The clinical and topographic spectrum of cerebellar infarcts: A clinical—magnetic resonance imaging correlation study

We studied 34 consecutive patients with non–mass-producing cerebellar infarcts using a standard protocol of investigations including magnetic resonance imaging (MRI). We analyzed the topography of infarcts to determine the involved arterial territories and we correlated the findings with neurological dysfunction and potential causes of stroke. Sixteen patients had an infarct in the territory of the posterior inferior cerebellar artery (PICA); 2, in the territory of the anterior inferior cerebellar artery (AICA); 13, in the territory of the superior cerebellar artery (SCA); and 8 had junctional infarcts between the territories of the medial and lateral branches of the PICA or PICA/SCA territories. PICA or medial PICA territory infarcts were manifested by acute vertigo and truncal ataxia, while the patients with lateral PICA territory infarcts presented with unsteadiness, limb ataxia and dysmetria without dysarthria. Patients with infarcts in the AICA territory were characterized by limb and trunk ataxia associated with signs of lateropontine involvement. Patients with SCA territory infarcts presented with dysarthria, unsteadiness and/or vertigo, limb ataxia, and dysmetria. Cardiac embolism was the main cause of large infarcts in the territories of the PICA (8/16) or SCA (4/7). Multiple small infarcts were associated with vertebrobasilar atherosclerosis (8/12). These clinical–MRI correlations allow better definition of the topographic and etiological spectrum of cerebellar infarction, which was previously based on pathological studies in subjects with severe infarction.     

Limb ataxia and proximal intracranial territory brain infarcts: clinical and topographical correlations

Background

Limb ataxia is classically attributed to cerebellar hemispheric lesions, although isolated lesions of the inferior cerebellar peduncle (ICP) in the medulla may also cause this sign. It is still unclear why only some patients with acute cerebellar infarcts in the posterior inferior cerebellar artery (PICA) territory present with limb ataxia. The proximal intracranial posterior circulation (P‐PC) territory includes structures fed by the intracranial vertebral arteries (ICVAs): the medulla, supplied by small ICVAs branches, and posterior inferior portion of the cerebellum, fed by PICA. ICP and PICA territory cerebellar infarcts most often occur independently but occasionally occur together.

Objective

To identify structures responsible for limb ataxia in acute P‐PC brain infarcts, correlating clinical and topographical findings.

Methods

Sixteen patients (8 women) were included, aged 30–82 years (mean 62 years), with isolated acute strokes in the P‐PC territory.

Results

The cases reported here indicate that limb ataxia in acute P‐PC territory infarcts may be associated with damage to the ICP in the dorsolateral medulla, regardless of a hemispheric cerebellar lesion. In fact, among the nine patients with PICA stroke, limb ataxia was observed only in the two patients who also presented damage to the dorsolateral medulla involving the ICP. Of the seven patients with isolated dorsolateral medullary infarct, only five patients with ICP damage had limb ataxia.

Conclusions

When correlating limb ataxia and acute P‐PC infarcts, it is important to take into account the entire ICVA territory.Limb ataxia is characterised by dysmetria, dyssynergia and intention tremor, and is clinically assessed by the finger‐to‐nose and heel‐to‐knee tests.¹ It is classically associated with hemispheric cerebellar lesions² and rarely with brainstem lesions.³ Previous reports on cerebellar strokes focused on the frequency of neurological signs in patients with different cerebellar arterial territory infarcts.^4,5 Limb ataxia was reported in only approximately 50% of cases of posterior inferior cerebellar artery (PICA) infarcts but it was not related to the histological or neuroradiological findings.^4,5 A very recent clinical and MRI study⁶ reported limb ataxia in only 4 of 13 patients with acute PICA stroke. The authors correlated this finding with impairment of the intermediate and lateral cerebellar cortex or of the cerebellar nuclei, which are involved in the control of limb coordination. However, it is well known that lesions of the inferior cerebellar peduncle (ICP) without involvement of the cerebellar hemisphere may also cause limb ataxia.⁷The proximal intracranial posterior circulation (P‐PC) territory includes structures fed by the intracranial vertebral arteries (ICVAs), the medulla and the posterior inferior portion of the cerebellum. The blood supply of the posterior inferior cerebellum and the ICP derive from different branches of the ICVAs. The lateral medulla is supplied by small branches that originate from the ICVA and course through the lateral medullary fossa to supply the ICP and the dorsolateral medulla. The ICVA also gives rise to the PICA. The medial branch of the PICA supplies a small portion of the dorsal medulla but not the ICP. ICP and PICA territory cerebellar infarcts most often occur independently but occasionally occur together. Only 1 in 5 proximal territory infarcts include both the lateral medulla and the PICA territory cerebellum.⁸ When both occur together it is usually caused by a long occlusion of the ICVA which blocks flow in both the PICA and lateral medullary penetrators.Here we describe 16 patients with acute infarcts in the ICVA territory in order to understand the role of the cerebellum and of the ICP in the occurrence of limb ataxia.     

