Effect of current direction and muscle activation on motor cortex neuroplasticity induced by repetitive paired-pulse transcranial magnetic stimulation.

Repetitive paired-pulse transcranial magnetic stimulation (TMS) at indirect (I)-wave periodicity (iTMS) can increase plasticity in primary motor cortex (M1). Both TMS coil orientation and muscle activation can influence I-wave activity, but it remains unclear how these factors influence M1 plasticity with iTMS. We therefore investigated the influence of TMS coil orientation and muscle activation on the response to iTMS. Thirty-two young adults (24.2 ± 4.8 years) participated in three experiments. Each experiment included two sessions using a modified iTMS intervention with either a posterior-anterior orientation (PA) or anterior-posterior (AP) coil orientation over M1. Stimulation was applied in resting (Experiments 1 and 3) or active muscle (Experiments 2 and 3). Effects of iTMS on M1 excitability were assessed by recording motor evoked potentials (MEPs) and short-interval intracortical facilitation (SICF) with PA and AP orientations in both resting (all experiments) and active (Experiment 2) muscle. For the resting intervention, MEPs were greater after AP iTMS (Experiment 1, P = .046), whereas SICF was comparable between interventions (all P > .10). For the active intervention, responses did not vary between PA and AP iTMS (Experiment 2, all P > .14), and muscle activation reduced the effect of AP iTMS during the intervention (Experiment 3, P = .002). Coil orientation influenced the MEP response after iTMS, and muscle activation reduced the response during iTMS. While this suggests that AP iTMS may be beneficial in producing a neuroplastic modulation of I-wave circuits in resting muscle, further exploration of factors such as dosing is required.

Beta resting-state functional connectivity predicts tactile spatial acuity.

Tactile perception is a complex phenomenon that is processed by multiple cortical regions via the primary somatosensory cortex (S1). Although somatosensory gating in the S1 using paired-pulse stimulation can predict tactile performance, the functional relevance of cortico-cortical connections to tactile perception remains unclear. We investigated the mechanisms by which corticocortical and local networks predict tactile spatial acuity in 42 adults using magnetoencephalography (MEG). Resting-state MEG was recorded with the eyes open, whereas evoked responses were assessed using single- and paired-pulse electrical stimulation. Source data were used to estimate the S1-seed resting-state functional connectivity (rs-FC) in the whole brain and the evoked response in the S1. Two-point discrimination threshold was assessed using a custom-made device. The beta rs-FC revealed a negative correlation between the discrimination threshold and S1-superior parietal lobule, S1-inferior parietal lobule, and S1-superior temporal gyrus connection (all P < 0.049); strong connectivity was associated with better performance. Somatosensory gating of N20m was also negatively correlated with the discrimination threshold (P = 0.015), with weak gating associated with better performance. This is the first study to demonstrate that specific beta corticocortical networks functionally support tactile spatial acuity as well as the local inhibitory network.

Modulation of I-Wave Generating Pathways With Repetitive Paired-Pulse Transcranial Magnetic Stimulation: A Transcranial Magnetic Stimulation-Electroencephalography Study.

OBJECTIVES: Repetitive paired-pulse transcranial magnetic stimulation (iTMS) at indirect (I) wave intervals increases motor-evoked potentials (MEPs) produced by transcranial magnetic stimulation (TMS) to primary motor cortex (M1). However, the effects of iTMS at early and late intervals on the plasticity of specific I-wave circuits remain unclear. This study therefore aimed to assess how the timing of iTMS influences intracortical excitability within early and late I-wave circuits. To investigate the cortical effects of iTMS more directly, changes due to the intervention were also assessed using combined TMS-electroencephalography (EEG). MATERIAL AND METHODS: Eighteen young adults (aged 24.6 ± 4.2 years) participated in four sessions in which iTMS targeting early (1.5-millisecond interval; iTMS1.5) or late (4.0-millisecond interval; iTMS4.0) I-waves was applied over M1. Neuroplasticity was assessed using both posterior-to-anterior (PA) and anterior-to-posterior (AP) stimulus directions to record MEPs and TMS-evoked EEG potentials (TEPs) before and after iTMS. Short-interval intracortical facilitation (SICF) at interstimulus intervals of 1.5 and 4.0 milliseconds was also used to index I-wave activity. RESULTS: MEP amplitude was increased after iTMS (p < 0.01), and this was greater for PA responses (p < 0.01) but not different between iTMS intervals (p = 0.9). Irrespective of iTMS interval and coil current, SICF was facilitated after the intervention (p < 0.01). Although the N45 produced by AP stimulation was decreased by iTMS1.5 (p = 0.04), no other changes in TEP amplitude were observed. CONCLUSIONS: The timing of iTMS failed to influence which I-wave circuits were potentiated by the intervention. In contrast, decreases in the N45 suggest that the neuroplastic effects of iTMS may include disinhibition of intracortical inhibitory processes.

