A 61-year-old African American male with history of uncontrolled Type 2 diabetes mellitus, hypertension, anxiety, major depressive disorder, prior Bell’s palsy, and neuropathy, presented for worsening left upper extremity rhythmic movements and frequent falls over the last month. The movements worsened throughout the day, and he would hold his left arm at night to prevent hitting his partner.

On presentation, he was mildly hypertensive but otherwise normal vital signs. On physical exam, he was initially holding his left arm down, and when released, showed rhythmic, jerking movements. He also had diminished sensation to the left upper and lower extremities.

Diagnosis and Management

Patient’s history and physical were initially concerning for a neurological abnormality with unknown cause. The differential included ischemic stroke, focal seizure disorder, lesion of the cervical spine, sequalae of prior Bell’s palsy, hemorrhage, or psychological disorder. He was resting comfortably, holding his arm down, in no acute distress and hemodynamically stable. Because of the unclear etiology, a CT head was ordered alongside CBC and CMP. A capillary blood glucose was drawn which revealed his hyperglycemia. With concerns for diabetic ketoacidosis (DKA) or HHS, we broadened our workup to include urinalysis, osmolality, and venous blood gas. These showed a normal anion gap without acidosis and trace ketonuria, excluding DKA from the differential. Initial labs were significant for glucose 582, trace ketonuria, osmolality 303, pH 7.37, sodium 134, potassium 4.3, chloride 94, serum bicarbonate 29, Hgb A1c 14.1 percent. He did have a mildly elevated osmolality although not meeting diagnostic criteria for HHS.² He was given 2 liters lactated ringers, 50meq potassium chloride, and 10U IV regular insulin for treatment of hyperglycemia. CT of the brain was unremarkable, suggesting against any acute pathologies such as ischemic stroke, large hemorrhage, or tumor burden.

Neurology was consulted who recommended magnetic resonance imaging (MRI) of the brain and an electroencephalogram (EEG). The patient was admitted for aggressive glucose control in the setting of nonketotic hyperglycemic hemiballismus (NKHH). Brain MRI showed a small right-sided subdural hemorrhage and a nonspecific FLAIR hyperintense signal in the periventricular and supraventricular white matter and dorsal pons without evidence of acute ischemia. EEG was negative. Symptoms improved within 24 hours of starting an insulin regimen and resolved by discharge on day four. His diagnosis of NKHH was made from laboratory evaluation, physical exam, and improvement of symptoms with glucose control.

The patient was admitted to the medicine floor with neurology consultation. He was admitted for four days and discharged home after glucose was controlled and symptoms resolved. Uncontrolled hyperglycemia can have variable presentations, ranging from polyuria to neurological complications. Hemiballismus, a unilateral movement disorder, is a rare neurological process that is usually related to acute strokes but can also be a stroke mimicker.