Cerebellar infarction in the territory of the medial branch of the superior cerebellar artery

The authors studied 14 patients with an isolated cerebellar infarct in the territory of the medial branch of the superior cerebellar artery (MSCA). The most common clinical finding was severe gait ataxia with sudden falling (n = 9) or severe veering (n = 2). Cerebellar dysarthria was found in 8 patients. Eight patients had a mild unilateral limb ataxia. These findings emphasize that MSCA territory cerebellar infarction presented with the prominent gait ataxia and cerebellar dysarthria.     

Hemi- and Monoataxia in Cerebellar Hemispheres and Peduncles Stroke Lesions: Topographical Correlations

Limb ataxia of sudden onset is due to a vascular lesion in either the cerebellum or the brainstem (posterior circulation, PC, territory). This sign can involve both the upper and the lower limb (hemiataxia) or only one limb (monoataxia). The topographical correlates of limb ataxia have been studied only in brainstem strokes. Therefore, it is not yet known whether this sign is useful to localize the lesion within the entire cerebellar system, both the cerebellar hemisphere and the cerebellar brainstem pathways. Limb ataxia was semi-quantified according to the International Cooperative Ataxia Rating Scale in 92 consecutive patients with acute PC stroke. Limb ataxia was present in 70 patients. Four topographical patterns based on magnetic resonance imaging findings were identified: picaCH pattern (posterior inferior cerebellar artery infarct); scaCH pattern (superior cerebellar artery infarct); CH/CP pattern (infarct involving both the cerebellum and the brainstem cerebellar pathways); and CP pattern (infarct involving the brainstem cerebellar pathways). Hemiataxia was present in (47/70; 67.1%) and monoataxia in (23/70; 32.9%) of patients. Monoataxia involved the upper limb in (19/70; 27.1%) and the lower limb in (4/70; 5.7%) of patients. Limb ataxia usually localized the lesion ipsilaterally (picaCH, scaCH, CH/CP, and CP patterns involving the medulla and sometimes the pons) (53/70; 75.7%), but it might be due also to contralateral (CP pattern involving the pons or midbrain) (16/70; 22.9%) or bilateral lesions (1/70). Limb ataxia usually localizes the lesion ipsilaterally but the infarct might be sometimes contralateral. The occurrence of monoataxia may suggest that the cerebellar system is somatotopically organized.     

Bilateral Cerebellar Infarctions Caused by a Stenosis of a Congenitally Unpaired Posterior Inferior Cerebellar Artery

Bilateral symmetrical cerebellar infarcts in the territory supplied by the medial posterior inferior cerebellar artery (PICA) branches are extremely rare. In the few cases published, it has not been possible to clearly pinpoint the cause of this infarct pattern. The authors present the case history of a 58-year-old man who had acute headaches accompanied by pronounced rotatory vertigo with nausea and vomiting. The neurological examination revealed bilateral cerebellar signs. Cranial magnetic resonance imaging showed bilateral, nearly symmetrical infarcts in the territory of the medial branches of both PICAs. These bilateral PICA infarctions were caused by a stenosis of an unpaired PICA originating from the left vertebral artery supplying both cerebellar hemispheres.     

