Shaping Ankle Mechanical Impedance in Neurological Disorders

Sebastião Garcia Louro do Nascimento e Oliveira

Key information

Authors:

Sebastião Garcia Louro do Nascimento e Oliveira (Sebastião Garcia Louro do Nascimento e Oliveira)

Supervisors:

Jorge Manuel Mateus Martins (Jorge Manuel Mateus Martins); Rui Miguel de Moura Antunes e Valejo Coelho (Rui Miguel de Moura Antunes e Valejo Coelho)

Published in

November 28, 2024

Abstract

Neurological disorders like stroke and cerebral palsy impair movement control, reducing independence and quality of life. Upper motor neuron (UMN) lesions disrupt central nervous system function, causing limb control loss. Ankle impedance, influenced by joint properties and muscle co-activation via reflex and voluntary pathways, is notably affected during the stance phase of walking. This study presents a computational framework to evaluate how reflex pathways simulating spasticity-related UMN lesions affect ankle impedance. Focusing on ankle flexors (soleus, gastrocnemius, tibialis anterior), Geyer and Herr's reflex model was extended by adding pathways primarily impacting plantarflexor muscles, based on Bruel et al.'s work. The model’s reflex gains were optimized using a covariance matrix adaptation evolution strategy (CMA-ES) to achieve a more physiologically accurate gait pattern. Neural impairments were simulated by adjusting specific gains relative to the optimized solutions. Following Rouse et al.'s procedure, ankle impedance was estimated by perturbing the feet during stance, modeling stiffness, damping, and inertia. The second-order model replicated simulation torque with an average variance accounted for of 93\% across all estimations. Stiffness alterations suggested significant influence from the activation profiles of the SOL and GAS muscles, as well as variations in tendon lengths, while patterns in damping and inertia were less distinct.