Treatment of nasopharyngeal carcinoma and prevention of nonalcoholic Wernicke’s disease:A case report and review of literature

BACKGROUND Wernicke encephalopathy is a neurological disorder caused by thiamine deficiency,commonly seen in alcoholic populations but also involving other circumstances that may lead to thiamine deficiency.The recognition of Wernicke encephalopathy often depends on clinicians’keen ability to detect its typical triad of features;however,most cases do not present with the full constellation of signs,which complicates the timely identification of Wernicke encephalopathy.CASE SUMMARY This case report describes a patient with nasopharyngeal carcinoma who developed abnormal ocular function and ataxia following concurrent chemoradiotherapy,without a history of alcohol abuse.With the aid of radiological examinations,he received a timely diagnosis and treatment;however,his symptoms did not fully resolve during follow-up.CONCLUSION For patients with malignant tumors exhibiting neurological symptoms,clinicians should consider the possibility of Wernicke encephalopathy and provide prophylactic thiamine therapy.

Clinical analysis of Wernicke encephalopathy after liver transplantation

Background:Wernicke encephalopathy(WE)is an acute neurological disease resulting from vitamin B1 deficiency,and there are only very few case reports of WE after liver transplantation.The present study aimed to investigate the clinical characteristics,etiology,magnetic resonance imaging(MRI)features,treatment and prognosis of patients with WE after liver transplantation.Methods:Twenty-three patients with WE after liver transplantation from the First Affiliated Hospital,Zhejiang University School of Medicine and Jiangxi Provincial People’s Hospital between January 2011 and December 2021 were retrospectively analyzed.Results:Among the 23 patients diagnosed with WE after liver transplantation,6(26%)had a classic triad of impaired consciousness,oculomotor palsy and ataxia,and 17(74%)had two features.The misdiagno-sis rate was 65%.After treatment with high-dose vitamin B1,19(83%)patients showed improvement,whereas 4(17%)showed no improvement,including 3 with residual short-term memory impairments and 1 with residual spatial and temporal disorientation and ataxia.Conclusions:The misdiagnosis rate is high in the early stage of WE,and the prognosis is closely asso-ciated with whether WE is diagnosed early and treated timely.High-dose glucose or glucocorticoids can trigger WE and cannot be administered before vitamin B1 treatment.Vitamin B1 is suggested to be used as a prophylactic treatment for patients with WE after liver transplantation.

Pancreatic encephalopathy and Wernicke encephalopathy in association with acute pancreatitis: A clinical study

AIM： To investigate clinical characteristics and therapy of pancreatic encephalopathy （PE） and Wernicke encephalopathy （WE）. METHODS： In a retrospective study of 596 patients with acute pancreatitis （AP）, patients with PE were compared to those with WE in regards to history, clinical manifestation, diagnosis, treatment and outcome. RESULTS： There were 93 patients with severe acute pancreatitis （SAP）. Encephalopathies were discovered in 10 patients （1.7%）. Six patients with PE all developed in SAP （6.5%）, and three of them died （3% of SAP, 50% of PE）. Four patients with WE developed in AP （0.7%）, and two of them died （0.3% of AP, 50% of WE）. Two patients with WE were treated with parenteral thiamine and survived. Global confusions were seen in all patients with encephalopathy. Ocular abnormalities were found. Conjugate gaze palsies were seen in 1 of 6 （16.7%） patients with PE. Of 4 patients with WE, one （25%） had conjugate gaze palsies, two （50%） had horizontal nystagmus, three （75%） had diplopia, and one （25%） had myosis. Ataxia was not seen in all patients. None of patients with WE presented with the classic clinical triad. CSF examinations for 2 patients with WE showed lightlyincreased proteins and glucose. CT and MRI of the brain had no evidence of characteristic abnormalities. CONCLUSION： PE occurs in early or reiteration stage of SAP, and WE in restoration stage of SAP/AP. Ocular abnormalities are the hallmarks of WE, and horizontal nystagmus is common. It is difficult to diagnose earlier an encephalopathy as PE or WE, as well as differentiate one from the other. Long fasting, hyperemesis and total enteral nutrition （TPN） without thiamine are main causes of thiamine deficiency in the course of pancreatitis.

