Myoelectric interface for neurorehabilitation conditioning to reduce abnormal leg co-activation after stroke: a pilot study

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Myoelectric interface for neurorehabilitation conditioning to reduce abnormal leg co-activation after stroke: a pilot study

• Abed Khorasani,
• Joel Hulsizer,
• Vivek Paul,
• Cynthia Gorski,
• Yasin Y. Dhaher &
• Marc W. Slutzky 

Journal of NeuroEngineering and Rehabilitation volume 21, Article number: 11 (2024) Cite this article

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Abstract

Background

The ability to walk is an important factor in quality of life after stroke. Co-activation of hip adductors and knee extensors has been shown to correlate with gait impairment. We have shown previously that training with a myoelectric interface for neurorehabilitation (MINT) can reduce abnormal muscle co-activation in the arms of stroke survivors.

Methods

Here, we extend MINT conditioning to stroke survivors with leg impairment. The aim of this pilot study was to assess the safety and feasibility of using MINT to reduce abnormal co-activation between hip adductors and knee extensors and assess any effects on gait. Nine stroke survivors with moderate to severe gait impairment received 6 h of MINT conditioning over six sessions, either in the laboratory or at home.

Results

MINT participants completed a mean of 159 repetitions per session without any adverse events. Further, participants learned to isolate their muscles effectively, resulting in a mean reduction of co-activation of 70% compared to baseline. Moreover, gait speed increased by a mean of 0.15 m/s, more than the minimum clinically important difference. Knee flexion angle increased substantially, and hip circumduction decreased.

Conclusion

MINT conditioning is safe, feasible at home, and enables reduction of co-activation in the leg. Further investigation of MINT’s potential to improve leg movement and function after stroke is warranted. Abnormal co-activation of hip adductors and knee extensors may contribute to impaired gait after stroke.

Trial registration This study was registered at ClinicalTrials.gov (NCT03401762, Registered 15 January 2018, https://clinicaltrials.gov/study/NCT03401762?tab=history&a=4).

Background

Impaired lower limb function following stroke results in impaired walking and an increased risk of falling [1]. While some stroke survivors achieve independent walking status, about a third continue to face challenges related to lower limb coordination, gait speed, walking endurance, and balance [2, 3]. Impaired movement after a stroke is often caused by a combination of weakness, spasticity, and abnormal muscle co-activation [4,5,6,7]. While many rehabilitation approaches have been developed to address weakness and spasticity, gait dysfunction can remain severe despite reduction of these components [8,9,10]. This suggests that abnormal muscle co-activation is a crucial contributor to gait dysfunction in many hemiparetic stroke survivors.

Stroke survivors often exhibit abnormal gait kinematics, including abnormal pelvic and leg joint motion in both the sagittal (decreased knee flexion) and frontal planes (hip hiking, circumduction) [11,12,13]. These abnormal kinematics are mechanically inefficient and energetically costly, which increases fatigue [14,15,16]. There is some evidence that hip hiking and circumduction are compensatory mechanisms to ensure toe clearance in people with stiff-knee gait [17, 18]. However, when external assistance to knee flexion was applied to hemiparetic legs using an orthosis, no changes in the expression of hip hiking and circumduction was observed [13]. Further, neurotypical participants whose knee flexion was artificially restricted with an orthosis did not show compensatory circumduction [19]. These findings suggest that the abnormal kinematics may be the result of compensating for an abnormal coupling between hip adduction and knee extension, instead of compensating for reduced knee flexion [12, 20]. An increase in knee extension and hip adduction at or near toe-off reduces the minimum distance between the toe and the ground, and between the foot and the contralateral leg, respectively, thus increasing the risk of tripping. To clear the ground and avoid hitting the opposite leg, patients may hip hike and circumduct [21]. While multiple abnormal coactivation patterns are seen after stroke [22,23,24,25], abnormal hip adduction/knee extension, especially at toe-off, was the dominant pattern [12]. Further, in a multiple regression model incorporating both classical impairments (decreased flexion of hip, knee, or ankle) and abnormal hip/knee coupling, abnormal hip adduction/knee extension most strongly correlated with hip hiking and most strongly predicted overground walking speed [22]. These studies were largely correlational. We have developed a system to reduce co-activation, called a myoelectric interface for neurorehabilitation (MINT), and shown that it effectively reduces co-activation between arm muscles trained [26, 27] and may improve arm function [28, 29].

Here, we tested the hypothesis that reducing abnormal hip adduction/knee extension co-activation in leg muscles through MINT conditioning could lead to improved walking function and joint biomechanics. We investigated this in nine stroke survivors in the lab and at home.

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