Biology subjects

Wartzack, S.

Publications and source records attributed to Wartzack, S..

3 recordsLinked to original sources

bioRxiv2025

Does reduced reactivity explain altered postural control in Parkinson's disease? A predictive simulation study.

Postural instability represents one of the cardinal symptoms of Parkinsons disease (PD). Still, internal processes leading to this instability are not fully understood. Simulations using neuromusculoskeletal human models could help understand these internal processes leading to PD-associated postural deficits. In this paper, we investigated whether reduced reactivity amplitudes resulting from impairments due to PD can explain postural instability as well as increased muscle tone as often observed in individuals with PD. To simulate reduced reactivity, we gradually decreased previously optimized gain factors within the postural control circuitry of our model performing a quiet upright standing task. After each reduction step, the model was again optimized. Simulation results were compared to experimental data collected from 31 individuals with PD and 31 age- and sex-matched healthy control participants. Analyzing our simulation results, we showed that muscle activations increased with a models reduced reactivity, as well as joint angles ranges of motion (ROMs). However, sway parameters such as center of pressure (COP) path lengths and COP ranges did not increase as observed in our experimental data. These results suggest that a reduced reactivity does not directly lead to increased sway parameters, but could cause increased muscle tone leading to subsequent postural control alterations. To further investigate postural stability using neuromusculoskeletal models, analyzing additional internal model parameters and tasks such as perturbed upright standing requiring comparable reaction patterns could provide promising results. By enhancing such models and deepening the understanding of internal processes of postural control, these models may be used to assess and evaluate rehabilitation interventions in the future. Impact StatementAltered postural control in Parkinsons disease can be partly associated to reduced reactivity. Additional changes in the neural circuitry need to be further investigated to fully explain the observed differences.

bioengineering↗

bioRxiv2024

Investigating cerebellar control in slow gait adaptations: Insights from predictive simulations of split-belt walking

BackgroundDuring split-belt treadmill walking, neurotypical humans exhibit adaptations characterized by a gradual decrease in step length asymmetry (SLA) toward or beyond symmetry, whereas individuals with cerebellar damage do not show these motor adaptations. Neuromusculoskeletal simulations may help to better understand individual aspects of the underlying neural control, but are currently incapable of predicting adaptations to the continuous perturbations imposed by split-belt walking. MethodsWe extend a spinal reflex model with a biologically inspired model of the cerebellum, which enables error-based motor adaptation by modulating spinal control parameters in response to mismatches between a continuously updated internal prediction and actual motor outcomes. In this work, the cerebellum modulates only a single spinal control parameter, the timing of swing initiation in each leg, which allows examining its isolated contribution to gait adaptation as all other reflex pathways are held constant. We created 80 s predictive simulations of the model walking on a split-belt treadmill with a 2:1 belt-speed ratio, and compared predicted spatiotemporal parameters and kinematics to the reflex-only model and literature. ResultsThe reflex-only model could walk on the split-belt treadmill, but showed no step length adaptations. In contrast, the extended model adapted SLA from an initial asymmetric value toward symmetry or beyond, following an exponential time course similar to that observed in experiments. The model could adapt at varying rates and converge to different asymmetry levels. We found that, in simulation, SLA adaptation during split-belt walking is possible without changes in reflex gains, by adapting the timing of swing initiation. The modulation of timing alone also predicted the experimentally observed exponential adaptation in the temporal domain, but only a linear change in the spatial domain, indicating that additional control mechanisms are likely required to reproduce the full spatial adaptation observed in split-belt walking. ConclusionWe propose a computational model of the cerebellum which, when integrated into a spinal reflex model, autonomously drives feedforward gait adaptations during split-belt walking. This advances the current state of predictive simulations and may eventually help to better understand specific adaptation processes. The modular framework can be extended to test different hypotheses about motor control and adaptation during continuous perturbation tasks.

neuroscience↗

bioRxiv2024

A sensorimotor enhanced neuromusculoskeletal model for simulating postural control of upright standing

The humans upright standing is a complex control process that is not yet fully understood. Postural control models can provide insights into the bodys internal control processes of balance behaviour. Using physiologically plausible models can also help explaining pathophysiological motion behaviour. In this paper, we introduce a neuromusculoskeletal postural control model using sensor feedback consisting of somatosensory, vestibular and visual information. The sagittal plane model was restricted to effectively six degrees of freedom and consisted of nine muscles per leg. Physiological plausible neural delays were considered for balance control. We applied forward dynamic simulations and a single shooting approach to generate healthy reactive balance behaviour during quiet and perturbed upright standing. Control parameters were optimized to minimize muscle effort. We showed that our model is capable of fulfilling the applied tasks successfully. We observed joint angles and ranges of motion in physiological plausible ranges and comparable to experimental data. This model represents the starting point for subsequent simulation of pathophysiological postural control behaviour.

bioengineering↗