Cranial Magnetic Resonance Imaging and Angiography Findings in a Patient With Hyperglycemic Hemichorea-Hemiballism

Although there are reports of hyperintense lesions in hyperglycemic hemichorea-hemiballism by brain magnetic resonance imaging (MRI) (1, 2), such findings by magnetic resonance angiography (MRA) are rare. An 82-year-old man presented with a 1-month history of left-sided involuntary movements of his face and limbs. Laboratory data revealed a blood glucose level of 20.8 mmol/L, glycosylated hemoglobin of 11.5%, and serum C-peptide of 2.20 ng/mL. There were no urinary ketones or metabolic acidosis. T1-weighed brain MRI showed a hyperintense lesion in the putamen and caudate nucleus, whereas cranial MRA showed an irregular perivascular hyperintense lesion and an arteriostenosis in the middle cerebral artery (MCA) (Figure 1A, arrows). After a diagnosis of hyperglycemic hemichorea-hemiballism, he was treated with insulin. Upon correction of blood glucose levels, the ballistic movements improved. At the 1-month follow-up visit, the abnormal hyperintense areas had improved slightly (Figure 1B), and they had disappeared completely at the 6-month follow-up visit (Figure 1C). His glycosylated hemoglobin improved to 7.6%. Hyperglycemic hemichorea-hemiballism is more common among patients with type 2 diabetes, Asians, and the elderly. Possible underlying mechanisms include microhemorrhages due to blood-brain-barrier failure (3), reactive astrocytes associated with ischemia (4), and decreased -aminobutyric acid production after dehydration (5), and they present as a high-intensity signal on T1-weighed MRI. We observed high perivascular signal intensity on MRA, along with stenosis of the MCA at the bifurcation of the lenticulostriate arteries, which supply the putamen and caudate nucleus. This suggests that these lesions have vascular fragility and they are vulnerable to ischemia and metabolic disorders associated with hyperglycemia.