Predictive value of clinical lacunar syndromes for lacunar infarcts on magnetic resonance brain imaging

OBJECTIVE: We prospectively investigated the predictive value of clinical and CT-supported lacunar syndromes for lacunar infarcts on magnetic resonance (MR) brain imaging. PATIENTS AND METHODS: The 54 prospective, consecutive patients had clinical lacunar syndromes of acute onset and early computed tomography (CT; on admission day, i.e. < or =48 h after onset of symptoms) showing either a small deep infarct or no corresponding lesion. Taking MR (at day 2 to 4 after admission) as the gold standard, the positive predictive value of the CT-supported clinical syndrome for corresponding lacunar lesions was calculated. RESULTS: In 27 (50%) patients, early CT showed a lacunar infarct corresponding to the clinical syndrome, a further 27 (50%) patients had no fresh ischemic lesion. In 51 patients (94%), MR showed a recent lacunar infarct (hyperintense lacune in T2-weighted scans, no demarcation on T1-weighted scans and/or positive gadolinium-enhancement) corresponding to the clinical syndrome (positive predictive value 0.94, 95%, CI: 0.88 to 0.98). In 3 (6%) patients MR was normal. Aside from old unrelated ischemic (macro- and/or microangiopathic) lesions, MR revealed no acute non-lacunar infarct. CT and MR sites of lacunar lesions were matching. Compared to gold standard MR, the sensitivity of early CT for suspected lacunar lesions was 0.53 (95% CI: 0.38 to 0.67). CONCLUSION: Lacunar syndromes were highly predictive for small deep infarcts on MR. Magnetic resonance brain imaging may be redundant in the setting of a lacunar syndrome supported by a CT that excludes non-ischemic causes of stroke; it may therefore be abandoned in order to reduce costs in the health care system.     

Relation of leukoaraiosis to lesion type in stroke patients

Nonspecific periventricular white matter lucencies on computed tomograms (leukoaraiosis) were found in 141 (38%) of 367 patients with ischemic or hemorrhagic strokes. Patients with leukoaraiosis were significantly older than those without it and were significantly more likely to have hypertension, diabetes mellitus, general vascular disease, and lacunar infarcts on computed tomograms but were less likely to have cortical infarcts. Because many of these variables may be mutually dependent, we performed a logistic regression analysis examining all clinical and computed tomographic variables. The analysis demonstrated that increasing age, lacunar infarcts, and hemorrhages were significant determinants of leukoaraiosis; cortical infarcts were also significantly, but negatively, correlated with leukoaraiosis. In patients with hemorrhages, leukoaraiosis occurred significantly more often when aneurysms or arteriovenous malformations were not demonstrated. These findings suggest that in patients with cerebrovascular disorders leukoaraiosis is associated with small-vessel disease.     

133例腔隙性脑梗死患者DSA结果及临床特点分析

目的 探讨腔隙性脑梗死患者的临床表现、影像学资料及DSA特点.方法 南方医科大学珠江医院神经内科自2002年5月至2008年4月共收治经头颅CT或MR证实并行DSA检查、初次出现临床症状的腔隙性脑梗死患者133例,回顾性分析患者的临床表现、影像学资料及DSA特点.结果 133例患者中临床表现为纯运动性卒中42例(31.6%),感觉运动性卒中36例(27.1%);CT/MR检查共发现梗死灶283个,梗死灶位于内囊78个(27.6%),放射冠+半卵圆中心121个(91.0%);DSA结果显示颅内大血管病变44例(101处),其中大血管狭窄38例(95处,其中责任血管34处,非责任血管61处),烟雾病6例,单发颅内动脉动脉瘤1例.DSA阳性患者中以纯运动性卒中(21例)和感觉运动性卒中(10例)居多,梗死部位以内囊(23个)和放射冠+半卵圆中心(31个)居多,44例患者存在至少1个脑血管病高危因素.结论 腔隙性脑梗死的病因多样,部分患者易出现颅内大血管狭窄,以纯运动性卒中和感觉运动性卒中最多,基底节和放射冠梗死灶为主,多存在脑血管病高危因素.

