Teaching Points:
- Wernicke’s Syndrome presents as a clinical triad of:
- Encephalopathy
- Ataxia
- Ophthalmoplegia
- The presence of all three characteristics is not needed in order to make the clinical diagnosis.
- An under-recognized disease
- Due to the lack of vitamin B1 (thiamine).
- Most common presentation is encephalopathy.
- Can manifest as indifference, confusion, poor attention span.
- Can rarely present as agitation in the setting of alcohol withdrawal.
- Severe cases can progress to stupor and coma
- Second most common sign is ataxia
- Ataxia can present itself before encephalopathy
- Ophthalmoplegia
- Presence of lateral right and left nystagmus, lack of smooth pursuit
- Severe cases can cause pupillary defects
- Patients do not have to be alcoholics in order to get Wernicke’s disease.
- Can be seen in those with poor oral intake, malnutrition, high catabolic states (sepsis), and those with poor utilization of thiamine (poor overall body substrate).
- Initiation of glucose prior to thiamine administration may actually precipitate Wernicke’s syndrome.
- Treatment involves high dose thiamine administration, with 500mg IV q8 hours x 2 days, then daily for 5-7 days.
- Response can be seen within hours to days.
- Untreated and prolonged Wernicke’s may lead to Korsakoff psychosis.
- Presents with anterograde and retrograde amnesia (long term memory retained), and confabulation.
- A more irreversible disease course.