Focal precentral gyrus involvement in osmotic demyelination

THE CASE A previously well 59-year-old woman was admitted to a regional hospital with subacute encephalopathy and found to have severe hyponatraemia (101mmol/L). She had taken indapamide for hypertension over the preceding 3months. Before referral to neurological services, she had received intravenous hypertonic saline. Her serum sodium concentration normalised within a few days, but was associated with a deteriorating conscious level. She was referred to our tertiary neurological centre with suspected osmotic demyelination where she presented in a ‘locked in’ state, involving quadriplegia and absent vertical eye movements. MR scan of the brain showed typical symmetrical pontine and basal ganglia changes, but also focal hyperintensity of the precentral gyri (figure 1). Nearly 6months after the initial admission to hospital, the patient had made some recovery of limb strength, but with persistent loss of fine dexterity and unable to stand independently. Hyponatraemia secondary to thiazide diuretics is well recognised, and cautious correction of chronic hyponatraemia is generally advised to minimise the risk of osmotic demyelination. This unusual extension of MRI changes in extrapontine myelinolysis is uncommon, and our case also shared the bilateral hyperintensity in the posterolateral nuclei of the Figure 1 MR scan of the brain. Axial fluid-attenuated inversion recovery (FLAIR) images show symmetrical pontine (A), basal ganglia (B) and a ‘ribbon’ of cortical T2 hyperintensity in the posterior precentral gyri (C). The precentral gyral changes are strikingly similar to a focal pattern of MRI changes described in cases of amyotrophic lateral sclerosis.