Neural Mechanisms Underlying the Control of Dynamic Muscle Contractions in Human Spinal Cord Injury

Spinal cord injury (SCI) severely diminishes an individual’s ability to generate the requisite muscle force for purposeful, voluntary movements. Motor deficits associated with SCI are frequently accompanied by sensory impairments, further contributing to altered patterns of voluntary muscle activation. Significantly, strength and voluntary activation post-SCI have been studied primarily during isometric contractions, where muscle length and joint angle are kept constant. Although isometric measurements are important, nearly all movements require combinations of lengthening (eccentric) and shortening (concentric) contractions. Hence, the focus of this dissertation was to address the gap in knowledge regarding the neural control of dynamic contractions in individuals with incomplete SCI. Three studies were conducted on 14 individuals with chronic motor incomplete SCI. The first study examined central motor drive of the knee extensors during single and repeated lengthening, isometric, and shortening maximal voluntary contractions. Data collected during isolated maximal contractions suggest individuals with incomplete SCI demonstrate a markedly distinct pattern of muscle activation compared to healthy, uninjured control subjects. That is, despite overall deficits in voluntary muscle activation, SCI subjects generated markedly increased central motor drive during lengthening compared to isometric or shortening maximal contractions. In contrast, controls demonstrated a depression of motor drive during lengthening contractions relative to the other contraction types. Additional results also suggest separate control mechanisms in SCI subjects for repeated maximal efforts during lengthening versus isometric or shortening contractions. The second study examined spinal mechanisms which may contribute to unique activation patterns following SCI. This study provided evidence that the facilitation of motoneuron activity during lengthening contractions demonstrated by SCI subjects is partly due to increased excitability of the monosynaptic stretch reflex within agonist muscles. The third study examined supraspinal contributions to the control of dynamic contractions. In this study, specific changes in intracortical inhibitory circuits involved in the control of dynamic contractions were observed in SCI subjects. Combined, these studies suggest voluntary muscle activation is facilitated during lengthening contractions by increased stretch reflex inputs, and that supraspinal modulation of descending commands is also altered following chronic SCI. Findings from this dissertation may provide the physiological basis for targeted rehabilitation interventions.