Autogenic and intermuscular pathways in cats with partial spinal cord lesions

Abstract

Bipeds, like humans, stand with two-thirds of their body mass at about two-thirds of their body height above the ground, which, distributed within a relatively narrow base of support, makes us an inherently unstable system. It is not surprising that in the background of all motor control activities, such as standing or walking, are fundamental and dynamic processes that are aimed at maintaining and restoring the stability of the entire body. By exerting forces via their limbs against the ground, humans and animals can counteract both intrinsic and extrinsic perturbative forces and maintain their stability. The sensory feedback throughout the body contributes to the restorative forces developed by the limb muscles, with feedback from muscle mechanoreceptors being the most crucial. Briefly, length-dependent feedback from muscle spindle receptors increases joint stiffness locally, and intermuscular, widely-distributed inhibitory force-dependent feedback from Golgi tendon organs reduces limb stiffness, while excitatory force-feedback enhances joint coupling during locomotion. These pathways have shown remarkable task-dependent modulation by supraspinal tracts. Thus, the inability to modulate the gain and/or bias of these proprioceptive pathways properly after spinal cord injury could contribute to the crouched gait deficit often observed, even after functional recovery of stepping. Utilizing mechanographic method, in this study, we provided a comprehensive overview of changes in these pathways. This research ultimately contributes four major findings; i.) following lateral hemisection, the gain of length-feedback arising from knee and ankle extensors is selectively amplified, ii.) a strong, bilateral and chronic inhibitory force-feedback bias is directed toward ankle extensors, iii.) which likely contributes to the inability to maintain static equilibrium and potentially to difficulty during the weight acceptance phase of a step cycle, and iv.) we provided evidence that supraspinal tract(s) that modulate force-feedback bias are likely located ventrally, whereas the dorsal tracts control the group III and IV pathways.