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Brain oscillations in its physiology and pathophysiology

開催日 2014/9/11
時間 9:00 - 11:00
会場 Room C(502)
Chairperson(s) 池田 昭夫 / Akio Ikeda (京都大学大学院医学研究科 てんかん・運動異常生理学講座 / Department of Epilepsy, Movement Disorders and Physiology, Kyoto University Graduate School of Medicine, Japan)
美馬 達哉 / Tatsuya Mima (京都大学大学院医学研究科附属脳機能総合研究センター / Human Brain Research Center, Kyoto University Graduate School of Medicine, Japan)

Non-invasive oscillatory brain stimulation coupling with rhythmical movements and induction of brain plastic change

  • S1-C-1-4
  • 小金丸 聡子 / Satoko Koganemaru:1 
  • 1:京都大院・医 / Dept Med, Kyoto Univ, Japan 

Recently, oscillatory non-invasive brain stimulation such as transcranial alternative current stimulation (tACS) and transcranial slow oscillatory stimulation (tSOS), has been reported to change brain activity, to enhance our cognitive function and to treat abnormal rhythmical movements such as tremor. Oscillatory non-invasive brain stimulation is likely to work more effectively by coupling with oscillatory brain activity.
Locomotion is one of the most familiar and essential activities in our daily life. As well as animals' quadripedal locomotion, principal patterned activities in peripheral nerves and lower-limb muscles exist during human bipedal locomotion. However, it is still unknown whether supraspinal oscillatory activities at the gait-cycle controls bipedal locomotion although descending supraspinal signals are critical for overall output of human locomotion. Studies using transcranial magnetic stimulation have shown different corticospinal activities between leg flexors and extensors in a phase-dependent manner during human bipedal locomotion.
We hypothesized that if oscillatory activities at the gait-cycle exist at a supraspinal level, non-invasive oscillatory brain stimulation simulating gait cycle would induce gait-specific changes by combining actual locomotion and real but not sham stimulation. Nine healthy subjects participated in the study. They were given SOS over the right M1 foot area during locomotion (SOS+gait) and on another day, given sham stimulation during locomotion (Sham+gait). As a result, they showed a significant enhancement of corticospinal excitability in the left tibialis anterior muscles (leg flexors) immediately and 30 min after SOS+gait, but neither in the left gastrocnemius muscles (leg extensors), nor after Sham+gait. In addition, they showed a significant prolongation of the cortical silent period in the left and right gastrocnemius muscles after SOS+gait, but nor after Sham+gait. We considered that SOS simulating gait cycle induced gait-specific plasticity by enhancing gait cycle-dependent oscillatory activities at a supraspinal level during locomotion. It might be a promising method for a treatment of gait disturbance by supraspinal neuronal damages such as stroke.

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