Double infarction in one cerebral hemisphere

Thirty-two patients whose first stroke was due to double infarct in one cerebral hemisphere were identified among 1,911 consecutive patients from the Lausanne Stroke Registry. The double infarct involved territories of the superficial middle cerebral artery, superficial posterior cerebral artery, lenticulostriate, anterior choroidal artery, or borderzone. The most common combination involved territories of the anterior middle cerebral artery plus the posterior middle cerebral artery. In the patients with the double infarct, the prevalence of potential cardiac sources of embolism (19%) was similar to that found in the registry in general, but the double infarct was closely associated with tight (greater than or equal to 90% of the lumen diameter) stenosis or occlusion (75%) of the internal carotid artery. The most common neurological picture mimicked large infarction in the middle cerebral artery territory, but nearly half of the patients with double infarct in one cerebral hemisphere had a specific clinical syndrome, which was not found in the 1,879 remaining patients from the registry, including hemianopia-hemiplegia (in 6), acute conduction aphasia-hemiparesis (in 2), and acute transcortical mixed aphasia (in 6), in relation to characteristic combinations of infarcts. These unique clinical and etiological correlates warrant the recognition of double infarct in one cerebral hemisphere from other acute ischemic strokes.     

Centrum ovale infarcts: subcortical infarction in the superficial territory of the middle cerebral artery.

The centrum ovale, which contains the core of the hemispheric white matter, receives its blood supply from the superficial (pial) middle cerebral artery (MCA) system through perforating medullary branches (MBs), which course toward the lateral ventricles. Though vascular changes in the centrum ovale have been emphasized in dementia, stroke from acute infarction in the centrum ovale is less well documented. We studied 36 patients with infarct limited to MB territory, without involvement of the lenticulostriate territory. Ten patients had a large infarct, associated with severe disease of the ipsilateral carotid artery and with neurologic-neuropsychological impairment not different from that of large MCA infarcts. In 26 patients, the infarct was small and round or ovoid, and was associated with hypertension or diabetes and with "lacunar syndromes," usually of progressive onset. These findings show that two forms of centrum ovale infarcts can be delineated according to infarct size and shape, clinical picture, risk factors, and associated vascular disease. We propose to classify subcortical infarcts in the carotid system into four main territory groups: (1) deep perforator territory (from the MCA trunk, carotid siphon, anterior choroidal artery, anterior cerebral artery trunk, Heubner's artery, and posterior communicating artery); (2) perforating MB territory (from the superficial MCA branches); (3) junctional (territory between 1 and 2); and (4) combined territories.     

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.     

Mechanisms of single and multiple borderzone infarct: transcranial Doppler ultrasound/magnetic resonance imaging correlates

BACKGROUND AND PURPOSE: Hemodynamic patterns after borderzone (BZ) infarction are variable and dynamic. However, stroke mechanisms in different types of BZ infarctions have not been systematically studied by magnetic resonance angiography (MRA) and transcranial Doppler ultrasonography (TCD). METHODS: Forty-nine patients who experienced a stroke limited to the territory of either the superficial or internal borderzone proved on MRI included in our registry, corresponding to 4% of 1,200 patients with ischemic stroke, were studied. All these patients underwent MRA, extracranial Doppler ultrasonography, TCD and other investigations from the standard protocol of our registry. Twenty of them (41%) had a posterior BZ infarct, 14 (29%) an anterior BZ infarct, 10 (20%) a subcortical BZ infarct and 5 (10%) bilateral BZ infarcts. RESULTS: Unilateral internal carotid artery (ICA) tight stenosis or occlusion ipsilateral to the lesion was present in 14 patients (70%) with a posterior BZ infarct, in 72% of those with an anterior BZ infarct, in 80% of those with a subcortical BZ infarct and in 80% of those with bilateral BZ infarcts. TCD showed cross-filling of the middle cerebral artery via the anterior communicating artery in 5 patients (25%) with a posterior BZ infarct and 10% had an increased mean flow velocity (MFV) in the ipsilateral P1 posterior cerebral artery (PCA). In patients with an anterior BZ infarct, 3 (23%) had an MFV increase in the contralateral A1 anterior cerebral artery (ACA), and 2 (15%) had a higher MFV in the ipsilateral PCA. An elevated velocity at midline depths with reversed A1 ACA flow direction was seen in 2 patients (20%) with a subcortical infarct, and 1 patient (10%) had an MFV increase in the ipsilateral P1 PCA. Left ventricular systolic dysfunction (ejection fraction <40%) was present in 50% of patients with a posterior BZ infarct, in 36% of those with an anterior BZ infarct, in 20% of those with a subcortical BZ infarct and bilateral BZ infarcts each. CONCLUSION: The association of severe ICA stenosis or occlusion with cardiopathies and left ventricular dysfunction may play a critical role in those with BZ infarcts having inadequate collateral supply, while a cardioembolism or acute ICA dissection may also cause BZ infarction due to the rapidity of the occlusive process and the inability of the cerebral vasculature to recruit collateral pathways quickly enough.     

