Wernicke's encephalopathy Flashcards
What is Wernicke’s encephalopathy?
Neurological disorder resulting from thiamine deficiency resulting in changes in mental state and oculomotor dysfunction.
What is the aetiology of Wernicke’s encephalopathy?
Acute or sub-acute thiamine (Vitamin B1) deficiency secondary to decreased intake and intestinal insult from alcohol. Can also be as a result of other malabsorptive disorders of the GI tract
What risk factors are there in Wernicke’s encephalopathy? (x5)
Alcohol dependence, AIDS, cancer, malnutrition, Hx of GI surgery.
What is the pathophysiology of Wernicke’s encephalopathy?
Thiamine can be stored for up to 18 days. It is an enzyme cofactor in the Kreb’s cycle. As such, deficiency leads to energy compromise which leads to neuronal death in neurones with high metabolic requirements. This predominantly affects areas of the brain related to memory, ocular motor function, vestibular nerve, and cerebellum.
What are the signs and symptoms of Wernicke’s encephalopathy?
Nystagmus, ophthalmoplegia (weakness of eye), ataxia, disorientation, apathy and memory loss
What are the investigations for Wernicke’s encephalopathy? (x3)
- PARENTERAL THIAMINE: clinical response to treatment is diagnostic.
- Test serum ammonia as this may cause metabolic encephalopathy.
- Serum Mg2+ as is common in alcohol misuse, and Mg2+ important co-factor in same enzymes as thiamine
How is Wernicke’s encephalopathy managed? (x4)
- THIAMINE: IV until improvement ceases
- Magnesium sulphate: IV
- Folic acid
- Oral thiamine in ongoing management (Pabrinex)
What are the complications of Wernicke’s encephalopathy?
Korsakoff’s psychosis: anterograde amnestic syndrome with confabulation as a result of irreversible damage to the mamillary bodies and hippocampus
What is anterograde amnesia?
Inability to make memories after the onset of amnesia. Retrograde amnesia is the inability to access memories from before the onset of amnesia