Abstract：

Objective To discuss the clinical manifestations, imaging data and DSA findings of lacunar infarction (LI). Methods One hundred and thirty-three patients, admitted to our hospital from May 2002 to April 2008, were chosen in our study; these patients with first onset as LI were confirmed by Head CT or MR; the clinical manifestations and imaging data were retrospectively analyzed; DSA was also performed on these patients and DSA findings were concluded. Results One hundred and thirty-three patients were clinically manifested as pure motor hemiplegia (PMH, n=42, 31.6%) and sensorimotor stroke (SMS, n=36, 27.1%). Two hundred and eighty-three lesions were noted by CT/MR examinations, including 78 locating at the endocyst (27.6%) and 121 locating at the corona radiate+greater oval center (91.0%). Forty-four patients were noted as having 101 intracranial vessel lesions by DSA, including 38 patients with angiostenosis, 6 with Moyamoya and 1 with single intracranial aneurysm; of the patients with angiostenosis, 95 lesions (34 in the offending vessels and 61 in other vessels) were found. Among the DSA (+) patients, PMH (n=21) and SMS (n=10) were mainly noted with their lesions locating at the endocyst (n=23) and the corona radiate+greater oval center (n=31); At least 1 high-risk factor such as hypertension, diabete, hyperlipemia, coronary heart disease and arial fibrillation was found in 44 patients. Conclusion The pathogeneses of LI are various. Main artery infarction may co-exist in some cases. PMH and SMS are common with their lesions frequently locating at basal ganglia area and corona radiate of the cerebral hemisphere. High risk factor exists in most patients with cerebrovascular diseases.     

不同临床类型的初发腔隙性脑梗死对患者认知功能的影响

目的 研究初次发病的腔隙性脑梗死患者的不同临床类型对认知功能的影响.方法 选择初次发病的腔隙性脑梗死患者91例,其中纯运动性轻偏瘫(PMH)25例(27.47%),纯感觉性卒中(PSS)13例(14.29%),感觉运动性卒中(SMS)17例(18.68%),共济失调性轻偏瘫(AH)和构音障碍-手笨拙综合征(DCHS)共15例(16.48%),其他类型21例(23.08%).于发病1周内进行神经心理学测验,包括简易精神状态检查量表、汉化的韦氏成人智力量表(数字广度、图片排列、数字符号和积木测验)、世界卫生组织-加利福尼亚洛杉矶大学听觉词语学习测验、简化的Rey复杂图形测验、Stroop测验、语义分类流畅性测验、加利福尼亚卡片分类测验和画钟测验.评估患者的认知功能情况.结果 SMS型的大部分认知功能测试为五型中最差.SMS型的WHO-UCLA听觉词语学习测验(F=4.074,P=0.005)与词语再认(击中-虚报)(F=2.952,P=0.024)评分低于其他四型,SMS型的大部分的记忆力评分较其他类型患者低(P＜0.05),尤其是低于PSS型和AH/DCHS型;SMS型在部分的执行能力和视空间结构能力方面较PMH型差(P＜0.05),差异有统计学意义.结论 SMS型患者在记忆力、执行能力和视空间结构能力方面的障碍较其他类型的初发腔隙性脑梗死患者更为严重,应加强重视和早期干预.     

Cognitive performance after lacunar stroke correlates with leukoaraiosis severity

BACKGROUND: This study investigates the effect of leukoaraiosis on patients presenting with cognitive impairment after lacunar stroke. METHODS: Fourty-six patients with cognitive impairment and newly discovered lacunar stroke detected by brain magnetic resonance imaging underwent neuropsychological testing. RESULTS: Patients with both lacunar infarct and leukoaraiosis performed less well on cognitive measures, compared to those with lacunar infarcts alone. Additionally, leukoaraiosis severity inversely correlated with cognitive performance. CONCLUSIONS: In patients with lacunar stroke, presence of leukoaraiosis is associated with worse performance in multiple cognitive domains. These findings suggest lacunar infarcts plus leukoaraiosis is a common etiology for vascular dementia.     

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.     

Diagnosis of lacunar infarcts within 6 hours of onset by clinical and CT criteria versus MRI.

