Reciprocal inhibition becomes facilitation after spinal cord injury: clinical application of a system identification...

Alteration in spinal inputs from descending pathways following spinal cord injury (SCI) affects different mechanisms including reciprocal Ia inhibition. However, whether there is a consistent pattern of change in reciprocal inhibition following SCI is uncertain. Typical attempts to evaluate reciprocal inhibition have been restricted to electrophysiological measurements, which may have limited translation to function. Our objective was to address the uncertainty regarding changes in reciprocal inhibition after SCI by quantitatively evaluating reciprocal inhibition of ankle extensors from ankle flexors using our novel, more functionally relevant system identification approach. To evaluate reciprocal inhibition using the system identification technique, a series of small-amplitude PseudoRandom Binary Sequence (PRBS) perturbations were applied to the ankle when subjects contracted their dorsiflexors. Depression of reflex stiffness with tibialis anterior (TA) activation was evaluated as reciprocal inhibition. Our results showed that reflex stiffness decreased continuously as dorsiflexor torque increased in the healthy control subjects whereas it remained almost unchanged in the SCI subjects, indicating the absence of reciprocal inhibition in patients. This pattern was consistent with the results obtained from electrophysiological measures in a exploratory control experiment revealing depression of the control H-reflex but no change to the SCI H-reflex. These findings suggest that our system identification mechanical technique is a reliable and valid approach for evaluating reciprocal inhibition. Furthermore, our results demonstrate that reciprocal inhibition can diminish or change to reciprocal facilitation after SCI, which in turn can result in reflex hyperexcitability and unwanted activity of ankle extensors triggered by TA activity. This suggests that reciprocal facilitation may play a major role in pathophysiology of spasticity and impaired function.