Present address: Department of Physiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
1460-9568/asset/EJN_left.gif?v=1&s=3d5223e01f3255a775e3d3fc8d54bc1c38677c6c)
Neuronal mechanism of mirror movements caused by dysfunction of the motor cortex
Article first published online: 16 SEP 2010
DOI: 10.1111/j.1460-9568.2010.07395.x
© 2010 The Authors. European Journal of Neuroscience © 2010 Federation of European Neuroscience Societies and Blackwell Publishing Ltd
Additional Information
How to Cite
Tsuboi, F., Nishimura, Y., Yoshino-Saito, K. and Isa, T. (2010), Neuronal mechanism of mirror movements caused by dysfunction of the motor cortex. European Journal of Neuroscience, 32: 1397–1406. doi: 10.1111/j.1460-9568.2010.07395.x
- †
Present address: Department of Physiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Publication History
- Issue published online: 15 OCT 2010
- Article first published online: 16 SEP 2010
- Received 25 March 2010, revised 12 June 2010, accepted 6 July 2010
Keywords:
- macaque monkey;
- mirror movements;
- muscimol;
- primary motor cortex
Abstract
Mirror movements (MMs) are often observed in hemiplegic patients after stroke, and are supposed to reflect some aspects of their recovery process. Therefore, understanding the neuronal mechanism of MMs is important, but from the currently available evidence in human case studies, the mechanism of MMs has not been clearly understood. Here we found that in monkeys, after reversible inactivation of the right primary motor cortex (M1) by microinjection of muscimol, MMs were induced in the right hand during voluntary grasping with the left hand, which were partially affected by the injection. Using this animal model, we investigated the origin of MMs after dysfunction of the M1. We found the MMs thus induced were completely abolished by additional blockade of the left M1. Electromyogram (EMG) activities in some homonymous muscle pairs in bilateral hands were co-activated. Detailed analysis of EMG activities suggested that the enhanced activation of the left M1, which led to MMs in the right hand, was not directly driven by the activity of the right M1, whose activity was likely to be affected by the injection. Rather, the present finding has suggested that common drive of bilateral M1 from higher-order structures and reduction in commissural inhibition from the affected side concomitantly enhanced the activity of the cortico-motoneuronal pathway of the intact side, and led to the MMs.