急性Wernicke脑病的MRI表现

Wernicke脑病1881年由Carl Wernicke首先进行了报道,它是由维生素B1(硫胺素)缺乏所致的急性神经系统疾病,酗酒、营养不良、妊娠剧吐、消化道手术、长期肠外营养等影响维生素B1吸收的因素均可引起。此病主要累及丘脑和下丘脑的脑室旁区域、第四脑室底和小脑的前上叶特别是蚓部,病变多呈对称性。此病病理上表现为毛细血     

Wernicke脑病12例临床分析

目的探讨Wernicke脑病患者的临床特点。方法回顾性分析12例Wernicke脑病患者的临床表现、实验室检查及影像学检查等临床资料。结果 12例Wernicke脑病患者男性6例,女性6例;有明确病因的患者为9例,如禁食、饮食差;恶心、呕吐、嗜酒;临床以"三主征"中的2个主征最多,为7例,1个主征得为4例,"三主征"仅为1例;辅助检查以头颅MR检查最有意义,12例患者中有6例出现典型的头颅MRI信号改变即短或等T1、长T2异常信号,多位于丘脑、小脑及中脑导水管周围;经维生素B1补充治疗后患者的症状有不同程度的好转。结论禁食、饮酒等诱因、临床表现及典型的头颅MR表现可为临床上该病的早期诊断提供重要线索。早期进行维生素B1的补充治疗在临床上可达到显著的疗效。     

腹部手术并发Wernicke脑病临床分析与护理

韦尼克氏(Wernicke)脑病是维生素B1缺乏所引起的中枢神经系统疾患[1].主要典型表现为眼球运动障碍、小脑性共济失调、精神意识障碍等三联征[2].Wernicke脑病起病隐匿,症状不典型,该病多发生于慢性乙醇中毒和妊娠呕吐者,外科重症患者并发Wernicke脑病少见.现将我院外科2003-02～2006-08手术患者术后并发Wernicke脑病临床与护理情况报告如下.……     

维生素B1缺乏致脚气病、Wernicke脑病3例报告

1 病例介绍 本文报告3例因维生素B_1缺乏致脚气病、Wernicke脑病者,其中例1因妊娠频繁呕吐2个月,出现四肢麻木,心悸,心率增快。就诊后在未补充维生素B_1情况下,静滴大量葡萄糖后出现精神异常,双眼运动障碍,双侧肢体共济障碍,经补充维生素B-1后好转。例2因“胃穿孔”手术,术中将胃与回肠吻合,空肠空置,术后消化吸收不良,出现心悸乏力,走路不稳。     

Wernicke脑病的MRI诊断与临床

目的探讨Wernicke脑病(WE)的MRI特征及其诊断价值。方法回顾性分析20例经临床证实的WE患者的临床及MRI检查资料。结果 WE的MRI特征主要表现为对称性T1WI低信号、T2WI高信号,在FLAIR序列中呈明显高信号,在DWI上呈明显高信号,ADC上呈低信号。主要累及部位为乳头体,第三、四脑室及中脑导水管周围灰质。结论WE早期缺乏特征性临床表现,但具有典型的MRI表现,头颅MRI检查对于该病的早期诊断具有重要的临床价值。     

Wernicke脑病四例的磁共振成像特征

Wernicke脑病（Wernicke encephalopathy,WE）有特征性磁共振成像（MRI）表现,磁共振弥散成像（DWI）可对WE早期诊断及预后判定提供帮助.我们2005年4-12月收治4例患者,报道如下.     

非酒精性Wernicke脑病二例

目的探讨Wernicke脑病患者的临床和影像学特点。方法分析2例非酒精性Wernicke脑病患者的临床资料。结果 2例患者均为消化道晚期肿瘤行手术治疗、术后有营养不均衡、发病前有葡萄糖注射液补液史。2例患者均有意识障碍和典型的头颅MRI信号改变,即双侧丘脑内侧、中脑顶盖及导水管周围的高T_2信号;维生素B_1补充治疗后患者的症状有不同程度的好转。结论导致维生素B_1缺乏的高危因素、临床表现及典型的头颅MRI表现是临床上Wernicke脑病早期诊断的重要线索。早期足量维生素B_1治疗效果好。高危患者应注意预防Wernicke脑病的发生。     

