Interaction of autonomic and motor reflexes in chronic human spinal cord injury
Abstract
The objective of this dissertation was to improve the understanding of the neural mechanisms that relate spastic motor reflexes and autonomic dysfunction in human spinal cord injury (SCI). This spinally mediated interaction is demonstrated in high-level SCI by the occurrence of increased spasticity during episodes of autonomic dysreflexia (AD). However, the neural mechanisms remain undetermined. This dissertation utilized indirect methods to examine the excitability of interneuronal and motoneuron pathways following SCI and the associated neuromodulation of these pathways during induced sympathetic activity. The first aim was to determine the sympathetic reflex responses to noxious electrocutaneous stimuli and bladder percussion in high and low-level SCI. Measurement of blood pressure and calf blood flow showed similar responses for both conditions. A novel finding was that both high and low-level SCI demonstrated similar lower extremity vasoconstriction. Additionally, high-level SCI showed evidence of a more widespread response, indicated by increased blood pressure. After the sympathetic response was characterized, we addressed the second and third aims, which was to describe the modulation of spastic motor reflexes during induced sympathetic reflexes. Briefly, joint torques and electromyograms were measured during separate experiments where flexor and hip triggered spastic reflexes were induced before, during and after the introduction of a conditioning stimulus. The data showed a decrease in the noxious stimulation induced flexor reflex amplitude and windup for both types of conditioning. This decrease was attributed to inhibition of the primary pain afferents, possibly through endogenous opioid or monoaminergic neuromodulation. Hip triggered extensor spasms incorporate a different afferent pathway and the data showed that they responded to conditioning by facilitation of the semitendinosis stretch reflex while multijoint reflexes remained essentially unchanged. This was interpreted as a general increase in motoneuron excitability as demonstrated by plateau potential like behaviors of the response. It is hoped that the findings of this dissertation will contribute to an improved understanding of spinal reflex function and lead to new methods for spasticity management and the treatment of autonomic dysfunction in SCI.
This paper has been withdrawn.