腔隙性梗死综合征的临床特点

腔隙性梗死临床极为常见,每种腔隙性梗死综合征通常提示为某一特定部位的病变,然而,临床观察发现同一腔隙综合征也可由不同部位的病变所致。同一部位病灶也可导致不同种类的腔隙综合征。腔隙综合征的临床表现复杂多变,远不止Fisher列举的21种腔隙综合征,如手-口综合征、面舌综合征、构音障碍-面轻瘫综合征、单独吞咽困难、单独偏身共济失调及四肢共济失调等多被归入某些综合征的变异型。另外,同时或相继以两组综合征起病的腔隙性梗死极少见,内囊后肢腔隙性梗死更具有其独特的特点。     

Haemorrhagic pure motor stroke

To describe the clinical characteristics of haemorrhagic pure motor stroke (PMS). Twelve patients with haemorrhagic PMS were identified. Haemorrhagic PMS accounted for 3.2% of all cases of pure motor hemiparesis ( n  = 380) and 3.3% of intracerebral haemorrhage ( n  = 364) entered in the database. When compared with PMS of ischaemic origin, patients with haemorrhagic PMS were more likely to be younger (62.2 vs. 75.2 years, P  = 0.003) and to have headache (33% vs. 6.3%, P  =0.007) and thalamus involvement (25% vs. 2.4%, P  = 0.005). Limb weakness (100% vs. 74.1%; P  = 0.03), involvement of the internal capsule (50% vs. 17.3%, P  = 0.012) and symptom free at discharge (25% vs. 3.7%, P  = 0.012) were significantly more frequent in patients with haemorrhagic PMS than in the remaining cases of haemorrhagic stroke, whereas nausea and vomiting (0% vs. 25.9%, P  = 0.03), altered consciousness (0% vs. 42.9%, P  = 0.001), sensory symptoms (8.3% vs. 46.9%, P  =0.007) and ventricular haemorrhage (0% vs. 26.1%, P  = 0.028) were significantly less frequent. Haemorrhagic PMS is a very infrequent stroke subtype. Headache at stroke onset may be useful sign for distinguishing haemorrhagic PMS from other causes of lacunar stroke. There are important differences between haemorrhagic PMS and the remaining intracerebral haemorrhages.     

腔隙性脑梗死患者的智能障碍

采用韦氏成人智力量表对186例腔隙性脑梗死患者进行测定，结果表明腔隙性脑梗死损害部位不同，其智能损害程度差异较大。左侧半球病变更易造成智能障碍，尤其左侧基底节及颞叶；多发病灶者其智能损害较单发病灶者重，单发的皮质下腔隙性梗死也可造成明显智能缺损。性别、年龄、职业与腔隙性脑梗死后引发的智能障碍无相关性，但受教育程度的高低与智能障碍的程度呈负相关。笔者认为提高国民文化素质，积极预防和治疗脑血管病，是减少和防治脑血管性痴呆发生的关键。     

Causes of small deep infarcts detected by CT

Clinical data of 83 patients with symptomatic CT detected small deep infarcts in one of the cerebral hemispheres were retrospectively reviewed. 61 Percent had hypertension. In 15 percent a cardiac embolus was the most probable cause of a small deep infarct. In 22 cases angiography had been performed and ipsilateral internal carotid stenosis was present in 6 cases. It is suggested that small deep infarcts visible on CT may be caused by cardiac emboli and artery-to-artery emboli from carotid lesions, besides small vessel disease due to hypertension. Therefore anticoagulation or angiography. if need be. followed by carotid endarterectomy, may be indicated in a number of cases.     

Pure sensory stroke with lacunar infarction in the posterior ventral thalamus on CT

A hypertensive male patient is described who suffered a pure sensory stroke. CT revealed a small lacunar infarct in the contralateral posterior part of the ventral thalamus. This is the second described case with a CT verified single ischemic lesion restricted to the thalamus.     

Clinical study of 39 patients with atypical lacunar syndrome

The aim of this study was to describe the clinical characteristics of atypical lacunar syndrome (ALS) based on data collected from a prospective acute stroke registry. In total, 2500 acute stroke patients were included in a hospital based prospective stroke registry over a 12 year period, of whom 39 were identified as having ALS and radiologically proven (by computed tomography or magnetic resonance imaging) lacunes. ALS accounted for 1.8% of all acute stroke patients, 2.1% of acute ischaemic stroke, and 6.8% of lacunar syndromes. ALS included dysarthria facial paresis (n = 12) or isolate dysarthria (n = 9), isolated hemiataxia (n = 4), pure motor hemiparesis with transient internuclear ophthalmoplegia (n = 4), pure motor hemiparesis with transient subcortical aphasia (n = 3), unilateral (n = 2) or bilateral (n = 3) paramedian thalamic infarct syndrome, and hemichorea hemiballismus (n = 2). Atypical lacunar syndromes were due to small vessel disease in 96% of patients. Atherothrombotic infarction occurred in one patient and cardioembolic infarct in another, both presenting pure dysarthria. Outcome was good (in hospital mortality 0%, symptom free at discharge 28.2%). After multivariate analysis, the variables of speech disturbances, nausea/vomiting, ischaemic heart disease, and sensory symptoms were found to be significantly associated with ALS. In conclusion, atypical lacunar syndrome is an infrequent stroke subtype (one of each 14 lacunar strokes). ALS occurred in 6.8% of lacunar strokes. Isolated dysarthria or dysarthria facial paresis were the most frequent presenting forms. The prognosis of this infrequent non-classic lacunar syndrome is good.     