Multiple large and small cerebellar infarcts

To assess the clinical, topographical, and aetiological features of multiple cerebellar infarcts,18 patients (16.5% of patients with cerebellar infarction) were collected from a prospective acute stroke registry, using a standard investigation protocol including MRI and magnetic resonance angiography. Infarcts in the posterior inferior cerebellar artery (PICA)+superior cerebellar artery (SCA) territory were most common (9/18; 50%), followed by PICA+anterior inferior cerebellar artery (AICA)+SCA territory infarcts (6/18; 33%). One patient had bilateral AICA infarcts. No infarct involved the PICA+AICA combined territory. Other infarcts in the posterior circulation were present in half of the patients and the clinical presentation largely depended on them. Large artery disease was the main aetiology. Our findings emphasised the common occurrence of very small multiple cerebellar infarcts (<2 cm diameter).These very small multiple cerebellar infarcts may occur with (13 patients/18; 72%) or without (3/18; 22%) territorial cerebellar infarcts. Unlike previous series, they could not all be considered junctional infarcts (between two main cerebellar artery territories: 51/91), but also small territorial infarcts (40/91). It is suggested that these very small territorial infarcts may be endzone infarcts, due to the involvement of small distal arterial branches. It is possible that some very small territorial infarcts may be due to a microembolic process, but this hypothesis needs pathological confirmation.     

Presentation and prognosis of bilateral infarcts in the territory of the superior cerebellar artery.

Unilateral cerebellar infarcts in the territory of the superior cerebellar artery (SCA) have been studied in recent years to delineate the clinical presentation and stroke mechanism, but most studies excluded bilateral infarctions. We have studied patients with bilateral SCA infarctions to provide data on clinical findings, stroke distribution and outcome. We collected data of 8 patients with bilateral SCA infarctions recognized by computed tomography and/or magnetic resonance imaging. The most common clinical presentation of patients with bilateral SCA infarctions were nausea, vomiting or vertigo (6 patients), often associated with ataxia and dysarthria (5 patients). Further symptoms were variable and depended on additional infarcts in other vascular territories. Infarcts were often partial or scattered with equal distribution between the medial and lateral branches of the SCA. Complete infarction within the SCA area occurred in less than half of the cases. Clinical outcome was either benign (full recovery in 3 patients) or fatal (5 patients). Predictors for a good clinical recovery were young age, few vascular risk factors, only partial involvement of the SCA territory without involvement of other vascular territories, and absent limb weakness on clinical presentation.     

Spectrum of the posterior inferior cerebellar artery territory infarcts. Clinical-diffusion-weighted imaging correlates

BACKGROUND AND PURPOSE: The clinical, etiological and stroke mechanisms are defined well before but the detailed clinical and etiologic mechanisms regarding to all clinical spectrum of posterior inferior cerebellar artery (PICA) infarcts were not systematically studied by diffusion-weighted imaging (DWI). METHODS: Seventy-four patients with PICA territory ischemic lesion proved by DWI with decreased apparent diffusion coefficient and FLAIR (fluid attenuation inversion recovery) included in our Registry, corresponding to 2% of 3,650 patients with ischemic stroke, were studied. The presence of steno-occlusive lesions in the posterior circulation were sought by magnetic resonance angiography, and reviewed with a three-dimensional rotating cineangiographic method. RESULTS: We found six subgroups of PICA territory infarcts according clinico-topographical relationship: (1) 9 patients with lesion in the territory lateral branch of PICA; (2) 23 patients with an infarct in the territory of medial branch of PICA; (3) 9 patients with a lesion involving both medial and lateral branches of the PICA; (4) 9 patients with cortical infarcts at the boundary zones either between medial and lateral branches of the PICA or between PICA and m/l superior cerebellar artery (SCA); (5) 10 patients with a lesion at the deep boundary zones either between medial and lateral PICA, or between PICA and medial/lateral SCA; (6)14 patients with concomitant multiple lesions in the PICA and in other vertebrobasilar artery territories. The main cause of PICA infarcts was extracranial large-artery disease in 30 patients (41%) patients, cardioembolism and in situ branch disease in 15 patients (20%) each. CONCLUSIONS: Multiple PICA territory lesions on DWI were not uncommon and could be caused by multiple emboli originating from break-up of atherosclerotic plaque in the subclavian/innominate-vertebral arterial system. DWI findings of single or multiple small lesions could account for some cases with transient and subtle cerebellar symptoms which have been considered before as 'vertebrobasilar insufficiency' without morphologic lesion. Different clinical-DWI correlations allow us to determine better definition of the topographical and etiological spectrum of acute PICA territory lesions, which was previously defined by pathological and conventional MRI studies.     

