MRI对非乙醇中毒性韦尼克脑病的诊断价值(附五例临床分析)

目的 分析非乙醇中毒性韦尼克脑病(WE)患者的临床和颅脑MRI成像特点,探讨颅脑MRI对其的诊断价值. 方法 深圳市第二人民医院放射科自2007年6月至2010年2月应用MRI检查非乙醇中毒性WE患者5例,回顾性分析患者的临床特征、颅脑MRI成像特点及治疗转归等资料. 结果 非乙醇中毒性WE患者缺乏特征性临床表现,颅脑MRI主要表现为丘脑内侧,侧脑室,第三脑室,中脑导水管周围脑组织对称性高信号,2例患者可见大脑皮层受累.增强扫描后部分病变可见强化.2例患者死亡,3例患者应用维生素B1治疗后预后良好. 结论 颅脑MRI对非乙醇中毒性WE具有诊断价值,其显示的损害范围可反映WE的疾病严重程度.

Abstract：

Objective To analyze the clinical features and MR imaging features of patients with nonalcoholic Wemicke's encephalopathy (WE). Methods A retrospective review of the data,consisting of clinical and cranial MRI features, and the treatment results, was conducted on 5 patients with nonalcoholic WE, who admitted to our hospital fiom June 2007 to February 2010. Results The clinical features of nonalcoholic WE were non-characterized and most of them had no specific value for diagnosis. MR imaging showed symmetrical high signal in the medial thalamus, lateral ventricle, third ventricle and surrounding area of the aqueduct of midbrain; involvement of the cerebral cortex was found in 2 patients. Enhancement in some of the lesions was noted after performing contrast-enhanced scan.Favorable prognosis was given to the 3 patients treated with vitamin B1; 2 patients died. Conclusion Cerebral MRI enjoys great value in diagnosing nonalcoholic WE and reflects appropriately the pathological severity of this disease by demonstrating the scope of the lesions.     

颅脑MRI检查在非乙醇中毒性韦尼克脑病诊断中的价值

目的评价颅脑MRI检查在非乙醇中毒性韦尼克脑病(WE)诊断中的价值。方法对6例非乙醇中毒性WE患者的临床特征、颅脑MRI影像及治疗转归等资料进行分析。结果本组颅脑MRI显示．丘脑内侧及侧脑室、第三脑室、中脑导水管周围脑组织对称性T2W及Flair成像异常高信号,1例成为持续性植物状态的患者伴有部分皮质T2W及Flair成像异常高信号。随访显示4例康复患者,随临床表现好转其颅脑MRI异常信号逐渐消失,1例持续性植物状态患者随访2年,异常信号无变化：结论顷脑MRI对非乙醇中毒性WE具有诊断价值,其显示的损害范围可反映WE患者的疾病严重程度。     

韦尼克脑病三例的磁共振表现

韦尼克脑病(Wernicke encephalopathy)是一种由于硫胺缺乏所致的严重的营养代谢性脑病,常发生于乙醇中毒患者。磁共振成像(MRI)检查的普及对本病早期诊断很有帮助,国外已经有关于韦尼克脑病影像表现特点的报道[1-4]。我们确诊3例韦尼克脑病患者,对他们的影像学表现进行报道,并与既往我院报道的3例病理诊断的非乙醇中毒性韦尼克脑病的临床病理[5]加以对比,以提高临床医生对于该病影像学表现的认识。临床资料例1男性,46岁,因“头晕、呕吐、复视23d,意识模糊9d”于2004年2月10日入院。2001年7月患者因胃窦癌于我院行手术切除及术后化疗,术后…     

韦尼克脑病20例临床分析

目的探讨韦尼克脑病(Wernicke’s encephalopathy,WE)的病因、发病机制、临床表现及治疗,提高对韦尼克脑病的认识和早期临床诊断率,减少临床误诊率。方法对济宁医学院附属医院肾内科、消化科、产科、神经内科、胃肠外科2005-01—2015-12收治的20例(男12例,女8例,年龄21～72岁)WE患者的病史、临床特征、诊断、治疗以及预后进行分析。结果饮酒为韦尼克脑病最常见的病因,临床表现多种多样,典型的临床表现为眼球运动麻痹、共济失调和意识精神障碍三大主征,但典型的WE"三联征"很少同时出现,20例患者中只有2例(10%)表现为典型的三联征。绝大多数患者经大剂量补充维生素B_1后疗效显著。结论 WE病因及临床表现复杂多样,早期诊断十分困难,颅脑MRI可作为诊断此病的重要辅助检查。及时大量补充维生素B_1可以明显改善患者预后情况。     

