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Many people with neurological conditions experience challenges with movement. Although rehabilitation is often provided acutely and sub-acutely following the onset of a condition, motor deficits commonly persist in the long-term and are exacerbated by disuse and inactivity. Notably, motor rehabilitation approaches that incorporate exercise and physical activity can support gains in motor function even in the chronic stages of many neurological conditions. However, delivering motor rehabilitation on a long-term basis to people with chronic neurological conditions is a challenge within health care systems, and the onus is often placed on patients to find and pay for services. While neurological motor rehabilitation is largely the domain of physical and occupational therapists, kinesiologists may be able to complement existing care and support delivery of long-term neurological motor rehabilitation, specifically through provision of supported exercise and physical activity programs. In this perspective style review article, we discuss potential contributions of kinesiologists to advancing the field through exercise programming, focusing on community-based interventions that increase physical activity levels. We conclude with recommendations on how kinesiologists’ role might be further optimized towards improving long-term outcomes for people with chronic neurological conditions, considering issues related to professional regulation and models of care.

Acute cycling exercise can modulate motor cortical circuitry in the non-exercised upper-limb. Within the primary motor cortex, measures of intracortical inhibition are reduced and intracortical facilitation is enhanced following acute exercise. Further, acute cycling exercise decreases interhemispheric inhibition between the motor cortices and lowers cerebellar-to-motor cortex inhibition. Yet, investigations into the effects of acute exercise on sensorimotor integration, referring to the transfer of incoming afferent information from the primary somatosensory cortex to motor cortex, are lacking. The current work addresses this gap in knowledge with two experimental sessions. In the first session, we tested the exercise-induced changes in somatosensory and motor excitability by assessing somatosensory (SEP) and motor evoked potentials (MEPs). In the second session, we explored the effects of acute cycling exercise on short- (SAI) and long-latency afferent inhibition (LAI), and afferent facilitation. In both experimental sessions, neurophysiological measures were obtained from the non-exercised upper-limb muscle, tested at two time points pre-exercise separated by a 25-min period of rest. Next, a 25-min bout of moderate-intensity lower-limb cycling was performed with measures assessed at two time points post-exercise. Acute lower-limb cycling increased LAI, without modulation of SAI or afferent facilitation. Further, there were no exercise-induced changes to SEP or MEP amplitudes. Together, these results suggest that acute exercise has unique effects on sensorimotor integration, which are not accompanied by concurrent changes in somatosensory or motor cortical excitability.

Context Sport-related concussion (SRC) often presents with multidimensional and subtle neurologic deficits that are difficult to detect with standard clinical tests. New assessment approaches that efficiently quantify deficits across multiple neurologic domains are needed. Objective To quantify impairments in postural movements during an assessment of rapid, bimanual motor ability in athletes within 10 days of experiencing an SRC and evaluate relationships between impairments in upper extremity and postural performance. Design Cohort study. Setting Sports medicine clinic. Patients or Other Participants Initial baseline assessments were completed for 711 athletes. Seventy-five athletes (age = 15.8 ± 3.3 years at baseline) sustained SRCs and were reassessed within 10 days. Seventy-eight athletes (age = 15.5 ± 2.0 years) completed 2 assessments in a healthy state. Main Outcome Measure(s) Athletes stood on force plates and performed a rapid, bimanual motor task, termed the object-hit task, delivered using a Kinesiological Instrument for Normal and Altered Reaching Movements endpoint robot. Measures of postural stability that quantified center-of-pressure movements and measures of upper extremity performance were used to characterize task performance. Results Performance changes across assessments were converted to reliable change indices. We observed a difference in reliable change indices values between athletes with SRC and healthy control athletes on the combined postural measures (P = .01). Using measures to evaluate the change in postural movements from the early, easier portion of the task to the later, more difficult portion, we identified the highest levels of impairment (19%–25% of the sample impaired). We also noted a difference between individuals with concussion and healthy individuals on the combined upper extremity measures (P = .003), but these impairments were largely unrelated to those identified in the postural movements. Conclusions Measurement of postural movements during the object-hit task revealed impairments in postural stability that were not related to impairments in upper extremity performance. The findings demonstrated the benefits of using assessments that simultaneously evaluate multiple domains of neurologic function (eg, upper extremity and postural control) after SRC.