双侧小脑梗死模式的探讨

目的探寻双侧小脑梗死的模式和机制。方法经MRI弥散成像(DWI)证实急性期小脑梗死的患者,根据梗死灶的分布将患者分为单侧小脑梗死组(UCI)和双侧小脑梗死组(BCI),并对两组的人口学特征、血管分布、小脑以外梗死灶以及病因进行了比较。结果因急性卒中入院的115例后循环脑梗死患者中,56例为小脑梗死或小脑合并其它部位梗死,其中单侧小脑梗死36例(64.3%),双侧小脑梗死20例(35.7%)。基线资料比较显示,脑卒中史(P=0.002)、纤维蛋白元水平(P=0.036)和入院时NIHSS评分(P=0.001)在双侧小脑梗死组明显高于单侧小脑梗死组。按血管分布区划分,小脑后下动脉(PICA)供血区小脑梗死发生率最高,且更多发生单侧小脑梗死(P=0.006);而双侧小脑梗死更常见于PICA+小脑上动脉(SCA)供血区(P=0.004)。双侧小脑梗死组合并小脑以外梗死灶的发生率明显高于单侧小脑梗死组(P=0.002),特别是合并幕下梗死灶常见(P=0.022)。在卒中机制上,双侧小脑梗死以大动脉粥样硬化性病变更多见(P=0.041),责任动脉病变主要是在椎动脉V4段、V4段与BA接合处的重度狭窄或闭塞。结论双侧小脑梗死并不少见,常见于PICA+SCA供血区;大动脉粥样硬化所致动脉源性栓塞是其卒中重要机制之一。     

Atherothrombotic cerebellar infarction: vascular lesion-MRI correlation of 31 cases.

BACKGROUND AND PURPOSE: Correlation of MRI findings with atherosclerotic vascular lesions has rarely been attempted in patients with cerebellar infarction. The aim of this study was to correlate the MRI lesions with the vascular lesions seen on conventional cerebral angiography in cerebellar infarction. METHODS: The subjects included 31 patients with cerebellar infarcts who underwent both MRI and conventional cerebral angiography. We analyzed the risk factors, clinical findings, imaging study, and angiography results. We attempted to correlate MRI lesions with the vascular lesions shown in the angiograms. RESULTS: The vascular lesions seen on angiograms were subdivided into 3 groups: large-artery disease (n=22), in situ branch artery disease (n=6), and no angiographic disease with hypertension (n=3). The proximal segment (V1) lesions of vertebral artery were the most common angiographic features in patients with large-artery disease in which stroke most commonly involved the posterior inferior cerebellar artery (PICA) cerebellum. The V1 lesions with coexistent occlusive lesions of the intracranial vertebral and basilar arteries were correlated with cerebellar infarcts, which had no predilection for certain cerebellar territory. The intracranial occlusive disease without V1 lesion was usually correlated with small cerebellar lesions in PICA and superior cerebellar artery (SCA) cerebellum. The subclavian artery or brachiocephalic trunk lesion was associated with small cerebellar infarcts. The in situ branch artery disease was correlated with the PICA cerebellum lesions, which were territorial or nonterritorial infarct. No angiographic disease with hypertension was associated with small-sized cerebellar infarcts within the SCA, anterior inferior cerebellar artery, or SCA cerebellum. CONCLUSIONS: Our study indicates that the topographic heterogeneity of cerebellar infarcts are correlated with diverse angiographic findings. The result that large-artery disease, in which nonterritorial infarcts are more common than territorial infarcts, is more prevalent than in situ branch artery disease or small-artery disease, suggest that even a small cerebellar infarct can be a clue to the presence of large-artery disease.     