Stroke in a young man with fibromuscular dysplasia of the cranial vessels with anticardiolipin antibodies: a case report

A case of fibromuscular dysplasia (FMD), presenting with a non-hemorrhagic infarct is reported. Positivity of anticardiolipin antibodies suggested an immune response. A 40-year-old man presented with sudden onset of stroke, preceded by similar ischemic attacks. Computed tomography (C1) of the brain showed a recent non-hemorrhagic infarct in the left middle cerebral artery (MCA) territory and an old right MCA territory infarct. Serum was positive for anticardiolipin antibodies. These above findings were confirmed at autopsy. A portion of the internal carotid artery and the middle cerebral arteries on both sides revealed features of FMD, with thrombosis. This case suggests an immune mechanism for FMD, hitherto unobserved in the cerebral circulation. Received: 27 November 2000 / Accepted in revised form: 3 April 2001     

Effects of mild whole body hyperthermia on graded focal ischaemia-reperfusion in a rat stroke model

The influence of body temperature on focal cerebral ischaemia-reperfusion was investigated by using a well established rat stroke model. Three different degrees of ischaemia were created in the cerebral cortex of the right middle cerebral artery territory by varying the duration of clamping of the bilateral common carotid arteries and the right middle cerebral artery with full reperfusion. Mild hyperthermic (body temperature 38-39 degrees C) influence during ischaemia significantly enhanced the severity of infarction in mild (30 min) ischaemia, mean infarct volume was 78% greater than normothermic (body temperature 36.5-37.5 degrees C) group (P < 0.001); and in moderate (60 min) ischaemia, mean infarct volume was 23% greater than in the normothermic group (P < 0.05); but no difference between the two groups was observed in severe (90 min) ischaemia. Our data suggest that mild whole body hyperthermia during focal ischaemia-reperfusion has a detrimental effect on the infarct volume only in mild and moderate ischaemia in this model.     

Spectrum of superficial posterior cerebral artery territory infarcts

Posterior cerebral artery (PCA) territory infarction is not uncommon. Published series were concentrated either on isolated deep PCA territory infarcts or on incomplete calcarine artery territory infarcts. Although, correlations between clinical symptoms, causes of stroke and outcome at 6-months in patients with superficial PCA territory stroke are less well known. We sought prospectively stroke causes, infarct topography, and clinical findings of 137 patients with superficial PCA territory infarcts with or without mesencephalic/thalamic involvement, representing 11% of patients with posterior circulation ischemic stroke in our Stroke Registry. We analyzed patients by subdividing into three subgroups; (1). cortical infarct (CI) group; (2). cortical and deep infarcts (CDI) (thalamic and/or mesencephalic involvement) group; (3). bilateral infarcts (BI) group. We studied the outcomes of patients at 6-month regarding clinical findings, risk factors and vascular mechanisms by means of comprehensive vascular and cardiac studies. Seventy-one patients (52%) had cortical (CI) PCA infarct, 52 patients (38%) had CDI, and 14 patients (10%) had bilateral PCA infarct (BI). In the CDI group, unilateral thalamus was involved in 38 patients (73%) and unilateral mesencephalic involvement was present in 27% of patients. The presumed causes of infarction were intrinsic PCA disease in 33 patients (26%), proximal large-artery disease (PLAD) in 33 (24%), cardioembolism in 23 (17%), co-existence of PLAD and cardioembolism in 7 (5%), vertebral or basilar artery dissection in 8 (6%), and coagulopathy in 2. The death rate was 7% in our series and stroke recurrence was 16% during 6-month follow-up period. Features of the stroke that was associated with significant increased risk of poor outcome included, consciousness disturbances at stroke onset (RR, 66.6; 95% CI, 8.6-515.5), mesencephalic and/or thalamic involvement (RR, 3.79; 95% CI, 1.49-9.65), PLAD (RR, 2.71; 95% CI, 1.09-6.73), and basilar artery disease (RR, 5.94; 95% CI, 1.73-20.47). The infarct mechanisms in three different types of superficial PCA territory stroke were quite similar, but cardioembolism was found more frequent in those with cortical PCA territory infarction. Although, the cause of stroke could not reliably dictate the infarct topography and clinical features. Visual field defect was the main clinical symptom in all groups, but sensorial, motor and neuropsychological deficits occurred mostly in those with CDI. Outcome is good in general, although patients having PLAD and basilar artery disease had more risk of stroke recurrence and poor outcome rather than those with intrinsic PCA disease.     