Continuous theta burst stimulation (cTBS) is a form of noninvasive repetitive brain stimulation that, when delivered over the contralesional hemisphere, can influence the excitability of the ipsilesional hemisphere in individuals with stroke. cTBS applied prior to skilled motor practice interventions may augment motor learning; however, there is a high degree of variability in individual response to this intervention. The main objective of the present study was to assess white matter biomarkers of response to cTBS paired with skilled motor practice in individuals with chronic stroke. We tested the effects of stimulation of the contralesional hemisphere at the site of the primary motor cortex (M1c) or primary somatosensory cortex (S1c) and a third group who received sham stimulation. Within each stimulation group, individuals were categorized into responders or nonresponders based on their capacity for motor skill change. Baseline diffusion tensor imaging (DTI) indexed the underlying white matter microstructure of a previously known motor learning network, named the constrained motor connectome (CMC), as well as the corticospinal tract (CST) of lesioned and nonlesioned hemispheres. Across practice, there were no differential group effects. However, when categorized as responders vs. nonresponders using change in motor behaviour, we demonstrated a significant difference in CMC microstructural properties (as measured by fractional anisotropy (FA)) for individuals in M1c and S1c groups. There were no significant differences between responders and nonresponders in clinical baseline measures or microstructural properties (FA) in the CST. The present study identifies a white matter biomarker, which extends beyond the CST, advancing our understanding of the importance of white matter networks for motor after stroke.

Background. Severity of arm impairment alone does not explain motor outcomes in people with severe impairment post stroke.Objective. Define the contribution of brain biomarkers to upper limb motor outcomes in people with severe arm impairment post stroke.Methods. Paretic arm impairment (Fugl-Meyer upper limb, FM-UL) and function (Wolf Motor Function Test rate, WMFT-rate) were measured in 15 individuals with severe (FM-UL ≤ 30/66) and 14 with mild–moderate (FM-UL > 40/66) impairment. Transcranial magnetic stimulation and diffusion weight imaging indexed structure and function of the corticospinal tract and corpus callosum. Separate models of the relationship between possible biomarkers and motor outcomes at a single chronic (≥6 months) time point post stroke were performed.Results. Age (ΔR20.365,p=0.017) and ipsilesional-transcallosal inhibition (ΔR20.182,p=0.048) explained a 54.7% (p=0.009) variance in paretic WMFT-rate. Prefrontal corpus callous fractional anisotropy (PF-CC FA) alone explained 49.3% (p=0.007) variance in FM-UL outcome. The same models did not explain significant variance in mild–moderate stroke. In the severe group, k-means cluster analysis of PF-CC FA distinguished two subgroups, separated by a clinically meaningful and significant difference in motor impairment (p=0.049) and function (p=0.006) outcomes.Conclusion. Corpus callosum function and structure were identified as possible biomarkers of motor outcome in people with chronic and severe arm impairment.

Background. Conventionally, change in motor performance is quantified with discrete measures of behavior taken pre- and postpractice. As a high degree of movement variability exists in motor performance after stroke, pre- and posttesting of motor skill may lack sensitivity to predict potential for motor recovery. Objective. Evaluate the use of predictive models of motor learning based on individual performance curves and clinical characteristics of motor function in individuals with stroke. Methods. Ten healthy and fourteen individuals with chronic stroke performed a continuous joystick-based tracking task over 6 days, and at a 24-hour delayed retention test, to assess implicit motor sequence learning. Results. Individuals with chronic stroke demonstrated significantly slower rates of improvements in implicit sequence-specific motor performance compared with a healthy control (HC) group when root mean squared error performance data were fit to an exponential function. The HC group showed a positive relationship between a faster rate of change in implicit sequence-specific motor performance during practice and superior performance at the delayed retention test. The same relationship was shown for individuals with stroke only after accounting for overall motor function by including Wolf Motor Function Test rate in our model. Conclusion. Nonlinear information extracted from multiple time points across practice, specifically the rate of motor skill acquisition during practice, relates strongly with changes in motor behavior at the retention test following practice and could be used to predict optimal doses of practice on an individual basis.