Recent Advances in Cerebellar Ischemic Stroke Syndromes Causing Vertigo and Hearing Loss

Cerebellar ischemic stroke is one of the common causes of vascular vertigo. It usually accompanies other neurological symptoms or signs, but a small infarct in the cerebellum can present with vertigo without other localizing symptoms. Approximately 11 % of the patients with isolated cerebellar infarction simulated acute peripheral vestibulopathy, and most patients had an infarct in the territory of the medial branch of the posterior inferior cerebellar artery (PICA). A head impulse test can differentiate acute isolated vertigo associated with PICA territory cerebellar infarction from more benign disorders involving the inner ear. Acute hearing loss (AHL) of a vascular cause is mostly associated with cerebellar infarction in the territory of the anterior inferior cerebellar artery (AICA), but PICA territory cerebellar infarction rarely causes AHL. To date, at least eight subgroups of AICA territory infarction have been identified according to the pattern of neurotological presentations, among which the most common pattern of audiovestibular dysfunction is the combined loss of auditory and vestibular functions. Sometimes acute isolated audiovestibular loss can be the initial symptom of impending posterior circulation ischemic stroke (particularly within the territory of the AICA). Audiovestibular loss from cerebellar infarction has a good long-term outcome than previously thought. Approximately half of patients with superior cerebellar artery territory (SCA) cerebellar infarction experienced true vertigo, suggesting that the vertigo and nystagmus in the SCA territory cerebellar infarctions are more common than previously thought. In this article, recent findings on clinical features of vertigo and hearing loss from cerebellar ischemic stroke syndrome are summarized.     

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.     

Multiple acute infarcts in the posterior circulation.

OBJECTIVE--to evaluate clinical, radiological, and prognostic features of patients with multiple acute infarcts in remote arterial territories of the posterior circulation. DESIGN--Data analysis from a prospective acute stroke registry in a community based primary care centre using a standard protocol including MRI and MRA. RESULTS--In three and a half years, 27 of the 236 patients (11%) with posterior circulation stroke had multiple acute infarcts in the posterior circulation as shown by gadolinium enhancement on MRI. Eighteen patients had multiple infratentorial and supratentorial infarcts including the cerebellum and posterior cerebral artery territory, with coexisting brainstem involvement in seven patients. Fourteen patients had a rostral basilar artery syndrome and cerebellar signs; four patients had a visual field defect with cerebellar signs. Causes were vertebral (six) or basilar (four) artery atheromatosis, and cardioembolism (four). Seven patients had multiple acute infarcts in the posterior circulation of the cerebellum and lower brainstem. Brainstem and cerebellar signs were found in most patients (five); aetiologies were small vessel disease (four), cardioembolism (one), and vertebral artery dissection (one). Two patients with large artery atheromatosis had multiple acute infarcts in the posterior circulation in the brainstem and posterior cerebral artery territory. One month after stroke more than 25% of the patients were dependent or had died. There was no difference in the outcome between the three groups, and recovery was linked to the size of infarcts rather than to a high number of infarcts. CONCLUSIONS--multiple acute infarcts in the posterior circulation usually involve the cerebellum. Simultaneous brainstem and posterior cerebral artery territory infarcts sparing the cerebellum are uncommon. They can be suspected clinically before neuroimaging, mainly when supratentorial and infratentorial infarcts coexist. This may be important, because different patterns of infarction are associated with different causes of stroke.     

Neuro-Otological Aspects of Cerebellar Stroke Syndrome

Cerebellar stroke is a common cause of a vascular vestibular syndrome. Although vertigo ascribed to cerebellar stroke is usually associated with other neurological symptoms or signs, it may mimic acute peripheral vestibulopathy (APV), so called pseudo-APV. The most common pseudo-APV is a cerebellar infarction in the territory of the medial branch of the posterior inferior cerebellar artery (PICA). Recent studies have shown that a normal head impulse result can differentiate acute medial PICA infarction from APV. Therefore, physicians who evaluate stroke patients should be trained to perform and interpret the results of the head impulse test. Cerebellar infarction in the territory of the anterior inferior cerebellar artery (AICA) can produce a unique stroke syndrome in that it is typically accompanied by unilateral hearing loss, which could easily go unnoticed by patients. The low incidence of vertigo associated with infarction involving the superior cerebellar artery distribution may be a useful way of distinguishing it clinically from PICA or AICA cerebellar infarction in patients with acute vertigo and limb ataxia. For the purpose of prompt diagnosis and adequate treatment, it is imperative to recognize the characteristic patterns of the clinical presentation of each cerebellar stroke syndrome. This paper provides a concise review of the key features of cerebellar stroke syndromes from the neuro-otology viewpoint.     

