Division of Neurology, Kaohsiung Veterans General Hospital, Taiwan, R.O.C.; Faculty of Medicine, School of Medicine, National Yang-Ming University, Taiwan, R.O.C.; Department of Nursing, Yuh-Ing Junior College of Health Care & Management, Taiwan, R.O.C.
Mov Disord. 2015 Feb;30(2):198-205. doi: 10.1002/mds.25940. Epub 2014 Jun 11.
Hemichorea-hemiballism (HC-HB) in uncontrolled diabetes mellitus is an uncommon manifestation of hyperglycemia. The pathophysiology of hyperglycemic HC-HB is not well understood. A previous report showed increased intracortical inhibition in the motor cortex in a patient with diabetes with HC-HB. The objective of this study is to investigate motor cortex excitability in patients with hyperglycemic HC-HB. We hypothesized that intracortical inhibition measured with transcranial magnetic stimulation, which likely reflects the excitability of cortical γ-aminobutyric acid (GABA)ergic circuits, would be impaired in patients with hyperglycemic HC-HB. We studied 15 patients with mean age 71.5 years (range, 48-94 y) and 12 age-matched healthy subjects. The motor cortex contralateral to the hemichorea was tested. Transcranial magnetic stimulation measures included motor evoked potential, recruitment curve, GABAA mediated short interval intracortical inhibition, intracortical facilitation, and GABAB mediated silent period duration and long interval intracortical inhibition. No significant difference was found in motor threshold, recruitment curve response, short interval intracortical inhibition, or intracortical facilitation in both rest and active conditions between patients with hyperglycemic HC-HB and normal subjects. However, long interval intracortical inhibition was significantly increased during muscle activation but not at rest in patients with hyperglycemic HC-HB. The silent period duration is also increased in patients with hyperglycemic HC-HB. We concluded that long interval intracortical inhibition and silent period are increased in the motor cortex contralateral to the hemichorea in hyperglycemic HC-HB, but only during muscle activation. Hemichorea-hemiballism may be associated with increased GABAB receptor-mediated inhibitory activity in the motor cortex.
未控制的糖尿病患者出现的偏侧舞蹈-投掷症（HC-HB）是一种少见的高血糖表现。高血糖性 HC-HB 的病理生理学尚不清楚。先前的一份报告显示，糖尿病伴 HC-HB 的患者运动皮层的皮质内抑制增加。本研究的目的是研究高血糖性 HC-HB 患者运动皮层的兴奋性。我们假设，经颅磁刺激测量的皮质内抑制（可能反映皮质γ-氨基丁酸（GABA）能回路的兴奋性）在高血糖性 HC-HB 患者中会受损。我们研究了 15 名平均年龄 71.5 岁（范围，48-94 岁）的患者和 12 名年龄匹配的健康受试者。对舞蹈对侧的运动皮层进行了测试。经颅磁刺激测量包括运动诱发电位、募集曲线、GABAA 介导的短间隔皮质内抑制、皮质内易化和 GABAB 介导的静默期持续时间和长间隔皮质内抑制。高血糖性 HC-HB 患者与正常受试者在静息和活动状态下的运动阈值、募集曲线反应、短间隔皮质内抑制或皮质内易化均无显著差异。然而，高血糖性 HC-HB 患者在肌肉激活时但不在静息时，长间隔皮质内抑制明显增加。静默期持续时间在高血糖性 HC-HB 患者中也增加。我们得出结论，高血糖性 HC-HB 患者舞蹈对侧运动皮层的长间隔皮质内抑制和静默期增加，但仅在肌肉激活时增加。偏侧舞蹈-投掷症可能与运动皮层中 GABA B 受体介导的抑制活性增加有关。
