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In this review, we elaborate on how musculoskeletal (MSK) modeling combined with dynamic movement simulation is gradually evolving from a research tool to a promising in silico tool to assist medical doctors and physical therapists in decision making by providing parameters relating to dynamic MSK function and loading. This review primarily focuses on our own and related work to illustrate the framework and the interpretation of MSK model-based parameters in patients with 3 different conditions, that is, degenerative joint disease, cerebral palsy, and adult spinal deformities. By selecting these 3 clinical applications, we also aim to demonstrate the differing levels of clinical readiness of the different simulation frameworks introducing in silico model-based biomarkers of motor function to inform MSK rehabilitation and treatment, with the application for adult spinal deformities being the most recent of the 3. Based on these applications, barriers to clinical integration and positioning of these in silico technologies within standard clinical practice are discussed in the light of specific challenges related to model assumptions, required level of complexity and personalization, and clinical implementation. [ABSTRACT FROM AUTHOR]

The metabolic energy rate of individual muscles is impossible to measure without invasive procedures. Prior studies have produced models to predict metabolic rates based on experimental observations of isolated muscle contraction from various species. Such models can provide reliable predictions of metabolic rates in humans if muscle properties and control are accurately modeled. This study aimed to examine how muscle-tendon model individualization and metabolic energy models influenced estimation of muscle-tendon states and time-series metabolic rates, to evaluate the agreement with empirical data, and to provide predictions of the metabolic rate of muscle groups and gait phases across walking speeds. Three-dimensional musculoskeletal simulations with prescribed kinematics and dynamics were performed. An optimal control formulation was used to compute muscle-tendon states with four levels of individualization, ranging from a scaled generic model and muscle controls based on minimal activations, inclusion of calibrated muscle passive forces, personalization of Achilles and quadriceps tendon stiffnesses, to finally informing muscle controls with electromyography. We computed metabolic rates based on existing models. Simulations with calibrated passive forces and personalized tendon stiffness most accurately estimate muscle excitations and fiber lengths. Interestingly, the inclusion of electromyography did not improve our estimates. The whole-body average metabolic cost was better estimated with a subset of metabolic energy models. We estimated metabolic rate peaks near early stance, pre-swing, and initial swing at all walking speeds. Plantarflexors accounted for the highest cost among muscle groups at the preferred speed and were similar to the cost of hip adductors and abductors combined. Also, the swing phase accounted for slightly more than one-quarter of the total cost in a gait cycle, and its relative cost decreased with walking speed. Our prediction might inform the design of assistive devices and rehabilitation treatment. The code and experimental data are available online. Author summary: Simulations of the musculoskeletal system can provide insights into motion mechanics and energetics. To increase confidence in the approach, it is important to establish how predictions are affected by modelling assumptions. In this study, we evaluated how simulations with increasing levels of sophistication and metabolic energy models from the literature agreed with recorded muscle excitations, fiber lengths, and whole-body metabolic rates during walking at different speeds. We found that calibrating muscle passive components: muscle passive forces, and tendon stiffness, estimated better muscle excitations and fiber lengths than using original musculoskeletal model values. The metabolic energy cost of walking was closely estimated with only a subset of metabolic energy models. We estimated that the metabolic energy demands are the highest during three periods of the gait cycle—early stance, pre-swing, and initial swing, at all walking speeds. In all walking speeds, muscles that support plantarflexion accounted for the highest metabolic cost among all the muscle groups. As walking speed increases, the metabolic cost of the stance phase also increases. Our detailed description of metabolic costs at muscle groups and gait phases might help to design assistive devices and rehabilitation treatments. [ABSTRACT FROM AUTHOR]