Cerebellar infarction in the area of the posterior cerebellar artery. Clinicopathology of 28 cases

We report a neuropathological study of cerebellar infarctions involving the territory of the posterior inferior cerebellar artery (PICA) in 28 cases. Fifteen cases involved the PICA territory only. In 13 cases infarctions in the anterior inferior cerebellar artery (AICA) territory and/or in the superior cerebellar artery (SCA) territory were also present. A thorough post-mortem study of the arterial supply of the brain from the heart up to the cerebellar arteries, including the cervical spine segment of the vertebral arteries was performed in 27 cases. The territory of the cerebellar infarcts has been ascertained. In 15/28 cases (54 percent), infarction involved the PICA territory only (17 infarcts). All of these cases had a benign outcome and death was due to another cause. Six of these were recent infarctions. None had evidence of swelling and tonsillar herniation. Infarcts were generally of small size and involved the entire PICA territory in only 2 cases. Most of these cases were unexpected discovered at autopsy. Cerebellar infarction in the territory of the medial branch of the PICA (9/17 infarcts) drew grossly a set square with a dorsal base and a ventral top headed for the IVth ventricle. Five out of these cases were associated with infarction in the dorsal and lateral medullary territories. Retrospective clinical study showed that they had been unnoticed or overshadowed by other neurological disorders (4 cases), or presented as Wallenberg's syndromes (4 cases), or as a pure vestibular syndrome (due to an infarction involving only the cerebellum) mimicking an acute labyrinthine disorder (1 case). Infarctions in the territory of the lateral branch of the PICA (5/17 infarcts) always occurred without medullary involvement. All of them were unexpectedly discovered at autopsy, and were unnoticed during the life (3 infarcts) or were overshadowed by other neurological disorders (2 infarcts). That was also the case in 2 cases of infarction in the whole PICA territory (3/17 infarcts). Thus infarctions strictly localized to the entire PICA territory only were rare. Thirteen/28 cases (46 p. 100) of infarction in the whole PICA territory were associated with infarction in the AICA and/or the SCA territories. This resulted from an association with other infarctions and not from an abnormally large territory of the PICA. Cerebellar swelling with brain stem compression and tonsillar herniation occurred 8/13 cases (62 p. 100). There were other massive median and paramedian brain stem infarctions involving midbrain, pons or medulla in 55 p. 100 of 13 cases.(ABSTRACT TRUNCATED AT 400 WORDS)     

The Usefulness of the TOAST Classification and Prognostic Significance of Pyramidal Symptoms During the Acute Phase of Cerebellar Ischemic Stroke

Cerebellar stroke is a rare condition with very nonspecific clinical features. The symptoms in the acute phase could imitate acute peripheral vestibular disorders or a brainstem lesion. The aim of this study was to assess the usefulness of the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification in cerebellar stroke and the impact of clinical features on the prognosis. We retrospectively analyzed 107 patients with diagnosed ischemic cerebellar infarction. We studied the clinical features and compared them based on the location of the ischemic lesion and its distribution in the posterior interior cerebellar artery (PICA), superior cerebellar artery (SCA), and anterior inferior cerebellar artery (AICA) territories. According to the TOAST classification, stroke was more prevalent in atrial fibrillation (26/107) and when the lesion was in the PICA territory (39/107). Pyramidal signs occurred in 29/107 of patients and were more prevalent when the lesion was distributed in more than two vascular regions (p?=?0.00640). Mortality was higher among patients with ischemic lesion caused by cardiac sources (p?=?0.00094) and with pyramidal signs (p?=?0.00640). The TOAST classification is less useful in assessing supratentorial ischemic infarcts. Cardioembolic etiology, location of the ischemic lesion, and pyramidal signs support a negative prognosis.     

