Anatomy of sensory findings in patients with posterior cerebral artery territory infarction.

BACKGROUND: Posterior cerebral arteries (PCAs) supply the ventrolateral thalamic sensory nuclei and white matter sensory tracts to the somatosensory parietal cortex. Patients with PCA territory strokes often have visual, memory, cognitive, and sensory signs. Clinicoanatomic correlation of visual, cognitive, and memory functions are well defined but, to our knowledge, no systematic study has analyzed the anatomy of sensory abnormalities. OBJECTIVE: To assess the frequency and anatomic correlation of sensory symptoms and signs in patients with PCA territory infarction. PATIENTS AND METHODS: Sixty patients with hemispheral and hemispheral and deep PCA territory infarcts apparent on computed tomographic and magnetic resonance imaging scans were studied for the presence of sensory findings and location of infarcts. RESULTS: Sensory symptoms or signs were present in 15 (25%) of 60 patients. Among patients with sensory findings, 11 of 15 had infarcts in the ventrolateral thalamus in the territory of the thalamogeniculate or lateral posterior choroidal arteries. The other 4 patients had no ventrolateral thalamic or white matter infarction but had severe proximal vascular occlusive lesions that could have caused temporary thalamic ischemia. One of these 4 patients had a medial thalamic infarct and transient hemisensory symptoms. Twelve patients had thalamic infarcts and no recorded sensory findings. Seven patients with thalamic infarcts (6 medial and 1 ventrolateral) had no sensory findings, and sensory findings could not be accurately assessed in 4 patients with ventrolateral and 1 patient with medial thalamic infarcts. CONCLUSIONS: All patients with PCA territory infarcts and sensory findings either had thalamic infarcts in thalamogeniculate or lateral posterior choroidal artery territory or had thalamic ischemia. Sensory findings in PCA territory infarction indicate ventrolateral thalamic ischemia.     

Bilateral thalamic infarction. Clinical, etiological and MRI correlates

To determine clinical, behavioral, topographic and etiological patterns in patients with simultaneous bilateral thalamic infarction in varied thalamic artery territories, we studied 16 patients who were admitted to our stroke unit over a 7-year period. Patients with bithalamic infarction represented 0.6% of our registry which included 2,750 ischaemic stroke patients. On computed tomography and magnetic resonance imaging with gadolinium enhancement, there were 4 topographic patterns of infarction: 1) bilateral infarcts in the territory of paramedian artery (8 patients [50%]); 2) bilateral infarcts in the territory of thalamogeniculate arteries (3 patients [19%]); 3) bilateral infarcts involving territory of paramedian and thalamogeniculate arteries (3 patients [19%]); 4) bilateral infarcts involving territory of polar and thalamogeniculate arteries (2 patients [13%]). A specific clinical picture was found in up to 50% of the patients with bithalamic infarction. This included patients with bilateral paramedian infarction having disorder of consciousness, memory dysfunctions, various types of vertical gaze palsy and psychic changes. Bilateral sensory loss predicted accurately bilateral infarction in the territory of thalamogeniculate arteries. The main cause of bilateral thalamic infarction was small artery-disease, followed by cardioembolism. Cognitive functions in patients with bilateral paramedian infarction did not change significantly during the follow-up, in contrast to those with infarcts in varied arterial territories. Acute bilateral infarction involving both thalamus is uncommon, although they are often associated with specific neurologic-neuropsychological patterns, allowing diagnosis before radiological examination.     

Hemiataxia-hypesthesia: a thalamic stroke syndrome.

