Motor Control

KM Steele, MH Schwartz (2022) “Causal Effects of Motor Control on Gait Kinematics After Orthopedic Surgery in Cerebral Palsy: A Machine-Learning Approach”

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Journal Article in Frontiers in Human Neuroscience

Altered motor control is common in cerebral palsy (CP). Understanding how altered motor control affects movement and treatment outcomes is important but challenging due to complex interactions with other neuromuscular impairments. While regression can be used to examine associations between impairments and movement, causal modeling provides a mathematical framework to specify assumed causal relationships, identify covariates that may introduce bias, and test model plausibility.

FIGURE 1 Directed Acyclic Graph (DAG) describing the assumed causal relationships between SEMLS (exposure) and 1GDI (outcome). The causal relationship between SEMLS and 1GDI is mediated by changes in impairments (1Imp). Baseline GDI (GDIpre) and 1GDI are related by measurement methods and other, unmeasured factors. Baseline impairment (Imppre), surgical history (Hx), and Age are also included as causal factors. The DAG also includes unmeasured factors related to general CP severity, which impact baseline impairment and surgical history. The step-by-step process and rationale for this DAG are available in the Supplementary Material and an interactive version is available on dagitty (http://dagitty.net/mUCSPWo).Aim: The goal of this research was to quantify the causal effects of altered motor control and other impairments on gait, before and after single-event multi-level orthopedic surgery (SEMLS).

Methods: We evaluated the impact of SEMLS on change in Gait Deviation Index (ΔGDI) between gait analyses. We constructed our causal model with a Directed Acyclic Graph that included the assumed causal relationships between SEMLS, ΔGDI, baseline GDI (GDIpre), baseline neurologic and orthopedic impairments (Imppre), age, and surgical history. We identified the adjustment set to evaluate the causal effect of SEMLS on ΔGDI and the impact of Imppre on ΔGDI and GDIpre. We used Bayesian Additive Regression Trees (BART) and accumulated local effects to assess relative effects.

Results: We prospectively recruited a cohort of children with bilateral CP undergoing SEMLS (N = 55, 35 males, age: 10.5 ± 3.1 years) and identified a control cohort with bilateral CP who did not undergo SEMLS (N = 55, 30 males, age: 10.0 ± 3.4 years). There was a small positive causal effect of SEMLS on ΔGDI (1.70 GDI points). Altered motor control (i.e., dynamic and static motor control) and strength had strong effects on GDIpre, but minimal effects on ΔGDI. Spasticity and orthopedic impairments had minimal effects on GDIpre or ΔGDI.

Interpretation: Altered motor control did have a strong effect on GDIpre, indicating that these impairments do have a causal effect on a child’s gait pattern, but minimal effect on expected changes in GDI after SEMLS. Heterogeneity in outcomes suggests there are other factors contributing to changes in gait. Identifying these factors and employing causal methods to examine the complex relationships between impairments and movement will be required to advance our understanding and care of children with CP.

EC Kuska, N Mehrabi, MH Schwartz, KM Steele (2022) “Number of synergies impacts sensitivity of gait to weakness and contracture”

Katie Landwehr JournalArticle, MotorControl, News, Projects, Publications , , , , , ,

Journal Article in Journal of Biomechanics

Muscle activity during gait can be described by a small set of synergies, weighted groups of muscles, that are theorized to reflect underlying neural control. For people with neurologic injuries, like cerebral palsy or stroke, even fewer synergies are required to explain muscle activity during gait. This reduction in synergies is thought to reflect altered control and is associated with impairment severity and treatment outcomes. Individuals with neurologic injuries also develop secondary musculoskeletal impairments, like weakness or contracture, that can impact gait. Yet, the combined impacts of altered control and musculoskeletal impairments on gait remains unclear.

A two-dimensional sagittal plane musculoskeletal model and synergy simulation framework tracked unimpaired gait kinematics. The model had nine degrees of freedom, including right and left leg hip, knee, and ankle flexion, actuated by eight muscles per leg. Fixed sets of synergies constrained control, forcing the direct collocation algorithm to solve for synergy activations. The objective function minimized deviations from unimpaired kinematics and the sum of muscle activations squared (neural demand). Weakness, simulated by a reduction in maximum isometric force, and contracture, simulated by a reduction in tendon slack length, were progressively increased for each muscle or muscle group until the simulation failed to replicate unimpaired gait. Kinematic deviations and convergence determined the success of the simulation. The primary outcomes were (1) musculoskeletal impairment thresholds, defined by the amount of weakness or contracture before failure, and (2) neural demand of each gait cycle.Aim: In this study, we use a two-dimensional musculoskeletal model constrained to synergy control to simulate unimpaired gait.

Methods: We vary the number of synergies, while simulating muscle weakness and contracture to examine how altered control impacts sensitivity to musculoskeletal impairment while tracking unimpaired gait.

Results: Results demonstrate that reducing the number of synergies increases sensitivity to weakness and contracture for specific muscle groups. For example, simulations using five-synergy control tolerated 40% and 51% more knee extensor weakness than those using four- or three-synergy control, respectively. Furthermore, when constrained to four- or three-synergy control, the model was increasingly sensitive to contracture and weakness of proximal muscles, such as the hamstring and hip flexors. Contrastingly, neither the amount of generalized nor plantarflexor weakness tolerated was affected by the number of synergies.