When aerobic exercise is performed following skilled motor practice, it can enhance motor memory consolidation. Previous studies have suggested that dopamine may play a role in motor memory consolidation, but whether it is involved in the exercise effects on consolidation is unknown. Hence, we aimed to investigate the influence of dopaminergic pathways on the exercise-induced modulation of motor memory consolidation. We compared the effect of acute exercise on motor memory consolidation between the genotypes that are known to affect dopaminergic transmission and learning. By combining cluster analyses and fitting linear models with and without included polymorphisms, we provide preliminary evidence that exercise benefits the carriers of alleles that are associated with low synaptic dopamine content. In line with previous reports, our findings implicate dopamine as a modulator of the exercise-induced effects on motor memory consolidation, and suggest exercise as a potential clinical tool to counteract low endogenous dopamine bioavailability. Further experiments are needed to establish causal relations.

Introduction An important problem in the field of sport-related concussion is the lack of a ‘gold-standard’ clinical assessment tool. Currently, the diagnosis relies heavily on self-reporting of symptoms and observation of clinical signs by medical professionals. To address this, our group has been motivated to develop objective measures of neurological impairment following concussion. Spatial working memory is an important aspect of cognitive function that might be impaired following concussion. In the present study, we measured spatial working memory using a robotic spatial span task. We first assessed test–retest reliability in 82 healthy athletes who underwent baseline testing across two athletic seasons using intraclass correlation coefficients. We then assessed spatial span performance relative to baseline in 47 athletes acutely following sport-related concussion using a reliable change index with 80% confidence limits to define impairment on an individual basis. Results We found good test–retest reliability for the mean span (a measure of spatial working memory span length; intraclass correlation coefficient = 0.79), and moderate reliability for the response duration (time taken per spatial target; intraclass correlation coefficient = 0.64) in healthy athletes. However, only 19% of acutely concussed athletes showed evidence of impairment relative to baseline in mean span, and even fewer (9%) showed evidence of impairment in response duration. Analysis of serial position curves revealed primacy and recency effects for this task, but no group-level differences between concussed and healthy athletes. Analysis of specific types of errors showed a higher rate of substitution errors in the concussed group at baseline, suggesting possible malingering in a small number of athletes. Conclusion Overall, few athletes showed evidence of impaired spatial working memory acutely following concussion, suggesting either that spatial working memory is not commonly impaired acutely post-concussion, or that the present task is not sufficiently demanding.

There is a need for better tools to objectively, reliably, and precisely assess neurological function after sport-related concussion (SRC). The aim of this study was to use a robotic device (Kinesiological Instrument for Normal and Altered Reaching Movements; KINARM) to quantify neurological impairments in athletes acutely and when clinically asymptomatic post-SRC. Robotic assessments included five KINARM standard tasks that evaluate aspects of motor, sensory, and cognitive function. We hypothesized that acutely concussed athletes would demonstrate significant rates of impairment on the robotic assessment, and that impairments would be associated with acute symptom severity. Pre-season assessments were conducted from 2011 to 2016 on 1051 athletes. Eighty-four athletes were reassessed acutely (≤10 days post-injury) and while symptomatic post-SRC and 89 when clinically asymptomatic. Forty-four parameters were measured from the KINARM assessment to characterize neurological function. Reliable change indices (80% confidence interval) identified impairments in healthy and concussed individuals for each parameter. In concussed individuals, impairment rate varied across parameters from 4% to 27% at the acute time point and from 2% to 18% when clinically asymptomatic. Healthy athlete impairment rates were between 2% and 16% across all testing time points. We identified relationships between acute symptom severity and task performance for only two parameters, both of which evaluated attributes of motor function. Overall, the KINARM identified impairments in motor, sensory, and cognitive function in athletes with SRC; however, impairment rates were low and largely did not relate to symptom severity. More complex tasks may be necessary to identify potentially subtle neurological impairments post-SRC.

In individuals with multiple sclerosis (MS), transcranial magnetic stimulation (TMS) may be employed to assess the integrity of corticospinal system and provides a potential surrogate biomarker of disability. The purpose of this study was to provide a comprehensive examination of the relationship between multiple measures corticospinal excitability and clinical disability in MS (expanded disability status scale (EDSS)). Bilateral corticospinal excitability was assessed using motor evoked potential (MEP) input–output (IO) curves, cortical silent period (CSP), short-interval intracortical inhibition (SICI), intracortical facilitation (ICF) and transcallosal inhibition (TCI) in 26 individuals with MS and 11 healthy controls. Measures of corticospinal excitability were compared between individuals with MS and controls. We evaluated the relationship(s) between age and clinical demographics such as age at MS onset (AO), disease duration (DD) and clinical disability (EDSS) with measures of corticospinal excitability. Corticospinal excitability thresholds were higher, MEP latency and CSP onset delayed and MEP durations prolonged in individuals with MS compared to controls. Age, DD and EDSS correlated with corticospinal excitability thresholds. Also, TCI duration and the linear slope of the MEP amplitude IO curve correlated with EDSS. Hierarchical regression modeling demonstrated that combining multiple TMS-based measures of corticospinal excitability accounted for unique variance in clinical disability (EDSS) beyond that of clinical demographics (AO, DD). Our results indicate that multiple TMS-based measures of corticospinal and interhemispheric excitability provide insights into the potential neural mechanisms associated with clinical disability in MS. These findings may aid in the clinical evaluation, disease monitoring and prediction of disability in MS.