Wernicke脑病8例临床报告

Wernicke脑病,俗称“脑型脚气病”,是由维生素B1缺乏所致。多呈亚急性或慢性起病,既往认为该病罕见,但作者在临床实践中发现我国北方及内蒙等地区实际发病率并不太低,只是许多非典型病例被临床医生所忽略,造成误诊、漏诊。为引起同道注意,提高对该病应有的警惕性,现将近年来作者遇到的8例Wernicke脑病报道如下。1临床资料1.1一般资料8例均为男性,年龄32岁~64岁,平均49.5岁。饮酒史13年~38年不等,平均22.5年。饮酒量0.7~1.5市斤/天,其中有6例超1市斤/天。2例急性起病,6例缓慢发病。病程3个月~5年,平均2.2年。1.2主要临床表现8例均有不同程…     

Wernicke脑病6例临床分析

Ｗｅｒｎｉｃｋｅ脑病是由于维生素Ｂ１缺乏引起的中枢神经系统综合征。本文就６例病人的临床表现,病因,ＭＲＩ,诊断和治疗方面,结合文献资料进行回顾性分析。     

Wernicke脑病的临床诊断与治疗

目的探讨Wernicke脑病的病因、临床特点及治疗。方法回顾分析8例患者的临床表现及辅助检查结果并复习文献。结果酒精中毒引起的Wernicke脑病只占37.5%（3/8），更多的见于顽固性呕吐、院内长期单纯补液。临床可表现为典型的或不典型的“三联征”、“四联征”。头颅MRI检查有助于诊断。结论Wernick脑病尽管临床少见，但各种医师都可能遇到。其预后与治疗是否及时密切相关，应提高对本病的认识。     

Wernicke脑病综合征10例临床分析

目的:探讨Wernicke脑病(WE)的病因、临床表现特点、MRI表现及预后。方法:对10例WE患者的病因、临床表现、头颅MRI特点和预后进行了回顾性分析。结果:WE病因多与维生素B1缺乏有关,主要临床表现为眼肌麻痹,共济失调、精神异常三联症,但也可以表现为周围神经病、言语障碍等。头颅MRI有特异性部位的异常信号改变。及时予以维生素B1治疗者预后多良好。结论:提高临床对WE的认识,有利于早诊断、早干预,有助于改善WE的预后。     

急性腹泻继发韦尼克脑病1例

1临床资料患者,女,38岁,于25d前出现腹泻,次日发现呼之不应,口吐白沫,小便失禁,四肢抽搐,至当地医院就诊,测体温38．5℃,血糖低于正常（具体不详）,血清钾3．15mmol／L,血清钠123．3mmol／L,腰穿结果“正常”（具体不详）,头颅CT示“脑水肿”,予“补糖、醒脑静”等治疗,后因反复肢体抽搐、双眼上翻、     

Magnetic Resonance Reflects the Pathological Evolution of Wernicke Encephalopathy

BACKGROUND AND PURPOSE: Wernicke encephalopathy (WE) is an acute phase of Wernicke-Korsakoff syndrome. Pathologic findings change between acute and chronic phases. Only a few magnetic resonance imaging (MRI) studies have been done to date. METHODS: To correlate the MRI findings in acute and chronic stages of WE with the known pathologic information, 15 consecutive patients with WE were examined with MRI: 3 before thiamine treatment, 7 within 24 hours of thiamine treatment, 4 between the second and sixth day after thiamine treatment, and 1 fifty-five days after thiamine treatment. Nine of the patients had follow-up MRI between 2 days and 33 months. T1-weighted, proton, and T2-weighted axial images were obtained with additional 5-mm-thick T1-weighted sagittal and coronal images to better visualize the mammillary bodies. RESULTS: In the acute WE, MRI showed high signal intensityon T2-weighted images in periaqueduct and medial thalamic regions. In a few patients with alcoholism, vermian and mammillary body atrophies and third ventricular enlargements were noted. In the chronic phase of WE, T2 hyperintensity disappeared but mammillary bodies and cerebellar vermis became atrophic and third ventricular enlargements were evident. High signal intensity on T2-weighted images disappeared as early as 2 days, and atrophic changes appeared as early as 1 week. CONCLUSION: MRI is useful for in vivo monitoring and reflects the pathological evolution in acute and chronic phases of WE.     