Six patients had isolated hemiataxia and ipsilateral sensory loss, as a manifestation of thalamic infarction in the thalamogeniculate territory. Acute hemiataxia-hypesthesia was not found in 1075 other patients from the Lausanne Stroke Registry who were admitted during the same period. Stroke onset was progressive in five patients and immediately complete in one. Five patients had an objective sensory loss. In two patients this affected light touch, pain and temperature sense, and in another three light touch, pain temperature, position and vibration sense. One patient had a purely subjective sensory disturbance. The sensory deficit cleared or was clearing although the ataxia persisted in all patients. On lesion mapping on CT or MRI, all patients had involvement of the lateral part of the thalamus (ventral posterior nucleus and ventral lateral nucleus). The presumed causes of stroke were cardioembolism in one patient, posterior cerebral artery occlusion in one patient and meningovascular syphilis in one patient, hypertensive small vessel disease in two patients, and undetermined in one patient. Hemiataxia-hypesthesia is a new stroke syndrome involving the perforating branches to the lateral thalamus, but in which small vessel disease may not be the leading cause.     

Basilar branch pontine infarction with prominent sensory signs

We identified 10 patients with acute pontine infarction and specific sensory findings. Two patients had pure sensory symptoms, two had sensory complaints of the hand and mouth, and the other six had hemisensory loss referable to medial lemniscal or spinothalamic tract dysfunction but localized to one limb, to an arm and leg, or to the face, characteristic of stroke localized to the cerebral hemisphere. All patients had magnetic resonance imaging showing infarction of the medial or lateral pontine tegmentum and a patent basilar artery. No definite source for cardiogenic thromboembolism was found. Infarcts in the midline extending from the base of the pons posteriorly into the tegmentum suggested basilar branch occlusion, while infarcts involving only part of the tegmentum probably resulted from small penetrator branch occlusion. Vertigo, light-headedness, or cranial nerve dysfunction suggested a pontine location of neurological dysfunction in these patients, but the nature of the sensory findings did not always predict the lateral, medial, inferior, or superior extent of tegmental infarction.     

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.     

The syndrome of posterior choroidal artery territory ifarction

Posterior choroidal artery (PChA) territory infarcts remain the least well-known type of thalamic infarcts. Our study of 10 personal cases, selected from 2,925 stroke patients admitted consecutively to a community-based primary care center, and 10 published cases of unilateral PChA territory infarct suggests that they can often be differentiated clinically from other thalamic infarcts. Patients with PChA territory infarct associated with superficial posterior cerebral artery territory infarct or with another infarct were excluded. Damage was characteristically limited to the lateral geniculate body, pulvinar, posterior thalamus, hippocampus, and parahippocampal gyrus, without involvement of the upper midbrain and the anterior nucleus of thalamus. In lateral PChA territory infarct, the most common clinical manifestations included homonymous quadrantanopsia, with or without hemisensory loss and neuropsychological dysfunction (trans-cortical aphasia, memory disturbances). A homonymous horizontal sectoranopsia is exceptional but particularly suggestive of the involvement of the lateral geniculate body in this territory. Medial PChA territory infarct was less frequent. Its neurologic picture was dominated by eye movement disorders not particularly suggestive of thalamic involvement. Late disability was usually absent or slight, being related to pain and delayed abnormal movements. The most common stroke etiology was presumed small-vessel occlusive disease.     

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.     

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.     

Vaskul?re Syndrome des Thalamus

The thalamus comprises numerous nuclei that can be grouped into five major functional domains: (1) the reticular and intralaminar nuclei influence arousal and nociception, (2) sensory nuclei handle afferent pathways, (3) the effector nuclei are involved in motor function and language, (4) associative nuclei participate in higher cognitive functions and (5) limbic nuclei influence mood and motivation. The thalamic nuclei are mainly supplied by the following four cerebral arteries: paramedian artery, anterior thalamoperforating artery, thalamogeniculate artery and posterior choroidal artery (lateral branches). Occlusions of these arteries affect the thalamic nuclei to varying degrees and produce partly characteristic and partly overlapping deficits. This article describes the clinical pictures.     

Thalamic infarcts in young adults: relationship between clinical-topographic features and pathogenesis.

