Wernicke-Korsakoff Syndrome

  • Demographics: 0-2% worldwide prevalence, ?12.5% of heavy drinkers
  • Cause:
    • Vitamin B1 (thiamine) deficiency typically in context of alcohol dependence
    • Other causes include decreased absorption and nutrition eg. bariatric surgery, cancer, recurrent vomiting or chronic diarrhoea
  • Differential diagnoses: TODO
  • Comorbidities: TODO
  • Pathophysiology
    • Alcohol use to thiamine deficiency:
      • Dependence > empty calories > inadequate nutrition
      • Ethanol inhibits thiamine transport in GIT and thiamine phosphorylation
    • Wernicke encephalopathy to Korsakoff syndrome:
      • If untreated, delirium clears up within a month with residual amnesia in 85% of cases
    • Neurobiological correlations: damage of anterior thalami and mamillary bodies (memory), as well as cerebellar degeneration (ataxia)
  • Wernicke encephalopathy
    • Clinical manifestations: acute onset of confusion (80%), horizontal nystagmus or ophthalmoplegia (30%) and ataxia (20-25%). Less than 20% present with complete triad.
    • Diagnosis: Caine criteria requires two of (cause or any symptom)
    • Investigations: thiamine blood tests do not correlate clinically and take time. Treat empirically.
    • Management
      • Thiamine replacement prior to glucose replacement
        • 500mg IM/IV TDS for 5 days then 300mg PO TDS for 2 weeks then 100mg PO daily [eTG]
        • Thiamine is considered a necessary cofactor for glucose replacement. Some evidence suggests that the order of replacement does not matter. Acute glucose replacement (not prolonged) may be relatively safe.
      • Correct magnesium (required as thiamine cofactor), potassium and phosphate (refeeding syndrome)
    • Prognosis: acute and reversible with thiamine
  • Korsakoff syndrome aka alcohol amnestic disorder
    • Clinical manifestations: insidious onset of confabulation, retrograde and anterograde amnesia. Frontal lobe changes including apathy, avolition, change in personality.
      • Ribot’s law: newer memories are lost first
    • Management: thiamine prevents further progression, likely requires institutionalisation. Memory rehabilitation may assist with procedural memory (less impaired than declarative memory)
    • Prognosis: complete resolution in 20% of patients, irreversible in 25% of patients
  • Beriberi: severe and chronic form of thiamine deficiency. WK syndrome is a form of dry beriberi. Rare in first-world nations.
  • References: Kaplan’s Synopsis, eTG

Confabulation

  • Definition: umbrella term in regards to memory falsification in association with organically derived amnesia whilst in clear consciousness
  • Cause: faulty impairment of retrieval of memories with wrong cue-memory associations and search strategies
  • Features
    • Most apparent in autobiographical memory
    • Patients have no insight. Nil attempt to correct contradictory statements. Will act on false memories.
    • Confabulation diminishes as memory impairment worsens
  • Phenomenology types:
    • Provoked / embarrassment: patient attempts to cover up memory gaps with false memories thus revealing social awareness. Patients may recall reality memories displaced in time. More common type.
    • Spontaneous / fantastical: frontal lobe impairment with non-elicited announcements. More rare type. Patients may incorrectly classify previous fantastical memories as reality memories.
  • References: Sim’s, Fish’s

Last modified: Tue Aug 13 17:31:07 2024