MON-652 - Transient Hemiballismus Triggered by Nonketotic Hyperglycemia Following A High-Sugar Meal in an Elderly Female: A Case Report

Background:
Hemiballismus is a rare hyperkinetic movement disorder characterized by involuntary, large-amplitude flinging movements, classically due to lesions of the contralateral subthalamic nucleus. While vascular etiologies are most common, nonketotic hyperglycemia (NKH) is an underrecognized but reversible metabolic cause, particularly in older adults with poorly controlled diabetes. Of note, hemiballismus associated with nonketotic hyperglycemia may present with a delayed onset, occurring days after the initial hyperglycemic insult, even as serum glucose levels begin to normalize.

Case Presentation:
A 73-y/o woman with poorly controlled T2DM (Hgb A1c 15.2%, from 5.9% over three months) presented with sudden-onset, continuous, involuntary flailing movements of the left upper and lower extremities. Movements were non-rhythmic, non-patterned, large in amplitude, and resolved during sleep—features consistent with hemiballismus. Symptoms began shortly after ingestion of a large high-sugar meal and worsened over 24 hours. Notably, she had been discharged one day prior following a hospitalization for hyperosmolar hyperglycemic state with blood glucose >600. Review of outpatient records revealed recent insulin nonadherence and dietary indiscretion.
On presentation, she denied personal history of movement disorders, focal weakness, sensory changes, trauma, medication changes, toxin exposure, history of autoimmune disease. Neuroimaging (CT, CTA, and MRI of the brain) revealed no acute ischemia, hemorrhage, or basal ganglia abnormalities, with only stable postoperative changes from remote intracranial surgery that occurred over 40 years ago. Laboratory evaluation was notable for Na 135, K 4, HCO3 18, AG 17, Glu 323, Osm 296, AG 17, no ketones.
The patient was treated conservatively with subcutaneous insulin and glycemic control, resulting in marked improvement and subsequent resolution of her hyperkinetic movements.

Discussion:
NKH-associated hemiballismus, also referred to as diabetic striatopathy, is thought to result from metabolic and excitotoxic injury to the basal ganglia. While characteristic T1 hyperintensity of the contralateral striatum may be seen on MRI, imaging can be normal, and absence of radiographic findings does not exclude the diagnosis. The clear temporal association with hyperglycemia, rapid clinical improvement with glucose control, and lack of structural lesions argue against vascular or epileptic etiologies.

Conclusion:
This case highlights NKH as an important, reversible cause of hemiballismus. In patients presenting with acute involuntary movements and severe hyperglycemia, clinicians should prioritize metabolic etiologies, as prompt glycemic control can lead to rapid symptom resolution and prevent unnecessary interventions such as thrombolysis, anticoagulation, or antiepileptic therapy.

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