BACKGROUND: Most reports on thalamic infarcts have focused on clinicoanatomical correlations while the mechanisms of stroke have rarely been investigated. Moreover, most series have included mainly elderly stroke patients, whereas scarce information is available about the etiology of thalamic infarcts in the young. OBJECTIVE: To investigate the mechanisms of thalamic infarcts according to vascular territory in a series of young adults. METHODS: A sample of 24 consecutive patients with thalamic infarcts were found in an unselected series of 129 patients with cerebral infarction aged 18-45 years. Diagnostic investigation included computed tomography and magnetic resonance imaging scans, ultrasonic scanning of the extracranial and intracranial arteries, conventional angiography and magnetic resonance angiography, transthoracic and transesophageal echocardiography and extensive thrombophilic studies. The affected vascular territory within the thalamus was determined using standard templates. RESULTS: Thalamic infarcts constituted almost one fifth of the ischemic strokes in our series. Ten patients (42%) had infarct in the territory of the thalamogeniculate pedicle (group 1), 10 (42%) in the territory of the paramedian thalamosubthalamic artery (group 2) and 3 (12%) in the territory of the tuberothalamic artery (group 3). In 1 patient (4%), the lesion involved more than one vascular thalamic territory. A significant association between cardioembolism and paramedian infarcts was found when comparing the mechanisms of stroke of group 2 with those of the group including infarcts in other thalamic territories (p = 0.002) and with those of group 1 (p = 0.02). CONCLUSIONS: Our findings provide information about the epidemiology of thalamic infarcts in young adults and point to a differential association between the distribution of infarcts in specific vascular territories and the mechanism of stroke.     

Non-dominant hemisphere syndrome as a result of a right thalamic infarct: an anatomoclinical case

A 71 year old man had a massive left sensory deficit and hemiplegia, with left heminanopia, visual neglect and constructional apraxia. Moreover he experienced an extra-left arm and illusions of movements. 3 weeks later he suffered "thalamic" pain on left side; he died suddenly 6 weeks after the stroke. Post-mortem examination revealed: a) a right inner temporal and occipital infarction; b) a right thalamic infarction in the thalamogeniculate and paramedian territories; c) an infarction in the adjacent right internal capsule. Considering this case and pertinent literature on clinicopathological studies of right thalamic infarction, the authors suggest that a simultaneous ischaemia of thalamogeniculate and paramedian territories should be necessary to induce somatognosic and visuospatial disturbances.     

Chronic cognitive impairment following laterothalamic infarcts: a study of 9 cases

BACKGROUND: The occlusion of the lateral thalamic arteries leads to infarcts of ventrolateral thalamic nuclei, the ventroposterior nucleus, and the rostrolateral part of pulvinar, and produces hemisensory loss with or without hemiataxia. Cognitive impairment after such strokes has not been systematically studied. OBJECTIVE: To determine the nature and the extent of long-lasting cognitive deficits following lateral thalamic strokes. DESIGN: Case series. SETTING: Neurology department, Lausanne University Hospital, Lausanne, Switzerland. PATIENTS: Nine patients with hemisensory loss due to an isolated laterothalamic infarct. MAIN OUTCOME MEASURES: Three to 6 months after stroke onset, standard neuropsychologic evaluation, including testing of language, ideomotor and constructive praxis, visual gnosis, spatial attention, learning abilities, and executive functions. RESULTS: Six of 9 patients showed some degree of cognitive impairment. Executive functions tasks, particularly verbal fluency, were impaired in 5 patients (4 with right and 1 with left lesion). Learning and delayed recall in visuospatial and verbal tasks, but not in recognition, were impaired in 3 patients (2 with right and 1 with left lesion). Difficulties in visual gnosia were observed in 1 patient with right lesion while word-finding difficulties were observed in 1 patient with left lesion. CONCLUSIONS: Our observations show that while learning, naming, and gnosic difficulties fit with the classical verbal/nonverbal dichotomy (left and right hemisphere, respectively), executive dysfunctions, including verbal fluency tasks, were more dominant after right thalamic infarcts. Although the observed deficits appeared to be less severe than those generally found with dorsomedial and polar thalamic strokes, the dominance of executive dysfunction suggests that ventrolateral thalamic lesions may disrupt frontothalamic subcortical loops.     

