Ask your competent? doctor how this information is going to recover your walking ability. In my case since most of my motor and pre-motor cortex is dead, nothing here is useful. My dead brain destroyed any possible synergy there was. WHAT IS THE FIX?
Motor modules are largely unaffected by pathological walking biomechanics: a simulation study
Journal of NeuroEngineering and Rehabilitation volume 22, Article number: 16 (2025)
Abstract
Background
Motor module (a.k.a. muscle synergy) analysis has frequently been used to provide insight into changes in muscle coordination associated with declines in walking performance, to evaluate the effect of different rehabilitation interventions, and more recently, to control exoskeletons and prosthetic devices. However, it remains unclear whether changes in muscle coordination revealed via motor module analysis stem from abnormal walking biomechanics or neural control. This distinction has important implications for the use of motor module analysis for rehabilitation interventions and device design. Thus, this study aims to elucidate the extent to which motor modules emerge from pathological walking biomechanics, i.e. abnormal walking biomechanics commonly observed in individuals with neurological disease and/or injury.
Methods
We conducted a series of computer simulations using OpenSim Moco to simulate pathological walking biomechanics by manipulating speed, asymmetry, and step width in a three-dimensional musculoskeletal model. We focused on these spatiotemporal metrics because they are commonly altered in individuals with Parkinson’s disease, stroke survivors, etc. and have been associated with changes in motor module number and structure. We extracted motor modules using nonnegative matrix factorization from the muscle activations from each simulation. We then examined how alterations in walking biomechanics influenced the number and structure of extracted motor modules and compared the findings to previous experimental studies.
Results
The motor modules identified from our simulations were similar to those identified from previously published experiments of non-pathological walking. Moreover, our findings indicate that the same motor modules can be used to generate a range of pathological-like waking biomechanics by modulating their recruitment over the gait cycle. These results contrast with experimental studies in which pathological-like walking biomechanics are accompanied by a reduction in motor module number and alterations in their structure.
Conclusions
This study highlights that pathological walking biomechanics do not necessarily require abnormal motor modules. In other words, changes in number and structure of motor modules can be a valuable indicator of alterations in neuromuscular control and may therefore be useful for guiding rehabilitation interventions and controlling exoskeletons and prosthetic devices in individuals with impaired walking function due to neurological disease or injury.
Background
Motor module (a.k.a. muscle synergy) analysis has emerged over the last few decades as a useful method to characterize the complex coordination of the numerous muscles involved in movements such as walking. Motor modules reflect coordinated patterns of muscle activity that can be flexibly combined to meet the goals of different movement behaviors [1]. It is hypothesized that motor modules reflect an underlying nervous system strategy to overcome the complexity of controlling movement by grouping muscles into functional units. As such, many researchers are using motor modules to evaluate the effect of different rehabilitation interventions on neuromuscular control [2,3,4,5,6,7,8,9,10,11,12] and even to control exoskeletons and prosthetic devices [13,14,15,16,17,18,19,20,21]. However, since motor modules are identified from experimentally-recorded electromyography (EMG) data using numerical decomposition techniques such as principal component analysis or nonnegative matrix factorization [1, 22, 23], there is ongoing debate regarding whether they truly represent an underlying neural strategy or simply emerge from the biomechanics of the recorded movement. Incorporating EMG-derived motor modules into rehabilitation interventions and/or into controllers for exoskeletons and prosthetics introduces additional complexity compared to recording only movement biomechanics. If motor modules are simply emergent from movement biomechanics, then there may be no need to incorporate such complexity into these settings. Therefore, it is critical to understand to what extent EMG-derived motor modules reflect an underlying neural strategy to support their use in identifying neuromuscular deficits limiting walking function, guiding rehabilitation efforts, and facilitating control of exoskeleton and prosthetic devices.
Converging evidence suggests that recruiting a reduced number of motor modules to control walking contributes to impaired walking function. Several studies have identified that between four to six motor modules are needed to describe muscle activity in unimpaired walking [24,25,26]. Comparatively fewer motor modules are required to describe muscle activity in people with neurological deficits (e.g., stroke [7, 24, 27, 28] cerebral palsy [29] and Parkinson’s disease [30,31,32]) and musculoskeletal conditions such as osteoarthritis [33]. Given that each module in unimpaired walking is organized around producing biomechanical functions such as leg swing control and forward propulsion [34, 35], it is not surprising that individuals with a reduced number of motor modules typically walk with impaired walking function. For example, reduced motor module number in stroke survivors is associated with slower walking speeds and more asymmetrical steps [24, 27] and an inability to change speed, cadence, step length, and step height [28]. Moreover, increases in motor module number that occur with rehabilitation are associated with improved walking function [10, 36]. While the prevailing interpretation of these studies is that a decrease in motor module number causes impaired function, an alternative explanation is that the observed reduction in motor modules may be a consequence of the altered walking biomechanics rather than the cause.
Musculoskeletal modeling and simulation offer a means to disentangle the effects of neural control and biomechanics on motor modules in a carefully controlled manner. For example, Falisse et al., demonstrated a reduction in motor module number alone could not produce the crouch gait biomechanics often observed in cerebral palsy [37]. Moreover, Mehrabi et al., found that normal walking biomechanics could not be achieved with reduced motor module number [38]. Conversely, a recent experimental study provided some evidence that healthy individuals could emulate crouch gait patterns commonly observed in children with cerebral palsy without reducing motor module number [39]. Taken together, these studies suggest that although biomechanics may have some influence on motor modules, there remains room for them to have a neural basis. However, a limitation of these studies is their focus on a single gait type, preventing insights into the extent of biomechanics versus neural control on motor module structure across the diverse walking biomechanics often observed in populations with neurological disease and/or injury.
The purpose of this study was to explore the extent to which motor modules are emergent from pathological walking biomechanics. Or in other words, does pathological walking biomechanics require a reduced number and/or altered structure of motor modules. Inspired by the work of De Groote et al. [26] in which motor modules were extracted from individual muscle-driven simulations of unimpaired walking identical to how motor modules are identified experimentally from EMG, we compared motor modules extracted from 27 muscle-driven simulations of pathological gait biomechanics. We use the term “pathological walking biomechanics” to refer to measurable gait characteristics such as spatiotemporal parameters, kinematics, and kinetics resulting from injury or disease. In this study, we focused on the effect of varying speeds, step length asymmetry, and step widths commonly observed in populations with neurological disease or injury such as stroke survivors, persons with Parkinson’s disease, etc. We hypothesized that motor modules cannot be explained by biomechanics alone and thus reflect to some extent an underlying neural control strategy. Based on this hypothesis, we predicted that the number and structure of motor modules would not differ across simulations with different pathological walking biomechanics.
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