Eight adults and 3 children out of 85 patients who had neuropathologic examination after death following orthotopic liver transplantation showed central pontine myelinolysis (CPM). Four patients also had extrapontine myelinolysis. Eight patients had significant serum sodium changes. In 5, the fluctuation occurred perioperatively and 4 had a clinical picture consistent with CPM, although no patient had this as an antemortem diagnosis. We emphasize the role of hepatic dysfunction as a cause of CPM and recommend careful monitoring of electrolytes in the perioperative period of patients undergoing liver transplantation.

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SUMMARY A 45-year-old woman with long standing surgical hypoparathyroidism presented with right hemichorea of three months' duration. She had profound hypocalcaemia and hyperphosphataemia and extensive cerebral, cerebellar and basal ganglia calcification. Correction of the chemical abnormalities with I ol-hydroxycholecalciferol, calcium supplements and aluminium hydroxide resulted within 10 weeks in complete disappearance of the abnormal movements. 21-2-6) and serum inorganic phosphorus 1-9-2-1 mmol/l (normal range: 0-9-1-6). Electroencephalography, skull and chest radiography and a pertechnetate brain scan were all normal. In particular there was no calcification seen in the routine skull films. However, computed tomography (CT) showed extensive bilateral calcification in the basal ganglia, cerebellum and cerebral cortex (fig). An electrocardiogram showed a prolonged Q-T interval. Serum thyroxin was 124 nmol/l (normal range: 64-154) and serum thyrotropin was 0 5 uU/ml (normal range: 0-7).

SUMMARY To determine if alcoholic neuropathy which causes denervation of the distal muscles of chronic alcoholics also produces a subclinical myopathy of their proximal muscles, we studied 11 chronic alcoholics who had no muscular weakness or wasting. Six patients demonstrated distal hyporeflexic (ankle jerks) sensory neuropathy on clinical examination. Four patients, one of whom was asymptomatic, had slow peroneal motor nerve conduction velocities. Patterns of neuropathy were present in the electromyograms of the proximal muscles of two patients. Muscle biopsy studies with enzyme histochemistry indicated denervation atrophy and myopathic changes in the contralateral quadriceps muscles of eight patients. As denervation atrophy was present, we concluded that these myopathic changes represented the effects of denervation of these muscles. We conclude, therefore, that the proximal subclinical alcoholic myopathy, previously described as primary by ourselves and others, is the result of denervation due to the well-known alcoholic neuropathy.