Face-arm-trunk-leg sensory loss limited to the contralateral side in lateral medullary infarction: a new variant

Two patients are reported on who experienced loss of pain and temperature sensation in the entire contralateral hemibody but sparing the ispsilateral face (pure sensory stroke pattern) related to acute lateral medullary infarction. In both patients MRI showed a notch-like retro-olivary ischaemic lesion in the ventromedial tegmentum with preservation of the far lateral medulla. The mediolateral lesion involved the crossed lateral spinothalamic tract and the ventral trigeminothalamic tract, corresponding to sensory loss in the contralateral face, arm, and upper trunk. The ventrolateral extension of infarct damaged the far lateral part of the spinothalamic tract, corresponding to sensory loss in the contralateral lower trunk and leg. The findings suggest that hemisensory loss of the spinothalamic type involving—and limited to—the whole hemibody can occur in infarction in the lower brainstem. This form of pure sensory stroke may be classified as type IV of sensory loss in lateral medullary infarction.

     

Mechanisms involved in large subcortical infarcts]

Large subcortical infarcts(maximum diameter of infarct > or = 20 mm) result from various stroke patterns, including striatocapsular infarcts (SCI), corona radiata infarcts, centrum semiovale infarcts, and internal borderzone infarcts. A systematic investigation of stroke pathogenesis involved in large subcortical infarcts, however, has not been performed. This study attempted to clarify the stroke mechanisms involved in large subcortical infarcts, by examining 50 patients with large subcortical infarcts out of 430 ischemic stroke patients consecutively registered in our department. The subjects were divided into two groups according to the vascular territories involved on the MRI: 1) the lenticulostriate arteries group for 39 patients whose infarcts were restricted to within the vicinity of the lenticulostriate arteries; 2) the internal borderzone group for 11 patients whose infarcts mainly involved the internal borderzone (the upper part of the corona radiata and the centrum semiovale) between the territories of the deep perforating branches from the basal cerebral arteries and the medullary branches from the superficial pial arteries. Stroke pathogenesis were classified into the following 6 categories: A) cardiogenic embolism, 9 patients; B) artery-to-artery embolism, 6 patients; C) cryptogenic embolism, 2 patients; D) thrombotic MCA (M1) occlusion, 9 patients; E) thrombotic ICA occlusion, 10 patients; F) undetermined cause, 14 patients. The lenticulostriate arteries group consisted of 9 patients with cardiogenic embolism, 6 with artery-to-artery embolism, 2 with cryptogenic embolism, 8 with thrombotic M1 occlusion, and 14 with undetermined cause. The internal borderzone group consisted of 10 patients with thrombotic ICA occlusion and 1 patient with thrombotic M1 occlusion. The stroke pathogenesis of the undetermined cause is considered to be thrombotic occlusion at the orifice of the lateral lenticulostriate artery, a so-called "branch atheromatous disease (BAD)". The patients in this group experienced a gradual onset, and did not have a cardiac source of the embolism or proximal large artery disease. Among the patients reported as having SCI, BAD may play a role in some cases, especially in those whose the cause was classified as "undetermined". In conclusion, the lenticulostriate arteries group exhibited a higher frequency of cerebral embolisms (cardiogenic embolism, artery-to-artery embolism, and cryptogenic embolism) and thrombotic M1 occlusion, whereas the internal borderzone group had a higher frequency of thrombotic ICA occlusion.     

Proximal posterior cerebral artery occlusion simulating middle cerebral artery occlusion

We describe 12 cases of acute stroke in which clinical features of proximal posterior cerebral artery occlusion simulated the clinical syndrome of middle cerebral artery occlusion. The majority of patients developed contralateral hemiparesis, homonymous hemianopia, hemispatial neglect, and sensory loss or sensory inattention. All 8 patients with dominant hemisphere lesions were aphasic. Accurate diagnosis in each case was achieved only after a head CT, showing occipital lobe, thalamic, and inferomesial temporal lobe infarction. "Cortical" signs are probably explained by thalamic involvement. Recognition of this syndrome has implications for management and prognosis.     

Posterior cerebral artery territory infarcts in the New England Medical Center Posterior Circulation Registry.

