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Background: Slowed balance and mobility after stroke have been well-characterized. Yet the effects of unilateral cortical lesions on whole-body neuromechanical control is poorly understood, despite increased reliance on cortical resources for balance and mobility with aging. Objective. We tested whether individuals post stroke show impaired cortical responses evoked during reactive balance, and the effect of asymmetrical interlimb contributions to balance recovery and the evoked cortical response., Methods: Using electroencephalography, we assessed cortical N1 responses evoked over fronto-midline regions (Cz) during backward support-surface perturbations loading both legs and posterior-lateral directions that preferentially load the paretic or nonparetic leg in individuals' post-stroke and age-matched controls. We tested relationships between cortical responses and clinical balance/mobility function, as well as to center of pressure (CoP) rate of rise (RoR) during balance recovery., Results: Cortical N1 responses were smaller and delayed after stroke ( P  < .047), regardless of perturbation condition. In contrast to controls, slower cortical response latencies associated with lower clinical function in stroke (Mini Balance Evaluation Systems Test: r  = -.61, P  = .007; Timed-Up-and-Go: r  = .53, P  = .024; walking speed: r  = -.46, P  = .055). Paretic-loaded balance recovery revealed slower CoP RoR ( P  = .012) that was associated with delayed cortical response latencies ( r  = -.70, P  = .003); these relationships were not present during bilateral and nonparetic-loaded conditions, nor in the older adults control group., Conclusions: Individuals after stroke may be limited in their balance ability by the slowed speed of their cortical responses to destabilization. In particular, paretic leg loading may reveal cortical response impairments that reflect reduced paretic motor capacity., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Background and Purpose: Aerobic exercise can elicit positive effects on neuroplasticity and cognitive executive function but is poorly understood after stroke. We tested the effect of 4 weeks of aerobic exercise training on inhibitory and facilitatory elements of cognitive executive function and electroencephalography markers of cortical inhibition and facilitation. We investigated relationships between stimulus-evoked cortical responses, blood lactate levels during training, and aerobic fitness postintervention., Methods: Twelve individuals with chronic (>6 months) stroke completed an aerobic exercise intervention (40 minutes, 3×/wk). Electroencephalography and motor response times were assessed during congruent (response facilitation) and incongruent (response inhibition) stimuli of a Flanker task. Aerobic fitness capacity was assessed as o2peak during a treadmill test pre- and postintervention. Blood lactate was assessed acutely (<1 minute) after exercise each week. Cortical inhibition (N2) and facilitation (frontal P3) were quantified as peak amplitudes and latencies of stimulus-evoked electroencephalographic activity over the frontal cortical region., Results: Following exercise training, the response inhibition speed increased while response facilitation remained unchanged. A relationship between earlier cortical N2 response and faster response inhibition emerged postintervention. Individuals who produced higher lactate during exercise training achieved faster response inhibition and tended to show earlier cortical N2 responses postintervention. There were no associations between o2peak and metrics of behavioral or neurophysiologic function., Discussion and Conclusions: These preliminary findings provide novel evidence for selective benefits of aerobic exercise on inhibitory control during the initial 4-week period after initiation of exercise training and implicate a potential therapeutic effect of lactate on poststroke inhibitory control., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Academy of Neurologic Physical Therapy, APTA.)

Importance: For walking rehabilitation after stroke, training intensity and duration are critical dosing parameters that lack optimization., Objective: To assess the optimal training intensity (vigorous vs moderate) and minimum training duration (4, 8, or 12 weeks) needed to maximize immediate improvement in walking capacity in patients with chronic stroke., Design, Setting, and Participants: This multicenter randomized clinical trial using an intent-to-treat analysis was conducted from January 2019 to April 2022 at rehabilitation and exercise research laboratories. Survivors of a single stroke who were aged 40 to 80 years and had persistent walking limitations 6 months or more after the stroke were enrolled., Interventions: Participants were randomized 1:1 to high-intensity interval training (HIIT) or moderate-intensity aerobic training (MAT), each involving 45 minutes of walking practice 3 times per week for 12 weeks. The HIIT protocol used repeated 30-second bursts of walking at maximum safe speed, alternated with 30- to 60-second rest periods, targeting a mean aerobic intensity above 60% of the heart rate reserve (HRR). The MAT protocol used continuous walking with speed adjusted to maintain an initial target of 40% of the HRR, progressing up to 60% of the HRR as tolerated., Main Outcomes and Measures: The main outcome was 6-minute walk test distance. Outcomes were assessed by blinded raters after 4, 8, and 12 weeks of training., Results: Of 55 participants (mean [SD] age, 63 [10] years; 36 male [65.5%]), 27 were randomized to HIIT and 28 to MAT. The mean (SD) time since stroke was 2.5 (1.3) years, and mean (SD) 6-minute walk test distance at baseline was 239 (132) m. Participants attended 1675 of 1980 planned treatment visits (84.6%) and 197 of 220 planned testing visits (89.5%). No serious adverse events related to study procedures occurred. Groups had similar 6-minute walk test distance changes after 4 weeks (HIIT, 27 m [95% CI, 6-48 m]; MAT, 12 m [95% CI, -9 to 33 m]; mean difference, 15 m [95% CI, -13 to 42 m]; P = .28), but HIIT elicited greater gains after 8 weeks (58 m [95% CI, 39-76 m] vs 29 m [95% CI, 9-48 m]; mean difference, 29 m [95% CI, 5-54 m]; P = .02) and 12 weeks (71 m [95% CI, 49-94 m] vs 27 m [95% CI, 3-50 m]; mean difference, 44 m [95% CI, 14-74 m]; P = .005) of training; HIIT also showed greater improvements than MAT on some secondary measures of gait speed and fatigue., Conclusions and Relevance: These findings show proof of concept that vigorous training intensity is a critical dosing parameter for walking rehabilitation. In patients with chronic stroke, vigorous walking exercise produced significant and meaningful gains in walking capacity with only 4 weeks of training, but at least 12 weeks were needed to maximize immediate gains., Trial Registration: ClinicalTrials.gov Identifier: NCT03760016.

