Description:

Abstract:

The corticospinal tract is an important target for motor recovery after spinal cord injury (SCI) in humans. Using noninvasive electrophysiological techniques we have demonstrated the presence of reorganization in corticospinal projections targeting spinal motor neurons of muscles located close and at a distance from the injury site in individuals with chronic anatomically incomplete cervical SCI. Our physiological findings indicate that corticospinal transmission change in a task-dependent manner and to a different extent in individuals with and without spasticity. We have used transcranial magnetic stimulation over the primary motor cortex and peripheral nerves to reinforce spinal function using principles of spike-timing dependent plasticity and to mimic the periodicity of descending volleys in the corticospinal tract in humans with and without SCI. This data, along with information about the extent of the injury, provide a new framework for exploring the contribution of the corticospinal tract to recovery of function following SCI.

Speaker Info: 

Monica A. Perez received his PhD in Physical Therapy from the University of Miami and previously held faculty positions at the University of Miami and the University of Pittsburgh. She is currently the Scientific Chair of the Arms & Hands AbilityLab and Professor in the Department of PM & R, Feinberg School of medicine at Northwestern University. Her work is focused on understanding how the brain and spinal cord contribute to the control of movement in humans with and without spinal cord injury. This theme is mainly investigated from a neurophysiological point of view, using a combination of transcranial magnetic stimulation, magnetic resonance imaging, and peripheral nerve stimulation techniques. Current research projects focus on topics such as examining: (a) the contribution of the primary motor cortex, the corticospinal system, and subcortical pathways to the control of grasping, (3) the use of spike-time dependent like plasticity to enhance the activity of residual corticospinal projections after spinal cord injury, and (3) the contribution of descending motor pathways to spasticity and muscle spasms.