Evidence for force-feedback inhibition in chronic stroke.
The presence of force-feedback inhibition was explored during reflex responses in five subjects with known incidence of stroke. Using constant velocity stretches, it was previously found that after movement onset, active reflex force progressively increases with increasing joint angle, at a rate proportional to a fractional exponent of the speed of stretch. However, after the reflex force magnitude exceeds a particular level, it begins rolling off until maintaining a steady-state value. The magnitudes of these force plateaus are correlated with the speed of stretch, such that higher movement speeds result in higher steady-state forces. Based upon these previous studies, we hypothesized that force plateau behavior could be explained by a force-feedback inhibitory pathway. To help facilitate an understanding of this stretch reflex force roll off, a simple model representing the elbow reflex pathways 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 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 parameters from the model fits indicate that the force threshold for force-sensitive receptors is relatively high, suggesting that the inhibition may arise from muscle free nerve endings rather than Golgi tendon organs. The experimental results coupled with the simulations of elbow reflex responses suggest the possibility that after stroke, the effectiveness of force-feedback inhibition may increase to a level that has functional significance. Practical implications of these findings are discussed in relation to muscle weakness commonly associated with stroke.
Hidler
Joseph M
JM
Department of Biomedical Engineering, Catholic University, Washington, DC 20064, USA. hidler@cua.edu
Schmit
Brian D
BD
D002908:Chronic Disease; D003198:Computer Simulation; D003936:Diagnosis, Computer-Assisted / Q000379:methods; D004551:Elbow Joint / Q000503:physiopathology; D004576:Electromyography / Q000379:methods; D019317:Evidence-Based Medicine / Q000379:methods; D005246:Feedback; D006801:Humans; D008959:Models, Neurological; D009119:Muscle Contraction; D009128:Muscle Spasticity / Q000209:etiology / Q000503:physiopathology*; D018482:Muscle, Skeletal / Q000294:innervation* / Q000503:physiopathology*; D009433:Neural Inhibition; D010291:Paresis / Q000209:etiology / Q000503:physiopathology*; D012018:Reflex; D013314:Stress, Mechanical; D020521:Stroke / Q000150:complications / Q000503:physiopathology*