Sudden bilateral hearing loss with vertigo due to vertebral artery occlusion]

We report a case of sudden bilateral hearing loss associated with an occlusion of the right vertebral artery. A 66-year-old man was admitted to hospital suffering from sudden onset vertigo, deafness, and vomiting. He could not walk due to truncal ataxia. There was positional nystagmus to the right; spontaneous and gaze-evoked nystagmus were absent. He had no facial nerve palsy, dysarthria, pyramidal tract signs, limb ataxia, and sensory impairment. Pure tone audiometry demonstrated a profound sensorineural deafness of both ears. A tentative diagnosis of sudden deafness was made. He was treated with intravenous infusion of corticosteroid; hearing loss of the left ear slightly improved. Cranial MR imaging demonstrated fresh small infarcts in the right cerebellar tonsil, the left cerebellar medulla, and the left middle cerebellar peduncle. MR angiography demonstrated an occlusion of the right vertebral artery. It is possible that reduced perfusion of the anterior inferior cerebellar arteries and internal auditory arteries on both sides resulted in multiple "border zone" infarcts and damage to the inner ear. Clinicians should be aware of the possibility of vertebrobasilar occlusive disease in case of sudden bilateral hearing impairment, even when brainstem or cerebellar signs are absent.     

119例小脑梗死的临床分析

目的探讨小脑梗死的中国缺血性脑卒中分型诊断(CISS)、受累血管区域、合并小脑外梗死病灶以及临床表现。方法回顾性分析自2012年1月至2015年12月119例急性小脑梗死住院患者的头颅MRI影像、病因学检查以及临床表现等资料。结果 119例小脑梗死患者中,单侧小脑梗死78例(UCI组),双侧小脑梗死41例(BCI组)。两组的CISS分型无明显差异。UCI组以小脑后下动脉区梗死发生率最高(35.9%),与BCI组比较,差异有显著统计学意义(P0.01);BCI组中小脑后下动脉+小脑上动脉区梗死发生率最高(39.0%),但两组间比较差异无显著性;其余区域的梗死发生率在两组中差异无显著性。63/119例(52.9%)同时合并小脑外梗死灶。BCI组合并小脑外后循环梗死的发生率(53.7%)较单侧UCI组高(P0.05),而UCI组合并前循环梗死较BCI组更多(P0.05)。主要症状、体征包括:头晕/眩晕、眼球震颤、眼倾斜反应、听觉减退、小脑性构音障碍、共济失调,浅感觉障碍、锥体束征以及意识障碍等。意识障碍在BCI组的发生率高于UCI组(P0.01),其余各项两组间比较差异无显著性。结论小脑梗死的主要病因为大动脉粥样硬化;小脑后下动脉区梗死在UCI中最常见,BCI常合并小脑外的后循环供血区梗死;UCI和BCI的受累小脑动脉以及合并小脑外梗死的区域有一定差异,提示两者病因机制存在不同;意识障碍等严重神经功能缺损表现在BCI更为常见。     

Vascular ataxic hemiparesis: a re-evaluation.

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

椎动脉优势对基底动脉弯曲及椎基底动脉连接部脑梗死的影响

目的 探讨椎动脉优势对基底动脉弯曲及椎基底动脉连接部脑桥和小脑梗死的影响. 方法 回顾性分析郑州人民医院神经内三科自2009年1月至2011年1月收治的91例单侧脑桥或小脑后下动脉脑梗死患者的影像学资料,包括梗死侧别、椎动脉优势、基底动脉弯曲及其方向性关系等,应用多元logistic回归分析寻找基底动脉弯曲的预测因素. 结果 旁正中动脉供血区的脑桥中央是脑桥梗死最多的受累部位,右侧小脑内下部是小脑后下动脉梗死最多的受累部位.椎动脉优势常发生于左侧(69.2％,63/91).91例患者中有76例在椎动脉优势和基底动脉弯曲之间存在相反方向的关系.椎动脉内径是基底动脉中重度弯曲的唯一预测因素,其OR值为2.70,95％CI为1.22～5.98. 结论 椎动脉优势是基底动脉弯曲的重要预测因素,且弯曲多朝向优势椎动脉的对侧.椎动脉优势及其造成的基底动脉弯曲增加了椎基底动脉连接部脑梗死的发生率.