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Content - **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

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