[Wernicke encephalopathy in alcoholic patients]

Area of Science:

• Neurology
• Internal Medicine
• Nutritional Neuroscience

Background:

• Wernicke encephalopathy (WE) is a serious neurological complication primarily associated with thiamine (vitamin B1) deficiency.
• Chronic alcohol consumption is a leading risk factor for WE due to impaired thiamine absorption and storage.
• Malnutrition and limited dietary intake, as seen in this patient, further exacerbate thiamine deficiency.

Observation:

• A 67-year-old male presented with somnolence, bradypsychia (slowed thinking), and gait disturbance.
• Physical examination revealed stigmata of chronic liver disease.
• Neurological examination demonstrated right-sided cerebellar tremor, bilateral dysmetria, gait ataxia, and hyporeflexia, indicative of cerebellar and peripheral nerve dysfunction.

Findings:

• The patient's history of high ethanol intake (>100-120 g/day), poor diet, and clinical presentation strongly suggested Wernicke encephalopathy.
• The constellation of neurological signs, including ataxia and altered mental status, are classic manifestations of thiamine deficiency.

Implications:

• Early recognition and treatment of Wernicke encephalopathy with thiamine supplementation are critical to prevent irreversible neurological damage and mortality.
• This case underscores the importance of considering Wernicke encephalopathy in patients with risk factors such as alcoholism and malnutrition presenting with neurological symptoms.
• Effective management requires prompt neurological assessment and aggressive thiamine repletion, often intravenously, followed by oral supplementation.