Wernicke encephalopathy in a patient after liver transplantation: A case report

Wernicke encephalopathy(WE) is an acute neurological disorder resulting from vitamin B1 deficiency, which is common in chronic alcoholism and is rare in acute liver failure. So far, there are 2 cases of WE reported after liver transplantation. Here, we report a case of a 45-year-old nonalcoholic male patient who developed psychiatric and neurological disturbance 15 d after receiving orthotopic liver transplantation because of hepatitis B-related cirrhosis and portal hypertension. Brain magnetic resonance imaging(MRI) showed symmetric high-signal intensities in the periaqueductal area. The patient was diagnosed with WE and given intravenous high-dose vitamin B1 immediately. His neurological disturbance resolved in 7 d after receiving the vitamin B1. Brain MRI after 5 mo showed nearly complete recovery. Most WE cases may be misdiagnosed in patients after liver transplantation, and we should pay more attention to its onset.

Magnetic resonance imaging in the assessment of brain involvement in alcoholic and nonalcoholic Wernicke's encephalopathy

AIMTo present the typical and atypical magnetic resonance (MR) imaging findings of alcoholic and non-alcoholic Wernicke’s encephalopathy.METHODSThis study included 7 patients with Wernicke’s encephalopathy (2 men, 5 women; mean age, 52.3 years) that underwent brain MR examination between January 2012 and March 2016 in a single institution. Three patients were alcoholics and 4 patients were non-alcoholics. MR protocol included a T2-weighted sequence, a fluid attenuation inversion recovery (FLAIR) sequence, a diffusion-weighted sequence (b = 0 and 1000 s/mm2), and a contrast-enhanced MR sequence. All MR images were retrospectively reviewed at baseline and follow-up by two radiologists.RESULTSAll patients with Wernicke’s encephalopathy had bilateral areas showing high signal intensity on both T2-weighted and FLAIR MR images in the typical sites (i.e., the periaqueductal region and the tectal plate). Signal intensity abnormalities in the atypical sites (i.e., the cerebellum and the cerebellar vermis) were seen in 4 patients, all of which had no history of alcohol abuse. Six patients had areas with restricted diffusion in the typical and atypical sites. Four patients had areas showing contrast-enhancement in the typical and atypical sites. Follow-up MR imaging within 6 mo after therapy (intravenous administration of thiamine) was performed in 4 patients, and demonstrated a complete resolution of all the signal intensities abnormalities previously seen in all patients.CONCLUSIONMR imaging is valuable in the diagnosis of Wernicke’s encephalopathy particularly in patients presenting with atypical clinical symptoms, or with no history of alcohol abuse.

Non-alcoholic Wernicke encephalopathy in an esophageal cancer patient receiving radiotherapy:A case report

BACKGROUND, Wernicke encephalopathy is a rare but potentially fatal adverse event caused by thiamine deficiency. Reports of non-alcoholic Wernicke encephalopathy due to malignancy are scarce in the literature, with those reported mainly being on haematological cancer, followed by gastrointestinal cancer. As a result, there is considerable under-recognition and delay in the diagnosis and treatment of Wernicke encephalopathy in oncology departments. To our knowledge, there has been no report of Wernicke encephalopathy in a patient with esophageal cancer while receiving radiotherapy.CASE SUMMARY A 64-year-old man presented to the oncology outpatient clinic with a history of dysphagia for 2 mo, and was diagnosed with locally advanced esophageal squamous cell carcinoma(stage ⅢB). Radiotherapy was initiated to alleviate dysphagia due to malignant esophageal stenosis;however, the patient exhibited consciousness disturbances starting on day 10 of radiotherapy. Brain magnetic resonance imaging indicated the development of Wernicke encephalopathy. Subsequent treatment with thiamine led to rapid improvement in the patient’s neurological symptoms.CONCLUSION Wernicke encephalopathy may develop in non-alcoholic patients undergoing radiotherapy for esophageal cancer. Early diagnosis and sufficient thiamine supplementation during radiotherapy are essential.

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.

