Basilar artery stenosis mimicking the lacunar syndrome of pure motor hemiparesis

BACKGROUND: Stereotyped, repeated transient ischemic attacks manifesting as pure motor hemiparesis are most often attributed to ischemia of the internal capsule or ventral pons resulting from in situ disease of the small penetrating arteries. CASE DESCRIPTION: We report a 61-year-old man presenting with recurrent episodes of left-sided weakness consistent with the lacunar syndrome of pure motor hemiparesis. Subsequent neuroimaging revealed infarction of the right ventral pons and a critical basilar artery stenosis as the inciting lesion. Despite maximal antithrombotic therapy, he continued to have repeated symptoms. Angioplasty and stenting were attempted but both failed due to plaque recoil and technical difficulties. After the procedure, the patient had no further ischemic episodes and remained symptom-free at two months. CONCLUSIONS: This case illustrates the imprecise and discordant relationship between the mode of presentation of a stroke syndrome and its presumed pathophysiology. The lacunar syndrome of pure motor hemiparesis should be recognized by clinicians as a mode of stroke presentation due not only to small vessel disease, but also to large artery atherosclerotic disease such as basilar artery stenosis. Prompt institution of treatment can lead to a good clinical outcome.     

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.     

Acute isolated capsular stroke. A clinical study of 148 cases

The objectives of the study were to assess differential features between capsular stroke of ischemic and hemorrhagic origin, and to compare capsular strokes with all other (non-capsular) strokes. Data of 148 patients with isolated capsular stroke were collected from a prospective hospital-based stroke registry in which 2000 consecutive acute stroke patients were included. Isolated capsular stroke accounted for 8.4% of strokes included in the registry (8.4% of ischemic strokes and 10.5% of intracerebral hemorrhages). Capsular stroke of hemorrhagic origin (n = 24) was more severe than ischemic capsular stroke (n = 124) as determined by a significantly higher in-hospital mortality, length of stay, and lower number of patients free of functional deficit at discharge. After multivariate analysis, limb weakness, sudden onset, and sensory symptoms were independently associated with capsular hemorrhage, whereas pure motor hemiparesis appeared to be associated with capsular infarction. In summary, one of each 12 patients with acute ischemic stroke and one of each 10 patients with acute intracerebral hemorrhage had an isolated capsular stroke. Lacunar syndrome was the most frequent clinical presentation being more common (particularly pure motor hemiparesis) in ischemic than in hemorrhagic capsular stroke. Capsular hemorrhage and capsular infarction showed identical risk factor profiles suggesting the same underlying vascular pathology for both conditions.     

Spectrum of medial medullary infarction: clinical and magnetic resonance imaging findings

Among 4200 consecutive patients admitted to three hospitals with acute ischemic stroke, we found only 11 patients in whom magnetic resonance imaging (MRI) had proved that they had medial medullary infarction (MMI). In our centers, patients with MMI were less than 1 % of those with vertebrobasilar stroke. The infarcts documented by MRI were unilateral in 10 patients and bilateral in one. On clinico-topographical analysis there were four clinical patterns: (1) Classical Dejerine's syndrome was the most frequent, consisting of contralateral hemiparesis, lemniscal sensory loss and ipsilateral lingual palsy in 7 of the eleven patients. (2) Pure hemiparesis was present in 2 patients; (3) Sensorimotor stroke was present in 1 patient with contralateral hemiparesis, hypesthesia and mild decrease in pain sensation without lingual palsy; (4) Bilateral MMI syndrome in 1 patient, accompanied by tetraparesis, bilateral loss of deep sensation, dysphagia, dysphonia and anarthria. Presumed causes of MMI were intrinsic branch penetrator artery disease with concomitant vertebral artery stenosis in 6 of the 11 patients, vertebral artery occlusion in 2, dolichoectatic vertebrobasilar arteries in 2, a source of cardiac embolism in 1. Prognosis at 3 months was favorable in 8 patients, but the patient with bilateral MMI syndrome had persisting motor deficit causing limitation of daily activities, and 2 died from systemic causes. The classical triad of acute MMI facilitates the diagnosis, although the recognition of this syndrome in patients with incomplete manifestations can be difficult and occurs more frequently than commonly thought. Moreover, vertebral artery atherosclerosis and branch atheromatous disease of the penetrating arteries are the main causes of medullary infarction. Received: 21 February 2001, Received in revised form: 22 February 2001, Accepted: 17 May 2001     