BACKGROUND: The diagnosis of small deep infarcts (SDIs) based on clinical and noncontrast CT findings is often employed to triage stroke patients for emergent endovascular interventions. Few studies have evaluated the accuracy of <6 hours presentation with lacunar clinical syndromes in predicting the presence of a SDI and the absence of large vessel occlusion. METHODS: Consecutive patients were identified with symptoms suggestive of acute stroke, diffusion-weighted magnetic resonance imaging (DW-MRI) and CT performed within 6 hours of onset, and absence of hemorrhage on imaging. Patients were given a diagnosis of SDI if they met the defined clinical and CT criteria. Diagnoses of large vessel occlusion absent (LVOA) and final diagnoses of SDI versus non-SDI incorporated hyperacute multimodal MRI data. RESULTS: Of 64 patients, 15 were diagnosed as SDI at <6 hours based on clinical/CT criteria. Fourteen of 15 patients (93%) had a final diagnosis of LVOA. Ten of 15 (67%) had a final MR-DWI-confirmed diagnosis of SDI. Clinical/CT diagnosis of SDI showed sensitivity of 44%, specificity 97%, positive predictive value (PPV) 93%, and negative predictive value (NPV) of 61% in predicting LVOA and sensitivity 83%, specificity 90%, PPV 67%, and NPV 96% compared to the final diagnosis of SDI. Most patients incorrectly diagnosed with SDIs harbored small cortical branch infarcts. CONCLUSIONS: Diagnoses of SDI <6 hours from symptom onset based on a classic lacunar syndrome and CT criteria show only modest predictive value in predicting the presence of a small-vessel territory infarct but perform fairly well in identifying patients without large-vessel occlusions amenable to endovascular therapy.     

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.     

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.     

Late epileptic seizures after cerebral infarction

OBJECTIVES: To determine the profile of late epileptic seizures following cerebral infarcts and the predictive clinical and radiological factors associated with their development. METHODS: We compared 86 patients who developed late seizures after cerebral infarction with 285 similar patients who did not develop seizures for at least 1 year after their stroke. Patients who had seizures only at the onset of the stroke were excluded. Odds' ratios were used for statistical analysis. RESULTS: Simple partial, and mainly motor seizures, with or without secondary generalization, accounted for 80% of the classifiable seizures but it was not possible to determine the seizure type in half of the cases. Factors that appeared to be predictive of seizure development were the presence of large cortical infarcts and the presence of apparently preserved cerebral tissue within the infarcted area. Seizures were rare in patients with lacunar infarction but the presence of associated leukoaraiosis increased the risk. The risk was also increased in patients with other medical problems known to lower seizure threshold, such as renal failure.     

Early CT changes and outcome of ischemic stroke

Although recombinant tissue plasminogen activator (rt-PA) was rapidly implemented as part of the emergency care of acute stroke, its use in daily clinical practice still remains controversial in many countries. The most important question is criteria for careful selection of subgroup of patients for this treatment. It has been hypothesized that early computed tomography (CT) changes of ischemia are risk factors for symptomatic intracerebral hemorrhage and poor outcome. We conducted a prospective outcome study of patients with acute ischemic stroke (IS) admitted to the hospital within 6 h of symptom onset. Experienced neuroradiologists blind to the clinical outcome of the patients read all CT scans carried out in the emergency room. Early CT changes were defined as in European Cooperative Acute Stroke Study (ECASS) 2. There were 150 patients (75 males, mean age 72.5 +/- 9.0) with acute IS (54.7% with mild stroke and 45.3% with severe stroke). Early CT changes were presented with tissue hypodensity - 55.7%, effacement of sulci - 41.3%, hyperdensity of middle cerebral artery (MCA) - 13.3%, hypodensity of lentiform - 20.7%, loss of insular ribbon sign - 28.7%. Follow-up after 30 days showed that 44% of the patients were discharged home, 20% were discharged to rehabilitation facilities, 22% were discharged to chronic care institutions and 14% died. Data were statistically analyzed. Our data suggest that early signs on CT scan could not predict outcome of patients with acute IS.     

Pure motor hemiparesis due to non-hypertensive putaminal haemorrhage

Summary The syndrome of pure motor hemiplegia (PMH) has been traditionally regarded to be due to lacunar infarcts at various places in the brain. Recently, attention has been drawn towards various other aetiological factors which have been responsible for this clinical presentation. PMH as a result of hypertensive putaminal haemorrhage is extremely uncommon. A case of PMH as a result of non-hypertensive putaminal haemorrhage is described.     

