Biology subjects

Van Campenhout, A.

Publications and source records attributed to Van Campenhout, A..

4 recordsLinked to original sources

bioRxiv2025

Estimating the contribution of musculoskeletal impairments to altered gait kinematics in children with cerebral palsy using predictive simulations

1.BackgroundCerebral palsy (CP) is caused by a brain lesion around birth leading to impaired motor control, bony deformities, muscle contractures, and weakness resulting in altered gait. Since the brain lesion cannot be cured, treatment aims at improving mobility. Multilevel surgery targets muscle and bony impairments but the outcome of multilevel surgery is variable and unpredictable due to our limited insight in the contribution of musculoskeletal impairments to gait alterations. MethodsHere, we used predictive simulations based on personalized musculoskeletal models to identify the contribution of musculoskeletal impairments to altered gait in eight individuals with CP scheduled for multilevel surgery. For each individual, we generated gait patterns based on eight models with different levels of personalization. We modeled muscle weakness, muscle contractures, and/or bony deformities of hip and knee and evaluated the contribution of these impairments to deviations in kinematics by comparing simulated and experimental kinematics. ResultsThe contribution of musculoskeletal impairments varied largely between participants. All modeled musculoskeletal impairments explained little to 39% of the kinematic deficits, in line with the limited and variable effect of multilevel surgery. Muscle contractures had the largest effect on the predicted kinematics. ConclusionOur results suggest an important contribution of motor control and unmodeled musculoskeletal impairments (e.g. shank and foot deformities) to alterations in the gait pattern. Model-based simulations are a promising tool to determine the contribution of musculoskeletal impairments to alterations in gait kinematics in individuals with CP.

bioengineering↗

bioRxiv2023

Identification of neural and non-neural origins of joint hyper-resistance based on a novel neuromechanical model.

Joint hyper-resistance is a common symptom in neurological disorders. It has both neural and nonneural origins, but it has been challenging to distinguish different origins based on clinical tests alone. Combining instrumented tests with parameter identification based on a neuromechanical model may allow us to dissociate the different origins of joint hyper-resistance in individual patients. However, this requires that the model captures the underlying mechanisms. Here, we propose a neuromechanical model that, in contrast to previously proposed models, accounts for muscle shortrange stiffness and its interaction with muscle tone and reflex activity. We collected knee angle trajectories during the pendulum test in 15 children with cerebral palsy (CP) and 5 typically developing children. We did the test in two conditions - hold and pre-movement - that have been shown to alter knee movement. We modeled the lower leg as an inverted pendulum actuated by two antagonistic Hill-type muscles extended with SRS. Reflex activity was modeled as delayed, linear feedback from muscle force. We estimated neural and non-neural parameters by optimizing the fit between simulated and measured knee angle trajectories during the hold condition. The model could fit a wide range of knee angle trajectories in the hold condition. The model with personalized parameters predicted the effect of pre-movement demonstrating that the model captured the underlying mechanism and subject-specific deficits. Our model thus allows us to determine subject-specific origins of joint hyper-resistance and thereby opens perspectives for improved diagnosis and consequently treatment selection in children with spastic CP.

pathology↗

bioRxiv2023

Adult stem cell characterization from the Medial Gastrocnemius and Semitendinosus muscles in early development of cerebral palsy pathology

Cerebral palsy (CP) is one of the most common lifelong conditions leading to childhood physical disability. Literature reported previously altered muscle properties such as lower number of satellite cells (SCs), with altered fusion capacity. However, these observations highly vary among studies, possibly due to heterogeneity in patient population, lack of appropriate control data, methodology and different assessed muscle. In this study we aimed to strengthen previous observations and to understand the heterogeneity of CP muscle pathology. Myogenic differentiation of SCs from the Medial Gastrocnemius (MG) muscle of patients with CP (n=16, 3-9 years old) showed higher fusion capacity compared to age-matched typically developing children (TD, n=13). Furthermore, we uniquely assessed cells of two different lower limb muscles and showed a decreased myogenic potency in cells from the Semitendinosus (ST) compared to the MG. Longitudinal assessments, one year after the first botulinum toxin treatment, showed slightly reduced SC representations and lower fusion capacity. Finally, we proved the robustness of our data, by assessing in parallel the myogenic capacity of two samples from the same TD muscle. In conclusion, these data confirmed previous findings of increased SC fusion capacity from MG muscle of young patients with CP compared to age-matched TD. Further elaboration is reported on potential factors contributing to heterogeneity, such as assessed muscle, CP progression and reliability of primary outcome parameters.

developmental biology↗

bioRxiv2019

Physics-based predictive simulations to explore the differential effects of motor control and musculoskeletal deficits on gait dysfunction in cerebral palsy: a retrospective case study

Model-based simulations of walking have the theoretical potential to support clinical decision making by predicting the functional outcome of treatments in terms of walking performance. Yet before using such simulations in clinical practice, their ability to identify the main treatment targets in specific patients needs to be demonstrated. In this study, we generated predictive simulations of walking with a medical imaging based neuro-musculoskeletal model of a child with cerebral palsy presenting crouch gait. We explored the influence of altered muscle-tendon properties, reduced neuromuscular control complexity, and spasticity on gait function in terms of joint kinematics, kinetics, muscle activity, and metabolic cost of transport. We modeled altered muscle-tendon properties by personalizing Hill-type muscle-tendon parameters based on data collected during functional movements, simpler neuromuscular control by reducing the number of independent muscle synergies, and spasticity through delayed muscle activity feedback from muscle force and force rate. Our simulations revealed that, in the presence of aberrant musculoskeletal geometries, altered muscle-tendon properties rather than reduced neuromuscular control complexity and spasticity were the primary cause of the crouch gait pattern observed for this child, which is in agreement with the clinical examination. These results suggest that muscle-tendon properties should be the primary target of interventions aiming to restore a more upright gait pattern for this child. This suggestion is in line with the gait analysis following muscle-tendon property and bone deformity corrections. The ability of our simulations to distinguish the contribution of different impairments on walking performance opens the door for identifying targeted treatment strategies with the aim of designing optimized interventions for neuro-musculoskeletal disorders.

bioengineering↗