# When Stroke Is Not a Stroke: Wernicke’s Encephalopathy in a Patient With Chronic Alcohol Misuse

## TL;DR

This paper describes a case where a patient with chronic alcohol misuse showed stroke-like symptoms due to Wernicke’s encephalopathy, highlighting the importance of early thiamine treatment and the unpredictability of cognitive recovery.

## Contribution

The case emphasizes that radiological improvement in Wernicke’s encephalopathy does not guarantee cognitive recovery, especially after severe presentations.

## Key findings

- The patient's neurological condition rapidly deteriorated, mimicking a stroke but was diagnosed with Wernicke’s encephalopathy.
- High-dose thiamine led to radiological improvement, but the patient had persistent severe cognitive deficits.
- The case underscores the need for immediate thiamine administration in suspected cases and warns against assuming good outcomes from imaging recovery.

## Abstract

Wernicke’s encephalopathy (WE) is a neurological emergency caused by thiamine deficiency and is a recognised stroke mimic. While prior reports often describe subacute presentations, we present a uniquely instructive case characterised by abrupt neurological collapse, with a rapid decline in Glasgow Coma Scale from 14 to 3 within 48 hours, closely simulating catastrophic cerebrovascular disease. Initial computed tomography was unremarkable; however, magnetic resonance imaging demonstrated classic, symmetrical involvement of the medial thalami, periaqueductal grey matter, tectal plate, mammillary bodies, and pyramidal tracts, consistent with acute WE. High-dose intravenous thiamine was initiated promptly, resulting in marked radiological improvement within five days. Despite recovery of consciousness and imaging resolution, the patient exhibited persistent and severe cognitive impairment on follow-up (Montreal Cognitive Assessment score 12/30), including prominent memory deficits. This case highlights an important and under-emphasised clinical lesson: radiological reversibility in WE does not reliably predict cognitive recovery, particularly following extreme presentations with abrupt coma. The report reinforces the need for immediate empirical thiamine administration in patients with acute unexplained neurological deterioration and risk factors for thiamine deficiency and cautions against interpreting early imaging improvement as evidence of a favourable neurological outcome.