School of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, United States
Guglielmo Foffani
CINAC, Hospital Universitario HM Puerta del Sur, Universidad CEU-San Pablo, Madrid, Spain; Hospital Nacional de Parapléjicos, Servicio de Salud de Castilla-La Mancha, Toledo, Spain
Patrick D Ganzer
School of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, United States
John R Bethea
Department of Biology, Drexel University, Philadelphia, United States
School of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, United States; Department of Biomedical Engineering, University of California, Davis, United States
After paralyzing spinal cord injury the adult nervous system has little ability to ‘heal’ spinal connections, and it is assumed to be unable to develop extra-spinal recovery strategies to bypass the lesion. We challenge this assumption, showing that completely spinalized adult rats can recover unassisted hindlimb weight support and locomotion without explicit spinal transmission of motor commands through the lesion. This is achieved with combinations of pharmacological and physical therapies that maximize cortical reorganization, inducing an expansion of trunk motor cortex and forepaw sensory cortex into the deafferented hindlimb cortex, associated with sprouting of corticospinal axons. Lesioning the reorganized cortex reverses the recovery. Adult rats can thus develop a novel cortical sensorimotor circuit that bypasses the lesion, probably through biomechanical coupling, to partly recover unassisted hindlimb locomotion after complete spinal cord injury.
