[Gayet-Wernicke encephalopathy with normal thiamine level: a case report]. / Encéphalopathie de Gayet-Wernicke avec taux de thiamine normale: à propos d'un cas.

Gayet-Wernicke encephalopathy is a neuropsychiatric emergency due to thiamine deficiency (vitamin B1), secondary to several factors. We here report a case of Gayet-Wernicke encephalopathy in a 43-year-old woman who didn't consume alcoholic beverages, presenting with disorders of consciousness and diplopia with normal thiamine level. Classic triad of symptoms and Magnetic resonance imaging (MRI) played an important role, in particular, in the diagnosis of Gayet-Wernicke encephalopathy with normal thiamine levels in the absence of alcohol abuse.

[Gayet-Wernicke encephalopathy: clinical features and radiological anomalies]. / L'encéphalopathie de Gayet Wernicke: aspects cliniques et anomalies radiologiques.

Gayet Wernicke encephalopathy (EGW) is a neurological emergency secondary to thiamine deficiency (vitamin B1). This is more often secondary to chronic alcoholism. The purpose of this study is to remind clinicians of some clinical signs different from ethylism, suggesting EGW as well as to report four cases characterized by different types of anomalies shown by MRI. The average age of patients was 40 years (2 females 2 males). The neurological picture was characterized by disorders of vigilance in all patients, oculomotor disorders in 2 cases, and cerebellar ataxia in one patient. Chronic vomiting was reported in two cases, prolonged fasting in the first case and alcoholism in the second case. MRI of the brain showed anomalies suggesting EGW in all patients with contrast enhancement in one case. Thiamin deficiency was confirmed in two patients. In our context EGW seems to be more frequent in pathological circumstances other than chronic alcoholism (chronic vomiting, severe malnutrition, severe starvation, and chemotherapy...). The clinical signs can suggest other pathologies such as cerebral venous thrombosis, stroke, or other metabolic disorders but MRI excluded them and allowed the diagnosis of EGW. MRI of the brain has an essential role in the diagnosis of EGW. Absence or delay in treatment may influence the prognosis.

Hyperemesis-induced Wernicke-Korsakoff Syndrome due to Hypergastrinemia during Long-term Treatment with Proton Pump Inhibitors.

We herein report a patient with Wernicke-Korsakoff syndrome (WKS) who had neither a history of alcoholism or of history of gastric surgery. A 56-year-old woman was transferred to our hospital because of the loss of consciousness and she was diagnosed to have Wernicke encephalopathy. She showed proton pump inhibitor-induced refractory hypergastrinemia with the subsequent development of hyperemesis and a vitamin B1 deficiency.

Comprehensive review of Wernicke encephalopathy: pathophysiology, clinical symptoms and imaging findings.

Wernicke's encephalopathy (WE) is a severe and life-threatening illness resulting from vitamin B1 (thiamine) deficiency. The prevalence of WE has been estimated from 0.4 to 2.8%. If not treated properly, severe neurologic disorders such as Korsakoff psychosis and even death may occur. The classical triad of clinical symptoms (abnormal mental state, ataxia, and ophthalmoplegia) is found in only 16-33% of patients on initial examination. The originally described underlying condition of WE is alcoholism, but it accounts for about 50% of causes of WE. Nonalcoholic patients are also affected by WE and likely to present symptoms and radiological imaging findings different from patients with alcoholism, which further complicates the diagnosis of WE. Being familiar with predisposing causes, symptoms and radiological imaging findings of WE is important for radiologists and clinicians when making the diagnosis to start immediate treatment. This review discusses pathophysiologies, underlying causes, clinical symptoms, imaging findings and their mimics.

Focal hyperemia in Wernicke's encephalopathy: a preliminary arterial spin labeling MRI study.