Correlations between CT scan and sensorimotor EEG rhythms in patients with cerebrovascular disorders

Fifty subjects with cerebrovascular disorders and motor deficits, all able to perform a voluntary hand movement and aged between 33 and 78 years, were involved in this study. CT scan and computerized analysis of sensorimotor rhythms (mu rhythm and central beta rhythm) were performed for all patients. From the mu rhythm, the hemispheric asymmetry in amplitude and ERD during movement (ERD = event-related desynchronization) was measured and referred to a group of 38 neurologically normal subjects. Comparisons of CT scan data and EEG findings indicate a high correlation between morphological and functional findings. This correlation can be used to predict the localization of a lesion in the territory of the middle cerebral artery (MCA) based only on the amplitude and reactivity pattern of the mu rhythm. Thus, for example, an ipsilaterally enhanced mu rhythm in connection with a symmetric ERD indicates with a probability of 95% a deep, and with only 5%, a superficial lesion. Hemispheric mu amplitude symmetry and asymmetric ERD indicate a superficial cortical ischemia with a probability of 81%. An ipsilaterally attenuated mu rhythm accompanied by an asymmetric or abolished ERD indicates with 62% and 55%, respectively, a large extension of the infarct over the whole territory of the MCA.     

Cause of cerebral infarction in the carotid territory. Its relation to the size and the location of the infarct and to the underlying vascular lesion

Seventy-three patients with acute nonhemorrhagic stroke in the carotid territory were investigated for the cause of the stroke: middle cerebral artery (MCA) occlusion/stenosis or internal carotid artery (ICA) occlusion/stenosis; embolus from the heart and extra-cranial arteries or thrombosis. The study is prospective and consecutive comprising stroke patients below the age of 75 years, admitted in the acute state i.e. within 3 days after stroke onset. Excluded were patients with intracerebral hematoma, subarachnoid hemorrhage, vertebrobasilar stroke and patients in whom another severe disease was present. Cerebral angiography and CT-scan were performed in all patients within one and two days after admission. CT-scan was repeated 2 weeks and 6 months later. Forty percent had MCA occlusion, none had MCA stenosis, 12% had ICA occlusion, 14% had severe ICA stenosis (half of these were associated with MCA occlusion) and 41% were without significant MCA/ICA lesions. Twenty-seven percent had large infarcts with a diameter greater than 3 cm; 34% had medium-sized infarcts with a diameter between 3 and 1.5 cm; 21% had small infarcts with a diameter less than 1.5 cm; 18% had no identifiable infarct on CT-scan. MCA occlusion was responsible for 62% of the large or medium-sized infarcts. ICA occlusion or severe ICA stenosis were responsible for only 27% of the large or medium-sized infarcts. Only 11% of the patients with small or no infarct on CT-scan had significant MCA/ICA lesion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Opercular cheiro-oral syndrome

Perioral and distal upper limb sensory dysfunction (cheiro-oral syndrome) has classically been attributed to cortical involvement. In previously reported cases of the syndrome, caused by stroke, however, the thalamus or brain stem has been the actual site of the lesion. We have studied two patients with infarct in the superficial middle cerebral artery territory involving the parietal operculum. Sensory involvement was purely subjective in the face, but severe hypoesthesia was present in the distal upper limb, involving mainly position sense, stereognosis, and graphesthesia. Temperature and pain sensation were involved in one patient. These findings correlated with involvement of the lower part of the postcentral gyrus, more caudal parts of the parietal operculum, and underlying white matter. This opercular cheiro-oral syndrome seems more uncommon than faciobrachiocrural hemihypesthesia associated with anterior parietal artery territory infarct. A double supply to the parietal opercular region through branches of the temporal arteries and anterior parietal artery may explain the rarity of cheiro-oral syndrome resulting from hemisphere stroke, because simultaneous and partial compromise to two different pial artery networks is uncommon.     