To examine the relationship of transcallosal pathway microstructure and transcallosal inhibition (TCI) with motor function and impairment in chronic stroke.Diffusion-weighted magnetic resonance imaging and transcranial magnetic stimulation (TMS) data were collected from 24 participants with chronic stroke and 11 healthy older individuals. Post-stroke motor function (Wolf Motor Function Test) and level of motor impairment (Fugl-Meyer score) were evaluated.Fractional anisotropy (FA) of transcallosal tracts between prefrontal cortices and the mean amplitude decrease in muscle activity during the ipsilateral silent period evoked by TMS over the non-lesioned hemisphere (termed NL-iSPmean) were significantly associated with level of motor impairment and motor function after stroke (p0.05). A regression model including age, post-stroke duration, lesion volume, lesioned corticospinal tract FA, transcallosal prefrontal tract FA and NL-iSPmean accounted for 84% of variance in motor impairment (p0.01). Both transcallosal prefrontal tract FA (ΔR(2)=0.12, p=0.04) and NL-iSPmean (ΔR(2)=0.09, p=0.04) accounted for unique variance in motor impairment level.Prefrontal transcallosal tract microstructure and TCI are each uniquely associated with motor impairment in chronic stroke.Utilizing a multi-modal approach to assess transcallosal pathways may improve our capacity to identify important neural substrates of motor impairment in the chronic phase of stroke.

Background Current assessment tools for sport-related concussion are limited by a reliance on subjective interpretation and patient symptom reporting. Robotic assessments may provide more objective and precise measures of neurological function than traditional clinical tests. Objective To determine the reliability of assessments of sensory, motor and cognitive function conducted with the KINARM end-point robotic device in young adult elite athletes. Methods Sixty-four randomly selected healthy, young adult elite athletes participated. Twenty-five individuals (25 M, mean age±SD, 20.2±2.1 years) participated in a within-season study, where three assessments were conducted within a single season (assessments labeled by session: S1, S2, S3). An additional 39 individuals (28M; 22.8±6.0 years) participated in a year-to-year study, where annual pre-season assessments were conducted for three consecutive seasons (assessments labeled by year: Y1, Y2, Y3). Forty-four parameters from five robotic tasks (Visually Guided Reaching, Position Matching, Object Hit, Object Hit and Avoid, and Trail Making B) and overall Task Scores describing performance on each task were quantified. Results Test-retest reliability was determined by intra-class correlation coefficients (ICCs) between the first and second, and second and third assessments. In the within-season study, ICCs were ≥0.50 for 68% of parameters between S1 and S2, 80% of parameters between S2 and S3, and for three of the five Task Scores both between S1 and S2, and S2 and S3. In the year-to-year study, ICCs were ≥0.50 for 64% of parameters between Y1 and Y2, 82% of parameters between Y2 and Y3, and for four of the five Task Scores both between Y1 and Y2, and Y2 and Y3. Conclusions Overall, the results suggest moderate-to-good test-retest reliability for the majority of parameters measured by the KINARM robot in healthy young adult elite athletes. Future work will consider the potential use of this information for clinical assessment of concussion-related neurological deficits.

The objective of the current work was to evaluate whether the effects of acute aerobic exercise on motor learning were dependent on genetic variants impacting brain-derived neurotrophic factor (BDNF val66met polymorphism) and the dopamine D2 receptor (DRD2/ANKK1 glu713lys polymorphism) in humans. A retrospective analysis was performed to determine whether these polymorphisms influence data from our two previous studies, which both demonstrated that a single bout of aerobic exercise prior to motor practice enhanced implicit motor learning. Here, our main finding was that the effect of acute aerobic exercise on motor learning was dependent on DRD2/ANKK1 genotype. Motor learning was enhanced when aerobic exercise was performed prior to skill practice in glu/glu homozygotes, but not lys allele carriers. In contrast, the BDNF val66met polymorphism did not impact the exercise effect. The results suggest that the dopamine D2 receptor may be involved in acute aerobic exercise effects on motor learning. Such genetic information could inform the development of individualized aerobic exercise strategies to promote motor learning.