Although a perturbed cerebral blood flow (CBF) has been reported in patients with Wernicke's encephalopathy (WE), its clinical meaning is still elusive. A retrospective analysis of 10 patients (male, 6; mean age, 57.7 years) with WE between October 2012 and May 2018 was performed. Brain imaging was performed using fluid-attenuated inversion recovery (FLAIR), diffusion-weighted imaging (DWI), arterial spin labeling (ASL) perfusion-weighted imaging (PWI), and contrasted enhanced T1-weighted imaging. All patients had symmetric high signal intensity lesions in the vulnerable areas on FLAIR or DWI with focal hyperintensity on ASL-PWI (100% sensitivity). CBFlesion was variable (from 70 mL/100 g/min to 190.0 mL/100 g/min). CBFlesion/CBFwhite matter was elevated, ranging from 2.5 to 5.5. Focal hyperintensity on ASL in the vulnerable areas can be a diagnostic clue for WE.

Wernicke Encephalopathy-Clinical Pearls.

Wernicke encephalopathy (WE) was first described by Carl Wernicke in 1881. WE is caused by thiamine deficiency. Alcoholism is the most common etiologic factor associated with WE in the United States, but it can occur in any patient with a nutritional deficiency state such as hyperemesis gravidarum, intestinal obstruction, and malignancy. WE is a clinical diagnosis. The common findings include mental status changes, ocular dysfunction, and a gait apraxia, present in only 10% of cases. Only a few cases of WE are diagnosed before death. Approximately 80% of patients with untreated WE have development of Korsakoff syndrome, which is characterized by memory impairment associated with confabulation. The initial clinical diagnosis of WE is critical, keeping in mind that the classic triad of symptoms is often absent. Recognition of nutritional deficiency and any portion of the classic triad should prompt treatment. Additionally, hypothermia, hypotension, and coma should raise clinical suspicion for the disease. Primary treatment includes timely administration of thiamine, for which the route and dosage remain controversial. Clinical judgment should be exercised in diagnosis and treatment (dosage, frequency, route of administration and duration) in all cases of WE. Overdiagnosis and overtreatment may be preferred to prevent prolonged or persistent neurocognitive impairments given the excellent safety profile of thiamine. Further prospective research is warranted to better understand the disease biology, risk factors, and treatment recommendations.

Cognitive and Motor Impairment Severity Related to Signs of Subclinical Wernicke's Encephalopathy in HIV Infection.

BACKGROUND: Wernicke's encephalopathy (WE) is a neurological condition resulting from thiamine deficiency. Although commonly associated with alcoholism, nonalcoholic WE has been described in individuals with HIV infection, but subclinical WE may be underdiagnosed. The current study questioned whether the presence of subclinical WE signs underlies cognitive and motor deficits in HIV individuals as observed in alcoholism. SETTING: Fifty-six HIV-positive individuals (HIV+) and 53 HIV-negative controls (HIV-) were assessed on 6 cognitive and motor domains: attention/working memory, production, immediate and delayed episodic memory, visuospatial abilities, and upper-limb motor function. METHODS: Based on a rating scheme by Caine et al, HIV+ individuals were categorized by subclinical WE risk factors (dietary deficiency, oculomotor abnormality, cerebellar dysfunction, and altered mental state). Performance was expressed as age- and education-corrected Z-scores standardized on controls. RESULTS: Sorting by Caine criteria yielded 20 HIV+ as Caine 0 (ie, meeting no criteria), 22 as Caine 1 (ie, meeting one criterion), and 14 as Caine 2 (ie, meeting 2 criteria). Comparison among HIV+ Caine subgroups revealed a graded effect: Caine 0 performed at control levels, Caine 1 showed mild to moderate deficits on some domains, and Caine 2 showed the most severe deficits on each domain. CONCLUSION: This graded severity pattern of performance among Caine subgroups suggests that signs of subclinical WE can partly explain the heterogeneity in HIV-related cognitive and motor impairment. This study highlights the utility of Caine criteria in identifying potential causes of HIV-related neurocognitive disorders and has implications for disease management.

