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。     

无共济失调小脑梗死12例临床分析

目的:探讨无共济失调小脑梗死的临床特点、梗死区域及早期诊断对疾病预后的意义。方法:回顾性分析12例以眩晕为主要症状但无共济失调表现的小脑梗死的临床资料。结果:患者年龄58～78岁,CT检查未发现梗死灶,MRI阳性率为100%。脑梗死主要危险因素为高血压、糖尿病、高脂血症和心房颤动。11例患者小脑梗死的病灶主要位于单侧小脑半球后下部,属于小脑后下动脉(PICA)供血区域;1例小脑梗死的病灶位于小脑蚓部后部及其附近的两侧小脑半球,属于小脑后下动脉中间支(mPICA)供血区域。结论:无共济失调小脑梗死常见于PICA供血区。对于中老年眩晕患者,无论有无共济失调表现,都应完善MRI检查明确有无小脑梗死。     

急性双侧小脑梗死

目的 探讨急性小脑梗死的临床和影像学表现特点和相互关系,病因和发生机制以及预后.方法 选择我科住院的15例双侧小脑多发性梗死患者,对其血管危险因素、临床表现、MRI病变形态、分布和临床的关系,可能的病因性发病机制以及预后进行分析.结果 本组双侧小脑梗死占全部小脑梗死患者的23.8%.急性双侧小脑梗死以双侧PICA供血区的多发性梗死最多见(66.7%).主要临床表现为头晕/眩晕(93.3%)、恶心、呕吐(93.3%)、共济失调(60%)和构音障碍(58.7%).双侧小脑梗死多表现为大病变侧的单侧体征如共济失调.除上述小脑症状外,双侧PICA供血区梗死,特别是内侧支分布区受累(6例)时,突出的临床表现为眩晕,其中4例表现为孤立性假性眩晕;AICA梗死患者的特征表现为双侧耳聋;而SCA供血区梗死的临床表现特点是构音障碍、单侧共济失调,偶可出现大病变对侧的耳聋.Rankin评分均在3分或3分以下,死亡1例.结论 急性小脑多发性梗死主要发生于双侧PICA供血区,主要临床症状和体征为头晕/眩晕、恶心呕吐、共济失调等体征多数限局于单侧肢体,出现于小脑梗死较大的一侧.病因多数为心源性栓塞或主动脉粥样硬化性栓塞所致.预后较好.     

小脑梗死20例误诊分析

小脑梗死是由小脑上动脉、小脑后下动脉、小脑前下动脉等闭塞所致，常有眩晕、恶心、呕吐、眼震、共济失调、站立不稳、肌张力降低、脑干受压及颅内压增高症状。占全部脑梗死的5％～10％，因梗死部位、病灶大小而症状各异，特别是大面积小脑梗死，形成占位效应，临床症状及体征缺乏特异性，诊断困难，易误诊为前庭神经疾病、脑干梗死、高血压病、椎基底动脉供血不     

小脑梗死20例误诊分析

小脑梗死是由小脑上动脉、小脑后下动脉、小脑前下动脉等 闭塞所致,常有眩晕、恶心、呕吐、眼震、共济失调、站立不稳、肌 张力降低、脑干受压及颅内压增高症状。占全部脑梗死的5％ -10％,因梗死部位、病灶大小而症状各异,特别是大面积小脑 梗死,形成占位效应,临床症状及体征缺乏特异性,诊断困难,易 误诊为前庭神经疾病、脑干梗死、高血压病、椎基底动脉供血不 足等,延误治疗。现将我院1993-01-2003-10间收治的经头颅 MRI证实误诊的小脑梗死20例报告如下。 1 临床资料     

26例小脑梗死的临床分析

目的 对26例小脑梗死患者的临床特点分析探讨，加深临床医师对小脑梗死的进一步认识，减少小脑梗死的误诊、漏诊率。方法对26例经头颅CT、MRI确诊的小脑梗死病人从病因、临床及影像学表现特点进行归纳分析。结果 高血压动脉硬化仍是小脑梗死的主要病因，眩晕、恶心、呕吐是其主要临床表现，头颅CT、MRI是确诊依据。临床小脑梗死极易误诊为椎基动脉供血不足。结论对临床上出现有高血压病史而又以急性眩晕为首发症状的病人应及时行头颅CT、MRI等有效影像学检查，减少小脑梗死的误诊、漏诊率。     

小脑梗死与眩晕

1临床资料1.1一般资料本组30例患者均经头部CT或MRI确诊为小脑梗死,男22例,女8例,年龄38～72岁,平均58．9岁。有意识障碍者除外。1．2小脑梗死分类①小脑后下动脉（PICA）;小脑前下动脉（AICA没小脑上动脉（SCA）的区域性梗死,②小脑动脉和终末区之间的交界区梗死,③小脑深部小校死。1.3眩晕分类为便于观察,将眩晕分为①轻度;患者感眩晕,可进行适活动,无呕吐。②中度;患者眩晕明显,头部稍活动即恶心,呕吐;③重度;患者卧床时仍有剧烈的眩晕,频繁呕吐。1.4临床表现及影像学改变30例患者中,24例有程度不同的眩晕,16…     

