Background

The major causes of unilateral hemichorea–hemiballismus include vascular insult (stroke), traumatic brain injury and neoplasms.1 The present case reports a patient who presented with unilateral hemichorea–hemiballismus, which was reversed by the treatment of hyperglycaemia. Hyperglycaemia thus represents a reversible cause of unilateral hemichorea–hemiballismus and should be considered in each and every case presenting with hemichorea–hemiballismus as prompt treatment is curative. Usually unilateral manifestations are a sequel of structural/vascular pathology, whereas in this case it was due to a reversible metabolic cause.1 ,2

Case presentation

A 71-year-old woman, presented with a history of osmotic symptoms since 10 days and the acute onset involuntary movements of right forearm, arm and fingers, of 2 days duration. The movements were jerky, irregular involving right forearm and arm with abnormal posturing of fingers. Initially the movements were of low amplitude and occurred every 2–3 h but progressed to occur four to five times every hour in last 4 h. They were not suppressed by activity and did not occur during sleep. The patient was conscious but bit confused. She had poorly controlled type 2 diabetes mellitus and hypertension since last 10 years. There was no history of trauma, fever or consumption of medications other than antidiabetics and antihypertensives. There was no past or family history of movement disorders.

On examination she was conscious and oriented. She was dehydrated, had a pulse 110/min and blood pressure 100/70 mm Hg. On neurological examination, the patient was conscious but bit confused (Glasgow Coma Scale 15/15, Mini-Memtal Status Examination 26/30). Asterexis were present. Abnormal involuntary movements suggestive of hemichorea and hemiballismus were present. Cranial nerve examination including the fundus was normal. There were no cerebellar signs. The sensorimotor examination in upper limbs was normal, but in lower limbs all modalities of sensations were diminished below the ankle joints. The deep tendon reflexes including the ankle were depressed and plantars were flexor. Other systemic examination was normal.

Investigations

Investigations on admission revealed a random blood glucose 650 mg/dL. Glycated haemoglobin was 13.5%. Her blood urea nitrogen and creatine were 30 and 2.2 mg/dL, respectively. Plasma osmolality was 336 mOsm/L, sodium 145 mEq/L, potassium 4.8 mEq/L. Arterial blood gas analysis showed pH was 7.41, partial pressure of oxygen=83.6 mm, partial pressure of carbon dioxide=36 and HCO₃=18 mEq/L. Haemoglobin was 12.1 gm/dL and total leucocyte count was 11 400/mm³ with polymorphonuclear predominance. Serum calcium was 9.2 mg%. The liver function and thyroid function tests were normal. Urine routine showed urine glucose was 4+ and ketones were negative with field full of pus cells. Specific gravity was 1.020.

MRI of the brain performed 3 days later, once the patient was stable, showed no abnormality.

Differential diagnosis

The major differential for hemichorea–hemiballismus include structural/vascular lesions such as stroke, neoplasms, granulomatous disorders, neurodegenerative disorders like amyotrophic lateral sclerosis and demyelinating disorders involving basal ganglia, as well as complication of HIV infection. These can be ruled out by neuroimaging, which should be performed irrespective of finding an underlying reversible metabolic cause such as hyperglycaemia, because metabolic cause might be unmasking-underlying structural problem.1

Treatment

The patient was started on intravenous fluids for rehydration followed by insulin infusion and antibiotics for urosepsis. Her blood sugar normalised over 6–8 h. Involuntary movements completely disappeared in 1 day. She had no involuntary movements during the rest of her hospital stay. Urine culture performed after 14 days of intravenous antibiotics was not showing any growth.

Outcome and follow-up

The patient was shifted on subcutaneous insulin (basal bolus regimen glargine and actrapid) and discharged.