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 Wernicke脑病尽管临床少见,但各科医师都可能遇到。其预后与治疗是否及时密切相关,应提高对本病的认识。     

典型韦尼克脑病1例

正1病例患者男性,55岁,因"大量饮酒30年,性格改变伴记忆力下降3年"入院。30年前因工作原因出现饮酒,为社交性,每次饮52°白酒约50~100 g/次,每次均和他人一起饮酒,至3年前酒量逐渐增加至400 g/d,未诉有特殊躯体不适及精神上的依赖,3年前,出现晨起饮酒,喝寡酒,从早上喝到晚上,最少400 g/d,最多600 g/d,并逐渐出现了手抖、头晕、心慌、     

韦尼克脑病16例临床分析

目的探讨韦尼克脑病(Wernicke’s encephalopathy,WE)的病因、发病机制、临床表现及治疗。方法回顾性分析我院2002~2009年16例WE患者的临床资料。结果 WE病因复杂,饮酒为其最常见的病因。主要临床表现包括行走不稳、眼征、精神神志障碍三联征,但典型的WE三联征很少同时出现,往往以其中一种或两种表现为主。头部MRI大多为腔隙性脑梗死、脑萎缩等非特异性表现,丘脑、下丘脑、乳头体及脑室周围等部位对称性长T1、长T2信号的特征性表现并不多见。绝大多数患者经大剂量补充Vit-B1后疗效显著。结论 WE病因及临床表现复杂多样,早期诊断困难,头部MRI可作为WE重要的辅助检查。及时补充大剂量Vit-B1预后良好。     

35例韦尼克脑病临床分析

目的探讨韦尼克脑病(Wernicke’s encephalopathy,WE)的病因、临床表现、磁共振特征、误诊原因和治疗转归。方法回顾性分析我院2012年10月~2015年6月收治的35例WE患者的临床资料。结果饮酒是WE最常见原因,其次是胃、胆囊、胰腺病变导致呕吐和进食差。具有典型的精神意识障碍、眼肌麻痹、共济失调三联征者占11.4%,具备三联征中两项者占42.9%,仅有三联征中一项者占45.7%。头部MRI可见双侧丘脑、侧脑室周围、导水管周围、第三脑室、四脑室旁、乳头体、皮质、胼胝体等部位对称性异常信号。本组患者的误诊率达60%,其中酒精中毒性WE误诊率为54.17%,非酒精中毒性WE误诊率为72.73%。住院期间91.42%患者(32/35)好转,8.58%患者无好转。出院5 m时9例失访,随访的26例中6例死亡(死亡率23.07%),13例痊愈(50%),5例遗留记忆力障碍,2例完全卧床。结论 WE病因及临床表现多样,MRI有特征性改变,但早期误诊率高,预后与是否诊断和治疗及时密切相关。     

饮酒致韦尼克脑病的护理干预

现将我科近年来在韦尼克脑病(wernicke encephalopathy,WE)护理工作的经验介绍如下。1资料与方法1.1一般资料2002-06~2006-12我科收治确诊饮酒所致韦尼克脑病患者15例。均为男性,年龄30~55岁,其中农民3例,工人5例,无固定职业4例,干部3例;文盲1例,小学文化程度3例,初中文化程度8     

韦尼克脑病误诊为精神分裂症1例

本文报道了1例误诊为精神分裂症的韦尼克脑病病例。患者1月余前在当地精神专科医院住院,诊断为精神分裂症。12天前逐渐出现流涎、进食困难、双手发抖、行走不稳、舌后坠等情况,按照药物不良反应处理后效果差,并出现意识障碍。转入我院并完善检查后考虑为韦尼克脑病合并周围神经病,因患者病情进展,家属放弃治疗、要求出院,患者于院外死亡。通过本案例报道,旨在提高对精神障碍患者韦尼克脑病的认识和早期预防,以改善预后。     

Wernicke encephalopathy and Creutzfeldt-Jakob disease

We assessed the prevalence of Wernicke encephalopathy (WE) in all 657 cases suspected of Creutzfeldt-Jakob (CJD) referred from 2001 to 2006 to the French Neuropathology Network of CJD. Clinical, biological and imaging data were reviewed when the diagnosis of WE was made at autopsy. No CJD was found in five cases suspected of sporadic CJD. In these five cases, myoclonus had been observed in four, CSF 14-3-3 protein in two. In 14 other cases, WE was combined with CJD, 13 of which were sporadic. These belonged mainly to the molecular variants of sporadic CJD associated with a long duration of disease. This stresses the necessity of remaining alert to the diagnosis of WE when CJD is suspected.     