Posterior cerebral artery territory infarcts: clinical features, infarct topography, causes and outcome. Multicenter results and a review of the literature

Only a few large series of posterior cerebral artery (PCA) stroke exist, and clinical features and causes have not been studied as extensively as in other vascular territories. The PCA syndrome includes more clinical signs than the well-known visual field deficits. Concomitant findings are frequently sensory, slight motor and neuropsychological deficits. Unilateral headaches are the common presenting symptom making complicated migraine an important differential diagnosis. Combined deep and superficial PCA territory infarcts involving the lateral thalamus are more frequent than commonly assumed and are mostly associated with sensory and reversible slight motor deficits. Occlusion of the precommunal PCA segment with associated paramedian midbrain infarction causes severe motor deficits, oculomotor signs, and decreased consciousness and has a poorer outcome than other PCA territory infarcts. Embolism from a cardiac or undetermined source is the leading mechanism accounting for up to half of the cases, whereas arterial embolism from significant proximal vertebrobasilar disease is less frequent. Local atherothrombotic stenosis or occlusion of the PCA is uncommon. In spite of thorough diagnostic evaluation, the etiology of PCA territory infarction cannot be determined in at least one quarter of patients. Among the rare causes of PCA territory infarction carotid artery disease is important while the significance of migraine remains controversial.     

不同病因分型的穿支动脉供血区梗死患者的临床及影像学研究

目的 利用高分辨率磁共振成像诊断穿支动脉疾病及载体动脉斑块堵塞穿支动脉的大动脉粥样硬 化型卒中,比较不同病因穿支动脉供血区梗死患者的临床特征。 方法 收录豆纹动脉及脑桥旁正中动脉供血区急性脑梗死患者作为研究对象,依据中国缺血性卒中 分型诊断（Chinese Ischemic Stroke Subclassification,CISS）分型标准排除心源性、其他病因及原因未明 性卒中,对所有入组患者的载体动脉行高分辨率磁共振管壁成像（high-resolution magnetic resonance i magi ng,HR -MRI）检查,将载体动脉存在粥样硬化斑块患者定义为载体动脉斑块堵塞穿支动脉 （parent artery plaque occluding penetrating artery,POPA）组,载体动脉无异常者定义为穿支动脉疾病 （penetration artery disease,PAD）组,比较不同病因卒中患者的危险因素及临床特征。 结果 本研究共连续纳入64例穿支动脉供血区急性脑梗死患者,其中48例（75%）为POPA患者,且 其中21例患者常规血管影像学检查难以发现载体动脉管壁病变,经HR -MRI 明确诊断。比较两组 不同病因卒中患者的一般资料,POPA组中吸烟患者比例显著高于PAD组,比较差异有统计学意义 （P =0.028）。POPA组中26例为基底节区或侧脑室旁梗死,22例为脑桥梗死。POPA组患者影像学表现 特点为病灶相对较大、呈多灶或簇状分布,脑桥梗死患者病灶多累及脑桥基底部呈脑桥旁正中梗死, 且POPA组患者运动功能缺损易进展;而PAD患者病变部位多位于脑桥深部近背侧,小灶性改变。 结论 本研究穿支动脉供血区梗死患者中75%属于POPA,HR-MRI提高了卒中病因分型的准确性。 POPA型卒中患者的病因、病灶体积、形态及预后不同于单纯穿支病变患者。     

Spectrum of anterior cerebral artery territory infarction: clinical and MRI findings