Psychogenic anorexia and non-alcoholic Wernicke's encephalopathy: Complete clinicoradiological recovery with thiamine

Rationale:Prolonged undernutrition may arise out of depression and lead to Wernicke's encephalopathy if timely diagnosis and intervention are missed.Wernicke's encephalopathy is potentially treatable,and appropriate treatment may revert clinical depression and cognitive dysfunction to some extent.Patient's concern:A 69-year-old female who had been taking escitalopram for one year developed tremor,ophthalmoplegia,ataxia,progressive cognitive decline,and convulsions.Diagnosis:Non-alcoholic Wernicke's encephalopathy and hypomagnesemia due to psychogenic anorexia.Interventions:High dose intravenous thiamine and magnesium were supplemented.Outcomes:The patient showed remarkable improvement in neurological complications and even in depressive features.Lessons:Wernicke's encephalopathy should not be ignored in the treatment of depression.

Clinical manifestation, imageological and pathological characteristics of Wernicke encephalopathy

BACKGROUND: The clinical manifestations of Wernicke encephalopathy(WE) are atypical and short of effective auxiliary examination means. The effects of magnetic resonance imaging (MRI) in the diagnosis of WE have been reported successively. But its imageological detection needs to be further investigated. OBJECTIVE: To analyze the characteristics of clinical manifestations, skull MRI examination and pathological results in patients with WE. DESIGN: Retrospective analysis. SETTING: The General Hospital of Chinese PLA. PARTICIPANTS: Ten patients of WE admitted to the Department of Neurology, General Hospital of Chinese PLA were recruited. Among them, five patients were diagnosed pathologically after death. Their pathological changes accorded with the pathological characteristics of WE. The other 5 patients were diagnosed clinically before death. Their pathological changes accorded with clinical and imageological manifestations and had definite reaction to the treatment of thiamine. Ten patients, 7 males and 3 females, were aged (47±13) years ranging from 33 to 73 years. Their disease courses averaged 6 weeks ranging from 3 to 10 weeks. They all were non-alcoholics. Four patients developed WE after acute pancreatitis, two patients after the recurrence of gastric cancer, two patients after cholecystectomy, one patient after hepatitis medicamentosa, one patient after Alzheimer disease. Informed consents were obtained from all the patients and their relatives. METHODS: After admission, clinical manifestations of patients were observed and recorded. Five patients underwent skull MRI examination and their detected results were recorded. Five dead patients underwent autopsy and brain pathological examinations. Neuropathological examination involved cerebrum, cerebellum and brain stem. MAIN OUTCOME MEASURES: Clinical manifestations, MRI examination results, pathological analysis results and prognosis of all the patients. RESULTS: Ten patients with WE were involved in the final analysis. ①Nine patients presented various degrees of mental and conscious disturbance. Six patients initially presented vertigo, nausea, and vomiting. Five patients showed opthalmoplegia. Three patients presented hypotension (BP < 120/60 mm Hg, 1 mm Hg= 0.133 kPa). Two patients showed ataxia. One patient showed severe polyneuropathy. Both lower extremities were more severe. EMG showed axonal degeneration. ②Five patients accepted skull MRI examination. Three patients showed typical high signals in periaqueductal regions and circumference of third and fourth ventriculus in T2 -weighted and flair-weighted images, two of them showed high signals in fornixes in T2 -weighted and flair-weighted images, and one of them showed high signals in optic chiasma, both mammillary bodies, and subcortical white matter. No abnormality was found in the other two patients. Two patients who accepted the supplements of thiamine showed obviously improvements in the second MRI examination. ③Macroscopically, the border between gray and white matters was clear in the coronal section of cerebrum. Congestions, edema and multiple petechial hemorrhages were found in periaqueductal regions, circumference of third and fourth ventriculus, and both mammillary bodies. Microscopically, various degrees of necrosis of parenchymal structures, loss of nerve cells and ischemic changes were found. Myelinated fibers were more affected than neurons. There were focal capillary proliferation and multiple petechial hemorrhages. Prominent astrocytic proliferations were found in gelatinous fiber staining. And demyelinations were found in myelin staining. These pathological findings were all in accord with the diagnostic criteria of WE. ④In the diagnosis before death, 4 of 5 patients who were supplemented with thiamine had obvious improvement 2 weeks later and 1 of them abandoned therapy due to progressive aggravation of jaundice caused by recurrence of stomach cancer. The other 5 patients who were not diagnosed definitely before death and not supplemented with thiamine died. Final diagnosis was performed in autopsy examination. CONCLUSION: The clinical manifestations of this group of WE patients are atypical. MRI and pathological examination results are corresponding, and both have the characteristic manifestations of WE.

