of embolism in patients with lacunar versus cortical infarct? 3) What is the frequency of vascular risk factors in these two groups of patients? METHODS: The study was performed in a well-defined prospective series of 103 patients with a first-ever lacunar infarct and 144 other patients with a first-ever infarct involving the cortex. RESULTS: Sensitivity and specificity of the lacunar syndromes in diagnosing lacunar infarction were 95% and 93%, respectively. Positive and negative predictive values of diagnosing lacunar infarction in patients with lacunar syndromes were 90% and 97%, respectively. Risk factor analysis showed no differences for either group of cerebral infarction. A cardiac source of embolism was significantly less frequent in patients with lacunar infarction (odds ratio = 0.32, 95% confidence interval = 0.17-0.61, p less than 0.001). Significant carotid stenosis (diameter reduction greater than or equal to 50%) was also less frequent in patients with lacunar infarction (odds ratio = 0.35, 95% confidence interval = 0.16-0.76, p less than 0.001). CONCLUSIONS: These findings show that the lacunar syndrome is an excellent clinical test for diagnosing lacunar infarction and that cardiac and carotid embolism are unlikely causes of lacunar infarction, supporting the hypothesis that lacunar infarcts are usually caused by small vessel disease.     

Plasma lipoproteins in cortical versus lacunar infarction

We investigated the relation of plasma lipids to the risk for ischemic stroke by comparing clinical and biochemical characteristics of survivors of cortical (n = 48) and lacunar (n = 36) brain infarction. By analysis of variance, no differences were observed in the concentrations of total cholesterol, triglycerides, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, or apoproteins A1 and B. Patients with lacunar infarction, however, had higher concentrations of high density lipoprotein (HDL)-cholesterol than patients with cortical stroke. This HDL-cholesterol difference was due primarily to a strikingly low HDL-cholesterol content in white patients with cortical stroke. These data suggest that previously demonstrated differences in HDL-cholesterol concentrations between patients with ischemic stroke and control subjects without stroke may apply to patients with cortical but not lacunar infarction. Separation of cerebral infarction into subtypes based on mechanism may help clarify lipid-related risk factors in cerebrovascular disease.     

Hypodensity of the cerebral white matter in patients with transient ischemic attack or minor stroke: influence on the rate of subsequent stroke. Dutch TIA Trial Study Group.

In a prospective study of 3,017 patients with transient ischemic attack or minor ischemic stroke from the Dutch Transient Ischemic Attack Trial, the presence or absence of diffuse hypodensity of the white matter on a baseline computed tomography (CT) scan of the brain was related to the occurrence of subsequent stroke. On entry, 337 patients were judged to have diffuse hypodensity of the white matter on CT; they were older (71.4 +/- 7.4 years versus 64.4 +/- 9.9 years), more often had hypertension (50% versus 41%), and more often had lacunar infarcts on CT scan (40% versus 26%) than did patients with normal white matter. Strokes, fatal or nonfatal, occurred in 51 (15%) of the patients with diffuse hypodensity of the cerebral white matter, compared to 217 (8%) in the group with normal white matter (crude hazard ratio, 2.0; 95% confidence interval, 1.4-2.7). After adjustment for age and other relevant entry variables, the hazard ratio was 1.6 (95% confidence interval, 1.2-2.2). In patients younger than 70 years the crude hazard ratio was 2.7 (95% confidence interval, 1.7-4.2). The distribution between the main subtypes of stroke was similar for patients with and those without diffuse hypodensity of the cerebral white matter: Intracerebral hemorrhage occurred in 6 and 9%, cortical infarction in 47 and 45%, and lacunar infarction in 34 and 29%, respectively. We conclude that hypodensity of the cerebral white matter in patients with transient ischemic attack or minor stroke is associated with an extra risk of future stroke, from large as well as from small vessels, and particularly in patients under 70 years old; this increase of risk is independent of other risk factors for stroke.     