To evaluate and review the clinical spectrum of anterior cerebral artery (ACA) territory infarction, we studied 48 consecutive patients who admitted to our stroke unit over a 6-year period. We performed magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) in all patients, and diffusion magnetic resonance imaging (DWI) in 21. In our stroke registry, patients with ACA infarction represented 1.3% of 3705 patients with ischemic stroke. The main risk factors of ACA infarcts was hypertension in 58% of patients, diabetes mellitus in 29%, hypercholesterolemia in 25%, cigarette smoking in 19%, atrial fibrillation in 19%, and myocardial infarct in 6%. Presumed causes of ACA infarct were large-artery disease and cardioembolism in 13 patients each, small-artery disease (SAD) in the territory of Heubner's artery in two and atherosclerosis of large-arteries (<50% stenosis) in 16. On clinico-radiologic analysis there were three main clinical patterns depending on lesion side; left-side infarction (30 patients) consisting of mutism, transcortical motor aphasia, and hemiparesis with lower limb predominance; right side infarction (16 patients) accompanied by acute confusional state, motor hemineglect and hemiparesis; bilateral infarction (two patients) presented with akinetic mutism, severe sphincter dysfunction, and dependent functional outcome. Our findings suggest that clinical and etiologic spectrum of ACA infarction may present similar features as that of middle cerebral artery infarction, but frontal dysfunctions and callosal syndromes can help to make a clinical differential diagnosis. Moreover, at the early phase of stroke, DWI is useful imaging method to locate and delineate the boundary of lesion in the territory of ACA.     

Neuropsychological abnormalities associated with lacunar infarction

The objective of this study was to assess neuropsychological abnormalities in 40 patients with lacunar infarction. Topography of infarction, presence of isolated or multiple silent infarcts and white matter hyperintensities were correlated with results of neuropsychological tests and subtypes of lacunar infarction. Patients were studied within 1 month after stroke. A total of 21 patients were males and the mean age was 70.7 years; 30% had a single infarction (mean number of infarctions was 3.4). Twelve patients had pure motor hemiparesis, 9 pure sensory stroke, 8 dysarthria-clumsy hand/ataxic hemiparesis, 8 atypical lacunar syndrome, and 3 sensorimotor stroke. The mean score of the Mini-Mental State Examination was 28.4. Mild cognitive impairment of subcortical vascular features occurred in 23 patients and isolated executive disturbances in 4. Neuropsychological results showed that patients with atypical lacunar syndrome followed by pure motor hemiparesis showed significantly more cognitive executive disturbances. Patients with dysarthria-clumsy hand/ataxic hemiparesis accounted for the best scores in some tests of visuoconstructive function and visual memory. In summary, mild neuropsychological disturbances (57.5%) are not infrequent in acute lacunar infarcts especially in patients with atypical lacunar syndrome and pure motor hemiparesis. Neuropsychological impairment should be considered as common clinical feature in acute lacunar infarction.     

Discrete lesions in the sensorimotor control system. A clinical-topographical study of lacunar infarcts.

In 50 patients with computed tomography-verified small, deep, lacunar, infarcts from a prospective stroke registry, we studied the lesion site in relationship with the clinical syndromes pure motor stroke, sensorimotor stroke and ataxic hemiparesis. Seventy per cent (95% confidence interval: 57-83%) of the lesions were located in the posterior limb of the internal capsule or adjacent paraventricular region, affecting the corticospinal tract in pure motor stroke, as well as the thalamocortical tract in sensorimotor stroke, and the cerebellar (dentato(rubro)thalamocortical and corticopontocerebellar) pathways in ataxic hemiparesis. This most frequently involved area is supplied by the anterior choroidal artery, indicating that this artery is the predominant deep, penetrating artery involved in small vessel disease causing lacunar stroke syndromes.     

Lateral thalamic infarcts

A patient with occlusion of the proximal posterior cerebral artery (PCA), a lateral thalamic infarct, and hemisensory loss later developed hemianopia and hemiparesis and had extensive PCA territory infarction in the midbrain, the lateral portion of the thalamus, and the occipital lobe noted at necropsy. Two other patients had lateral thalamic infarcts on computed tomography, normal angiographic findings, and presumed thalamogeniculate artery branch occlusion. There are three clinical syndromes associated with lateral thalamic infarction: (1) hemisensory loss, hemiataxia, and involuntary movements; (2) pure sensory stroke; and (3) sensory-motor stroke. Ataxia, adventitious movements, and sensory loss are due to infarction of the lateral, posterolateral, and posteromedial ventral nuclei caused by occlusion of the PCA proximal to the thalamogeniculate artery branches or by occlusion of large thalamogeniculate arteries. Pure sensory and sensory-motor strokes are due to smaller infarcts in the posterolateral-posteromedial ventral complex and adjacent internal capsule caused by occlusion of penetrating artery branches of the thalamogeniculate arteries.     