Gastrointestinal beriberi: a forme fruste of Wernicke's encephalopathy?

Gastrointestinal symptoms, such as anorexia, nausea, vomiting and abdominal pain, are very common in patients with Wernicke's encephalopathy (WE). Mild thiamine deficiency may have only gastrointestinal symptoms. We are reporting two patients with thiamine deficiency who predominantly had gastrointestinal symptoms. Case 1: a 38-year-old man had gastrointestinal problems for about 2-3 years. It gradually became severe. The patient came to the neurology outpatient department for his recent-onset vertigo and headache. Clinical examinations fulfilled Caine's criteria of WE. Gastrointestinal symptoms responded dramatically to intravenous thiamine. Case 2: a 21-year-old woman developed drug-induced hepatitis and gastritis. Associated nausea, vomiting and abdominal pain progressively increased over the weeks. The patient responded only to intravenous thiamine administration.We suggest that a suspicion for gastrointestinal beriberi should arise if gastrointestinal symptoms (anorexia, nausea, vomiting and abdominal pain) are refractory to the usual therapies.

Wernicke encephalopathy without delirium that appeared as agitation in a patient with lung cancer.

OBJECTIVE: Wernicke encephalopathy (WE) is a neuropsychiatric disorder caused by thiamine deficiency, and is sometimes overlooked because of the diversity of clinical symptoms. METHOD: From a series of WE patients with cancer, we report a lung cancer patient who developed WE, the main symptom of which was agitation.ResultA 50-year-old woman with lung cancer was referred to our psycho-oncology clinic because of agitation lasting for three days. No laboratory findings or drugs explaining her agitation were identified. Although the patient did not develop delirium, ophthalmoplegia, or ataxia, WE was suspected because she experienced a loss of appetite loss lasting 5 weeks. This diagnosis was supported by abnormal serum thiamine and disappearance of agitation one hour after intravenous thiamine administration.Significance of resultsThis report emphasizes the clinical diversity of WE and indicates the limits of the ability to diagnose WE from typical clinical symptoms. The presence of a loss of appetite for more than two weeks may be the key to the accurate diagnosis of WE.

A case report: Non-alcoholic Wernicke encephalopathy associated with polyneuropathy.

We report a rare case of non-alcoholic Wernicke encephalopathy (WE) with polyneuropathy. A 24-year-old woman who had recently served a 4-month prison sentence and underwent a short period of dieting manifested slow response, weakness, language disorder and amnesia. Brain magnetic resonance imaging (MRI) revealed typical lesions of WE. Examination of nerve conduction velocity revealed sensory-motor axonal polyneuropathy. The patient was immediately treated with thiamine. Neurological symptoms were alleviated in a few days and abnormal signals were markedly decreased in a follow-up MRI 1 week later. Polyneuropathy symptoms ameliorated during hospital therapy and significantly improved after 4 months. This case suggests that WE may be associated with polyneuropathy in non-alcoholic patients. Early thiamine treatment in symptomatic patients may improve prognosis.

Wernicke Encephalopathy in Adolescents After Bariatric Surgery: Case Report and Review.

Roughly 1% of all weight loss surgery is performed in adolescents. There is strong evidence demonstrating significant postsurgical weight loss, improvement in quality of life, and reduction in comorbidities such as hypertension and diabetes. Reports of postoperative complications in adolescents are few because of the small sample size in most series. Despite vitamin supplementation, nutritional deficiencies requiring hospitalization occur occasionally after Roux-en-Y gastric bypass. Wernicke encephalopathy, a triad of ophthalmoplegia, ataxia, and altered mental status, is a serious consequence of thiamine (vitamin B1) deficiency. Few cases of Wernicke encephalopathy after weight loss surgery have been reported in the literature and even fewer in the pediatric population. Here we describe a teenage girl who develops vomiting after Roux-en-Y gastric bypass and presented with nystagmus, irritability, and ataxia. The clinical presentation, diagnosis, and treatment of Wernicke encephalopathy in adolescents after bariatric surgery are discussed.