单侧孤立基底节区腔隙性脑梗死早期神经功能恶化的多因素分析及缺血耐受的相关性研究

目的 探讨单侧孤立的基底节区腔隙性脑梗死早期神经功能恶化（early neurological deterioration, END）的相关因素及其与脑缺血耐受（brain ischemic tolerance,BIT）机制的研究。 方法 回顾性分析经磁共振证实的167例单侧新发孤立的基底节区腔隙性脑梗死患者的临床资 料,并排除大动脉狭窄患者。根据卒中发生后1周内动态的美国国立卫生研究院卒中量表（National Institutes of Health Stroke Scale,NIHSS）评分情况将167例患者分为END阳性及END阴性两组,使用 Logistic回归分析研究与脑梗死早期神经功能恶化有关的因素。 结果 167例患者中42例发生END,125例未发生END。多因素分析结果显示病灶累及内囊后肢侧脑室 旁放射冠后部是预测END的独立危险因素,两组比较差异有显著性（P <0.01）;而发病年龄、脑梗死 病史、糖尿病史、入院收缩压及脑白质病变与END有相关性,且比较差异有显著性（P <0.05）。分别 以有无合并糖尿病、不同病灶位置进行分层并层间的单因素及多因素分析,结果显示,有无合并糖尿 病、病灶部位的不同不影响年龄、卒中史、脑白质与END阳性的关系,END与既往脑梗死病史、脑白质 病变、发病年龄存在相关性,比较差异有显著性（P <0.05）。 结论 单侧孤立基底节区腔隙性脑梗死早期END与病灶是否累及内囊后肢侧脑室体旁后部密切相关, 同时也与是否合并脑白质病变、既往脑梗死病史、糖尿病史、年龄等因素相关。年龄≥65岁、收缩压 高、卒中史、脑白质病变是END阳性的保护因素。缺血不耐受为腔隙性脑梗死发生END的主要机制。     

Cranial computed tomographic observations in multi-infarct dementia. A controlled study.

BACKGROUND AND PURPOSE: We compared cranial computed tomography findings among 58 multi-infarct dementia index cases and 74 multi-infarct control subjects without cognitive impairment to identify potential determinants of multi-infarct dementia. METHODS: The cranial computed tomography records of acute ischemic stroke patients with a history of multiple cerebral infarcts were compared to determine the number, location, and size of cerebral infarcts; the pattern of infarction; brain volume loss; and the degree of white matter lucency, sulcal enlargement, and ventricular enlargement. Multi-infarct patients were divided into two groups: 1) index cases were defined as those with multi-infarct dementia as defined by the Diagnostic and Statistical Manual of Mental Disorders, edition 3 (DSM-III) criteria; and 2) control subjects were defined as those multi-infarct patients without dementia or multi-infarct dementia according to DSM-III criteria. RESULTS: Overall, multi-infarct index cases had more cerebral infarcts, more cortical and subcortical left hemisphere infarcts, higher mean ventricular volume to brain volume ratio, more extensive enlargement of the body of the lateral ventricles and cortical sulci, and a higher prevalence of white matter lucencies. Among multi-infarct cases and control subjects the most frequent site of infarction was the subcortical region, and the most frequent pattern of infarction was lacunar. Stepwise logistic regression analysis examined cranial computed tomography as well as other factors and showed that level of education, stroke severity, left cortical infarction, and diffuse enlargement of the left lateral ventricle were the best overall predictors of multi-infarct dementia. CONCLUSIONS: Level of education, stroke severity, and left hemisphere infarction may be predictors of multi-infarct dementia.     

Little association between intracranial arterial stenosis and lacunar stroke

Atheromatous middle cerebral artery (MCA) stenosis could cause lacunar stroke by occluding lenticulostriate artery origins, but atheroma is common, and previous studies lacked suitable controls. We aimed to determine if intracranial atheroma was more common in lacunar than in cortical ischaemic stroke. We recruited patients with lacunar stroke and controls with mild cortical stroke, confirmed the stroke subtype with magnetic resonance imaging and used transcranial Doppler ultrasound imaging to record flow velocity and focal stenoses in the basal intracranial arteries 1 month after stroke. We compared ipsi- and contralateral MCA mean flow velocities between stroke subtypes and tested for associations using linear mixed models. Amongst 67 lacunar and 67 mild cortical strokes, mean age 64 and 67 years, respectively, we found no difference in MCA mean flow velocity between cortical and lacunar patients. Increasing age and white matter lesion scores were independently associated with lower MCA flow velocities (0.2 cms(-1) fall in velocity per year increase in age, p = 0.045; 3.75 cms(-1) fall in flow velocity per point increase in white matter lesion score, p = 0.004). We found no intracranial arterial stenoses. MCA atheromatous stenosis is unlikely to be a common cause of lacunar stroke in white populations. Falling velocities with increasing white matter lesion scores may reflect progressive brain tissue loss leaving less tissue to supply.