The objectives of the present study were to evaluate the impact of a single bout of high-intensity aerobic exercise on 1) long-term potentiation (LTP)-like neuroplasticity via response to paired associative stimulation (PAS) and 2) the temporal and spatial components of sequence-specific implicit motor learning. Additionally, relationships between exercise-induced increases in systemic brain-derived neurotrophic factor (BDNF) and response to PAS and motor learning were evaluated. Sixteen young healthy participants completed six experimental sessions, including the following: 1) rest followed by PAS; 2) aerobic exercise followed by PAS; 3) rest followed by practice of a continuous tracking (CT) task and 4) a no-exercise 24-h retention test; and 5) aerobic exercise followed by CT task practice and 6) a no-exercise 24-h retention test. The CT task included an embedded repeated sequence allowing for evaluation of sequence-specific implicit learning. Slope of motor-evoked potential recruitment curves generated with transcranial magnetic stimulation showed larger increases when PAS was preceded by aerobic exercise (59.8% increase) compared with rest (14.2% increase, P = 0.02). Time lag of CT task performance on the repeated sequence improved under the aerobic exercise condition from early (−100.8 ms) to late practice (−75.2 ms, P < 0.001) and was maintained at retention (−79.2 ms, P = 0.004) but did not change under the rest condition ( P > 0.16). Systemic BDNF increased on average by 3.4-fold following aerobic exercise ( P = 0.003), but the changes did not relate to neurophysiological or behavioral measures ( P > 0.42). These results indicate that a single bout of high-intensity aerobic exercise can prime LTP-like neuroplasticity and promote sequence-specific implicit motor learning.

Recovery of motor function after stroke involves relearning motor skills and is mediated by neuroplasticity. Recent research has focused on developing rehabilitation strategies that facilitate such neuroplasticity to maximize functional outcome poststroke. Although many molecular signaling pathways are involved, brain-derived neurotrophic factor (BDNF) has emerged as a key facilitator of neuroplasticity involved in motor learning and rehabilitation after stroke. Thus, rehabilitation strategies that optimize BDNF effects on neuroplasticity may be especially effective for improving motor function poststroke. Two potential poststroke rehabilitation strategies that consider the importance of BDNF are the use of aerobic exercise to enhance brain function and the incorporation of genetic information to individualize therapy. Converging evidence demonstrates that aerobic exercise increases BDNF production and consequently enhances learning and memory processes. Nevertheless, a common genetic variant reduces activity-dependent secretion of the BDNF protein. Thus, BDNF gene variation may affect response to motor rehabilitation training and potentially modulate the effects of aerobic exercise on neuroplasticity. This perspective article discusses evidence that aerobic exercise promotes neuroplasticity by increasing BDNF production and considers how aerobic exercise may facilitate the acquisition and retention of motor skills for poststroke rehabilitation. Next, the impact of the BDNF gene val66met polymorphism on motor learning and response to rehabilitation is explored. It is concluded that the effects of aerobic exercise on BDNF and motor learning may be better exploited if aerobic exercise is paired more closely in time with motor training. Additionally, information about BDNF genotype could provide insight into the type and magnitude of effects that aerobic exercise may have across individuals and potentially help guide an individualized prescription of aerobic exercise to enhance motor rehabilitation poststroke.

