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J Neurophysiol (April 30, 2008). doi:10.1152/jn.00020.2008
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Submitted on January 8, 2008
Accepted on April 16, 2008

Shaping appropriate locomotive motor output through interlimb neural pathway within spinal cord in humans

Noritaka Kawashima1*, Daichi Nozaki2, Masaki O Abe3, and Kimitaka Nakazawa4

1 Dept. of Rehabilitation for Movement Functions, Research Institute, National Rehabilitation Center for the Disabled, Tokorozawa City, Japan; Rehabilitation Engineering Lab, Toronto Rehabilitation Institute, 520 Sutherland Drive, Toronto, M4G 3V9, Canada
2 Department of Physical and Health Education, University of Tokyo, Tokyo, Japan
3 Department of Kinesiology, The Pennsylvania State University, United States
4 Research Institute, National Rehabilitation Center for the Disabled, Tokorozawa, Japan

* To whom correspondence should be addressed. E-mail: nori.kawashima{at}utoronto.ca.

Direct evidence supporting the contribution of upper limb motion on the generation of locomotive motor output in humans is still limited. Here, we aimed to examine the effect of upper limb motion on locomotor-like muscle activities in the lower limb in persons with spinal cord injury (SCI). By imposing passive locomotion-like leg movements, all cervical incomplete (n=7) and thoracic complete SCI subjects (n=5) exhibited locomotor-like muscle activity in their paralyzed soleus muscles. Upper limb movements in thoracic complete SCI subjects did not affect the electromyographic (EMG) pattern of the muscle activities. This is quite natural since neural connections in the spinal cord between regions controlling upper and lower limbs were completely lost in these subjects. On the other hand, in cervical incomplete SCI subjects, in whom such neural connections were at least partially preserved, the locomotor-like muscle activity was significantly affected by passively imposed upper limb movements. Specifically, the upper limb movements generally increased the soleus EMG activity during the backward swing phase. Although some subjects showed a reduction of the EMG magnitude when arm motion was imposed, this was still consistent with locomotor-like motor output because the reduction of the EMG occurred during the forward swing phase corresponding to the swing phase. The present results indicate that the neural signal induced by the upper limb movements contributes not merely to enhance, but to shape the lower limb locomotive motor output. Such neural interaction between upper and lower limb motion could be an underlying neural mechanism of human bipedal locomotion.







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