BACKGROUND: Infarcts in the territory of the posterior cerebral arteries (PCAs) are common. Although associated clinical symptoms and signs are known, the mechanisms of stroke and the anatomical distribution of PCA territory lesions caused by the various stroke mechanisms are less well defined. Published reports have selected only special subgroups of patients. PATIENTS AND METHODS: We studied stroke mechanisms, infarct distribution, and clinical findings among 79 patients in the New England Medical Center Posterior Circulation Registry in whom brain imaging scans showed infarcts that involved 1 or more cortical territories of the PCA. RESULTS: Forty-eight patients (61%) had infarcts limited to the PCA territory (pure PCA), while 31 (39%) also had infarcts in other territories (PCA+). Infarcts were in the cortical territory of the PCA in 47 patients (59%) and were cortical and deep in 32 (41%). Infarcts that were cortical and deep were more common in PCA+ lesions. Stroke mechanisms were embolism of cardiac origin (32 [41%]), proximal arterial disease (25[32%]), cryptogenic embolism (8[10%]), intrinsic PCA disease (7[9%]), vasoconstriction (4[5%]), and coagulopathy (3[4%]). Patients with cardiogenic embolism and intrinsic PCA disease often had pure PCA territory infarcts, while patients with proximal arterial disease more often had PCA+ infarcts. Visual abnormalities were present in 66 patients (84%). Motor weakness, cognitive and behavioral abnormalities, and ataxia were found in 20 patients (25%); only 12 (15%) had sensory signs. CONCLUSIONS: The great majority of pure PCA and PCA+ territory infarcts are caused by cardiac or intra-arterial embolism. Intrinsic PCA disease, vasoconstriction, and coagulopathy are less common causes of infarction.     

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.     

Bilateral paramedian thalamic infarction with hypothalamic dysfunction

Unilateral thalamic lesions cause transient or permanent behavioral, sensory and oculomotor disturbances; bilateral lesions of thalamus result in more severe and longer lasting symptoms. We present an atypical case of bilateral paramedian thalamic infarct with concomitant hypothalamic dysfunction. The only risk factor of ischaemic stroke found in the patient was a short lasting episode of atrial fibrillation. Bilateral paramedian thalamic infarcts may result from occlusion of one paramedian thalamic artery, which arises from the posterior cerebral artery, either with separated or with a common trunk, thus supplying the thalamus bilaterally. Independently of anatomical variants of thalamus blood supply, the most probable cause of infarct in our patient was unilateral or bilateral occlusion of the posterior cerebral artery by cardioembolism, probably in the course of basilar artery occlusion. Hypothalamic dysfunction may accompany thalamic infarcts; thus hypothalamo-pituitary function should be routinely assessed in bithalamic infarcts.     

脑白质区域非腔隙性梗死灶与颅内外血管狭窄关系的探讨

目的 探讨脑白质区域非腔隙性梗死灶与颅内外血管狭窄的关系.方法 对30例脑白质区域非腔隙性梗死患者的头颅MRI以及主动脉弓、全脑数字减影血管造影(DSA)检查资料进行分析.结果 本组MRI示12例单侧基底节区片状异常信号中,DSA表现为一侧颈内动脉(ICA)起始部闭塞或高度狭窄9例,一侧大脑中动脉(MCA)M1段高度狭窄2例,无明确血管病变1例.6例基底节以及侧脑室旁白质区域病灶中,一侧ICA起始部闭塞或高度狭窄3例,一侧ICA C5段闭塞1例,一侧MCA M1段闭塞2例.4例侧脑室旁或半卵圆中心白质区域病灶中,一侧ICA C6段闭塞1例,一侧MCA M1段高度狭窄2例,无明确血管病变1例.8例皮质下上型或皮质下侧型分水岭脑梗死患者中,一侧ICA起始部闭塞或高度狭窄6例,双侧ICA起始部闭塞1例,一侧MCA M1段高度狭窄1例.结论 脑白质区非腔隙性梗死灶的发生与ICA系统大血管的狭窄或闭塞有密切的关系.