Introduction: Hyperglycemic hemichorea-hemiballism (HC-HB) in uncontrolled diabetes mellitus is an uncommon manifestation of hyperglycemia and typically shows high signal intensity lesions in the putamen and sometimes in the caudate head on T1-weighted MRI. However, the pathophysiology of hyperglycemic HC-HB is not well understood.
Objective: To investigate motor cortex (MC) excitability in patients with hyperglycemic HC-HB.
Patients and Methods: We studied 15 patients with mean age 71.5 years (range 48 to 94 years) and 12 age-matched healthy subjects. TMS studies included motor evoked potential, recruitment curve, GABAA mediated short interval intracortical inhibition (SICI), intracortical facilitation (ICF) and GABAB mediated silent period (SP) duration and long interval intracortical inhibition (LICI). The conditioning and test pulses were applied to the same MC at the ISI of 2 ms for SICI, 10 ms for ICF, and 50, 100, 150 and 200 ms for LICI in both rest and active conditions.
Results: There was no significant difference in motor threshold, recruitment curve response, SICI, ICF in both rest and active conditions between patients with hyperglycemic HC-HB and normal subjects. However, LICI was significantly increased during muscle activation (p = 0.0005) but not at rest in patients with hyperglycemic HC-HB. The SP duration is also increased in patients with hyperglycemic HC-HB (p = 0.0005).
Conclusion: LICI and SP are increased in the MC contralateral to the hemichorea in hyperglycemic HC-HB, but only during muscle activation. This suggests that HC-HB is associated with increased GABAB receptor mediated inhibitory activity in the MC.
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