Paramedian thalamic and midbrain infarcts: Clinical and neuropathological study

The clinical and neuropathological findings in 28 cases of paramedian thalamic and midbrain infarcts are reported. The 4 instances of unilateral paramedian thalamic infarct were characterized by mood and behavioral changes, limitation of the infarct to the center of the anatomical paramedian territory, and symmetrical configuration of the paramedian thalamic arteries. Basilar artery occlusion was found in 1 patient. The 5 cases of bilateral paramedian thalamic infarcts were characterized by disturbances of consciousness and behavior, extension of the infarct (to the mammillothalamic tracts in 4 cases, the red nuclei in 3, and the hypothalamus in 2), and a variable paramedian thalamic arterial pattern. The arterial pattern was symmetrical in 2 cases, asymmetrical in 1, and unilateral in 1. The basilar artery was occluded in 1 case, the basilar communicating and posterior cerebral arteries in 1, and a third patient had occlusion involving an aneurysm of the basilar artery. The 19 patients with paramedian thalamopeduncular infarcts had marked disturbances of consciousness (hypersomnia, deep coma, akinetic mutism) associated with ocular motility changes. Later, abnormal movements—always delayed—and memory, disturbances were observed in some. Thalamic changes were restricted to the paramedian territory in only 3 cases. The arterial pattern was symmertical in 5. The basilar and posterior cerebral arteries were occluded in 4 patients each. Paramedian infarcts were rarely found as isolated lesions and were always bilateral when there was only one arterial pedicle. The paramedian thalamic pedicle can supply the polar thalamic territory.     

Aphasia and infarction of the posterior cerebral artery territory

Spoken language disorders are rarely mentioned in superficial infarction of the posterior cerebral (PCA) territory. Two clinical types have been reported: transcortical sensory and amnesic aphasia. Between 1979 and 1990, we studied retrospectively 76 patients suffering from an occipitotemporal infarction located in the superficial territory of the posterior cerebral artery, all well documented by CT. Aphasia was one of the first and prominent signs in 18 cases. Middle cerebral artery concomitant infarction could have been the cause of language impairment in 10. In 8 patients aphasia was only explained by a PCA territory infarct. Three patients showed features of transcortical sensory aphasia. CT localization showed internal lobe and thalamic involvement of the dominant hemisphere. Five patients exhibited word finding impairment with various degrees of amnestic syndrome. The dominant internal temporal lobe was always afffected. Dominant thalamus involvement was found in one case only. Some correlations between clinical features and anatomical support (vascular supply and anatomical structure) might be suggested in our 8 cases of aphasic disorders due to PCA infarcts. They are discussed and compared with data in the literature.     

Borderzone infarctions distal to internal carotid artery occlusion: prognostic implications

Bilateral watershed (WS) infarction at the borderzone of the middle cerebral artery territory are typically related to severe hypotensive events. Unilateral WS infarctions have sometimes been reported in occlusion of the ipsilateral internal carotid artery (ICA), but their pathogenesis and prognostic implications are poorly known. Twenty-six of 154 (17%) consecutive patients with ICA occlusion had a computed tomography-proved ipsilateral WS infarct. Severe active heart disease with hypotension and syncope (p less than 0.0001), severe contralateral ICA disease (p less than 0.001), and elevated venous hematocrit values (p less than 0.001) related to heavy smoking were more frequent in the patients with WS infarction than in other patients. Delayed infarctions in the territory of the main branches of the middle cerebral artery distal to the ICA occlusion correlated with a visible stump or emboligenic changes (ulcerated or irregular stenosis) on the collateral channels, but this was not true for delayed WS infarctions. These findings suggest that most of the WS infarctions were hemodynamic. The patients with WS infarct had a higher death rate (9.9% per year) than did the patients without WS infarct (2.3% per year), suggesting that heart disease should be particularly closely managed in patients with WS infarctions. As WS infarctions were the most frequent type of infarction distal to an occluded ICA, appropriate treatment of all potential causes of systemic hemodynamic disturbances may be crucial in the long-term management of patients with ICA occlusion.     

