Wernicke encephalopathy

Result from Thiamine (vitamin B-1) deficiency 

Characteristically associated with chronic alcoholism, because it affects thiamine uptake and utilization. However, may develop in nonalcoholic conditions, such as prolonged starvation, hyperemesis gravidarum, bariatric surgery, and HIV.

Triad of Wernicke encephalopathy are: 

1-Encephalopathy: profound disorientation, indifference, and inattentiveness

2-Ataxic gait:combination of polyneuropathy, cerebellar involvement, and vestibular dysfunction

3-Oculomotor dysfunction:Nystagmus is the most common finding and is typically evoked by horizontal gaze to both sides

All 3 features of the triad are recognized in only about one third of cases.

Other features: long-term alcohol abuse and/or malnutrition and any of the following: 

-acute confusion, 

-ataxia, 

-ophthalmoplegia, 

-memory disturbance, 

-hypothermia with hypotension.

-delirium tremens.

A high proportion of patients with acute Wernicke encephalopathy who survive develop Korsakoff psychosis, characterized by:

-potentially irreversible retrograde amnesia 

-anterograde amnesia (inability to assimilate new information)

-confabulation

-Hallucination ( visual/auditory)

-varying degrees of other cognitive deficits

Diagnosis:

Clinical, however tests to exclude other causes.

FBC

Blood glucose

Toxocology screen

Erythrocyte transketolase activity assay

Blood pyruvate and lactate measurements

MRI: not usually required. mamilary body haemorrhage and atropy.

Treatment:

Thiamine until the patient resumes a normal diet.

Empirical parenteral magnesium sulfate

Wernicke's encephalopathy may be precipitated by administration of intravenous glucose solutions to individuals with thiamine deficiency. In susceptible individuals glucose administration should be preceded or accompanied by thiamine 100 mg IV.

Thiamine supplementation, along with other multivitamin supplementation, is recommended for patients at risk for thiamine deficiency.