Background: Stroke survivors experience chronic gait impairments, so rehabilitation has focused on restoring ambulatory capacity. High-intensity speed-based treadmill training (HISTT) is one form of walking rehabilitation that can improve walking, but its effectiveness has not been thoroughly investigated. Additionally, cortical priming with transcranial direct current stimulation (tDCS) and movement may enhance HISTT-induced improvements in walking, but there have been no systematic investigations. The objective of this study was to determine if motor priming can augment the effects of HISTT on walking in chronic stroke survivors. Methods: Eighty-one chronic stroke survivors participated in a controlled trial with stratification into four groups: 1) control-15 min of rest (n = 20), 2) tDCS-15 min of stimulation-based priming with transcranial direct current stimulation (n = 21), 3) ankle motor tracking (AMT)-15 min of movement-based priming with targeted movements of the ankle and sham tDCS (n = 20), and 4) tDCS+AMT-15 min of concurrent tDCS and AMT (n = 20). Participants performed 12 sessions of HISTT (40 min/day, 3 days/week, 4 weeks). Primary outcome measure was walking speed. Secondary outcome measures included corticomotor excitability (CME). Outcomes were measured at pre, post, and 3-month follow-up assessments. Results: HISTT improved walking speed for all groups, which was partially maintained 3 months after training. No significant difference in walking speed was seen between groups. The tDCS+AMT group demonstrated greater changes in CME than other groups. Individuals who demonstrated up-regulation of CME after tDCS increased walking speed more than down-regulators. Conclusions: Our results support the effectiveness of HISTT to improve walking; however, motor priming did not lead to additional improvements. Upregulation of CME in the tDCS+AMT group supports a potential role for priming in enhancing neural plasticity. Greater changes in walking were seen in tDCS up-regulators, suggesting that responsiveness to tDCS might play an important role in determining the capacity to respond to priming and HISTT. Trial registration: ClinicalTrials.gov, NCT03492229. Registered 10 April 2018retrospectively registered, https:// clinicaltrials.gov/ct2/show/NCT03492229.
Background-Walking speed is used to assess functional status, predict recovery, prescribe exercise, and track functional progress after stroke. Determining concurrent validity ensures that results from different tests of walking speed can be compared or used interchangeably. The GAITRite electronic walkway and the 10-meter walk test (10MWT) are popular measurement tools of walking speed in the laboratory and in clinical settings, respectively.Research Question-Do walking speeds in chronic stroke survivors measured with the 10meter walk test and GAITRite electronic walkway demonstrate concurrent validity? Methods-77 participants with chronic stroke performed four trials of 10MWT and four trials of GAITRite-two trials at comfortable walking speed and two trials at maximal walking speed. Intraclass correlations [ICC (3,1), absolute agreement] and Bland-Altman plots were used to assess the relationship between gait speed from these two measures.Results-Walking speed showed poor to good absolute agreement between 10MWT and GAITRite for comfortable walking speed [ICC: 0.77 (95% CI: 0.46, 0.89; P<0.001)] and excellent absolute agreement for maximal walking speed [ICC: 0.94 (95% CI: 0.91, 0.96; P<0.001)]. Mean difference value (systematic bias) was different from 0 for comfortable walking [10MWT was faster; P<0.001 (95% CI: 0.05, 0.10)] but not for maximal walking [P=0.16 (95% CI: −0.01, 0.04)]. Limits of agreement were broad (comfortable walking speed, 0.43; maximal walking speed, 0.37), and there was proportional bias at both speeds whereby participants who walked faster tended to have a faster walking speed during 10MWT vs. GAITRite (comfortable walking speed, R 2 =0.22, P<0.001; maximal walking speed, R 2 =0.08, P=0.01).Significance-Systematic bias, proportional bias, and broad limits of agreement suggest that caution should be used when comparing walking speeds from 10MWT and GAITRite. It may not be appropriate to use them interchangeably. Conducting 10MWT and GAITRite tests at maximal walking speeds may allow more accurate comparisons between measures.
Stroke-related damage to the crossed lateral corticospinal tract causes motor deficits in the contralateral (paretic) limb. To restore functional movement in the paretic limb, the nervous system may increase its reliance on ipsilaterally descending motor pathways, including the uncrossed lateral corticospinal tract, the reticulospinal tract, the rubrospinal tract, and the vestibulospinal tract. Our knowledge about the role of these pathways for upper limb motor recovery is incomplete, and even less is known about the role of these pathways for lower limb motor recovery. Understanding the role of ipsilateral motor pathways to paretic lower limb movement and recovery after stroke may help improve our rehabilitative efforts and provide alternate solutions to address stroke-related impairments. These advances are important because walking and mobility impairments are major contributors to long-term disability after stroke, and improving walking is a high priority for individuals with stroke. This perspective highlights evidence regarding the contributions of ipsilateral motor pathways from the contralesional hemisphere and spinal interneuronal pathways for paretic lower limb movement and recovery. This perspective also identifies opportunities for future research to expand our knowledge about ipsilateral motor pathways and provides insights into how this information may be used to guide rehabilitation.
Objective: To understand whether lower limb asymmetry in chronic stroke is related to paretic motor impairment or impaired interlimb coordination. Methods: Stroke and control participants performed conventional, unilateral, and bilateral uncoupled pedaling. During uncoupled pedaling, the pedals were mechanically disconnected. Paretic mechanical work was measured during conventional pedaling. Pedaling velocity and muscle activity were compared across conditions and groups. Relative limb phasing was examined during uncoupled pedaling. Results: During conventional pedaling, EMG and mechanical work were lower in the paretic than the non-paretic limb (asymmetry). During unilateral pedaling with the paretic limb, muscle activity was larger, but velocity was slower and more variable than during conventional pedaling (evidence of paretic motor impairment). During uncoupled pedaling, muscle activity increased further, but velocity was slower and more variable than in other conditions (evidence of impaired interlimb coordination). Relative limb phasing was impaired in stroke participants. Regression analysis suggested that interlimb coordination may be a stronger predictor of asymmetry than paretic motor impairment. Conclusions: Paretic motor impairment and impaired interlimb coordination may contribute to asymmetry during pedaling after stroke. Significance: Rehabilitation that addresses paretic motor impairment and impaired interlimb coordination may improve symmetry and maximize improvement.
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