Clinical awareness for health care professionals: Fatal encephalopathy complicating persistent vomiting in pregnancy.

Women with persistent vomiting during pregnancy need early referral to appropriate health facilities. Delayed referral and inappropriate management may lead to metabolic encephalopathy from a variety of causes, including electrolyte derangements or thiamine deficiency (Wernicke's encephalopathy) (WE). We present a case of persistent vomiting in pregnancy in which there was delayed referral, inappropriate treatment and failure to associate neurological signs such as terminal neck stiffness with WE, resulting in poor fetomaternal outcomes. In this report, we discuss the following lessons: (i) the need for early transfer of a patient with persistent vomiting and enigmatic clinical features to a higher healthcare facility; (ii) failure to associate neurological signs with complications of hyperemesis gravidarum/WE; (iii) lack of thiamine supplementation; and (iv) the advantages of magnetic resonance imaging over a computed tomography scan in the diagnosis of WE.

Consecuencia del abuso de alcohol / A consequence of alcohol abuse

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Wernicke's encephalopathy in crack-cocaine addiction.

HYPOTHESIS: Crack-cocaine addiction is associated with a variety of conditions that increase risk of thiamine deficiency and Wernicke's encephalopathy. EVIDENCE: We report a case of Wernicke's encephalopathy in a crack-cocaine addict who did not habitually consume alcohol. We list some conditions associated with crack-cocaine addiction that may contribute to thiamine deficiency. IMPLICATIONS: Clinicians should bear in mind that crack-cocaine addiction may be associated with Wernicke's encephalopathy, mainly due to malnutrition. We suggest that routine Wernicke's encephalopathy prophylaxis with parenteral thiamine be provided to patients with chronic crack-cocaine addiction, as is already established practice in chronic alcoholics, so as to prevent cognitive damage in this population.

Encephalopathy after persistent vomiting: Three cases of non-alcohol-related Wernicke's encephalopathy.

Wernicke's encephalopathy (WE) is a medical emergency. Although WE is commonly viewed in the context of alcoholism, it can be caused by thiamine deficiency secondary to persistent vomiting. Non-alcohol-related WE may be more catastrophic in onset and less likely to present with the classic features than WE with alcoholism as a cause. We describe three cases of WE due to persistent vomiting without alcoholism in patients with hyperemesis gravidarum, drug-induced hyperlactataemia, and an acute gastrointestinal illness in an already malnourished individual. Our cases highlight the importance of recognising WE when undernutrition, which may be caused by gastrointestinal disease or surgery, or malignancy, is compounded by vomiting. Expert guidelines suggest that WE must be considered in the emergency room in any individual with disturbed consciousness of unknown cause. Treatment is with parenteral thiamine before glucose administration.

Wernicke Encephalopathy.

INTRODUCTION AND PURPOSE: This paper reviews the complaints and associated symptoms/consequences of lacking essential nutrients and vitamins in our central and peripheral nervous systems. This has become important as there has been a rise in malnutrition following the increasing incidence of bariatric surgery for obesity. METHODS: A case report example involving review of the clinical presentation and treatment. RESULTS: A 30-year-old Caucasian woman who had gastric sleeve surgery did not take the recommended capsules as they were too large to swallow. She noted diplopia and oscillopsia 2 months later, which led her to have full orthoptic and neuro-ophthalmic evaluations. After being treated with chewable vitamins with thiamine, she noted a tremendous improvement in her symptoms. CONCLUSION: Wernicke encephalopathy is a disease that was seen more in the 1940s and 1950s, following war times and mostly in underdeveloped countries. However, with the increasing utilization of bariatric surgery for obesity, neurological offices are seeing more patients with neurological impairments. We recommend inquiring about any obesity surgery in one's history and including Wernicke encephalopathy in possible differential diagnoses in those patients who have a recent onset of strabismus or nystagmus, altered mental status, and/or gait ataxia.