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。     

非酒精性 Wernicke 脑病临床特征分析

目的：探讨非酒精性Wernicke脑病（Wernicke’s encephalopathy ,WE）的病因、临床表现、影像学检查及治疗。方法回顾性分析我院住院的18例非酒精性W E患者的临床资料。结果各种原因所引起的体内维生素B1缺乏均可导致非酒精性WE的发生;临床可表现为精神及意识障碍、眼外肌麻痹和共济失调三联征,但典型的 WE 三联征仅有3例（16.7％）,其余往往以其中1种或2种表现为主,精神及意识障碍最常见（77.8％）,而眼外肌麻痹（33.3％）和共济失调（27.8％）相对较少;影像学检查以头颅M RI为首选,病灶多对称性分布于脑中线结构附近,最常见累及部位是丘脑内侧、第三脑室周围（61.1％）、中脑导水管周围区域（55.6％）、乳头体（38.9％）;18例患者经及时的大剂量补充维生素B1,临床表现均有不同程度的改善。结论各种引起维生素B1缺乏的因素均可为W E的病因,识别不典型的临床表现及特征性头颅M RI改变,对WE早期诊断及治疗具有重要意义。     

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8例临床分析

<正> 临床资料:1 一般资料:男7例,年龄48～65岁,平均55.7岁,女1例,为27岁。长期酗酒(饮酒史11～40年,饮酒量5～10两/日)5例,胆道胰腺疾病长时间静脉营养1例,胃溃疡术后消化不良1例,妊娠呕吐1例。主要症状体征:消瘦3例,     

Wernicke脑病

Wernicke脑病（WE）是一种急性或亚急性起病的维生素B1缺乏症。表现为眼部体征、躯干性共济失调、意识障碍和情感淡漠及多发性周围神经病。M砌的表现有助于提示本病。WE是由于胃肠道手术、酗酒和胰腺炎等病因引起,补充维生素B1有助于恢复。     

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。     

Wernicke脑病3例报告

Ｗｅｒｎｉｃｋｅ脑病３例报告张霁帆，周维林近年来，因慢性酒中毒而住院的病人呈上升趋势，我科近１５年共收治１２４例，１９９０年以后收治的占５０％，而并发于中毒晚期的特征性综合征也较前多见，其中确诊为Ｗｅｒｎｉｃｋｅ脑病３例，现报告如下；例１．男，３６岁...     

Wernicke脑病二例

Wernicke脑病由维生素B1缺乏引起,临床主要表现为眼外肌麻痹、共济失调、精神和意识障碍,病变部位多位于邻第3脑室的丘脑、下丘脑、乳头体,中脑导水管旁和第4脑室底,且双侧病变对称[1]。此文报道作者医院收治的2例Wernicke脑病患者。1临床资料例1:患者女,76岁。因患慢性胰腺炎1年半、急性发作3 h于2004-08-22被收入作者医院ICU。患胰腺炎以来一直进食不佳,且未额外补充维生素。住院后病情平稳。2005-08-25,坐位说话过程中突发意识丧失,急查头颅CT未见异常。次日行头颅MRI检查,平扫发现长T1长T2信号,DWI发现第四脑室底部散在稍高信号,…     

Wernicke脑病2例临床分析

例1,女,28岁,因早孕反应,恶心、呕吐2个月后出现视物模糊20天,逐渐出现厌食,在当地医院补液治疗无好转,后出现胸闷、气短、心慌、声嘶无力,说话声小来我院。入院查体:T37℃、P102次/分、R22次/分、Bp120/70mmHg,神清反应迟钝,情绪低落,少言,体质消瘦,语利但声小,颅神经未见异常,双上肢肌力V级,双下肢肌力Ⅳ级,双上肢肱二、三头肌腱反射、桡骨骨膜反射对称存在,双膝腱、跟腱反射消失,左上肢痛觉减退,双巴氏征( )。心电图示:窦性心动过速,ST-T广泛下移。头MRI示:双丘脑、大脑脚、视束、窟窿柱、乳头体、导水管周围中脑等可见对称的稍等T…     

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.     

