Hemichorea–hemiballismus due to hyperglycaemia

A 77‐year‐old man with a history of type 2 diabetes was admitted to hospital for acute hyperglycaemia (glucose, 577mg/dL; glycated haemoglobin, 139mmol/mol), with positive ketonaemia (2mmol/L). Forty‐eight hours later, he had psychomotor agitation and involuntary, poorly patterned movements affecting the left hemibody, suggesting a hemichorea diagnosis. An unenhanced computed tomography scan found hyperdensity of the right striatum (Figure, A). Magnetic resonance imaging found a T1 hypersignal of the right putamen (Figure, B). Hemichorea–hemiballismus due to hyperglycaemia was diagnosed, as neurological work‐up ruled out other toxic, vascular, infectious, inflammatory or neoplastic causes. He was discharged ten days later, with initial improvement of abnormal movements.

After three weeks, he had a recrudescence of hemichorea–hemiballismus despite euglycaemia and required treatment with tetrabenazine and haloperidol. Two months later, he no longer displayed abnormal movements, the T1 hypersignal had decreased (Figure, C), and neurological treatments could be gradually discontinued (stopped at six months). At ten months, the T1 hypersignal disappeared (Figure, D).

Hemichorea–hemiballismus related to hyperglycaemia (non‐ketotic in most cases) is part of the spectrum of diabetic striatopathy, a rare disorder with a largely unknown pathophysiology (petechial haemorrhage, ischaemia or mineral deposition are among the suggested mechanisms). Antichorea treatments are required in patients unresponsive to aggressive glucose control.1