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脑病的临床、影像学及病理特点

目的探讨Wernicke脑病的临床、影像学及病理特点。方法回顾性分析10例Wernicke脑病患者的临床、影像学及病理资料。结果本组10例均非乙醇中毒患者,临床表现为不同程度的精神及意识障碍9例,首发症状为眩晕、恶心和呕吐6例,眼肌瘫痪5例,低血压3例,共济失调2例,严重的周围神经病变1例。5例行头颅MRI检查,3例表现为第三、四脑室及中脑导水管周围对称性的长T1长T2异常信号,2例无阳性发现。经补充维生素B1明显好转4例,死亡5例,放弃治疗1例。5例尸检脑部表现为第三、四脑室及中脑导水管周围灰质充血、水肿和点状出血。结论Wernicke脑病临床表现不典型,MRI检查可为Wernicke脑病的早期诊断提供帮助,及早补充维生素B1是治疗的关键。     

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's encephalopathy in infancy

Summary Wernicke's encephalopathy documented by characteristic involvement of the mammillary bodies developed in a premature infant during parenteral nutrition. This case illustrates the need for thiamine supplementation in seriously ill patients with inadequate intake of the vitamin.     

Wernicke's encephalopathy induced by hyperemesis gravidarum

A report is presented on a patient with Wernicke's encephalopathy secondary to hyperemesis gravidarum. The 25-year-old female presented 11 weeks into pregnancy with prolonged vomiting. Neurological examination 8 weeks later demonstrated obtunded sensations, nystagmus and ataxia of gait. MR imaging revealed bilateral lesions in the mediodorsal nuclei of thalami, in the hypothalamus and in the periaqueductal gray matter (1). The neurological signs and the MRI findings pointed to a diagnosis of Wernicke's encephalopathy. The patient was treated with intramuscular vitamin B1 followed by oral thiamine until the end of pregnancy. The subsequent course of the pregnancy was uncomplicated, and resulted in the delivery of a healthy 2970 g male infant. A review of the literature published during the last 30 years revealed an additional 20 cases of Wernicke's encephalopathy induced by hyperemesis gravidarum. Only half of these pregnancies resulted in the birth of a normal infant.     

Vascular changes in acute Wernicke's encephalopathy

The nature and distribution of vascular changes in acute Wernicke's encephalopathy (WE) were analyzed in three autopsy cases. Lesions of the lateral vestibular nucleus of the medulla oblongata (three cases) and lateral ventricular wall (one case) were examined by reconstruction of 200 serial sections, and the capillary diameter in the tegmentum of the medulla oblongata was measured morphometrically in all cases. The vascular changes commonly found in and around the parenchymal lesions in all cases were: (1) dilatation and endothelial swelling of almost all vessels ranging from small arteries to veins, being especially severe with undulation in small arteries and arterioles, and (2) fibrinoid degeneration and hemorrhage involving selectively the arterioles and capillaries on the arterial side. These vascular changes in the medulla oblongata were essentially the same as those in the third ventricular wall, but differed in their severity. Capillary diameter in these cases was significantly larger than that in seven control cases. Such vascular changes, especially a dysoric change on the arterial side, could not be ascribed to secondary change following changes in the parenchyma, and were, therefore, considered to be a lesion essential to WE, as in the case of the parenchymal lesion.     

Anti-Ma encephalitis masquerading as Wernicke encephalopathy

BackgroundAnti-Ma encephalitis is a disease usually associated with testicular cancer in young male patients. Anti-Ma encephalitis presented as Wernicke encephalopathy-like symptoms and with gastric cancer is rare. Here, we report a case of anti-Ma encephalitis with gastric cancer in an elderly patient, which has been misdiagnosed of Wernicke encephalopathy.Case reportA 71-year old male with a history of alcohol abuse was admitted to the hospital because of progressive dizziness, diplopia and anorexia lasted for 1 month. He was initially diagnosed as Wernicke encephalopathy. However, this patient failed in the treatment of VitB1. The blood and cerebrospinal fluid examination found the presence of anti-Ma1/2 antibodies. ¹⁸F-FDG PET-MR showed symmetrical hypermetabolic changes on the bilateral hypothalamus, basal ganglion and brainstem, as well as gastric neoplasms with liver metastasis. The patient was finally diagnosed with anti-Ma encephalitis.ConclusionAnti-Ma encephalitis should be suspected in patient with Wernicke encephalopathy-like symptoms but failed VitB1 treatment.