In previous work, acute high-intensity aerobic exercise benefited continuous motor sequence task learning. As memory processes underlying motor sequence learning vary between tasks involving continuous and discrete movements, the objective of the current study was to determine whether the beneficial effects of acute aerobic exercise generalize to the learning of a discrete motor sequence task.Sixteen young healthy individuals practiced a discrete motor sequence task preceded by either a period of rest or a bout of high-intensity cycling. Participants moved a cursor with a computer mouse to a series of discretely presented targets on a screen. Target presentation followed either a repeated or a random sequence, which allowed the evaluation of implicit sequence-specific motor learning. The change in movement response time over practice (△-ACQ) and from practice to a 24-h "no-exercise" retention test (△-RET) and the rate of improvement over practice (α-ACQ) and during the retention test (α-RET) were calculated.α-RET was greater for the repeated sequence than random sequences after aerobic exercise (P = 0.01), but not rest (P = 0.33). Further, α-RET for the repeated sequence was greater after aerobic exercise than for either sequence (repeated, random) in the rest condition (P ≤ 0.01). There were no differences between sequences and/or conditions for △-ACQ, △-RET, or α-RET (P ≥ 0.57).Our findings show a positive effect of acute high-intensity aerobic exercise on implicit discrete motor sequence learning. Performing exercise before practice increased the rate of improvement at a 24-h delayed retention test, suggesting an effect on the rate of motor memory retrieval. Pairing acute aerobic exercise with motor practice may facilitate learning of discrete movement sequences in sport or rehabilitation settings.

Unilateral training involving voluntary contractions, neuromuscular electrical stimulation (NMES), or a combination of the two can increase the excitability of neural circuits bilaterally within the CNS. Many rehabilitation programs are designed to promote such "neuroplasticity" to improve voluntary movement following CNS damage. While much is known about this type of activity-dependent plasticity for the muscles that dorsi-flex the ankle, similar information is not available for the plantar-flexors. Presently, we assessed the excitability of corticospinal (CS) and spinal circuits for both soleus (SOL) muscles before and after voluntary contractions of the right plantar-flexors (VOL; 5 s on-5 s off, 40 min), NMES of the right tibial nerve (tnNMES; 5 s on-5 s off, 40 min), or both together (V + tnNMES). CS excitability for the right (rSOL) and left SOL (lSOL) muscles was assessed by quantifying motor evoked potentials elicited by transcranial magnetic stimulation. Spinal excitability was assessed using measures from the ascending limb of the M-wave versus H-reflex recruitment curve. CS excitability did not change for rSOL (the activated muscle) or lSOL following any condition. In contrast, there was a marked increase in spinal excitability for rSOL, but only following V + tnNMES; the slope of the M-wave versus H-reflex recruitment curve increased approximately twofold (pre = 7.9; post = 16.2) and H-reflexes collected when the M-wave was ~5 % of the maximal M-wave (M(max)) increased by ~1.5× (pre = 19 % M(max), post = 29 % M(max)). Spinal excitability for lSOL did not change following any condition. Thus, only voluntary contractions that were coupled with NMES increased CNS excitability, and this occurred only in the ipsilateral spinal circuitry. These results are in marked contrast to previous studies showing NMES-induced changes in CS excitability for every other muscle studied and suggest that the mechanisms that regulate activity-dependent neuroplasticity are different for SOL than other muscles. Further, while rehabilitation strategies involving voluntary training and/or NMES of the plantar-flexors may be beneficial for producing movement and reducing atrophy, a single session of low-intensity NMES and voluntary training may not be effective for strengthening CS pathways to the SOL muscle.

Neuromuscular electrical stimulation (NMES) generates contractions by depolarising axons beneath the stimulating electrodes. The depolarisation of motor axons produces contractions by signals travelling from the stimulation location to the muscle (peripheral pathway), with no involvement of the central nervous system (CNS). The concomitant depolarisation of sensory axons sends a large volley into the CNS and this can contribute to contractions by signals travelling through the spinal cord (central pathway) which may have advantages when NMES is used to restore movement or reduce muscle atrophy. In addition, the electrically evoked sensory volley increases activity in CNS circuits that control movement and this can also enhance neuromuscular function after CNS damage. The first part of this review provides an overview of how peripheral and central pathways contribute to contractions evoked by NMES and describes how differences in NMES parameters affect the balance between transmission along these two pathways. The second part of this review describes how NMES location (i.e. over the nerve trunk or muscle belly) affects transmission along peripheral and central pathways and describes some implications for motor unit recruitment during NMES. The third part of this review summarises some of the effects that the electrically evoked sensory volley has on CNS circuits, and highlights the need to identify optimal stimulation parameters for eliciting plasticity in the CNS. A goal of this work is to identify the best way to utilize the electrically evoked sensory volley generated during NMES to exploit mechanisms inherent to the neuromuscular system and enhance neuromuscular function for rehabilitation.

We present new evidence supporting the hypothesis that the effects of cardiovascular exercise on memory can be regulated in a time-dependent manner. When the exercise stimulus is coupled temporally with specific phases of the memory formation process, a single bout of cardiovascular exercise may be sufficient to improve memory.