Interpretation: These findings highlight the interactions between altered control and musculoskeletal impairments, emphasizing the importance of measuring and incorporating both in future simulation and experimental studies.

BR Shuman, M Goudriaan, K Desloovere, MH Schwartz, KM Steele (2019) “Muscle synergies demonstrate only minimal changes after treatment in cerebral palsy.” Journal of NeuroEngineering and Rehabilitation

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Journal Article in Journal of NeuroEngineering and Rehabilitation:

In collaboration with University Hospital Pellenberg we examined whether muscle synergies change following common treatments in CP.

Background: Children with cerebral palsy (CP) have altered synergies compared to typically-developing peers, reflecting different neuromuscular control strategies used to move. While these children receive a variety of treatments to improve gait, whether synergies change after treatment, or are associated with treatment outcomes, remains unknown.

Methods: We evaluated synergies for 147 children with CP before and after three common treatments: botulinum toxin type-A injection (n = 52), selective dorsal rhizotomy (n = 38), and multi-level orthopaedic surgery (n = 57). Changes in synergy complexity were measured by the number of synergies required to explain > 90% of the total variance in electromyography data and total variance accounted for by one synergy. Synergy weights and activations before and after treatment were compared using the cosine similarity relative to average synergies of 31 typically-developing (TD) peers.

Results: There were minimal changes in synergies after treatment despite changes in walking patterns. Number of synergies did not change significantly for any treatment group. Total variance accounted for by one synergy increased (i.e., moved further from TD peers) after botulinum toxin type-A injection (1.3%) and selective dorsal rhizotomy (1.9%), but the change was small. Synergy weights did not change for any treatment group (average 0.001 ± 0.10), but synergy activations after selective dorsal rhizotomy did change and were less similar to TD peers (− 0.03 ± 0.07). Only changes in synergy activations were associated with changes in gait kinematics or walking speed after treatment. Children with synergy activations more similar to TD peers after treatment had greater improvements in gait.

Conclusions: While many of these children received significant surgical procedures and prolonged rehabilitation, the minimal changes in synergies after treatment highlight the challenges in altering neuromuscular control in CP. Development of treatment strategies that directly target impaired control or are optimized to an individual’s unique control may be required to improve walking function.

Alyssa Spomer and Momona Yamagami Present at a Neurorehabilitation Conference in Spain

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Alyssa and Momona attended the Summer School on Neurorehabilitation (SSNR) in Baiona, Spain from September 16th to the 21st. Alyssa gave a podium presentation on a feedback system she is developing that aims to characterize and target altered motor control in cerebral palsy. Momona gave a poster presentation to share her recent quantifications of deficits in motor planning in cerebral palsy. Nice work, Alyssa and Momona!Alyssa at podium presenting "A Feedback System to Characterize and Target Altered Motor Control in Cerebral Palsy".

 

 

Monoma stands in front of her poster "Quantification of Deficits in Motor Planning in Cerebral Palsy", discussing with interested colleagues.

 

M Goudriaan, BR Shuman, KM Steele, M Van den Hauwe, N Goemans, G Molenaers, K Desloovere (2018) “Non-neural Muscle Weakness Has Limited Influence on Complexity of Motor Control during Gait.” Frontiers in Human Neuroscience

Nicole JournalArticle, MotorControl, Projects, Publications , , , , ,

Journal Article in Frontiers in Human Neuroscience:

Despite significant differences in kinematics children with Duchenne muscular dystrophy have similar control complexity to typically developing children.

Abstract: Cerebral palsy (CP) and Duchenne muscular dystrophy (DMD) are neuromuscular disorders characterized by muscle weakness. Weakness in CP has neural and non-neural components, whereas in DMD, weakness can be considered as a predominantly non-neural problem. Despite the different underlying causes, weakness is a constraint for the central nervous system when controlling gait. CP demonstrates decreased complexity of motor control during gait from muscle synergy analysis, which is reflected by a higher total variance accounted for by one synergy (tVAF1). However, it remains unclear if weakness directly contributes to higher tVAF1 in CP, or whether altered tVAF1 reflects mainly neural impairments. If muscle weakness directly contributes to higher tVAF1, then tVAF1 should also be increased in DMD. To examine the etiology of increased tVAF1, muscle activity data of gluteus medius, rectus femoris, medial hamstrings, medial gastrocnemius, and tibialis anterior were measured at self-selected walking speed, and strength data from knee extensors, knee flexors, dorsiflexors and plantar flexors, were analyzed in 15 children with CP [median (IQR) age: 8.9 (2.2)], 15 boys with DMD [8.7 (3.1)], and 15 typical developing (TD) children [8.6 (2.7)]. We computed tVAF1 from 10 concatenated steps with non-negative matrix factorization, and compared tVAF1between the three groups with a Mann-Whiney U-test. Spearman’s rank correlation coefficients were used to determine if weakness in specific muscle groups contributed to altered tVAF1. No significant differences in tVAF1 were found between DMD [tVAF1: 0.60 (0.07)] and TD children [0.65 (0.07)], while tVAF1 was significantly higher in CP [(0.74 (0.09)] than in the other groups (both p < 0.005). In CP, weakness in the plantar flexors was related to higher tVAF1 (r = −0.72). In DMD, knee extensor weakness related to increased tVAF1 (r = −0.50). These results suggest that the non-neural weakness in DMD had limited influence on complexity of motor control during gait and that the higher tVAF1 in children with CP is mainly related to neural impairments caused by the brain lesion.