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.     

Progressive stroke caused by CT-verified small deep infarcts; relation with the size of the infarct and clinical outcome

In 73 of 83 consecutive patients with a CT-verified small deep infarct, the course of the initial deficit was retrospectively assessed. Sixty-four percent showed their maximal deficit at stroke onset, while 36% had progression of the initial deficit. Between these 2 groups, there was no difference in the number of patients with hypertension and in the number of patients with a probable cardiac embolic cause of the lacunar stroke. Patients with progressive lacunar stroke had larger volume infarcts and showed less favourable outcome at one month. Our data suggest that progression of symptoms in patients suffering a small deep infarct is due to an increase of the infarcted area. This offers a rationale for early anticoagulant treatment in patients with small deep infarcts. However, since any beneficial effect of such treatment has not been established so far, a prospective controlled study is warranted.     

脑干腔隙性梗塞的MRI,TCD与临床

本文对８５例脑干腔隙性梗塞（腔梗）患者的头颅ＭＲＩ、部分ＴＣＤ及临床特征作回顾性分析。结果：本组患者发病年龄较大，７５％有长期高血压史，临床表现为复杂性、多样化特点，且多数缺乏典型的交叉或脑干孤立症征。ＭＲＩ扫描显示腔隙灶以桥脑腹侧居多，病灶＜０．５ｃｍ者可无症状或症状轻微。ＴＣＤ可很好反映椎－基底动脉系统的血管弹性及血流速度，对脑干腔梗的诊断有一定的帮助，但定位不甚准确。ＭＲＩ仍是诊断脑干腔梗的最佳手段。     

Prevalence of silent myocardial ischemia in single and multiple lacunar infarcts and large vessel disease stroke

Background and purpose

The relationships between single (SLI) and multiple lacunar infarcts (MLI) and occult coronary artery disease (CAD) have not yet been sufficiently evaluated. We aimed to investigate the prevalence of silent CAD in patients with SLI, MLI and large vessel disease (LVD) stroke, and to identify factors associated with its presence.

Methods

We enrolled 125 patients who had suffered their first non-cardioembolic ischemic stroke but had no documented history of CAD. According to their pathologies, these patients were assigned to one of three groups: MLI (n = 21), SLI (n = 50) or LVD (n = 54). Asymptomatic CAD was detected by myocardial perfusion SPECT imaging.

Results

Silent CAD was detected in 40 patients (32% of the total); of those that experienced CAD, 15 (30%) were from the SLI group, 7 (33%) had MLI, and 18 (33%) had an LVD stroke. Differences between the groups were not significant. During a median follow-up of 48 months, the overall stroke recurrence was 8.8%; the stroke recurrence rates for each subgroup were 6% in patients with SLI, 7% in LVD and 19% in MLI. Mortality was higher in patients from the MLI and LVD groups (26% and 14%, respectively) than in those from the SLI group (6%; p = 0.02). We found no relationships between the various risk factors and silent CAD.

Conclusions

In this exploratory study, SPECT imaging results revealed that the prevalence of abnormal myocardial perfusion was similar in patients with either single or multiple lacunar infarcts and those that had experienced large vessel disease stroke.     

Restricted pain and thermal sensory loss in a patient with pontine lacunar infarction: a clinical MRI study

Pure sensory syndrome (PSS) is characterized by hemisensory symptoms without other major neurological signs. It was initially attributed to thalamic lacunar infarction, but several reports have shown the PSS can be due to small infarcts involving the posterior part of the internal capsula, the cerebral cortex and the brainstem. Paramedian and lateral pontine infarctions are associated respectively with lemniscal and spinothalmic (ST) sensory impairment. We describe a patient with an isolated impairment of the ST modalities caused by a segmental paramedian pontine infarction.     