Background: The inability to flexibly modulate motor behavior with changes in task demand or environmental context is a pervasive feature of motor impairment and dysfunctional mobility after stroke. Objective: The purpose of this study was to test the reactive and modulatory capacity of lower-limb primary motor cortical (M1) networks using electroencephalography (EEG) measures of cortical activity evoked by transcranial magnetic stimulation (TMS) and to evaluate their associations with clinical and biomechanical measures of walking function in chronic stroke. Methods: TMS assessments of motor cortex excitability were performed during rest and active ipsilateral plantarflexion in chronic stroke and age-matched controls. TMS-evoked motor cortical network interactions were quantified with simultaneous EEG as the post-TMS (0-300 ms) beta (15-30 Hz) coherence between electrodes overlying M1 bilaterally. We compared TMS-evoked coherence between groups during rest and active conditions and tested associations with poststroke motor impairment, paretic propulsive gait deficits, and the presence of paretic leg motor evoked potentials (MEPs). Results: Stroke ( n = 14, 66 ± 9 years, F = 4) showed lower TMS-evoked cortical coherence and activity-dependent modulation compared to controls ( n = 9, 68 ± 6 years, F = 3). Blunted reactivity and atypical modulation of TMS-evoked coherence were associated with lower paretic ankle moments for propulsive force generation during walking and absent paretic MEPs. Conclusions: Impaired flexibility of motor cortical networks to react to TMS and modulate during motor activity is distinctly associated with paretic limb biomechanical walking impairment, and may provide useful insight into the neuromechanistic underpinnings of chronic post-stroke mobility deficits.

Background/Objective . We investigated interhemispheric interactions in stroke survivors by measuring transcranial magnetic stimulation (TMS)-evoked cortical coherence. We tested the effect of TMS on interhemispheric coherence during rest and active muscle contraction and compared coherence in stroke and older adults. We evaluated the relationships between interhemispheric coherence, paretic motor function, and the ipsilateral cortical silent period (iSP). Methods . Participants with (n = 19) and without (n = 14) chronic stroke either rested or maintained a contraction of the ipsilateral hand muscle during simultaneous recordings of evoked responses to TMS of the ipsilesional/nondominant (i/ndM1) and contralesional/dominant (c/dM1) primary motor cortex with EEG and in the hand muscle with EMG. We calculated pre- and post-TMS interhemispheric beta coherence (15-30 Hz) between motor areas in both conditions and the iSP duration during the active condition. Results . During active i/ndM1 TMS, interhemispheric coherence increased immediately following TMS in controls but not in stroke. Coherence during active cM1 TMS was greater than iM1 TMS in the stroke group. Coherence during active iM1 TMS was less in stroke participants and was negatively associated with measures of paretic arm motor function. Paretic iSP was longer compared with controls and negatively associated with clinical measures of manual dexterity. There was no relationship between coherence and. iSP for either group. No within- or between-group differences in coherence were observed at rest. Conclusions . TMS-evoked cortical coherence during hand muscle activation can index interhemispheric interactions associated with poststroke motor function and potentially offer new insights into neural mechanisms influencing functional recovery.

