第 6 回 Motor Control 研究会
特別講演†
- 日時： 6 月 21 日（木） 17:10 〜 18:40
- 司会： 本田 学
柴崎 浩 京都大学名誉教授
Cortical activities associated with voluntary and involuntary movements
Recent advance in non-invasive physiological techniques has enabled investigation of control mechanism of voluntary movements and pathophysiology of involuntary movements in human. Epicortical recording with subdural electrodes in epilepsy patients complemented the findings obtained by the non-invasive techniques. Before self-initiated simple movement, activation occurs first in the pre-supplementary motor area (pre-SMA) and SMA proper bilaterally with some somatotopic organization, and the lateral premotor cortex and the primary motor cortex (M1) mainly contralaterally with precise somatotopic organization. Praxis movements used for daily activities are initiated by activation of the parietal cortex of the dominant hemisphere. Activation pattern in the self-initiated motor inhibition is identical to that of the self-initiated muscle contraction at least at the cortical level.
Generating mechanisms of involuntary movements have been studied by jerk-locked back averaging and cortico-muscular coherence, and the application of transcranial magnetic stimulation (TMS) has provided information on the state of excitability and inhibition of the sensorimotor cortex (SMC). SMC was shown to play an important role in generation of cortical myoclonus, essential tremor, Parkinson tremor, and focal dystonia. Cortical myoclonus is actively driven by SMC while essential tremor and Parkinson tremor are mediated by SMC which might serve as a relay center of the incoming oscillations arising from subcortical structures. Negative myoclonus is also caused by active process of the SMC and can be stimulus-sensitive. Unilateral asterixis seen in patients with lateral thalamic lesion was also shown to be mediated by SMC.
References
- Shibasaki H. Cortical activities associated with voluntary movements and involuntary movements. Clin Neurophysiol 2012;123:229-43.
- Inoue M, Kojima Y, Mima T, et al. Pathophysiology of unilateral asterixis due to thalamic lesion. Clin Neurophysiol (in press).
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