Wernicke encephalopathy☆ Clinical presentation and MR images in two nonalcoholic patients

The aim of the present study was to investigate the importance of and correlation between clinical presentations and magnetic resonance imaging （MRI） of two different cases of nonalcoholic Wernicke encephalopathy. Case l ： A 63-year-old man with a diagnosis of incomplete mechanical intestinal obstruction. His abdominal symptoms were improved by gastrointestinal decompression, but blurred vision, hypoacusis, dizziness, and unsteady gait were noted. His illness deteriorated to confusion on day seven. MRI showed hyperintense lesions in the medial thalami, tectum of the midbrain, and the periaqueduct region on T2- and diffusion-weighted images. Thiamine therapy was commenced immediately with good results. Case 2： A 22-year-old woman was admitted for sudden-onset confabulation and unsteady gait after hyperemesis gravidarum. She had no history of alcohol or any medication. Brain MRI was normal. The patient experienced relief after Vitamin B1 treatment. These results suggest that brain MRI can define characteristic abnormalities in Wernicke encephalopathy, and that diffusion-weighted imaging may improve the diagnosis sensitivity. In addition, the MRI images may be correlated to the clinical stage and severity of the disease. Nevertheless, the clinical features are essential for correct diagnosis.     

胼胝体病变的临床与CT、MRI表现

目的：分析胼胝体病变临床表现及CT、MRI影像学特征。材料与方法：搜集经CT、MRI检查后发现胼胝体病变37例（其中15例经手术及定向穿刺后病理证实）。结果与结论：37例胼胝体病变包括所胼胝体发育不全6例、脂肪瘤5例，外伤及脑血管意外致血肿11例、肿瘤13例（胶质母细胞瘤3例、Ⅰ～Ⅱ级星形细胞瘤5例、淋巴瘤3例、转移后2例）、血管畸形及多发性硬化各1例。除8例脑外伤以外，其他病人临床上均有长期头晕、头痛、突发意识障碍、癫痫等表现、但非特征性改变。CT、MRI对胼胝体病变（无论是原发或是继发）的发现、诊断及鉴别诊断均有重要的价值，MRI在定位上较CT更为精确．从而为术前手术方式的选择，术后放疗的定位准确提供更多有用信息。     

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。     

2例肥厚性硬脑膜炎的临床和磁共振影像学特征

目的:报道2例肥厚性硬脑膜炎(HCP),探讨其临床和磁共振(MRI)成像特征。方法:分析2例患者临床和MRI特点,结合文献讨论HCP的病因、临床表现和影像学特点等。结果:HCP病因多样。临床以头痛和多组脑神经损害为主。1例低颅压性头痛为HCP罕见症状。MRI增强扫描以颅内硬脑膜弥漫性异常增厚为特点。结论:HCP是以头痛和硬脑膜弥漫性增厚为特点。根据临床缓慢局灶和全脑功能障碍症状,结合增强MRI特点,有利于早期作出较明确的诊断。     

低血糖脑病的临床及脑部磁共振特征

目的探讨低血糖脑病的临床及脑部磁共振特征。方法回顾分析69例低血糖昏迷患者的临床、脑磁共振（MRI）成像资料。结果低血糖昏迷诱因较为复杂,常见的为进食减少、腹泻、上呼吸道感染、降糖药物应用不当等。临床表现复杂多样,除意识障碍外,还可表现为偏瘫、四肢瘫、凝视麻痹等,多数伴有Babinski征。69例患者中有18例出现脑MRIDWI异常高信号病灶,病灶主要累及海马、基底节、大脑皮质以及皮质下白质,多为对称性损害。3个月后随访,不伴有脑部MRI损害的患者预后良好率明显高于伴有脑部MRI损害的患者（94．12％对22．22％;P=0．0011）。伴有脑部MRI损害者有10例患者预后不良,其中9例（90％）发生于皮质受累患者。结论低血糖脑病临床表现不具有特异性,对于昏迷患者,应当考虑到低血糖的可能。降糖药物应用不当为低血糖脑病的主要诱发因素。脑部MRI要优于脑部CT检查,其中DWI序列对于检测低血糖所致的脑部损害有着非常重要的意义。皮质受累者预后不良。     

亚急性坏死性基底节脑病36例报告

目的;探讨亚急性坏死性基底节脑病(ＳＮＢＧＥ)与Ｌｅｉｇｈ病的关系。方法:对３６例ＳＮＢＧＥ的病因、临床特点、ＣＴ/ＭＲＩ进行分析。结果:发现３６例均因各种不同病因引起临床亚急性经过,出现锥体外系、锥体束损害等多种多样的症状、体征,而在颅脑ＣＴ或ＭＲＩ均呈双侧基底节对称性坏死、软化性改变。结论:颅脑ＣＴ或ＭＲＩ对ＳＮＢＧＥ可作生前诊断,根据病因不同,可分为原发性(即Ｌｅｉｇｈ病)和继发性,后者又可根据明确病因,冠以中毒性、缺氧性或感染性ＳＮＢＧＥ。