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。     

Acute vestibular syndrome in a patient with cerebral autosomal dominant leukoencephalopathy with subcortical infarcts and leukoencephalopathy (CADASIL)

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary form of small vessel disease in which the pons may show lacunar infarcts and leukoaraiosis. Acute pure vestibular syndrome may be due to caudal pontine lesions and is probably underestimated. We describe a case of CADASIL with acute vestibular syndrome mimicking peripheral vestibulopathy, and evidence of focal infarction in the ponto-medullary junction at gadolinium-enhanced MRI including diffusion-weighted imaging, involving the area of the right vestibular nucleus and root entry zone of the ipsilateral vestibular nerve bundle. In CADASIL, both focal brainstem lesions and leukoaraiosis may parallel supratentorial white matter changes and may be related to poor outcome. Their actual extent should be evaluated in longitudinal studies that might predict clinical outcome and progression of disability.     

Baseline Computed Tomography Changes and Clinical Outcome After Thrombolysis With Recombinant Tissue Plasminogen Activator in Acute Ischemic Stroke

OBJECTIVE: Intravenous recombinant tissue plasminogen activator (rt-PA) is the only therapy of proven value for patients with acute ischemic stroke (AIS). Controversy exists with regard to the prognostic significance of early computed tomography (CT) changes in patients receiving rt-PA for AIS. The authors retrospectively reviewed all cases of AIS who received intravenous rt-PA for AIS in University of South Alabama hospitals between January 1996 and May 1999. A neuroradiologist, blinded to clinical outcomes, reviewed all baseline CT scans for the presence of the following signs: hyperdense middle cerebral artery (HMCA), loss of gray-white differentiation (LGWD), insular ribbon sign (IRS), parenchymal hypodensity (PH), and sulcal effacement (SE). Modified Rankin Scale (mRS) score was recorded 90 days after thrombolysis, and clinical outcome was dichotomized as favorable (0-1) or unfavorable (2-6). The authors performed both univariate and multivariate analyses to investigate the relationship between early CT signs, baseline clinical variables, and functional outcome as measured by the 90-day mRS scores. Any one early CT finding was detected in 23(64%) patients. The frequency of specific findings were as follows: SE in 13 patients (36%), LGWD in 12 patients (33%), PH in 9 patients (25%), HMCA in 4 patients (11%), and IRS in 3 patients (8%) patients. There was no statistically significant association between the occurrence of these imaging findings and subsequent functional outcome after thrombolysis. The data suggest that the presence of subtle acute CT changes in AIS patients is not predictive of clinical outcome following administration of rt-PA as per National Institute of Neurological Disorders and Stroke protocol.     

Vascular ataxic hemiparesis: a re-evaluation.

Ataxic hemiparesis is commonly considered as one of the "typical" lacunar syndromes. Using the prospective stroke registries from Lausanne and Besançon, 100 patients were selected consecutively (73% men, 27% women; age 64.7 (SD 13.6) years) with a first stroke and ataxic hemiparesis (hemiparesis or pyramidal signs and ipsilateral incoordination without sensory loss). Brain CT or MRI was performed on all patients. A primary haemorrhage was present in 5%, an infarct in 72%, isolated leukoaraiosis in 9%, and no apparent abnormality in 14%. The locations of lesions were the internal capsule (39%), pons (19%), thalamus (13%), corona radiata (13%), lentiform nucleus (8%), cerebellum (superior cerebellar artery territory) (4%), and frontal cortex (anterior cerebral artery territory) (4%). The clinical features of ataxic hemiparesis with different locations were almost identical. Only minor associated signs allowed the localisation of the lesions (paraesthesiae with a lesion in the thalamus; nystagmus or dysarthria with a cerebellar or pontine location). Crural paresis with homolateral ataxia was seen only with cortical paramedian frontal lesions. Presumed hypertensive small artery disease was not always found, but was still the leading cause of stroke, being present in 59% of the patients and in 62% of those with small deep infarcts. A potential source of embolism (arterial or cardiac) was found in one fourth of the patients. Therefore no definite association can be made between ataxic hemiparesis and lacunar infarction. In particular, so called uncommon lesion locations may not be rare. After extensive investigations a diagnosis of lacunar infarct can be retained in only slightly more than half of the cases.     