Neurovascular territory involved in different etiological subtypes of ischemic stroke in the Perugia Stroke Registry

We studied the correlation between the potential causes of stroke (TOAST etiological groups) and the involvement of different vascular territories seen on computed tomography (CT) scans in patients with ischemic stroke. Information from consecutive patients with a first-ever stroke have been prospectively coded and entered into a computerized data bank (Perugia Stroke Registry). A population of 1,719 patients were evaluated: 1,284 patients (74.7%) had ischemic stroke. Large artery disease was the main cause of entire middle cerebral artery (MCA) territory infarcts (40.9%), superficial MCA territory infarcts (35.7%), and watershed infarcts (68.2%). The highest presence of emboligenic heart disease was found in the entire MCA territory infarcts (28.8%) or superficial (29.4%) supratentorial infarcts and in cerebellar infarcts (36.8%). Small artery disease was the most common presumed cause of deep MCA infarcts (75.0%) and posterior cerebral artery (PCA) territory infarcts (52.1%). In conclusion: stroke location could depend on its etiology. Lacunar infarcts are the most prevalent (36.7%), being mostly localized in the deep MCA territory; large artery disease includes more than two-thirds of watershed infarcts; the most prevalent territories involved in cardioembolic stroke are the entire MCA and posterior fossa.     

Anterior cerebral artery territory infarction in the Lausanne Stroke Registry. Clinical and etiologic patterns

We studied 27 patients with acute stroke and a corresponding infarct in the anterior cerebral artery territory, as disclosed using computed tomography. Patients were selected from 1490 patients (1.8%) admitted consecutively to a community-based primary care center who underwent standard investigations. An embolic phenomenon from the internal carotid artery or from the heart explained the infarct in 17 patients (63%). Anterior cerebral artery occlusion without a potential source of embolism was found only in one Vietnamese patient. Neurologic features correlated well with the topography and size of infarct, including hemiparesis, hemihypesthesia, mutism at onset, transcortical motor aphasia, conflictual tasks impairment, mood disturbances, and, more uncommonly, incontinence, grasp reflex, hemineglect, acute confusional state, and unilateral left apraxia. These findings suggest that the etiologic spectrum of anterior cerebral artery infarcts is the same as that of middle cerebral artery infarcts.     

利用激光散斑成像技术观察尤瑞克林对脑梗死大鼠脑血流的影响

目的 利用激光散斑成像技术研究尤瑞克林对大鼠脑梗死后局部脑血流的影响.方法 成年雄性SD大鼠24只,线栓法制备大鼠永久性大脑中动脉梗死模型.激光散斑成像系统观测缺血半球皮质及大脑中动脉供血区血流,2,3,5-三苯基氯化四氮唑(TTC)染色法测定脑梗死体积,并进行神经功能评分.结果 皮质及大脑中动脉供血区血流在大剂量组第1天及第2天给药后均有明显改善,部分大脑皮质血管增粗,血流速度加快,小剂量组及生理盐水组无明显变化,脑缺血48 h后,大、小剂量尤瑞克林组及生理盐水组的梗死体积分别为10.14%±3.02%,25.99%±3.90%,27.10%±3.32%,大剂量组与生理盐水组比较差异有统计学意义(F=61.14,P<0.01),小剂量组与生理盐水组比较差异无统计学意义.缺血后4 h,大剂量组神经功能损伤明显改善,小剂量组及生理盐水组无明显改变,36 h各组间的神经功能评分差异无统计学意义.结论 尤瑞克林可以减少大鼠局灶性脑缺血后梗死体积,延缓神经功能损伤,其作用可能与促进侧支循环的开放,增加大脑皮质和缺血区血流有关.     

Cerebellar infarction in the territory of the superior cerebellar artery: a clinicopathologic study of 33 cases

We reviewed the clinical and pathologic findings in 33 patients with infarcts in the territory of the superior cerebellar artery (SCA). The clinical manifestations included the rostral basilar artery syndrome (8); coma at onset, often with tetraplegia (11); cerebellar and vestibular signs (9, with delayed coma due to cerebellar swelling in 6); and, in only 1 patient, the "classic" syndrome of the SCA. Clinical features were overshadowed by an infarct in the territory of the middle cerebral artery in 3 other patients, and the diagnosis was made only at autopsy in a fourth. Pathologically, SCA infarcts occurred in isolation in 7 patients. The most striking finding was the high frequency of associated infarcts in the territory of the rostral part of the basilar artery (73%). One-third of patients also had an infarct in the territory of the posterior inferior cerebellar artery, sometimes associated with infarction of the anterior inferior cerebellar artery. Tonsillar herniation was observed in 15 patients, 8 of whom had no infarcts in other cerebellar territories. Occlusions occurred mainly in the distal basilar artery and distal vertebral artery. The infarcts were mostly caused by cardiac and artery-to-artery emboli.     

