Medicine

May 29th, 2021

Wernicke's encephalopathy

Clinicals - History

Introduction

Wernicke's encephalopathy (WE) is a neurological disorder caused by thiamine (vitamin B1) deficiency. Thiamine deficiency can occur in individuals with compromised absorption (e.g., hyperemesis), increased metabolism (e.g., sepsis), or increased carbohydrate intake (e.g., following IV dextrose administration). Chronic alcohol abuse is the most common etiology. The underlying pathophysiology involves lactic acid accumulation secondary to altered glucose metabolization in the absence of thiamine. This results in neurotoxic edema and oxidative stress that affects multiple brain structures.

Altered mentation

Altered mentation is the most frequent symptom. This can manifest as: cognitive impairment, including impairment of memory and an inability to concentrate; delirium; spatial disorientation; dizziness; drowsiness; apathy; coma; or, death. Altered mentation is believed to occur due to lesions affecting the dorsomedial thalamus, mammillary bodies, and cerebral cortex.

Visual disturbances

Diplopia is a classic symptom. This is thought to be due to lesions of cranial nerves III and IV.

Poor nutrition

Patients should be asked about their diet, and if they have any conditions that might impact nutrition, including: alcoholism, malignancies, gastrointestinal disease, gastrointestinal surgery. This is because an inadequate diet may cause thiamine deficiency.

Alcoholism

WE is more frequent in alcoholic patients, in whom it often presents as a subclinical syndrome.

Loss of balance

Patients may present with loss of balance and falls. This is due to ataxia.

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