Epidemiology

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Etiology

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Pathophysiology

• Thiamine deficiency → decreased cerebral glucose metabolism and mitochondrial dysfunction → depleted ATP and increased free radicals → injury of neuronal elements (e.g., myelin sheaths, blood-brain-barrier, decreased neurotransmitters, etc.) → impaired axonal conduction → symptoms of Wernicke encephalopathy and Korsakoff syndrome
• In patients with Korsakoff syndrome: long term thiamine deficiency → permanent damage to components of the limbic system (e.g., mammillary bodies, anterior thalamic nuclei) → atrophy of these components → memory loss, apathy, and disrupted emotional processing

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Clinical features

Wernicke encephalopathy (acute, reversible)

• Should be suspected in any patient with a history of chronic heavy alcohol use who presents with one/more symptoms of the classic triad of Wernicke encephalopathy
  1. Confusion (most common)
     • Disorientation, impaired vigilance, and cognitive deficits
  2. Oculomotor dysfunction
     • Due to involvement of the CN III, CN IV, and CN VI nuclei
     • Gaze-induced horizontal/vertical nystagmus (most common)
     • Diplopia
     • Conjugate gaze palsy
  3. Gait ataxia: wide-based, small steps
     • Due to a combination of peripheral neuropathy, vestibular dysfunction, and cerebellar dysfunction
     • Romberg test positive

When to suspect

Wernicke encephalopathy should be suspected in any patient with chronic alcohol abuse or any form of malnutrition and any of the following: acute altered mental status, ophthalmoplegia, ataxic gait, delirium, and hypotension.

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Diagnostics

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Treatment

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