An 83-year-old Japanese man was admitted for an acute onset of right hemichorea. At admission, initial blood glucose was 252 mg/dL and glycosylated hemoglobin A1c was 14.2% (National Glycohemoglobin Standardization Program: NGSP). The left lenticular nucleus and a lateral part of the globus pallidus showed high signals on T1-weighted magnetic resonance images (Fig. 1a). [123-Iodine]-fluoropropyl (FP)- 2 beta-carbomethoxy-3 beta-(4-iodophenylnortropane) (CIT) dopamine transporter single-photon emission computed tomography (SPECT) showed a reduced striatal uptake on the left side (Fig. 1b), with hyperperfusion on 99m Technetium (Tc) -ethylcysteinate dimer (ECD) SPECT (Fig. 1c). The pathogenesis of diabetic hemichorea remains unknown. Many different causes have been suggested, including petechial hemorrhage, temporary ischemia [123-Iodine]-fluoropropyl (FP)- 2 beta-carbomethoxy-3 beta-(4-iodophenylnortropane) (CIT), hyperglycemia-induced blood–brain barrier dysfunction, and the decreased synthesis of gamma-aminobutyric acid and acetylcholine secondary to metabolic changes. An imaging study showed a reduced rate of cerebral glucose metabolism on positron-emission tomography and hyperperfusion on SPECT, suggesting the subsequent regional metabolic failure.1 Our dopamine transporter SPECT findings provide new evidence of functional disturbance in presynaptic dopaminergic neurons secondary to failure in postsynaptic D2 receptors of the striatum, or dopamine reuptake inhibition of presynaptic dopaminergic terminals by the damage of striatum and/or globus pallidus. The authors declare no conflict of interest.