Acute infarction limited to the lenticular nucleus: clinical,etiologic, and topographic features

BACKGROUND: Chronic diseases involving the putamen and globus pallidus induce parkinsonism and other movement disorders. Sensory and motor dysfunction from deep middle cerebral artery infarction is usually due to an involvement of the internal capsule. The clinical picture associated with isolated infarction of the lenticular nucleus is less well established. OBJECTIVE: To analyze clinical features, topographic correlations, and cause of purely lenticular ischemic infarction. PATIENTS AND METHODS: We reviewed 820 consecutive patients with deep hemispheral infarct included in the Lausanne Stroke Registry between 1986 and 1998 and selected those with isolated lenticular involvement on computed tomography or magnetic resonance imaging. RESULTS: Thirteen patients had pure lenticular infarction. All had faciobrachiocrural hemisyndrome, while none showed acute or delayed parkinsonism or abnormal movement. Nine patients had a lesion restricted to the putamen. Two of them had ataxic motor hemisyndrome and 7 had sensorimotor hemisyndrome (with ataxia in 4, left hemineglect in 1, and deep pain in the arm and leg in 1). Four patients had a lesion of putamen and globus pallidus externus.Three of them had motor hemisyndrome (with nonfluent aphasia in 2 and ataxia in 1) and 1 had ataxic sensorimotor hemisyndrome. All infarcts were in the territory of the medial perforating branches of the medial cerebral artery. Presumed cause of stroke was small-artery disease in 5, artery-to-artery embolism in 4, cardioembolism in 3 and undetermined in 1. CONCLUSIONS: Acute lenticular infarction induces mainly hemiparesis but no movement disorder. Associated sensory deficits, aphasia, and hemineglect underline clinically the function of the lenticular nucleus in connection with the prefrontal, temporal, and parietal cortices.     

Risk factors and clinical manifestations of pathologically verified lacunar infarctions

Review of 2,859 autopsy reports disclosed lacunar infarctions in 169 patients (6%). Review of the charts of 167 of these patients revealed hypertension in 64%, diabetes in 34%, smoking in 46%, and no known risk factor for cerebrovascular disease in 18%. As many as 81% of the patients with lacunes were asymptomatic. Symptomatic lacunes presented most commonly as pure motor hemiparesis (31%), aphasia plus right hemiparesis (20%), or sensorimotor dysfunction (11%); none presented as pure sensory stroke. These results suggest that the spectrum of lacunar infarction is more heterogeneous than previously thought. Most lacunes are asymptomatic, and the majority of symptomatic patients do not present with "classical" lacunar syndromes.     

Posterior cerebral artery infarction from middle cerebral artery infarction

BACKGROUND: While it is known that posterior cerebral artery (PCA) infarction may simulate middle cerebral artery (MCA) infarction, the frequency and localization of this occurrence are unknown. OBJECTIVE: To determine the frequency of PCA infarction mimicking MCA infarction and the territory of the PCA most commonly involved in this simulation. DESIGN: We studied 202 patients with isolated infarction in the PCA admitted to our stroke center to determine the frequency of PCA infarction simulating MCA infarction, the involved PCA territory, and the patterns of clinical presentation. RESULTS: We found 36 patients (17.8%) with PCA ischemic stroke who had clinical features suggesting MCA stroke. The PCA territory most commonly involved was the superficial PCA territory (66.7%), followed by the proximal PCA territory (16.7%) and both the proximal and the superficial PCA territories (16.7%). The principal stroke mechanism was cardioembolic (54.1%) in the superficial PCA territory, lacunar (46.2%) in the proximal PCA territory, and undetermined (40.2%) in both the proximal and the superficial territories. Among the 36 patients, the most common clinical associations were aphasia (13 patients), visuospatial neglect (13 patients), and severe hemiparesis (7 patients). CONCLUSIONS: Posterior cerebral artery infarction simulating MCA infarction is more common than previously thought. Early recognition of the different stroke subtypes in these 2 arteries may allow specific management.     

Strokes in the subinsular territory: clinical, topographical, and etiological patterns

The authors studied 11 patients with subinsular stroke (subIS) located in a deep border zone between lenticulostriate arteries and small insular cortical penetrating branches of the middle cerebral artery. The typical clinical features of subIS were motor deficits (11 patients), sensory disturbances (6 patients), transcortical motor aphasia and hypophonia (2 patients), and transient dysphagia at stroke onset (5 patients). Large artery disease and cardioembolic mechanisms may give rise to subIS by hemodynamic mechanisms.     

