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.

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

AIM To present the typical and atypical magnetic resonance(MR) imaging findings of alcoholic and non-alcoholic Wernicke's encephalopathy.METHODS This 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/mm^2), and a contrast-enhanced MR sequence. All MR images were retrospectively reviewed at baseline and follow-up by two radiologists.RESULTS All 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 diffusionin 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. CONCLUSION MR 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.

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.

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.

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.

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.

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.

Case Report:Wernicke encephalopathy following splenectomy in a patient with liver cirrhosis:a case report and review of the literature

Objective:To report a case of Wernicke encephalopathy in the early stage after surgery.Methods:A nonalcoholic female patient with hepatitis B-related cirrhosis and hypersplenism underwent splenectomy in a local hospital.No surgical complications occurred and the patient recovered well.However,on the eighth postoperative day she developed psychiatric and neurological disturbance without an obvious cause.She was then admitted to our hospital.Brain magnetic resonance imaging(MRI) with FLAIR T2 showed symmetric high-signal intensities in the periaqueductal area of the midbrain,which were consistent with Wernicke encephalopathy.She was thus given in-tramuscular thiamine immediately.Results:After the administration of thiamine,the patient's confused mental state resolved within 3 d,and her dystaxia gradually improved over the next 5 d.The brain MRI with FLAIR T2 was re-examined one month after the episode,and showed nearly complete resolution of the previously abnormal signal intensities in the periaqueductal area of the midbrain.Conclusion:Physicians should be aware of the possibility of acute Wernicke encephalopathy,especially in patients with liver dysfunction.

Wernicke encephalopathy in children and adolescents

Background:Wernicke encephalopathy is caused by thiamine(vitamin B1)defi ciency.It is generally considered to be a disease of adult alcoholics.However,it is known to occur in the pediatric population and in non-alcoholic conditions.Data sources:We searched PubMed with the key words Wernicke,thiamine,pediatric,children and adolescents and selected publications that were deemed appropriate.Results:The global prevalence rates of hunger,poverty and resultant nutrient deprivation have decreased in the 21st century.However,several scenarios which may predispose to Wernicke encephalopathy may be increasingly prevalent in children and adolescents such as malignancies,intensive care unit stays and surgical procedures for the treatment of obesity.Other predisposing conditions include magnesium defi ciency and defects in the SLC19A3 gene causing thiamine transporter-2 deficiency.The classic triad consists of encephalopathy,oculomotor dysfunction and gait ataxia but is not seen in a majority of patients.Treatment should be instituted immediately when the diagnosis is suspected clinically without waiting for laboratory confi rmation.Common magnetic resonance findings include symmetric T2 hyperintensities in dorsal medial thalamus,mammillary bodies,periaqueductal gray matter,and tectal plate.Conclusions:Wernicke encephalopathy is a medical emergency.Delay in its recognition and treatment may lead to significant morbidity,irreversible neurological damage or even death.This article aims to raise the awareness of this condition among pediatricians.

Wernicke Encephalopathy in a Patient with Pulmonary and Abdominal Tuberculosis

Wernicke encephalopathy （WE） is an acute or subacute neurological syndrome caused by thiamine （Vitamin B 1） deficiency and is usually underestimated in clinical practice. WE is suspected in merely about 6% of non-alcoholic patients and one-third of alcoholic patients, Non-alcoholic causes include gastrointestinal surgery and disease, malnutrition, cancer and chemotherapeutic treatments, and long-term parenteral nutrition.However, few cases were reported about WE in patients with tuberculosis. Early diagnosis and medication are vital for the prognosis of this disease.

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.

Atypical miller-fisher syndrome after COVID-19 and sleeve gastrectomy:Contribution of neurochemical markers to early diagnosis

Background:The coronavirus disease 2019(COVID-19)pandemic,caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),began in late 2019.More recently,there have been sporadic case reports on devel-opment of Miller-Fisher Syndrome,a rare variant of Guillain-BarréSyndrome in COVID-19 patients.Case report:We reported herein the case of a French young women presenting with ophtalmoplegia,cerebellar ataxia,and universal areflexia following a bariatric surgery(sleeve gastrectomy).A concomitant COVID-19 diagnosis was retained based on microbiological testing.The patient was successfully treated after high-dose intravenous thiamine,but areflexia persisted.Underlying COVID-19 related Miller-Fisher Syndrome was established on physical examination and confirmed by pathologic neurophysiological findings and elevated level of phosphorylated neurofilament heavy chain protein in cerebrospinal fluid analysis.Conclusions:Guillain-BarréSyndrome and its variants after SARS-CoV-2 infection are extremely rare.The mea-surement of phosphorylated neurofilament heavy chain protein should be considered as an easy tool to detect an early affection of the peripheral nervous system.