The unique structure of the human foot is seen as a crucial adaptation for bipedalism. The foot's arched shape enables stiffening the foot to withstand high loads when pushing off, without compromising foot flexibility. Experimental studies demonstrated that manipulating foot stiffness has considerable effects on gait. In clinical practice, altered foot structure is associated with pathological gait. Yet, experimentally manipulating individual foot properties (e.g. arch height or tendon and ligament stiffness) is hard and therefore our understanding of how foot structure influences gait mechanics is still limited. Predictive simulations are a powerful tool to explore causal relationships between musculoskeletal properties and whole-body gait. However, musculoskeletal models used in three-dimensional predictive simulations assume a rigid foot arch, limiting their use for studying how foot structure influences three-dimensional gait mechanics. Here, we developed a four-segment foot model with a longitudinal arch for use in predictive simulations. We identified three properties of the ankle-foot complex that are important to capture ankle and knee kinematics, soleus activation, and ankle power of healthy adults: (1) compliant Achilles tendon, (2) stiff heel pad, (3) the ability to stiffen the foot. The latter requires sufficient arch height and contributions of plantar fascia, and intrinsic and extrinsic foot muscles. A reduced ability to stiffen the foot results in walking patterns with reduced push-off power. Simulations based on our model also captured the effects of walking with anaesthetised intrinsic foot muscles or an insole limiting arch compression. The ability to reproduce these different experiments indicates that our foot model captures the main mechanical properties of the foot. The presented four-segment foot model is a potentially powerful tool to study the relationship between foot properties and gait mechanics and energetics in health and disease. Author summary: During every step, the foot absorbs the shock as it strikes the ground, supports the body weight, and transfers calf muscle forces to the ground to push off towards the next step. Although experiments have shown that foot structure affects both foot and whole-body movement, a deep understanding of the role of different muscles, ligaments, and other tissues in the foot is still lacking. Examining the relation between alterations in individual foot properties, e.g. muscle strength or arch height, and walking is challenging in experiments, but can be done in model-based simulations. Yet, existing models that are suitable for simulating walking oversimplify the foot. Here, we present a new, more detailed foot model. Simulations with our model captured many features of human walking not captured by simulations with simple models. We found that the stiffness of the foot-ankle complex and especially the ability to stiffen the foot had a large effect on the walking pattern. A reduced ability to stiffen the foot resulted in simulated walking patterns resembling those observed in patients with flexible feet. In the future, we will use our model to investigate how foot deformities alter walking in patients and to design personalized treatments. [ABSTRACT FROM AUTHOR]

Balance impairments are common in cerebral palsy. When balance is perturbed by backward support surface translations, children with cerebral palsy have increased co-activation of the plantar flexors and tibialis anterior muscle as compared to typically developing children. However, it is unclear whether increased muscle co-activation is a compensation strategy to improve balance control or is a consequence of reduced reciprocal inhibition. During translational perturbations, increased joint stiffness due to co-activation might aid balance control by resisting movement of the body with respect to the feet. In contrast, during rotational perturbations, increased joint stiffness will hinder balance control as it couples body to platform rotation. Therefore, we expect increased muscle co-activation in response to rotational perturbations if co-activation is caused by reduced reciprocal inhibition but not if it is merely a compensation strategy. We perturbed standing balance by combined backward translational and toe-up rotational perturbations in 20 children with CP and 20 TD children. Perturbations induced forward followed by backward movement of the center of mass. We evaluated reactive muscle activity and the relation between center of mass movement and reactive muscle activity using a linear feedback model based on center of mass kinematics. In typically developing children, perturbations induced plantar flexor balance correcting muscle activity followed by tibialis anterior balance correcting muscle activity, which was driven by center of mass movement. In children with cerebral palsy, the switch from plantar flexor to tibialis anterior activity was less pronounced than in typically developing children due to increased muscle co-activation of the plantar flexors and tibialis anterior throughout the response. Our results thus suggest that a reduction in reciprocal inhibition causes muscle co-activation in reactive standing balance in children with CP. Author summary: Children with cerebral palsy often have balance impairments. When standing balance is perturbed using support-surface translations, children with cerebral palsy have high agonist-antagonist co-activation. Increasing joint stiffness by co-activating agonists and antagonists might aid standing balance control during translational, but not rotational perturbations. If children with cerebral palsy show muscle co-activation during rotational perturbations, we can assume that this co-activation is a consequence of neurological impairments (e.g., not be able to suppress antagonist activation upon stretch of the agonist). We found that both in typically developing children and children with cerebral palsy reactive muscle activity could be explained by delayed feedback of center of mass kinematics. Our combined translational and rotational perturbations induced a switch in center of mass movement (forward to backward). We found that upon this switch in center of mass movement, typically developing children switched from plantarflexor to tibialis anterior muscle activity. This switch in muscle activity was less clear in children with cerebral palsy, although center of mass movement was the same as in typically developing children, due to muscle co-activation. Therefore, our results suggest that neural impairments cause muscle co-activation in reactive standing balance in children with cerebral palsy. [ABSTRACT FROM AUTHOR]