Investigation of neural and biomechanical impairments leading to pathological toe and heel gaits using neuromusculoskeletal modelling.

This study investigates the pathological toe and heel gaits seen in human locomotion using neuromusculoskeletal modelling and simulation. In particular, it aims to investigate potential cause-effect relationships between biomechanical or neural impairments and pathological gaits. Toe and heel gaits are commonly present in spinal cord injury, stroke and cerebral palsy. Toe walking is mainly attributed to spasticity and contracture at plantar flexor muscles, whereas heel walking can be attributed to muscle weakness of biomechanical or neural origin. To investigate the effect of these impairments on gait, this study focuses on the soleus and gastrocnemius muscles as they contribute to ankle plantarflexion. We built a reflex circuit model based on previous work by Geyer and Herr with additional pathways affecting the plantar flexor muscles. The SCONE software, which provides optimisation tools for 2D neuromechanical simulation of human locomotion, is used to optimise the corresponding reflex parameters and simulate healthy gait. We then modelled various bilateral plantar flexor biomechanical and neural impairments, and individually introduced them in the healthy model. We characterised the resulting simulated gaits as pathological or not by comparing ankle kinematics and ankle moment with the healthy optimised gait based on metrics used in clinical studies. Our simulations suggest that toe walking can be generated by hyperreflexia, whereas muscle and neural weaknesses partially induce heel gait. Thus, this 'what if' approach is deemed of great interest as it allows investigation of the effect of various impairments on gait and suggests an important contribution of active reflex mechanisms to pathological toe gait. KEY POINTS: Pathological toe and heel gaits are commonly present in various conditions such as spinal cord injury, stroke and cerebral palsy. These conditions present various neural and biomechanical impairments, but the cause-effect relationships between these impairments and pathological gaits are difficult to establish clinically. Based on neuromechanical simulation, this study focuses on the plantar flexor muscles and builds a new reflex circuit controller to model and evaluate the potential effect of both neural and biomechanical impairments on gait. Our results suggest an important contribution of active reflex mechanisms to pathological toe gait. This 'what if' based on neuromechanical modelling is thus deemed of great interest to target potential causes of pathological gait.