Abstract
Walking after stroke is often described as requiring excessive muscle co-contraction, yet, evidence that co-contraction is a ubiquitous motor control strategy for this population remains inconclusive. Co-contraction, the simultaneous activation of agonist and antagonist muscles, can be assessed with electromyography (EMG) but is often described qualitatively. Here, our goal is to determine if co-contraction is associated with gait impairments following stroke. Fifteen individuals with chronic stroke and nine healthy controls walked on an instrumented treadmill at self-selected speed. Surface EMGs were collected from the medial gastrocnemius (MG), soleus (SOL), and tibialis anterior (TA) of each leg. EMG envelope amplitudes were assessed in three ways: (1) no normalization, (2) normalization to the maximum value across the gait cycle, or (3) normalization to maximal M-wave. Three co-contraction indices were calculated across each agonist/antagonist muscle pair (MG/TA and SOL/TA) to assess the effect of using various metrics to quantify co-contraction. Two factor ANOVAs were used to compare effects of group and normalization for each metric. Co-contraction during the terminal stance (TSt) phase of gait is not different between healthy controls and the paretic leg of individuals post-stroke, regardless of the metric used to quantify co-contraction. Interestingly, co-contraction was similar between M-max and non-normalized EMG; however, normalization does not impact the ability to resolve group differences. While a modest correlation is revealed between the amount of TSt co-contraction and walking speed, the relationship is not sufficiently strong to motivate further exploration of a causal link between co-contraction and walking function after stroke. Co-contraction does not appear to be a common strategy employed by individuals after stroke. We recommend exploration of alternative EMG analysis approaches in an effort to learn more about the causal mechanisms of gait impairment following stroke.
Highlights
After a stroke, most individuals experience lifelong walking impairments, including forward propulsion deficits, which contribute to metabolically inefficient gait [1,2,3,4]
Differences between healthy and stroke subjects are most relevant in terminal stance (TSt), where peak plantarflexor EMG tends to occur
TSt is the gait phase when plantarflexor EMG contributes to A2—the most robust measure of gait function employed in this study
Summary
Most individuals experience lifelong walking impairments, including forward propulsion deficits, which contribute to metabolically inefficient gait [1,2,3,4]. Especially excessive co-contraction, are commonly argued to be a major contributing factor to these walking impairments [5,6,7]. Co-contraction refers to simultaneous activity in agonist and. Co-Contraction after Stroke antagonist muscles across the same joint [6, 8]. This phenomenon is sometimes called agonist/antagonist co-activation or co-activation. Co-activation can refer to simultaneous activity in synergist muscles. We will use the term co-contraction and address the relationship between agonist and antagonist muscle co-activity
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