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。     

小脑前下动脉梗死的临床特征及病因探讨(附22例报告)

目的 分析小脑前下动脉(AICA)梗死的临床表现及MR改变，并探讨AICA梗死形成的原因。方法 对22例AICA梗死患者的临床表现、MRI及MRA进行分析。结果 AICA梗死的主要累及小脑中脚和(或)脑桥外下方，其症状体征以眩晕及共济失调为主，可合并多组颅神经受累，以Ⅷ对颅神经受累最具特征性。MRA上单纯AICA梗死单侧者，基底动脉(BA)显示良好，双侧AICA梗死及合并其它小脑梗死者BA未显影或显示狭窄。结论 AICA梗死的诊断主要依靠MRI，MRA对判定病因及预后有重要意义。     

26例小脑梗死的临床分析

目的　对 2 6例小脑梗死患者的临床特点分析探讨 ,加深临床医师对小脑梗死的进一步认识 ,减少小脑梗死的误诊、漏诊率。方法　对 2 6例经头颅CT、MRI确诊的小脑梗死病人从病因、临床及影像学表现特点进行归纳分析。结果　高血压动脉硬化仍是小脑梗死的主要病因 ,眩晕、恶心、呕吐是其主要临床表现 ,头颅CT、MRI是确诊依据。临床上小脑梗死极易误诊为椎基动脉供血不足。结论　对临床上出现有高血压病史而又以急性眩晕为首发症状的病人应及时行头颅CT、MRI等有效影像学检查 ,减少小脑梗死的误诊、漏诊率     

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.     

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.     

Infarcts in the territory of the lateral branch of the posterior inferior cerebellar artery.

The territory of the lateral branch of the posterior inferior cerebellar artery (1PICA) supplies the anterolateral region of the caudal part of the cerebellar hemisphere. Because infarcts in the territory of the 1PICA have rarely been studied specifically, 10 patients with this type of infarct are reported. An 1PICA infarct was isolated in only three patients, whereas it was associated with brainstem infarct in four, with occipital infarct in one, and with multiple infarcts in two patients. The most common symptom at onset was acute unsteadiness and gait ataxia without rotatory vertigo (six patients). Unilateral cerebellar dysfunction was found in all patients, with limb ataxia (nine patients), dysdiadochokinesia (five patients), and ipsilateral body sway (four patients), but dysarthria and primary position nystagmus were notably absent. In the patients with a coexisting infarct in the brainstem, cranial nerve and sensorimotor dysfunction was prominent and often masked the signs of cerebellar dysfunction. Unlike other infarcts in the PICA territory, 1PICA territory infarcts were mainly associated with vertebral artery atherosclerosis (six patients), whereas cardiac embolism was less common (three patients). Unilateral limb ataxia without dysarthria or vestibular signs suggests isolated 1PICA territory infarction and should allow its differentiation from other cerebellar infarcts.     

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.     

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)     

Anterior and posterior inferior cerebellar artery infarction with sudden deafness and vertigo

We report a patient with anterior and posterior inferior cerebellar artery infarction, which manifested as profound deafness, transient vertigo, and minimal cerebellar signs. We suspect that ischaemia of the left internal auditory artery, which originates from the anterior inferior cerebellar artery, caused the deafness and transient vertigo. A small lesion in the middle cerebellar peduncle in the anterior inferior cerebellar artery territory and no lesion in the dentate nucleus in the posterior inferior cerebellar artery territory are thought to explain the minimal cerebellar signs despite the relatively large size of the infarction. Thus a relatively large infarction of the vertebral-basilar territory can manifest as sudden deafness with vertigo. Neuroimaging, including magnetic resonance imaging, is strongly recommended for patients with sudden deafness and vertigo to exclude infarction of the vertebral-basilar artery territory.     

Repetitive Episodic Isolated Vertigo in a Patient with Cerebellar Infarction

Isolated vertigo is an important symptom of posterior circulation stroke. It has been reported that 11.3% of patients with isolated vertigo have a stroke and that most lesions are located in the cerebellum, particularly in the posterior inferior cerebellar artery. We report the case of a 63-year-old man with multiple atherosclerotic risk factors and atrial fibrillation who showed repeated episodes of isolated vertigo. His repeated vertigo was short-lasting and was often triggered by body position, mimicking benign paroxysmal positional vertigo. Cranial computed tomography on the third hospital day showed left cerebellar infarction within the territory of the posterior inferior cerebellar artery. The vertigo was ameliorated on the fifth hospital day and warfarin was prescribed for secondary prevention. Clinicians should pay special attention to cases in which a patient presents isolated vertigo, even if it shows transient recurrence or is triggered by a positional change, especially in patients with multiple cerebrovascular risk factors.     

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.     

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.