Wind-Up of Spinal Neurons Contributes To Supramaximal Volitional Torque in Human Spinal Cord Injury

Spinal cord injury (SCI) is a debilitating disease process that results in profound sensorimotor impairments. Deficits in volitional motor control generation are particularly devastating as the severity of impairments in torque generating capability, particularly of the knee extensors, are a primary determinant of walking ability in individuals with motor incomplete SCI. In contrast to previous research indicating greater fatigue following SCI using electrically stimulated contractions, recently published data indicates individuals with motor incomplete SCI are able to generate supramaximal torque during repeated maximal volitional effort contractions, with little evidence of fatigue. Such findings could potentially augment volitional force and contribute to gait improvements, although the mechanisms are poorly understood. As multiple sites across the segmental motor system may contribute to fatigue and/or potentiation, the goal of this thesis is to understand the mechanisms that contribute to this supramaximal volitional torque generation in humans with incomplete SCI. To this end, three electrophysiological and/or pharmacological experiments were performed on a total of 20 individuals with incomplete SCI. Data from the first experiment suggest supramaximal volitional torque generation is associated with increases in spinal neuron excitability, rather than alterations within peripheral structures, including neuromuscular transmission or excitation-contraction coupling. The second experiment demonstrates how a history of volitional activation will modulate both supramaximal volitional torque generation and increase short latency tendon reflexes. The third experiment demonstrates how serotonergic medications produce widespread alterations in both reflexive and volitional activation of the motor system, though serotonin induced co-contraction may limit volitional force production. These findings are consistent with the windup of spinal neurons during repeated maximal effort contractions in humans with incomplete SCI, possibly through intrinsic neuronal properties and/or their modulation by descending monoaminergic pathways. This work provides new insight on how people with incomplete SCI produce volitional force. It is proposed that this will provide a basis for novel rehabilitative interventions to overcome the profound impairments in volitional force generation that occurs following human incomplete SCI.