Background: Paired associative stimulation (PAS) combining repeated pairing of electrical stimulation of a peripheral nerve with transcranial magnetic stimulation (TMS) over the primary motor cortex (M1) can induce neuroplastic adaptations in the human brain and enhance motor learning in neurologically-intact individuals. However, the extent to which PAS is an effective technique for inducing associative plasticity and improving motor function in individuals post-stroke is unclear., Objective: The objective of this pilot study was to investigate the effects of a single session of PAS to modulate corticomotor excitability and motor skill performance in individuals post-stroke., Methods: Seven individuals with chronic stroke completed two separate visits separated by at least one week. We assessed general corticomotor excitability, intracortical network activity and behavioral outcomes prior to and at three time points following PAS and compared these outcomes to those following a sham PAS condition (PASSHAM)., Results: Following PAS, we found increased general corticomotor excitability but no significant difference in behavioral measures between PAS conditions. There was a relationship between PAS-induced corticomotor excitability increase and enhanced motor skill performance across post-PAS testing time points., Conclusion: These results provide preliminary evidence for the potential of PAS to increase corticomotor excitability that could favorably impact motor skill performance in chronic individuals post-stroke and are an important first step for future studies investigating the clinical application and behavioral relevance of PAS interventions in post stroke patient populations.

Background: Abnormal brain excitability influences recovery after stroke at which time a prolonged transcranial magnetic stimulation (TMS)-induced electromyographic silent period is thought to reflect abnormal inhibitory interneuron excitability. Cortical excitability can be probed directly during the silent period using concurrent electroencephalography (EEG) of TMS-evoked responses., Objective: The primary study objectives were to characterize TMS-evoked cortical potentials (TEPs) using EEG and to investigate associations with persistent hand and arm motor dysfunction in individuals with chronic stroke., Methods: Thirteen participants with chronic stroke-related mild-moderate arm motor impairment and 12 matched controls completed a single TMS-EEG cortical excitability assessment. TEPs recorded from the vertex during cortical silent period (CSP) assessment and while at rest were used to evaluate differences in cortical excitability between stroke and control participants. Associations between TEPs and CSP duration with measures of upper extremity motor behavior were investigated., Results: Significantly increased TEP component peak amplitudes and delayed latencies were observed for stroke participants compared with controls during CSP assessment and while at rest. Delayed early TEP component (P30) peak latencies during CSP assessment were associated with less manual dexterity. CSP duration was prolonged in stroke participants, and correlated with P30 peak latency and paretic arm dysfunction., Conclusions: Abnormal cortical excitability directly measured by early TMS-evoked EEG responses during CSP assessment suggests abnormal cortical inhibition is associated with hand dysfunction in chronic stroke. Further investigation of abnormal cortical inhibition in specific brain networks is necessary to characterize the salient neurophysiologic mechanisms contributing to persistent motor dysfunction after stroke.

Imbalance of corticomotor excitability between the paretic and nonparetic limbs has been associated with the extent of upper extremity motor recovery poststroke, is greatly influenced by specific testing conditions such as the presence or absence of volitional muscle activation, and may vary across muscle groups. However, despite its clinical importance, poststroke corticomotor drive to lower extremity muscles has not been thoroughly investigated. Additionally, whereas conventional gait rehabilitation strategies for stroke survivors focus on paretic limb foot drop and dorsiflexion impairments, most contemporary literature has indicated that paretic limb propulsion and plantarflexion impairments are the most significant limiters to poststroke walking function. The purpose of this study was to compare corticomotor excitability of the dorsi- and plantarflexor muscles during resting and active conditions in individuals with good and poor poststroke walking recovery and in neurologically intact controls. We found that plantarflexor muscles showed reduced corticomotor symmetry between paretic and nonparetic limbs compared with dorsiflexor muscles in individuals with poor poststroke walking recovery during active muscle contraction but not during rest. Reduced plantarflexor corticomotor symmetry during active muscle contraction was a result of reduced corticomotor drive to the paretic muscles and enhanced corticomotor drive to the nonparetic muscles compared with the neurologically intact controls. These results demonstrate that atypical corticomotor drive exists in both the paretic and nonparetic lower limbs and implicate greater severity of corticomotor impairments to plantarflexor vs. dorsiflexor muscles during muscle activation in stroke survivors with poor walking recovery. NEW & NOTEWORTHY The present study observed that lower-limb corticomotor asymmetry resulted from both reduced paretic and enhanced nonparetic limb corticomotor excitability compared with neurologically intact controls. The most asymmetrical corticomotor drive was observed in the plantarflexor muscles of individuals with poor poststroke walking recovery. This suggests that neural function of dorsi- and plantarflexor muscles in both paretic and nonparetic limbs may play a role in poststroke walking function, which may have important implications when developing targeted poststroke rehabilitation programs to improve walking ability., (Copyright © 2017 the American Physiological Society.)

