Refy, O. | Search bioRxiv

bioRxiv2024

Changes in Gait Asymmetry May Be Caused by Adaptation of Spinal Reflexes

In a recent human study, we found that adaptive changes in step length asymmetry (SLA) are correlated with similar changes in the H-reflex gains of the leg muscles during split-belt treadmill locomotion. While this observation indicated a closer link between gait asymmetry and spinal reflex adaptation, it did not reveal their causal relationship. To better understand this relationship, here we use a neuromuscular model of human walking whose control relies primarily on spinal reflexes. Subjecting the model to split-belt treadmill locomotion with different combinations of belt speed and reflex gain adaptation patterns, we find that belt speed changes increase the variability in SLA but do not result in consistent SLA patterns as observed in human experiments, whereas reflex gain adaptations do. Furthermore, we find that the model produces SLA patterns similar to healthy adults when its reflex gains are adapted in a way similar to the H-reflex changes we observed in our previous human study. The model also predicts SLA patterns similar to the ones observed for cerebellar degeneration patients when the reflexes do not adapt beyond a sudden dip at the time the ipsilateral belt speed is lowered. Our results suggest that SLA does not arise from imposing belt speed changes but requires the adaptation of the reflex gains, and that the dynamic adaptation of these gains may be an essential part of human gait control when encountering unexpected environment changes such as the uneven speed changes in split-belt treadmill locomotion.

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bioRxiv2022

Does Functional Recovery Imply Stable Circuitry in the Spinal Animal?

Spinal animals can regain locomotor function through gait training. However, the neural processes involved in this recovery are poorly understood. Here we use computer simulation to address if the reorganization of spinal circuits associated with the functional recovery leads to meaningful, stable circuitry function. Specifically, we develop a neuromuscular model of a spinalized rat whose circuitry can adapt based on two alternative Hebbian learning strategies, one designed to guide the circuitry back to its normal pre-injury state and the other designed to destabilize it and drive it into saturation. Exposing the model to simulated gait training, we find that both strategies lead to recovery of locomotor function as defined by the outcome measures reported in studies with spinal rats. If anything, the results obtained with the destabilizing learning strategy seem to agree more with animal observations, since it produces similarly excessive amplitudes in muscle activity. Our results suggest that gait training of spinalized animals does not necessarily effect a meaningful recovery of their spinal circuitry function. More experimental work should be directed to clarify this point, as it may have grave implications for the potential of gait rehabilitation in patients with motor complete injuries of the spinal cord.

neuroscience↗