Acute aerobic exercise facilitated long-term potentiation-like plasticity in the human primary motor cortex (M1). Here, we investigated the effect of acute aerobic exercise on cerebellar circuits, and their potential contribution to altered M1 plasticity in healthy individuals (age:24.8±4.1years). In Experiment 1, acute aerobic exercise reduced cerebellar inhibition (CBI) (n=10,p=0.01), elicited by dual-coil paired-pulse transcranial magnetic stimulation. In Experiment 2, we evaluated the facilitatory effects of aerobic exercise on responses to paired associative stimulation, delivered with a 25 ms (PAS25) or 21 ms (PAS21) interstimulus interval (n=16per group). Increased M1 excitability evoked by PAS25, but not PAS21, relies on trans-cerebellar sensory pathways. The magnitude of the aerobic exercise effect on PAS response was not significantly different between PAS protocols (interaction effect:p=0.30); however, planned comparisons indicated that, relative to a period of rest, acute aerobic exercise enhanced the excitatory response to PAS25(p=0.02), but not PAS21(p=0.30). Thus, the results of these planned comparisons indirectly provide modest evidence that modulation of cerebellar circuits may contribute to exercise-induced increases in M1 plasticity. The findings have implications for developing aerobic exercise strategies to “prime” M1 plasticity for enhanced motor skill learning in applied settings.

Neuromuscular electrical stimulation (NMES) increases the excitability of corticospinal (CS) pathways by altering circuits in motor cortex (M1). How NMES affects circuits interposed between the ascending afferent volley and descending CS pathways is not known. Presently, we hypothesized that short-latency afferent inhibition (SAI) would be reduced and afferent facilitation (AF) enhanced when NMES increased CS excitability. NMES was delivered for 40 min over the ulnar nerve. To assess CS excitability, motor evoked potentials (MEPs) were evoked using transcranial magnetic stimulation (TMS) delivered at 120% resting threshold for first dorsal interosseus muscle. These MEPs increased by ∼1.7-fold following NMES, demonstrating enhanced CS excitability. SAI and AF were tested by delivering a "conditioning" electrical stimulus to the ulnar nerve 18-25 ms and 28-35 ms before a "test" TMS pulse, respectively. Conditioned MEPs were compared to unconditioned MEPs evoked in the same trials. TMS was adjusted so unconditioned MEPs were not different before and after NMES. At the SAI interval, conditioned MEPs were 25% smaller than unconditioned MEPs before NMES but conditioned and unconditioned MEPs were not different following NMES. At the AF interval, conditioned MEPs were not different from unconditioned MEPs before NMES, but were facilitated by 33% following NMES. Thus, when NMES increases CS excitability there are concurrent changes in the effect of afferent input on M1 excitability, resulting in a net increase in the excitatory effect of the ascending afferent volley on CS circuits. Maximising this excitatory effect on M1 circuits may help strengthen CS pathways and improve functional outcomes of NMES-based rehabilitation programs.

The afferent volley generated during neuromuscular electrical stimulation (NMES) can increase the excitability of human corticospinal (CS) pathways to muscles of the leg and hand. Over time, such increases can strengthen CS pathways damaged by injury or disease and result in enduring improvements in function. There is some evidence that NMES affects CS excitability differently for muscles of the leg and hand, although a direct comparison has not been conducted. Thus, the present experiments were designed to compare the strength and specificity of NMES-induced changes in CS excitability for muscles of the leg and hand. Two hypotheses were tested: (1) For muscles innervated by the stimulated nerve (target muscles), CS excitability will increase more for the hand than for the leg. (2) For muscles not innervated by the stimulated nerve (non-target muscles), CS excitability will increase for muscles of the leg but not muscles of the hand. NMES was delivered over the common peroneal (CP) nerve in the leg or the median nerve at the wrist using a 1-ms pulse width in a 20 s on, 20 s off cycle for 40 min. The intensity was set to evoke an M-wave that was ~15% of the maximal M-wave in the target muscle: tibialis anterior (TA) in the leg and abductor pollicis brevis (APB) in the hand. Ten motor-evoked potentials (MEPs) were recorded from the target muscles and from 2 non-target muscles of each limb using transcranial magnetic stimulation delivered over the “hotspot” for each muscle before and after the NMES. MEP amplitude increased significantly for TA (by 45 ± 6%) and for APB (56 ± 8%), but the amplitude of these increases was not different. In non-target muscles, MEPs increased significantly for muscles of the leg (42 ± 4%), but not the hand. Although NMES increased CS excitability for target muscles to the same extent in the leg and hand, the differences in the effect on non-target muscles suggest that NMES has a “global” effect on CS excitability for the leg and a “focused” effect for the hand. These differences may reflect differences in the specificity of afferent projections to the cortex. Global increases in CS excitability for the leg could be advantageous for rehabilitation as NMES applied to one muscle could strengthen CS pathways and enhance function for multiple muscles.

