Abstract
Hemichorea-Hemiballism (HCHB) is a hyperkinetic condition characterized by abnormal, migratory, continuous, non-patterned movements of one side of the body. It results from involvement of contralateral basal ganglia that may be affected by metabolic, neoplastic, infectious, autoimmune [1], toxic or neurodegenerative processes [2]. The most common cause is ischemia from a focal vascular lesion [3]. Non-ketotic hyperglycemia has been reported as the second most common cause of HCHB in the Asian population [4]. It is usually seen in the elderly and has a female preponderance. The average reported age is 73 years. HCHB has been reported in patients with chronic diabetes and also in those with new onset hyperglycemia [5-7]. We describe a patient with HCHB in the setting of poorly controlled chronic diabetes, who also demonstrated basal ganglia atrophy on follow-up imaging. Basal ganglia atrophy in HCHB secondary to hyperglycemia is rarely reported.
Highlights
He had already failed a trial of muscle relaxants and benzodiazepines
The right lentiform nucleus appeared smaller than the left
Contrast enhanced brain MRI revealed T1 shortening within the head of the right caudate nucleus and putamen, which was more pronounced along the lateral aspect
Summary
A 58 year old diabetic male was admitted to the neurology service with a 6 weeks history of abnormal left sided involuntary movements. At onset, he experienced mild involuntary movements of the left arm that improved slightly, but worsened within the 2 weeks. The movements were constant, disabling and persistent even during sleep On examination he had chorea, ballismus and intermittent dystonic posturing of the left arm and leg. Unenhanced CT head revealed increased density in the head of right caudate nucleus and subtle increased density in the lateral aspect of the right putamen. Contrast enhanced brain MRI revealed T1 shortening (hyperintensity) within the head of the right caudate nucleus and putamen, which was more pronounced along the lateral aspect. His hemoglobin A1C was 12.7 % and plasma osmolality was 301mOsm/kg
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