腔隙性脑梗死所致抑郁的相关因素分析

目的探讨腔隙性脑梗死所致抑郁的相关因素。方法采用头颅CT或MPI确定诊断和病灶定位,并以SDS、ADL及NFA分别对患者进行测试,然后分析其发生抑郁的相关因素。结果本组腔隙性脑梗死所致抑郁的发生率为38．04％;与发生抑郁的相关因素有：梗死病灶系多发、且多分布于皮层下,存在脑室扩大,神经功能缺陷较重以及日常生活能力差等。结论腔隙性脑梗死所致抑郁是临床常见病,且为生物、心理因素协同作用所致。     

载脂蛋白E基因多态性与腔隙性梗死关系的研究

目的:探讨载脂蛋白E(ApoE)基因多态性与腔隙性梗死(lacunarinfarction)的相关性。方法:采用病例对照研究,对105例中老年腔隙性梗死患者和322例健康对照者进行研究。用多聚合酶链式反应(PCR)和限制性片段长度多态性测定ApoE基因多态性。结果:对照组ApoE基因的等位基因频率为e210%、e382.4%和e47.6%;腔隙性脑梗死组的等位基因频率为e28.2%、e384.3%和e47.5%。ApoE各基因型和等位基因频率在腔隙性脑梗死和对照组之间差异无显著性(P>0.05)。结论:未发现ApoE基因多态性与腔隙性梗死存在相关关系。     

血浆同型半胱氨酸与腔隙性脑梗死及认知功能关系

目的:探讨血浆同型半胱氨酸(Hcy)与腔隙性脑梗死的关系以及对认知功能的影响。方法:选取112例腔隙性脑梗死患者及50名健康对照者,检测血浆Hcy水平以及简易智能精神状态检查表(MMSE)评分。结果:①Hcy水平腔隙性脑梗死组明显高于对照组(P<0.05);②Logistic回归证实Hcy水平升高是腔隙性脑梗死的独立危险因素,OR为1.212;③Hcy水平与MMSE分值呈负相关(r=-0.552,P<0.001);④多元线性回归分析得出腔隙性脑梗死患者MMSE分数=45.771-7.314×logHcy-0.171×年龄。结论:血浆Hcy水平升高是腔隙性脑梗死的独立危险因素,对认知功能有独立的影响。     

ACE基因插入／缺失多态性与脑血管病的关联性研究

目的:探讨血管紧张素转换酶(ACE)基因插入(I)/缺失(D)多态性与脑血管病(CVD)的关系。方法:采用聚合酶链反应技术(PCR)检测19Z例卒中患者、95例高血压病人和124例正常人的ACE基因多态性。结果:CVD组ACE基因D等位基因频率为0.58,明显高于高血压对照组(P＜0.02)和正常对照组(P＜0.01),DD基因型频率明显高于正常对照组(P＜0.05)。腔隙性梗死(LACI)组的DD基因型显著高于对照组(P＜0.05)。多元回归分析发现ACE*DD基因型与卒中无明显相关性(P＜0.08),而与LACI存在明显相关性(P=0.048)。结论:ACE基因缺失多态性在LACI的形成中可能产生重要作用。     

Is TEE useful in patients with small subcortical strokes?

Although the role of transesophageal echocardiography (TEE) in the investigation of stroke mechanism is well established, the value of this test in patients with lacunar presentation is unclear. Review of 214 patients with acute cerebral ischemia referred for TEE to exclude cardioaortic sources of embolism after non-diagnostic basic work-up including carotid ultrasound and transthoracic echocardiography. TEE was considered positive when it showed large or complex aortic arch plaques, left atrial thrombus, mitral or aortic valve vegetations, or patent foramen ovale with atrial septal aneurysm. Multivariate regression analysis was performed to assess the value of lacunar syndrome and radiological small subcortical infarctions in predicting TEE result. Predictive values and likelihood ratios for these variables were calculated. Fifty-two patients (24%) had positive TEE. The most common embolic source was large or complex aortic plaques in 19% of patients. Neither clinical presentation with lacunar syndrome nor the presence of small subcortical infarction on CT scan predicted a negative TEE result on univariate or multivariate analysis. However, the combination of lacunar syndrome with radiological small subcortical infarction was uniformly associated with negative TEE (P=0.01; negative predictive value 100%). The combination of lacunar syndrome with small subcortical radiological infarct predicts the absence of cardioaortic sources of embolism on TEE in patients with acute cerebral ischemia.     

The classic lacunar syndromes: clinical and neuroimaging correlates

Background:  Although lacunar syndromes (LSs) are aimed to be linked to lacunar infarcts, the relation between both is still not very well defined.
Purpose:  The present retrospective study tries to define more specifically the clinical and the neuroimaging characteristics of the five most classic LSs.
Patients and methods:  Out of a series of 1617 consecutive stroke patients, admitted to the Ghent University Hospital, 293 presented a classic LS. Magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) was performed within 5 days after stroke onset in 227 patients. An acute territorial infarct was demonstrated in 54 patients. The study population finally consisted of 173 patients with a classic LS in whom the responsible lacune was demonstrated or in the absence of another type of infarct.
Results:  The responsible lacune was demonstrated with DWI in 104 patients. Pure motor stroke (MS) correlated significantly with the presence of the responsible lacune in the internal capsule ( P  = 0.000147) and with the stroke severity ( P  = 0.00724). No significant correlation was observed between the location of the lacunes and the other LS's.
Conclusion:  Pure MS has to be considered as the most specific lacunar syndrome.