The afferent volley generated during neuromuscular electrical stimulation (NMES) can increase the excitability of the human corticospinal (CS) pathway. This study was designed to determine the effect of different frequencies of NMES applied over the common peroneal nerve on changes in CS excitability for the tibialis anterior (TA) muscle. We hypothesized that higher frequencies of stimulation would produce larger increases in CS excitability than lower frequencies. NMES was applied at 10, 50, 100, or 200 Hz during separate sessions held at least 48 h apart. The stimulation was delivered in a 20 s on, 20 s off cycle for 40 min using a 1 ms pulse width. The intensity of stimulation was set to evoke an M-wave in response to a single pulse that was 15% of the maximal M-wave. CS excitability was evaluated by the amplitude of motor-evoked potentials (MEPs) in TA evoked by transcranial magnetic stimulation. MEPs were recorded immediately before and after the 40 min of NMES and in each 20 s “off” period. For each subject, MEPs recorded during three successive “off” periods were averaged together (n = 9 MEPs), providing a temporal resolution of 2 min for assessing changes in CS excitability. When delivering NMES at 100 Hz, MEPs became significantly elevated from those evoked before the stimulation at the 24th min, and there was a twofold increase in MEP amplitude after 40 min. NMES delivered at 10, 50, and 200 Hz did not significantly alter MEP amplitude. The amplitude of MEPs evoked in soleus and vastus medialis followed similar patterns as those evoked simultaneously in TA, but these changes were mostly not of statistical significance. There were no changes in the ratio of maximal H-reflex to maximal M-wave in TA or soleus. These experiments demonstrate a frequency-dependent effect of NMES on CS excitability for TA and show that, under the conditions of the present study, 100-Hz stimulation was more effective than 10, 50, and 200 Hz. This effect of NMES on CS excitability was strongest in the stimulated muscle and may be mediated primarily at a supraspinal level. These results contribute to a growing body of knowledge about how the afferent volley generated during NMES influences the CNS and have implications for identifying optimal NMES parameters to augment CS excitability for rehabilitation of dorsiflexion after CNS injury.

Background Complete recovery of motor function after stroke is rare with deficits persisting into the chronic phase of recovery. Diffusion tensor imaging (DTI) can evaluate relationships between white matter microstructure and motor function after stroke. The objective of this investigation was to characterize microstructural fiber integrity of motor and sensory regions of the corpus callosum (CC) and descending motor outputs of the posterior limb of the internal capsule (PLIC) in individuals with chronic stroke and evaluate the relationships between white matter integrity and motor function. Results Standardized measures of upper extremity motor function were measured in thirteen individuals with chronic stroke. Manual dexterity was assessed in thirteen healthy age-matched control participants. DTI scans were completed for each participant. Fractional anisotropy (FA) of a cross-section of sensory and motor regions of the CC and the PLIC bilaterally were quantified. Multivariate analysis of variance evaluated differences between stroke and healthy groups. Correlational analyses were conducted for measures of motor function and FA. The stroke group exhibited reduced FA in the sensory (p = 0.001) region of the CC, contra- (p = 0.032) and ipsilesional (p = 0.001) PLIC, but not the motor region of the CC (p = 0.236). In the stroke group, significant correlations between contralesional PLIC FA and level of physical impairment (p = 0.005), grip strength (p = 0.006) and hand dexterity (p = 0.036) were observed. Conclusions Microstructural status of the sensory region of the CC is reduced in chronic stroke. Future work is needed to explore relationships between callosal sensorimotor fiber integrity and interhemispheric interactions post-stroke. In addition, contralesional primary motor output tract integrity is uniquely and closely associated with multiple dimensions of motor recovery in the chronic phase of stroke suggesting it may be an important biomarker of overall motor recovery.