This 37-year-old man had insulin-dependent diabetes mellitus since age 5 with end-stage renal disease requiring kidney and pancreas transplant by the age of 30 years. He was admitted to the hospital for diabetic ketoacidosis. His calculated serum osmolarity fluctuated from 304 to 287 over a 6-hour period. Serum glucose reached 528 mg/dL (normal, 70 to 105 mg/dL). His mental status normalized in 2 days after insulin and intravenous
hydration. Three weeks later, he noted a “fidgety” right arm and right leg, rapidly growing in intensity.

Our patient had right hemichorea with a ballistic component associated with increased T1-weighted signal in the contralateral putamen and a T2-weighted central pontine hyperintensity sparing of the corticospinal fibers (Fig. 62.1). He was diagnosed with hemichorea-hemiballism (HC/HB) due to diabetic ketoacidosis, which was also complicated with osmotic demyelination expressed as a central pontine myelinolysis. He responded to haloperidol, which was discontinued after 1 month without hemichorea relapse. At the 3-month reevaluation, despite symptomatic resolution, serial brain magnetic resonance imaging (MRI) studies continued to demonstrate similar imaging abnormalities.