急性缺血性脑卒中CISS分型与危险因素相关性分析

目的探讨急性缺血性卒中中国缺血性卒中亚型（CISS）分型与不同危险因素的关系。方法回顾性分析连续登记的急性缺血性脑梗死患者,记录其危险因素,并按CISS分型标准将急性缺血性卒中分为5种类型并分析相关因素对其发生风险的影响。结果在纳入标准的212例急性缺血性卒中患者中,大动脉粥样硬化型99例（46.7%）、心源性卒中型35例（16.5%）、穿支动脉疾病45例（21.2%）、其他病因型5例（2.4%）、病因不确定型28例（13.2%）。吸烟者、高血压病、冠心病、心房颤动者在5亚型间比例差异具有统计学意义（P〈0.05）。相关和回归分析显示冠心病、心房颤动与心源性卒中亚型有正相关性（β=1.34、2.206,P〈0.05）,高血压病与穿支动脉疾病亚型有相关性,为正相关性（β=1.074,P〈0.05）。结论不同类型缺血性脑卒中与不同的危险因素有关,心房颤动、冠心病是心源性卒中亚型的危险因素,高血压病是穿支动脉疾病亚型的危险因素。     

Pure homonymous hemianopia due to anterior choroidal artery territory infarction

The most consistently observed neurological deficits in the anterior choroidal artery (AChA) territory infarction are pure motor or sensorimotor syndromes. Visual field defects and higher cortical dysfunction are occasionally accompanied, but pure homonymous hemianopia without motor and sensory symptom has never been reported yet. We present 2 patients with pure homonymous hemianopia, whose MRI disclosed cerebral infarction in the well-known territory of the AChA. In most patients with ischemic stroke, pure homonymous hemianopia indicates infarction in the posterior circulation, particularly in the posterior cerebral artery territory. However, the present cases provide evidence that it can also be caused by infarction in the anterior circulation, i.e. the AChA.     

Pure thalamic infarctions: Clinical findings

Our purpose in this study was to evaluate and review the risk factors, clinical profiles, and neuropsychologic abnormalities in patients with pure thalamic infarctions and to describe the clinical syndromes according to the thalamic arterial territory involved. We studied all patients with acute thalamic stroke admitted to our stroke unit over a 5-year period. We performed magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) on all patients. We classified patients into 4 thalamic artery territory subgroups based on MRI findings: thalamogeniculate, paramedian, polar, and posterior choroidal. Patients with pure thalamic infarction represented 2.4% of patients with ischemic stroke in our registry. There were 59 patients (39 men and 20 women; mean age, 62 ± 13 years) with thalamic infarctions that were confirmed by MRI. The main cause of thalamic infarction was small artery disease (75%). Hypertension (68%), hypercholesterolemia (29%), and diabetes mellitus (27%) were the most frequent risk factors. Hemisensory loss with or without motor and neuropsychologic deficit is highly associated with thalamogeniculate infarction, the most frequent type of thalamic stroke (51%). Paramedian infarction was the second most common type of thalamic infarction (34%) and is characterized by several neuropsychologic, oculomotor, and consciousness disturbances. Frontal-like syndrome with sensory motor findings is common in polar artery territory infarction (10%). Visual field defect is associated mainly with infarctions in the territory of the posterior choroidal artery (5%), probably caused by involvement of the lateral geniculate body. Approximately two thirds of the patients returned to their previous normal life. Cognitive deficits in patients with bilateral paramedian infarction persisted during the follow-up period, contrary to the other thalamic stroke subtypes. No patient died during follow-up. Acute thalamic stroke is a specific clinical picture that accurately predicts a small artery disease in the posterior circulation. The 4 arterial thalamic territories correspond well clinically to 4 different syndromes. Acute thalamic infarction appears to predict an overall good clinical recovery.     

