Reflex stiffness gain and dynamics in spinal cord injury: Abnormalities and underlying mechanisms

A parallel-cascade system identification method was used to characterize ankle dynamic stiffness in healthy and spastic spinal cord injured (SCI) subjects. Modulation of reflex stiffness gain and dynamics was studied by applying perturbations to the ankle at different ankle positions or different voluntary contraction levels of ankle extensors. Our results showed that reflex gain was significantly larger in SCI than healthy subjects and abnormally modulated with position and voluntary contraction. Furthermore, the reflex latency was shorter in SCI than healthy subjects. These abnormalities are likely due not only to a decrease in presynaptic inhibitory mechanisms but also to inappropriate recruitment of larger motoneurons or perhaps a disruption in the size-principle. Our results also revealed that the reflex dynamics represented by the frequency parameter was lower in SCIs and decreased with contraction level while it increased in healthy subjects. This was because of repeated activation of the motoneuron pools represented by extra peaks in the reflex activation dynamics, which are due to hyper-excitability of reflexes. These findings help better understanding of the origins of SCI-induced spasticity and its underlying mechanisms.