Therapeutic benefits of noninvasive somatosensory cortex stimulation on cortical plasticity and somatosensory function: A systematic review.

Optimal limb coordination requires efficient transmission of somatosensory information to the sensorimotor cortex. The primary somatosensory cortex (S1) is frequently damaged by stroke, resulting in both somatosensory and motor impairments. Noninvasive brain stimulation (NIBS) to the primary motor cortex is thought to induce neural plasticity that facilitates neurorehabilitation. Several studies have also examined if NIBS to the S1 can enhance somatosensory processing as assessed by somatosensory-evoked potentials (SEPs) and improve behavioural task performance, but it remains uncertain if NIBS can reliably modulate S1 plasticity or even whether SEPs can reflect this plasticity. This systematic review revealed that NIBS has relatively minor effects on SEPs or somatosensory task performance, but larger early SEP changes after NIBS can still predict improved performance. Similarly, decreased paired-pulse inhibition in S1 post-NIBS is associated with improved somatosensory performance. However, several studies still debate the role of inhibitory function in somatosensory performance after NIBS in terms of the direction of the change (i.e., disinhibition or inhibition). Altogether, early SEP and paired-pulse inhibition (particularly inter-stimulus intervals of 30-100 ms) may become useful biomarkers for somatosensory deficits, but improved NIBS protocols are required for therapeutic applications.

Cerebellar transcranial direct current stimulation disrupts neuroplasticity of intracortical motor circuits.

While previous research using transcranial magnetic stimulation (TMS) suggest that cerebellum (CB) influences the neuroplastic response of primary motor cortex (M1), the role of different indirect (I) wave inputs in M1 mediating this interaction remains unclear. The aim of this study was therefore to assess how CB influences neuroplasticity of early and late I-wave circuits. 22 young adults (22 ± 2.7 years) participated in 3 sessions in which I-wave periodicity repetitive transcranial magnetic stimulation (iTMS) was applied over M1 during concurrent application of cathodal transcranial direct current stimulation over CB (tDCSCB). In each session, iTMS either targeted early I-waves (1.5 ms interval; iTMS1.5), late I-waves (4.5 ms interval; iTMS4.5), or had no effect (variable interval; iTMSSham). Changes due to the intervention were examined with motor evoked potential (MEP) amplitude using TMS protocols measuring corticospinal excitability (MEP1mV) and the strength of CB-M1 connections (CBI). In addition, we indexed I-wave activity using short-interval intracortical facilitation (SICF) and low-intensity single-pulse TMS applied with posterior-anterior (MEPPA) and anterior-posterior (MEPAP) current directions. Following both active iTMS sessions, there was no change in MEP1mV, CBI or SICF (all P > 0.05), suggesting that tDCSCB broadly disrupted the excitatory response that is normally seen following iTMS. However, although MEPAP also failed to facilitate after the intervention (P > 0.05), MEPPA potentiated following both active iTMS sessions (both P < 0.05). This differential response between current directions could indicate a selective effect of CB on AP-sensitive circuits.

Threshold Tracked Short-Interval Intracortical Inhibition More Closely Predicts the Cortical Response to Transcranial Magnetic Stimulation.

OBJECTIVES: Short-interval intracortical inhibition (SICI) is a paired-pulse transcranial magnetic stimulation (TMS) technique that is commonly used to quantify intracortical inhibitory tone in the primary motor cortex. Whereas conventional measures of SICI (C-SICI) quantify inhibition by the amplitude of the motor evoked potential (MEP), alternative measures involving threshold tracked SICI (TT-SICI) instead record the TMS intensity required to maintain a consistent MEP amplitude. Although both C-SICI and TT-SICI are thought to reflect inhibition mediated by γ-aminobutyric acid type A (GABAA) receptors, recent evidence suggests that the mechanisms involved with each measure may not be equivalent. This study aimed to use combined TMS-electroencephalography (TMS-EEG) to investigate the cortical mechanisms contributing to C-SICI and TT-SICI. MATERIALS AND METHODS: In 20 young adults (30.6 ± 8.1 years), C-SICI and TT-SICI were recorded with multiple conditioning intensities, using both posterior-to-anterior (PA) and anterior-to-posterior (AP) induced currents, and this was compared with the TMS-evoked EEG potential (TEP). RESULTS: We found no relationship between the magnitude of C-SICI and TT-SICI within each current direction. However, there was a positive relationship between the slope (derived from multiple conditioning intensities) of inhibition recorded with C-SICI and TT-SICI, but only with a PA current. Furthermore, irrespective of conditioning intensity or current direction, measures of C-SICI were unrelated to TEP amplitude. In contrast, TT-SICI was predicted by the P30 generated with AP stimulation. CONCLUSIONS: Our findings further demonstrate that C-SICI and TT-SICI likely reflect different facets of GABAA-mediated processes, with inhibition produced by TT-SICI appearing to align more closely with TMS-EEG measures of cortical excitability.

