Original Research ARTICLE
Restoration of upper limb movement via artificial corticospinal and musculospinal connections in a monkey with spinal cord injury
- 1Department of Physiology & Biophysics, University of Washington, Seattle, WA, USA
- 2Washington National Primate Research Center, University of Washington, Seattle, WA, USA
- 3Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency, Tokyo, Japan
Functional loss of limb control in individuals with spinal cord injury or stroke can be caused by interruption of corticospinal pathways, although the neural circuits located above and below the lesion remain functional. An artificial neural connection that bridges the lost pathway and connects cortical to spinal circuits has potential to ameliorate the functional loss. We investigated the effects of introducing novel artificial neural connections in a paretic monkey that had a unilateral spinal cord lesion at the C2 level. The first application bridged the impaired spinal lesion. This allowed the monkey to drive the spinal stimulation through volitionally controlled power of high-gamma activity in either the premotor or motor cortex, and thereby to acquire a force-matching target. The second application created an artificial recurrent connection from a paretic agonist muscle to a spinal site, allowing muscle-controlled spinal stimulation to boost on-going activity in the muscle. These results suggest that artificial neural connections can compensate for interrupted descending pathways and promote volitional control of upper limb movement after damage of descending pathways such as spinal cord injury or stroke.
Keywords: brain–computer interface, artificial neural connection, hand, spinal cord injury, local field potential, muscle, spinal cord, monkey
Citation: Nishimura Y, Perlmutter SI, and Fetz EE (2013) Restoration of upper limb movement via artificial corticospinal and musculospinal connections in a monkey with spinal cord injury. Front. Neural Circuits 7:57. doi: 10.3389/fncir.2013.00057
Received: 01 November 2012; Paper pending published: 15 January 2013;
Accepted: 13 March 2013; Published online: 11 April 2013.
Edited by:Steve M. Potter, Georgia Institute of Technology, USA
Reviewed by:Liang Guo, Massachusetts Institute of Technology, USA
Abhishek Prasad, University of Miami, USA
Copyright: © 2013 Nishimura, Perlmutter, and Fetz. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
*Correspondence: Yukio Nishimura, Department of Developmental Physiology, National Institute for Physiological Sciences, National Institutes of Natural Sciences, 38 Nishigonaka, Myoudaiji, Okazki, Aichi 444-858, Japan. e-mail: email@example.com Eberhard E. Fetz, Department of Physiology & Biophysics, University of Washington, 1705 NE Pacific Street, HSB G424, Box 357290, Seattle, WA 98195, USA. e-mail: firstname.lastname@example.org
†Present address:Yukio Nishimura, Department of Developmental Physiology, National Institute for Physiological Sciences, National Institutes of Natural Sciences, Okazki, Japan.