Infarcts in the territory of the deep perforators from the carotid system

We studied risk factors and presumed causes of infarct in 100 consecutive patients with a first stroke, who had an appropriate CT-proven infarct in the territory of the deep perforators from the carotid system (ITDPCS). The infarct involved the territory of the lenticulostriate arteries in 65 cases, the anterior choroidal artery in 23 cases, watershed zones between these two territories in four cases, and another territory in eight cases. In 42% of the patients, we felt the cause of the infarct to be small-artery disease. In 36%, at least one source of embolism was present (in 27% from the internal carotid artery, in 17% from the heart), either with (25%) or without (10%) associated hypertension (HT) and diabetes mellitus (DM). Other possible less common etiologies included migraine, syphilitic angiitis, and systemic diseases. We have confirmed that HT or DM are the most common etiologic factors of ITDPCS. However, large-artery disease and cardioembolism may be more important than previously assumed.     

大脑中动脉狭窄患者急性脑梗死发病机制:一项弥散加权磁共振和微栓子监测研究

目的我们前瞻性研究了30例经颅多谱勒超声(TCD)和核磁血管成像(MRA)检查证实大脑中动脉(MCA)狭窄,并在该供血区域出现急性缺血性卒中患者,以探讨MCA狭窄的可能机制。方法全部病人均进行微栓子监测以及弥散加权磁共振(DWI)检查。急性梗死分成单发和多发梗死,梗死部位分成皮层梗死(CI)、交界区梗死(BI)和深穿支动脉梗死(PAI)。微栓子信号(MES)和DWI梗死病灶分别由两位不同的医生在不知道对方资料的情况下确认。结果DWI结果发现急性多发脑梗死和单发梗死各15例(50%)。多发梗死病人中,成链状排列的BI最常见(11例,占73%)。单发梗死中只有PAI是最常见的类型(10例,占67%)。10例(33%)病人检测到MES,每30min内MES的中位数为15(3-102)个。MES在多发梗死中的发生频率(9/15,60.0%)明显高于单发梗死(1/15,6.7%)(P=0.002)。MES的数目能预测DWI上脑梗死的数目(线性回归,调整后R2=0.475,P<0.01)。结论MCA狭窄梗死最常见的原因有两个:①穿支动脉闭塞引起的皮层下小的腔隙性梗死;②由动脉-动脉的栓子不能被清除而造成的多发小梗死,尤其是在交界区更明显。     

Mechanisms of acute cerebral infarctions in patients with middle cerebral artery stenosis: a diffusion-weighted imaging and microemboli monitoring study

Although most therapeutic efforts and experimental stroke models focus on the concept of complete occlusion of the middle cerebral artery as a result of embolism from the carotid artery or cardiac chamber, relatively little is known about the stroke mechanism of intrinsic middle cerebral artery stenosis. Differences in stroke pathophysiology may require different strategies for prevention and treatment. We prospectively studied 30 consecutive acute ischemic stroke patients with middle cerebral artery stenosis detected by transcranial Doppler and magnetic resonance angiography. Patients underwent microembolic signal monitoring by transcranial Doppler and diffusion-weighted magnetic resonance imaging. Characteristics of acute infarct on diffusion-weighted magnetic resonance imaging were categorized according to the number (single or multiple infarcts) and the pattern of cerebral infarcts (cortical, border zone, or perforating artery territory infarcts). The data of microembolic signals and diffusion-weighted magnetic resonance imaging were assessed blindly and independently by separate observers. Diffusion-weighted magnetic resonance imaging showed that 15 patients (50%) had single acute cerebral infarcts and 15 patients had multiple acute cerebral infarcts. Among patients with multiple acute infarcts, unilateral, deep, chainlike border zone infarcts were the most common pattern (11 patients, 73%), and for single infarcts, penetrating artery infarcts were the most common (10 patients, 67%). Microembolic signals were detected in 10 patients (33%). The median number of microembolic signals per 30 minutes was 15 (range, 3-102). Microembolic signals were found in 9 patients with multiple infarcts and in 1 patient with a single infarct (p = 0.002, chi(2)). The number of microembolic signals predicted the number of acute infarcts on diffusion-weighted magnetic resonance imaging (linear regression, adjusted R(2) =0.475, p < 0.001). Common stroke mechanisms in patients with middle cerebral artery stenosis are the occlusion of a single penetrating artery to produce a small subcortical lacuna-like infarct and an artery-to-artery embolism with impaired clearance of emboli that produces multiple small cerebral infarcts, especially along the border zone region.