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A 65-year-old man with a history of alcohol abuse was admitted with double vision, numbness and light-headedness. A physical examination showed no significant abnormality but a neurological examination showed right abducens palsy, left facial nerve palsy and internuclear ophthalmoplegia (failure to adduct on left side with nystagmus in the opposite, abducting eye). Blood results showed normal full blood count, renal and liver biochemistry, serum electrolytes, vasculitic screen, complement levels and autoimmune serology. A magnetic resonance scan of the brain (fig 1) showed ill-defined focal hyperintensity in the central part of the pons (circled) consistent with central pontine myelinosis (CPM). The patient was treated with an alcohol detoxification regimen and was advised to stop drinking alcohol. The neurological deficit improved slowly over months.
Victor et al were the first to identify CPM.1 It is a life-threatening condition, usually associated with the rapid correction of hyponatraemia.2 Other less common causes include alcohol abuse, malnutrition, liver failure/transplant, prolonged diuretic use and extensive burns. Focal neurological deficit is often attributed to stroke, requiring specific investigations and interventions. In the absence of cardiovascular risk factors for stroke, CPM should be considered in the differential diagnosis of neurological deficit, especially in a patient with a history of alcohol abuse.
This article has been adapted from Agarwal A K, Garg R, Kauser S A. When neurological deficit is not a stroke Emergency Medicine Journal 2007;24:751
Competing interests: none declared