Can Wernicke’s Encephalopathy Be Precipitated by Administering Glucose before Thiamine in Severely Malnourished or Alcoholic Patients?

We discuss the safety and controversy regarding the administration of glucose before thiamine with regards to precipitation of Wernicke’s Encephalopathy in the severely malnourished and alcoholic patient population. Herein we review clinical features, pathophysiology and the relevant literature to provide an evidenced-based recommendation that thiamine replacement should not delay glucose administration acutely in the malnourished patient population.

鼻咽癌同步放化疗致Wernicke脑病1例报道并文献复习

鼻咽癌是起源于鼻咽黏膜内侧的上皮性癌,其高发区域主要分布在我国东南沿海及东南亚地区[1],绝大多数患者就诊时,已处于中晚期[2]。“GP方案”诱导化疗后联合同步放化疗已成为我国局部晚期鼻咽癌的标准治疗模式[3],3年总生存率从90.3%提高到94.6%,具有里程碑意义[4]。Wernicke脑病是一种由维生素B1缺乏而引起的中枢神经系统急性代谢性疾病,临床上多见于慢性酒精中毒和具有长期酗酒史的患者[5],主要以“眼肌麻痹、精神意识障碍、共济失调”三联征为主要临床表现[6],临床诊断率仅0.06%~0.13%[7],若误诊或延缓治疗,可导致持久性功能障碍,死亡率高达15%~17%[8]。因鼻咽癌放化疗所致该疾病较为罕见,临床报道较少,为引起广大临床医务工作者警惕,现将我院诊治的1例鼻咽癌同步放化疗致Wernicke脑病的详细诊治经过报告如下。

儿童消化道疾病术后Wernicke′s脑病3例临床特征分析

Wernicke′s脑病(WE)是一种维生素B1缺乏所致急性脑病综合征,消化系统疾病及胃肠道手术为其常见诱因。本研究共收集到与消化道手术相关的WE患儿3例,回顾性分析患儿的临床表现、辅助检查和预后。旨在总结消化道疾病术后发生的WE的临床特点,提高对该病的认识,从而引导临床医师加强消化道疾病围术期患儿管理。3例患儿的临床表现包括言语障碍3例、共济失调3例、精神行为异常3例、眼震3例、视物模糊2例、不自主运动2例。头颅磁共振成像异常部位包括基底节、丘脑、脑干、中脑导水管和额叶病变。3例患儿长时间静脉营养,摄入维生素B_(1)较少,为0.1~0.3 mg/d。经过给予维生素B_(1)等积极治疗,在随访中,均获得了临床痊愈和头颅磁共振成像表现的恢复,恢复时间为1~2个月。我们认为对于消化道疾病围术期长期禁食水的患儿应警惕WE的发生,需注意每天维生素B_(1)的摄入量。

血清S-100B蛋白、可溶性凝集素样氧化低密度脂蛋白受体-1、胶质纤维酸性蛋白检测在新生儿缺血缺氧性脑病病情严重程度中的诊断价值

目的:探讨血清S-100B蛋白、可溶性凝集素样氧化低密度脂蛋白受体-1(sLOX-1)、胶质纤维酸性蛋白(GFAP)与新生儿缺血缺氧性脑病(HIE)病情严重程度的关系。方法:选择80例HIE患儿作为观察组,另选择90例健康新生儿作为对照组,收集所有患儿一般资料,并检测两组患儿血清S-100B蛋白、sLOX-1、GFAP水平,分析HIE患儿血清S-100B蛋白、sLOX-1、GFAP与病情严重程度的相关性及预后不良的影响因素。结果:对照组血清S-100B蛋白、sLOX-1、GFAP水平低于观察组(均P<0.05)。重度组血清S-100B蛋白、sLOX-1、GFAP水平高于中度组、轻度组和对照组(均P<0.05)。Pearson相关分析显示,疾病严重程度与HIE患儿血清S-100B蛋白、sLOX-1、GFAP水平呈正相关(均P<0.001)。随访预后良好患儿59例,预后不良21例,经多因素Logistic回归分析显示,产程异常、病情重度、S-100B蛋白、sLOX-1、GFAP为影响HIE患儿预后的危险因素(均P<0.05)。结论:HIE患儿病情严重程度和预后与血清S-100B蛋白、sLOX-1、GFAP水平有关,监测其水平变化有利于临床早期完善干预方案改善预后。

