UC Davis

Spinal cord injury (SCI) is a debilitating condition often resulting in motor deficits and loss of tactile sensation below the injury. The brain needs to relearn strategies to regain motor control after SCI. This ability of the brain to adapt after injury/rehabilitation is defined as neuroplasticity. Neuroplasticity in the motor cortex (M1) required to gain cortical control of trunk muscles below the injury level is not well understood after a clinically relevant incomplete mid-thoracic spinal contusion injury. After an incomplete SCI, there is a substantial spontaneous recovery of function that can be further facilitated by physical rehabilitation. The difference in cortical neuroplasticity associated with rehabilitation-assisted recovery and spontaneous recovery of function is unknown.

This thesis aimed to understand whether neuroplasticity in trunk M1 after rehabilitation is a mere enhancement of the learning strategy adopted by the cortex during spontaneous recovery or whether they represent a different strategy to regain control of muscle groups below the level of the lesion.

Regions within trunk M1 that control lower thoracic trunk muscle (LTM1) were specialized in the neuronal encoding of posture in intact animals. After an incomplete mid-thoracic spinal contusion injury, the network and cellular neuroplasticity in trunk M1 differed between animals that received physical rehabilitation and animals that spontaneously recovered. In animals that received the therapy, the lower thoracic trunk motor cortex (LTM1) maintained some control of trunk muscles below the injury, in addition to recruiting trunk muscles at/above the level of injury. Exercise therapy also prevented the degradation of neuronal responsiveness in the reorganized cortex to unexpected postural perturbation as well as during treadmill locomotion. This knowledge can help design activity-based therapy paradigms that improve cortical plasticity in the LTM1, relevant for postural control.