Background: Most cases of toe walking in children are idiopathic. We used pathology-specific neuromusculoskeletal predictive simulations to identify potential underlying neural and muscular mechanisms contributing to idiopathic toe walking. Methods: A musculotendon contracture was added to the ankle plantarflexors of a generic musculoskeletal model to represent a pathology-specific contracture model, matching the reduced ankle dorsiflexion range-of-motion in a cohort of children with idiopathic toe walking. This model was employed in a forward dynamic simulation controlled by reflexes and supraspinal drive, governed by a multi-objective cost function to predict gait patterns with the contracture model. We validated the predicted gait using experimental gait data from children with idiopathic toe walking with ankle contracture, by calculating the root mean square errors averaged over all biomechanical variables. Findings: A predictive simulation with the pathology-specific model with contracture approached experimental ITW data (root mean square error = 1.37SD). Gastrocnemius activation was doubled from typical gait simulations, but lacked a peak in early stance as present in electromyography. This synthesised idiopathic toe walking was more costly for all cost function criteria than typical gait simulation. Also, it employed a different neural control strategy, with increased length- and velocity-based reflex gains to the plantarflexors in early stance and swing than typical gait simulations. Interpretation: The simulations provide insights into how a musculotendon contracture combined with altered neural control could contribute to idiopathic toe walking. Insights into these neuromuscular mechanisms could guide future computational and experimental studies to gain improved insight into the cause of idiopathic toe walking.

Spasticity is a common impairment within pediatric neuromusculoskeletal disorders. How spasticity contributes to gait deviations is important for treatment selection. Our aim was to evaluate the pathophysiological mechanisms underlying gait deviations seen in children with spasticity, using predictive simulations. A cluster analysis was performed to extract distinct gait patterns from experimental gait data of 17 children with spasticity to be used as comparative validation data. A forward dynamic simulation framework was employed to predict gait with either velocity- or force-based hyperreflexia. This framework entailed a generic musculoskeletal model controlled by reflexes and supraspinal drive, governed by a multiobjective cost function. Hyperreflexia values were optimized to enable the simulated gait to best match experimental gait patterns. Three experimental gait patterns were extracted: (1) increased knee flexion, (2) increased ankle plantar flexion, and (3) increased knee flexion and ankle plantar flexion when compared with typical gait. Overall, velocity-based hyperreflexia outperformed force-based hyperreflexia. The first gait pattern could mostly be explained by rectus femoris and hamstrings velocity-based hyperreflexia, the second by gastrocnemius velocity-based hyperreflexia, and the third by gastrocnemius, soleus, and hamstrings velocity-based hyperreflexia. This study shows how velocity-based hyperreflexia from specific muscles contributes to different spastic gait patterns, which may help in providing targeted treatment.

Neuro-musculoskeletal modelling can provide insight into the aberrant muscle function during walking in those suffering cerebral palsy (CP). However, such modelling employs optimization to estimate muscle activation that may not account for disturbed motor control and muscle weakness in CP. This study evaluated different forms of neuro-musculoskeletal model personalization and optimization to estimate musculotendon forces during gait of nine children with CP (GMFCS I-II)and nine typically developing (TD)children. Data collection included 3D-kinematics, ground reaction forces, and electromyography (EMG)of eight lower limb muscles. Four different optimization methods estimated muscle activation and musculotendon forces of a scaled-generic musculoskeletal model for each child walking, i.e. (i)static optimization that minimized summed-excitation squared; (ii)static optimization with maximum isometric muscle forces scaled to body mass; (iii)an EMG-assisted approach using optimization to minimize summed-excitation squared while reducing tracking errors of experimental EMG-linear envelopes and joint moments; and (iv)EMG-assisted with musculotendon model parameters first personalized by calibration. Both static optimization approaches showed a relatively low model performance compared to EMG envelopes. EMG-assisted approaches performed much better, especially in CP, with only a minor mismatch in joint moments. Calibration did not affect model performance significantly, however it did affect musculotendon forces, especially in CP. A model more consistent with experimental measures is more likely to yield more physiologically representative results. Therefore, this study highlights the importance of calibrated EMG-assisted modelling when estimating musculotendon forces in TD children and even more so in children with CP.