Osmotic demyelination syndrome results from overly rapid serum sodium correction and is often iatrogenic. We report a 50-year-old hypertensive woman on Indapamide presenting with malaise, dizziness and serum sodium less than 100mmol/l who developed osmotic demyelination syndrome after correction of the hyponatremia. Good neurological recovery was seen after plasmapheresis.
Osmotic demyelination syndrome commonly affects the pons and infrequently involves the extrapontine region. We report a patient with severe hyponatraemia who developed osmotic demyelination syndrome as a consequence of rapid sodium correction. The condition manifested as acute severe parkinsonism, bilateral ptosis and gaze impairment. MRI revealed typical features of central pontine and extrapontine myelinolysis. The patient improved gradually after treatment with a combination of levodopa, intravenous immunoglobulin and dexamethasone. However, it is important to emphasise that the improvement of neurological symptoms is not necessarily causal with these experimental therapies.
This report deals with an elderly lady with Guillain-Barre Syndrome (GBS), who presented with features of unusually severe hyponatraemia. The hyponatraemia was probably due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The hyponatraemia resolved with water restriction and infusion of hypertonic saline; GBS was treated with human immunoglobulin (IVIG). This patient's experience stresses the importance of monitoring serum sodium levels as hyponatraemia has been identified to be a marker of poor prognosis in GBS.