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。     

以眩晕为首发症状的小脑梗死临床类型及供血区分布

目的:探讨以眩晕为首发症状的小脑梗死临床类型及病灶供血区分布特征。方法:对26例经MRI确诊、以眩晕为首发症状的小脑梗死患者的临床资料进行回顾性分析。结果:将眩晕为首发症状的小脑梗死分为2种临床类型:①稳定型:单纯自发性持续性眩晕伴平衡失调(19/26例,73.1%);②进展型:以持续性眩晕、平衡失调为首发症状,起病2d后伴有延迟神经功能受累症状(7/26例,26.9%)。梗死病灶以小脑后下动脉内侧支(16/26例,61.5%)受累最为常见;其次为小脑前下动脉区(6/26例,23.1%)及小脑上动脉区(2/26例,7.7%)。未见多发小脑供血动脉区梗死患者以单纯眩晕为首发症状。结论:以眩晕为首发症状的小脑梗死以小脑后下动脉内侧支受累最为常见,绝大多数患者呈良性病程,但需警惕可能出现的延迟神经功能受累症状和体征。     

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.     

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…     

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     

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     

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     

小脑后下动脉解剖变异致双侧小脑梗死2例报道并文献复习

目的 探讨小脑后下动脉(posterior inferior cerebellar artery, PICA)解剖变异致双侧小脑梗死的临床特征及发病机制。方法 对2例经颅脑MRI确诊的双侧小脑梗死患者采用CT血管造影(CTA)、磁共振血管成像(MRA)或数字减影血管造影(DSA)显示其头颈部血管,从而了解后循环血管的形态特征并复习相关文献。结果 病例1经DSA证实左侧椎动脉较细,远端管腔闭塞,通过右椎动脉代偿供血原左侧PICA供血区但欠充分,双侧PICA共同起源于右侧椎动脉。病例2经CTA证实右侧椎动脉较左侧明显细且远端显示欠清,MRA示双侧PICA共同起源于左侧椎动脉。结论 2例双侧小脑梗死患者均存在一侧椎动脉优势供血,且双侧PICA共同起源于该侧椎动脉。在该解剖变异基础上一侧椎动脉发生病变时可出现双侧小脑梗死。因此,在临床中出现双侧小脑梗死时临床医师不能忽略这一解剖变异基础。     

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。     

小脑性共济失调13例病例报道

目的:探讨以进行性小脑性共济失调为主要临床症状的疾病诊断。方法:回顾性分析13例以慢性进行性小脑共济失调为主要临床表现患者的临床资料、实验室、影像学和基因检查结果。结果:13例患者中,脊髓小脑性共济失调3例,多系统萎缩-小脑型6例,小脑肿瘤1例,桥小脑结合臂脓肿1例,小脑梗死后遗症2例。结论:对于以进行性小脑共济失调为主要体征的患者,临床上首先要排除占位性病变,其次多系统萎缩和脊髓小脑性共济失调为主要的遗传变性病因。     

小脑前下动脉梗死的临床与磁共振成像的研究

目的 研究小脑前下动脉(AICA)梗死的临床表现及磁共振成像(MRI)特征。方法 对我院1997年1月～2001年6月4年半间通过磁共振成像(MRI)确诊的19例AICA梗死患者进行临床及MRI观察。结果AICA梗死占同期急性脑梗死的1.47％,占同期小脑梗死22.1％。危险因素与一般缺血性脑卒中午相似,即高血压、高脂血症、糖尿病是其主要的危险因素。所有患者均有眩晕及小脑性共济失调的症状体征;除一名患者外均有颅神经受累,以Ⅷ、Ⅶ、v最多见。第Ⅶ颅神经受累是AIcA梗死的一个特征性改变。AICA梗死预后较好。结论 AICA梗死并非罕见,应提高对AICA梗死临床表现及MRI特征的认识,以降低临床误诊率。     

丁螺环酮治疗小脑性共济失调

目的 :探讨 5 HT1A受体激动剂丁螺环酮改善共济失调症状的作用。方法 :应用评分计分法观察丁螺环酮治疗 2 4例共济失调患者 3个月。结果 :治疗前后共济失调评分 ,包括稳定性、协调性、构音、眼球运动各方面的差异均有显著意义 (P <0 0 0 1) ;焦虑评分在治疗前后的差异无显著性 (P >0 0 5 )。结论 :丁螺环酮短期内可以有效地改善患者小脑性共济失调的症状     

Treatable causes of cerebellar ataxia

The cerebellar ataxia syndromes are a heterogeneous group of disorders clinically characterized by the presence of cerebellar dysfunction. Initial assessment of patients with progressive cerebellar ataxia is complex because of an extensive list of potential diagnoses. A detailed history and comprehensive examination are required for an accurate diagnosis and hierarchical diagnostic investigations. Although no cure exists for most of these conditions, a small group of metabolic, hereditary, inflammatory, and immune‐mediated etiologies of cerebellar ataxia are amenable to disease‐modifying, targeted therapies. Over the past years, disease‐specific treatments have emerged. Thus, clinicians must become familiar with these disorders because maximal therapeutic benefit is only possible when done early. In this article, we review disorders in which cerebellar ataxia is a prominent clinical feature requiring targeted treatments along with specific management recommendations. © 2015 International Parkinson and Movement Disorder Society     

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.     

Neurophysiological evidence for generalized sensory neuronopathy in cerebellar ataxia with neuropathy and bilateral vestibular areflexia syndrome

Introduction: Cerebellar ataxia with neuropathy and bilateral vestibular areflexia syndrome (CANVAS) is a recently described multisystem ataxia defined by the presence of cerebellar ataxia, bilateral vestibulopathy, and a somatosensory deficit. The characteristic clinical sign is an abnormal visually enhanced vestibuloocular reflex. The somatosensory deficit contributes to a significant level of disability in CANVAS. Methods: This study was a neurophysiological investigation of 14 patients with CANVAS. Results: Findings revealed uniformly absent sensory nerve action potentials in all limbs, abnormal blink reflexes in 13 of 14 patients, and abnormal masseter reflexes in 6 of 11 patients. Tibial H‐reflexes were absent in 11 of 14 patients. Somatosensory evoked potentials were abnormal in 10 of the 11 patients tested, and brainstem auditory evoked responses were abnormal in 3 of 8. Cutaneous silent period responses were abnormal in 7 of 14 patients. Conclusions: We suggest that a sensory neuronopathy should be sought in cerebellar and/or vestibular ataxias, particularly where the degree of ataxia is out of proportion to the clinically identified cerebellar and/or vestibular dysfunction. Muscle Nerve 51: 600–603, 2015     

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.     

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.