以急性意识障碍伴低血压为首发症状的非酒精性Wernicke脑病1例

目的探讨Wernicke脑病尤其是非酒精性Wernicke脑病的少见临床表现。方法回顾1例非酒精性Wernicke脑病患者的临床表现、辅助检查、治疗过程及预后,并复习该病相关文献。结果该例非酒精性Wernicke脑病患者以急性意识障碍伴低血压为首发症状,头部核磁(MRI)平扫+弥散加权成像(DWI)提示四叠体、双侧丘脑、双侧乳头体异常信号影,给予VitB1等对症治疗后,该例患者的临床症状得到改善。结论以急性意识障碍伴低血压为首发症状的非酒精性Wernicke脑病患者经常被误诊。结合可导致VitB1缺乏的病史以及头部MRI等检查有助于尽早明确诊断,及时补充VitB1可有效改善患者的预后。

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脑病的临床特点分析

目的探讨不同原因所致Wernicke脑病的临床特点。方法回顾性分析28例Wernicke脑病患者的临床资料,将病例分为饮酒组与非饮酒组,比较其临床表现、影像学、脑脊液、神经电生理等的差异。结果饮酒组最常见的神经系统症状为精神和意识异常(85.7%),少部分患者可见Wernicke脑病典型的"三联征",MRI示病灶最常见于丘脑内侧和第三脑室周围(78.6%),脑脊液检查均正常;非饮酒组症状亦为精神和意识的异常(85.7%),但眼部症状(42.9%)比饮酒组少,MRI示病灶最常见于丘脑内侧和第三脑室周围(85.7%),脑脊液(66.7%)示生化异常。饮酒组MRI乳头体增强明显高于非饮酒组(P=0.019)。结论不同原因所致Wernicke脑病的诊断均主要依靠临床特点;在饮酒组乳头体增强是一个特异性影像学表现,可以作为早期诊断的指标之一。

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。

MRI诊断Wernicke脑病

目的:探讨Wernicke脑病的MRI特点。材料和方法:回顾性分析6例Wernicke脑病的MRI表现并与病理对照。结果:6例中,男4例,女2例,年龄37～68岁,平均48岁。MRI表现为Ⅲ、Ⅳ脑室及中脑导水管周围对称性的长T1长T2异常信号4例,其余依次为穹隆柱(2／5)、乳头体(2／5)、视交叉(1／5)、小脑上蚓部(1／5)及皮质下白质(1／5)异常信号。1例尸检表现为Ⅲ、Ⅳ脑室及中脑导水管周围灰质充血、水肿和点状出血。结论:Wernicke脑病的临床表现不典型,MRI可对其早期诊断提供帮助。

Wernicke脑病的磁共振表现及其临床特点

目的探讨Wernicke脑病的临床特点及影像学MRI表现。材料与方法回顾性分析我院2010年2月至2015年6月经临床确诊的10例Wernicke脑病患者的临床及MRI影像资料。结果 10例患者中表现为意识障碍及精神症状者3例,视力障碍或眼肌麻痹者3例,共济失调者4例。10例均行MRI检查。10例患者中,6例患者表现为双侧丘脑内侧、第三、四脑室旁、中脑导水管周围出现,长T1WI信号,长T2WI信号,T2 FLAIR高信号;2例患者乳头体、穹隆柱出现对称性长T1WI信号,长T2WI信号,T2 FLAIR高信号;2例患者桥脑背盖、乳头体、中央导水管周围、双侧中央沟皮质出现对称性长T1WI信号,长T1WI信号,T2FLAIR高信号,弥散加权成像(diffusion weighted imaging,DWI)高信号。结论Wernicke脑病MRI具有一定特征性的表现,结合临床资料及临床症状可对本病作出早期的正确诊断。

长期全胃肠外营养并发Wernicke脑病的临床分析

目的：探讨因长期全胃肠外营养（TPN）引发Wernicke脑病（WE）的病因、患病机制及诊断和治疗方法。方法：回顾性分析我院1995—2005年，20例长期全胃肠外营养后并发WE的临床资料。结果：WE多发生在全胃肠外营养后第2—3周。其中18例经及时诊断后补充维生素B1症状消失，2例因误诊致死亡。结论：长期胃肠外营养病人及时补充维生素B1是预防及治疗WE发生的关键。