Force-feedback inhibition in chronic stroke

The presence of force-feedback inhibition was explored during reflex responses in thirteen stroke subjects. Using constant velocity stretches, it was previously found that after movement onset, active reflex force progressively increased with increasing joint angle. However after the reflex force magnitude exceeded a particular level, it began rolling off until maintaining a steady-state value. We hypothesized that the force plateau could be explained by a force-feedback inhibitory pathway. To help facilitate an understanding of this force roll off, a simple model representing the elbow reflex pathway was developed. This model contained two separate feedback pathways, one representing the monosynaptic stretch reflex originating from muscle spindle excitation, and another representing force-feedback inhibition arising from force sensitive receptors. It was found that force-feedback inhibition altered the otherwise linear stretch reflex response, resulting in a force response that followed a sigmoidal shape similar to that observed experimentally. Furthermore, simulated reflex responses were highly dependent on force-feedback gain, where predicted reflex force began plateauing at decreasing levels with increases in this force-feedback gain. The experimental results coupled with simulations of elbow reflex responses suggest the possibility that after brain injury, the effectiveness of force-feedback inhibition may increase to a level which has functional significance.