Wernicke's

Question 1

Wernicke’s

Answer 1

Wernicke’s encephalopathy is characterised by the triad of global confusion, ophthalmoplegia, and ataxia (though the complete triad is only present in 10% of cases). It results from prolonged thiamine deficiency which is normally seen in people with alcohol dependency. It also occurs in other conditions including:-

Anorexia nervosa
Following gastric surgery
Malignancy
AIDS
Hyperemesis gravidarum
Prolonged total parenteral nutrition

The onset of Wernicke’s is usually abrupt but may develop over several days to weeks.

It is a very serious condition and has an associated mortality of 10-20%.

The lesions of Wernicke’s encephalopathy occur in a symmetrical distribution in structures surrounding the third ventricle, aqueduct, and fourth ventricle. The mammillary bodies are involved in up to 80% of cases, atrophy of these structures is specific for Wernicke’s encephalopathy.

Pathological features include neuronal loss and demylination in periventricular grey matter, and haemorrhage and small vessel proliferation in the mamillary bodies, thalamus, cerebellar vermis, and pons.

Treatment involves intravenous thiamine (vitamin B1), as oral forms of B1 are poorly absorbed. Of those untreated, 80% go on to develop Korsakoff’s syndrome. IV glucose should be avoided when thiamine deficiency is suspected as it can precipitate or exacerbate Wernicke’s.

With treatment ophthalmoplegia and confusion usually resolve within days but the ataxia, neuropathy, and nystagmus may be prolonged or permenant.
Nystagmus (usually horizontal) is the most common ocular abnormality seen in Wernicke’s.

The classic clinical triad of Wernicke’s encephalopathy consists of confusion, ophthalmoplegia, and gait ataxia. However, the complete triad may be present in as few as 10% of cases.

MRI (not CT) is the preferred imaging technique used to assist in the diagnosis of Wernicke’s.