Prognosis of young ischemic stroke in Taiwan: impact of prothrombotic genetic polymorphisms

We investigated the effects of genetic factors on the prognosis of cerebral infarction in young adults in Taiwan. Because ischemic stroke with arterial occlusion or undetermined etiology is more likely to be related to a genetic prothrombotic state, 231 patients younger than 50 years (mean age 44.6 years, range 25 to 49 years) with acute ischemic stroke due to large artery atherosclerosis (n=90), small artery occlusion (n=114) or undetermined cause (n=27) were recruited and prospectively followed up for pre-determined outcome. On each patient, we screened the PlA1/PlA2 polymorphism of the platelet glycoprotein IIIa gene, 4G/5G polymorphism of the plasminogen activator inhibitor-1 gene, G10976A polymorphism of the factor VII gene, C677T polymorphism of the methylenetetrahydrofolate reductase gene, and 27 base-pair repeat polymorphism of the endothelial nitric oxide synthase gene. End points were the composite outcome events of stroke, myocardial infarction, and death from all causes. During a mean duration follow-up of 29 months, composite outcome events occurred in 33 patients. There was a higher annual incidence rate of composite outcome events during the first year (9.1%, 95% CI 5.9-13.9%) than in the subsequent 2 years (2.6%, 95% CI 1.2-5.6%, p=0.038). None of the genetic polymorphism was associated with the composite outcome events. Past history of coronary artery disease or cerebrovascular disease was the only independent predictor of the composite outcome events (HR 3.71, 95% CI 1.69-8.14, p=0.001) at the Cox regression analysis. Our data indicate that the prothrombotic genetic polymorphisms do not have a significant influence on the prognosis in young ischemic stroke due to arterial occlusion or undetermined causes in Taiwan.     

Clinical lacunar syndromes as predictors of lacunar infarcts. A comparison of acute clinical lacunar syndromes and findings on diffusion-weighted MRI

OBJECTIVES: To evaluate if patients with acute lacunar syndromes have acute lacunar infarcts or other types of cerebral lesions on diffusion-weighted MRI. METHODS: Patients with acute lacunar syndromes underwent echo-planar diffusion MRI of the brain within 3 days after stroke onset. Localization and size of lesions with hyperintense signal were determined, compared with clinical characteristics and with findings on follow-up T2-weighted MRI. RESULTS: Twenty-three patients participated in the study. Thirteen patients had pure motor stroke, 1 pure sensory stroke, 8 sensorimotor stroke, and 1 ataxic hemiparesis. Twenty-two patients had at least one lesion with increased signal on diffusion-weighted MR images. These acute lesions were in the internal capsule/ basal ganglia/thalamus in 13 patients, subcortical white matter in 5 patients, brainstem in 2 patients, cortex (multiple small lesions) in 1 patient, and cortex + basal ganglia in 1 patient. The median volume of the lesions was 0.6 ml on the initial examination and on follow-up, of 17 patients after 1 to 5 months, 0.5 ml. CONCLUSIONS: Almost all patients with acute ischemic lacunar syndromes have acute lesions on echo-planar diffusion-weighted MRI within 3 days after stroke onset. These lesions are mostly small and subcortical, compatible with lacunar infarcts caused by single penetrating artery occlusion, but in a minor proportion of patients (2 of 23 in our study) a cortical involvement is found.     

缺血性脑卒中患者动脉粥样硬化分布的临床研究

目的探讨急性缺血性脑卒中不同亚型与颈动脉粥样硬化分布的相关性。方法通过经颅多普勒超声(TCD)和颈动脉彩色多普勒血流成像(CDFI)方法检测颅内、外动脉粥样硬化程度,并结合病史、生化指标及影像学提示的病变部位进行综合分析。结果411例急性缺血性脑卒中患者,颅内动脉狭窄率为38.93%(160/411),颈动脉颅外段狭窄率24.09%(99/411)。颈动脉颅外段狭窄者年龄大、吸烟比例高,与无狭窄者比较差异有统计学意义(P=0.020,0.013);而颅内动脉狭窄者糖尿病发病率明显高于无狭窄者(P=0.005)。411例中皮质梗死49例、皮质下梗死108例、腔隙性梗死72例和短暂性脑缺血发作30例,颈动脉颅外段狭窄者以皮质梗死为主(P=0.001),并且动脉内-中膜层厚度明显增加(P=0.020);而颅内动脉狭窄者以腔隙性梗死更多见(P=0.016)。颅内、外动脉狭窄者的年龄、性别、血糖及血脂之间差异无统计学意义(均P>0.05)。结论临床和影像学检查所确定的急性缺血性脑卒中亚型与颅内、外动脉粥样硬化的病变部位相关,提示发病的原因可能不同。糖尿病与吸烟是引起颅内、外动脉病变的重要原因。