A Novel COL4A2 Mutation Associated with Recurrent Strokes

Mutations in type four collagens, specifically COL4A1 and COL4A2, have been associated with cerebral small vessel disease (SVD), defined as lacunar infarcts, deep intracerebral hemorrhages (ICH), and leukoaraiosis. We present a case of a man with recurrent cerebral infarcts, related to a novel COL4A2 mutation, the p.A1534S variant. Magnetic resonance imaging demonstrated multiple lacunar infarcts, numerous deep and lobar microhemorrhages and advanced leukoaraiosis. Evaluation for COL4A2 mutations should be considered when suspecting a genetic cerebral small vessel disease.     

MRI hyperintensities of the temporal lobe and external capsule in patients with CADASIL

BACKGROUND: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited, autosomal dominant condition caused by mutations of the Notch3 gene. Affected individuals have migraine, mood disturbance, and recurrent strokes, often progressing to subcortical dementia and premature death. MRI findings include focal lacunar infarcts and diffuse T2-weighted hyperintensity, or leukoaraiosis. However, such findings are seen much more commonly in patients with cardiovascular risk factors, particularly hypertension, where they are believed to represent cerebral small vessel disease. No previous study has sought to identify specific radiologic markers of CADASIL. METHODS: MRI scans from 20 consecutive patients with CADASIL and 20 patients with sporadic leukoaraiosis due to presumed small-vessel disease were compared using the previously validated semiquantitative MRI rating scale devised by Scheltens et al. Analysis was blinded to clinical category. RESULTS: Scores for hyperintensities of the temporal white matter and external capsule-insula region were significantly higher in patients with CADASIL. Hyperintensity confined to the pole of the temporal lobe was a characteristic finding in CADASIL, occurring in 19 patients with CADASIL but no patients with ischemic leukoaraiosis. Involvement of the external capsule, though less specific, was seen early in the disease course. In a few patients with CADASIL, involvement of the corpus callosum was observed. CONCLUSIONS: Temporal pole hyperintensity is a radiologic marker of CADASIL. Involvement of the external capsule and corpus callosum are also characteristic findings that may help to distinguish the disease.     

Are white matter lesions directly associated with cognitive impairment in patients with lacunar infarcts?

Forty-four patients (mean age 66, SD 8 years) with either clinical evidence of a focal lacunar syndrome (n=36) or with disorders of memory or gait (n=8) in the presence of a lacunar infarct on CT were studied for cognitive functioning and for the presence of white matter lesions on MRI. MR images were assessed by a neurologist and a neuro-radiologist blinded to the clinical data. Thirty-six patients had one or more lacunar infarets on CT or MRI (in the thalamus in 5, in the caudate nucleus in 3 and in the internal capsule or corona radiata in the remaining patients). Twelve patients had multiple infarcts. Severe lesions of the white matter were found in 13 patients, mild to moderate lesions in 20 patients. Scores on Digit Span, Digit Symbol and delayed recall of the 15-Words test were significantly lower in the group with severe lesions, whilst there was a trend in the same direction for the Cognitive part of the Cambridge Examination of Mental Disorders in the Elderly, the Trailmaking B, Stroop colour interference test and the delayed visual reproduction of the Wechsler Memory Scale. These findings suggest that diffuse lesions of the white matter are an independent factor in the pathogenesis of intellectual dysfunction, also in patients with lacunar infarcts, but a truly independent analysis is difficult because the most severe involvement of the white matter tended to be associated with the largest number of lacunar infarcts.     

Two mesencephalic lacunar infarcts presenting as Claude's syndrome and pure motor hemiparesis

Two exceptional cases of mesencephalic lacunar infarcts located both in the anterior vascular territory are reported. In patient 1, the infarct selectively involved the red nucleus, thus resulting in a Claude's syndrome. In patient 2, the lesion was limited to the external 2/3 of the cerebral peduncle, and was responsible for a pure motor hemiplegia (PMH). CT scan easily demonstrated the lesion in both cases. Claude's syndrome is very unusual, and PMH has only been reported once before in a mesencephalic infarct. The reasons why these lesions are so uncommon are discussed.