MR Atypical Wernicke Encephalopathy Showing Extensive Brain Stem and Diencephalic Involvement

Wernicke encephalopathy (WE) is a serious neurological disorder caused by thiamine (vitamin B1) deficiency. We report a case of atypical and extensive location of abnormal signal lesions on magnetic resonance imaging (MRI) in a man with alcohol abuse with WE. MRI performed on the first hospital day showed signal intensity alterations extending in the whole brain stem and diencephalon; the mismatch between diffusion‐weighted images and apparent diffusion coefficient map was highly suggestive of vasogenic edema. This report further supports the view that WE may represent a spectrum of radiological entities and can have a wide spectrum of manifestations on MRI; thus, clinical features are essential to diagnose it.     

非酒精性韦尼克脑病的临床与MRI影像特征

目的非酒精性韦尼克脑病(Wernicke encehalopathy,WE)易误诊,本文旨在提高对该病的认识。方法回顾性分析6例非酒精性WE患者临床及MRI特征。结果 6例患者均出现不同程度的意识障碍,其中仅2例表现为经典的三联征。6例患者均出现双侧对称性丘脑内侧、脑室及导水管周围、中脑顶盖异常信号典型表现,同时2例深昏迷患者分别表现出弥漫性皮层及面神经核受累。随访患者平均恢复时间为7.5个月,而MRI则为2.8个月。2例深昏迷患者预后较差,1例患者死亡,另1例2年后仍遗留严重四肢痉挛性瘫痪,并伴智能低下。2例深昏迷患者DWI上表现为广泛高信号。结论 MRI可为非酒精性WE提供早期诊断,而病变累及广泛皮层及颅神经核可能提示较差的预后,同时DWI序列可能有一定的预后作用。     

海洛因脑病的临床表现与影像学特征

目的:探讨海洛因脑病患者临床表现和影像学特点。方法:回顾性分析经临床和实验室确诊的7例海洛因脑病患者的相关资料。结果:所有患者有吸食海洛因病史,在突然戒断期间中发病,临床以言语障碍,共济失调、锥体束征阳性为特征,MRI表现为对称性大脑、小脑白质、内囊以及脑干的长T1、长T2信号,Gd～DTPA增强后无强化,脑脊液检查一般未见异常。结论:海洛因脑病多见于青年男性,有吸食海洛因史,临床表现多变,影像学有较典型的特点。     

Corpus Callosum Atrophy in Wernicke's Encephalopathy

Background and Purpose. Neuropathologic changes in Wernicke's encephalopathy (WE) involve variable brain structures. Corpus callosum involvement in WE, however, is largely unknown. The authors investigated the degree and the pattern of corpus callosum changes in WE according to the etiologies. Methods. Nineteen patients with WE (between 34 and 81 years) and 19 age‐ and sex‐matched control participants were included. The total cross‐sectional callosal area and 5 callosal subregions (C1‐C5) were measured by tracing outer margins in the midsagittal sections. Subregions were determined by placing radial dividers with 10 rays. The pixel numbers for corpus callosums were calculated, and the values obtained were adjusted for head size variations. Results. The causes of WE were alcoholism (10), intestinal surgery (5), anorexia (3), and hyperemesis gravidarum (1). The mean size of the total corpus callosum was significantly reduced in alcoholic WE (P< .001; 527.8 ± 70.8 mm 2for alcoholic WE; 664.6 ± 58.1 mm 2for the corresponding controls), but not in nonalcoholic WE. In subregion analysis, prefrontal callosum (C2) atrophy was the most prominent in alcoholic WE. In contrast, only splenium (C5) was atrophied in nonalcoholic WE. The degree of atrophy did not change throughout the follow‐up period (mean 5.3 weeks). Conclusion. This study suggests that the extent and location of corpus callosum atrophy differs between alcoholic WE and nonalcoholic WE, implying separate contribution of alcohol neurotoxicity and nutritional deficiency.