27 research outputs found

    Impaired limb shortening following stroke: what's in a name?

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    BackgroundDifficulty advancing the paretic limb during the swing phase of gait is a prominent manifestation of walking dysfunction following stroke. This clinically observable sign, frequently referred to as 'foot drop', ostensibly results from dorsiflexor weakness.ObjectiveHere we investigated the extent to which hip, knee, and ankle motions contribute to impaired paretic limb advancement. We hypothesized that neither: 1) minimal toe clearance and maximal limb shortening during swing nor, 2) the pattern of multiple joint contributions to toe clearance and limb shortening would differ between post-stroke and non-disabled control groups.MethodsWe studied 16 individuals post-stroke during overground walking at self-selected speed and nine non-disabled controls who walked at matched speeds using 3D motion analysis.ResultsNo differences were detected with respect to the ankle dorsiflexion contribution to toe clearance post-stroke. Rather, hip flexion had a greater relative influence, while the knee flexion influence on producing toe clearance was reduced.ConclusionsSimilarity in the ankle dorsiflexion, but differences in the hip and knee, contributions to toe clearance between groups argues strongly against dorsiflexion dysfunction as the fundamental impairment of limb advancement post-stroke. Marked reversal in the roles of hip and knee flexion indicates disruption of inter-joint coordination, which most likely results from impairment of the dynamic contribution to knee flexion by the gastrocnemius muscle in preparation for swing. These findings suggest the need to reconsider the notion of foot drop in persons post-stroke. Redirecting the focus of rehabilitation and restoration of hemiparetic walking dysfunction appropriately, towards contributory neuromechanical impairments, will improve outcomes and reduce disability

    Impaired Limb Shortening following Stroke: What's in a Name?

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    Abstract Background: Difficulty advancing the paretic limb during the swing phase of gait is a prominent manifestation of walking dysfunction following stroke. This clinically observable sign, frequently referred to as 'foot drop', ostensibly results from dorsiflexor weakness

    Evidence for shared neural information between muscle synergies and corticospinal efficacy.

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    Stroke survivors often exhibit gait dysfunction which compromises self-efficacy and quality of life. Muscle Synergy Analysis (MSA), derived from electromyography (EMG), has been argued as a method to quantify the complexity of descending motor commands and serve as a direct correlate of neural function. However, controversy remains regarding this interpretation, specifically attribution of MSA as a neuromarker. Here we sought to determine the relationship between MSA and accepted neurophysiological parameters of motor efficacy in healthy controls, high (HFH), and low (LFH) functioning stroke survivors. Surface EMG was collected from twenty-four participants while walking at their self-selected speed. Concurrently, transcranial magnetic stimulation (TMS) was administered, during walking, to elicit motor evoked potentials (MEPs) in the plantarflexor muscles during the pre-swing phase of gait. MSA was able to differentiate control and LFH individuals. Conversely, motor neurophysiological parameters, including soleus MEP area, revealed that MEP latency differentiated control and HFH individuals. Significant correlations were revealed between MSA and motor neurophysiological parameters adding evidence to our understanding of MSA as a correlate of neural function and highlighting the utility of combining MSA with other relevant outcomes to aid interpretation of this analysis technique

    Gait events and hip-floor height.

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    <p>(a) Toe clearance served as our indicator of limb clearance. We used the trajectory of the distal toe marker to quantify toe position. Minimal toe clearance (TC<sub>min</sub>) was defined as the lowest vertical position of the trajectory of the toe marker during swing. Normalized limb length was calculated as the instantaneous hip-toe distance (HT<sub>distance</sub>) divided by the instantaneous vertical distance from the hip joint center to the floor (HF<sub>distance</sub>). <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0110140#pone.0110140-Moosabhoy1" target="_blank">[30]</a> Limb shortening was quantified as the percent reduction in normalized limb length relative to the instantaneous height of the hip joint center. Maximal limb shortening (LS<sub>max</sub>) was defined as the highest percent reduction in normalized limb length during swing. (b) The vertical trajectory of the great toe marker, time normalized to the gait cycle. (c) Normalized limb length quantified as the hip-toe distance divided by the hip-floor distance. Values less than 1 indicate limb shortening. (d) Ipsilateral and (e) contralateral normalized hip-floor height quantified as the hip-floor height divided by the participant’s height. Controls are depicted in solid black, with participants post-stroke depicted with dashed lines in all panels. Vertical cursor lines represent: minimal toe clearance (b) and maximal limb shortening (c) for each group. Grey shaded regions (d and e) represent the range (across groups) of timing for minimal toe clearance (1<sup>st</sup>) and maximal limb shortening (2<sup>nd</sup>).</p

    Relative contributions to limb shortening.

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    <p>Cohen’s effect size for factorial ANOVA.</p>†<p>significant statistical interaction (group × joint) and the location of effect revealed upon post-hoc testing.</p><p>LS: limb shortening.</p><p>LS<sub>max</sub>: maximal limb shortening.</p><p>Data are mean (sd). Control values reflect the limb against which the stroke limb was tested (i.e., the right limb was designated for comparison against the paretic limb). Note paretic knee flexion and its contribution to limb shortening are limited post-stroke. Nonparetic hip flexion is exaggerated post-stroke.</p><p>Relative contributions to limb shortening.</p
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