Background: Recent rehabilitation efforts after stroke often focus on increasing walking speed because it is associated with quality of life. For individuals poststroke, propulsive force generated from the paretic limb has been shown to be correlated to walking speed. However, little is known about the relative contribution of the paretic versus the nonparetic propulsive forces to changes in walking speed., Objective: The primary purpose of this study was to determine the contribution of propulsive force generated from each limb to changes in walking speed during speed modulation within a session and as a result of a 12-week training program., Methods: Gait analysis was performed as participants (N = 38) with chronic poststroke hemiparesis walked at their self-selected and faster walking speeds on a treadmill before and after a 12-week gait retraining program., Results: Prior to training, stroke survivors increased nonparetic propulsive forces as the primary mechanism to change walking speed during speed modulation within a session. Following gait training, the paretic limb played a larger role during speed modulation within a session. In addition, the increases in paretic propulsive forces observed following gait training contributed to the increases in the self-selected walking speeds seen following training., Conclusions: Gait retraining in the chronic phase of stroke recovery facilitates paretic limb neuromotor recovery and reduces the reliance on the nonparetic limb's generation of propulsive force to increase walking speed. These findings support gait rehabilitation efforts directed toward improving the paretic limb's ability to generate propulsive force., (© The Author(s) 2015.)

Objective: A deficit in paretic limb propulsion has been identified as a major biomechanical factor limiting walking speed after stroke. The purpose of this study was to determine the influence of corticomotor symmetry between paretic and nonparetic plantarflexors on the propulsive strategy used to increase walking speed., Methods: Twenty-three participants with post-stroke hemiparesis underwent transcranial magnetic stimulation and biomechanical testing at their self-selected and fastest walking speeds. Plantarflexor corticomotor symmetry (CS(PF)) was calculated as a ratio of the average paretic versus nonparetic soleus motor evoked potential amplitude. The ratio of the paretic and nonparetic peak ankle plantarflexion moments (PF(sym)) was calculated at each speed., Results: CS(PF) predicted the ΔPF(sym) from self-selected and fastest speeds (R(2)=.629, F(1,21)=35.56, p<.001). An interaction between CS(PF) and ΔPF(sym) (β=.596, p=.04) was observed when predicting Δspeed ((adj)R(2)=.772, F(3,19)=20.48, p<.001). Specifically, the ΔPF(sym) with speed modulation was positively related to the Δspeed (p=.03) in those with greater CS(PF), but was not related in those with poor CS(PF) (p=.30)., Conclusions: Symmetry of the corticomotor input to the plantarflexors influences the propulsive strategy used to increase post-stroke walking speed., Significance: Rehabilitation strategies that promote corticomotor symmetry may positively influence gait mechanics and enhance post-stroke walking function., (Copyright © 2015 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.)

Objective: The role of cortical drive in stroke recovery for the lower extremity remains ambiguous. The purpose of this study was to investigate the relationship between cortical drive and gait speed in a group of stroke survivors., Methods: Eighteen individuals with stroke were dichotomized into fast or slow walking groups. Transcranial magnetic stimulation (TMS) was used to collect motor evoked potentials (MEPs) from the tibialis anterior of each lower extremity during rest, paretic muscle contractions, and nonparetic muscle contractions. An asymmetry-index (AI) was calculated using motor thresholds and compared between groups. The average MEP of the paretic leg during TMS at maximal intensity (MEP100) for each condition was compared within and between groups., Results: A significant positive correlation was found between AI and walking speed. Slow-walkers had greater MEP100s during the nonparetic contraction than during the paretic contraction or rest conditions. In contrast, fast-walkers had greatest MEP100s during the paretic contraction., Conclusions: Alterations in the balance of corticomotor excitability occur in the lower extremity of individuals with poor motor recovery post-stroke. This atypical cortical drive is dependent on activation of the unaffected hemisphere and contraction of the nonparetic leg., Significance: Understanding mechanisms underlying motor function can help to identify specific patient deficits that impair function., (Copyright © 2015 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.)

Information regarding how motor units are controlled to produce forces in individuals with stroke and the mechanisms behind muscle weakness and movement slowness can potentially inform rehabilitation strategies. The purpose of this study was to describe the rate coding mechanism in individuals poststroke during both constant (n = 8) and rapid (n = 4) force production tasks. Isometric ankle dorsiflexion force, motor unit action potentials, and surface electromyography were recorded from the paretic and nonparetic tibialis anterior. In the paretic limb, strength was 38% less and the rate of force development was 63% slower. Linear regression was used to describe and compare the relationships between motor unit and electromyogram (EMG) measures and force. During constant force contractions up to 80% maximal voluntary contraction (MVC), rate coding was compressed and discharge rates were lower in the paretic limb. During rapid muscle contractions up to 90% MVC, the first interspike interval was prolonged and the rate of EMG rise was less in the paretic limb. Future rehabilitation strategies for individuals with stroke could focus on regaining these specific aspects of motor unit rate coding and neuromuscular activation.