Effect of brain-derived neurotrophic factor gene polymorphisms on motor performance and motor learning: A systematic review and meta-analysis.

Brain-derived neurotrophic factor (BDNF) gene polymorphisms may modulate neurotransmitter efficiency, thereby influencing motor performance and motor learning. However, studies to date have provided no consensus regarding the genetic influence of BDNF genotypes (i.e., Val/Val, Val/Met, or Met/Met type). This study aimed to investigate the effect of BDNF genotype on motor performance and motor learning in healthy human adults via a systematic review and meta-analysis. A total of 19 relevant studies were identified using PubMed and Web of Science search for articles published between 2000 and 2021 with motor performance or motor learning as the primary outcome measures. The results of our systematic review suggest that the BDNF genotype is unlikely to contribute to motor performance and motor learning abilities because only 2/32 datasets (6.3%) from 16 studies on motor performance and 3/19 datasets (17.6%) from 13 studies on motor learning indicated a significant genetic effect. Moreover, a meta-analysis of motor learning publications involving 17 datasets from 11 studies revealed that there was no significant difference in the learning score normalized using baseline data between Val/Val and Met carriers (Val/Met + Met/Met or Val/Met; standardized mean differences = 0.08, P = 0.37) with zero heterogeneity (I2 = 0) and a relatively low risk of publication bias. Taken together, the BDNF genotype may have only a minor impact on individual motor performance and motor learning abilities.

Do Brain-Derived Neurotrophic Factor Genetic Polymorphisms Modulate the Efficacy of Motor Cortex Plasticity Induced by Non-invasive Brain Stimulation? A Systematic Review.

Techniques of non-invasive brain stimulation (NIBS) of the human primary motor cortex (M1) are widely used in basic and clinical research to induce neural plasticity. The induction of neural plasticity in the M1 may improve motor performance ability in healthy individuals and patients with motor deficit caused by brain disorders. However, several recent studies revealed that various NIBS techniques yield high interindividual variability in the response, and that the brain-derived neurotrophic factor (BDNF) genotype (i.e., Val/Val and Met carrier types) may be a factor contributing to this variability. Here, we conducted a systematic review of all published studies that investigated the effects of the BDNF genotype on various forms of NIBS techniques applied to the human M1. The motor-evoked potential (MEP) amplitudes elicited by single-pulse transcranial magnetic stimulation (TMS), which can evaluate M1 excitability, were investigated as the main outcome. A total of 1,827 articles were identified, of which 17 (facilitatory NIBS protocol, 27 data) and 10 (inhibitory NIBS protocol, 14 data) were included in this review. More than two-thirds of the data (70.4-78.6%) on both NIBS protocols did not show a significant genotype effect of NIBS on MEP changes. Conversely, most of the remaining data revealed that the Val/Val type is likely to yield a greater MEP response after NIBS than the Met carrier type in both NIBS protocols (21.4-25.9%). Finally, to aid future investigation, we discuss the potential effect of the BDNF genotype based on mechanisms and methodological issues.

Age-related changes in motor cortex plasticity assessed with non-invasive brain stimulation: an update and new perspectives.

It is commonly accepted that the brains capacity to change, known as plasticity, declines into old age. Recent studies have used a variety of non-invasive brain stimulation (NIBS) techniques to examine this age-related decline in plasticity in the primary motor cortex (M1), but the effects seem inconsistent and difficult to unravel. The purpose of this review is to provide an update on studies that have used different NIBS techniques to assess M1 plasticity with advancing age and offer some new perspective on NIBS strategies to boost plasticity in the ageing brain. We find that early studies show clear differences in M1 plasticity between young and older adults, but many recent studies with motor training show no decline in use-dependent M1 plasticity with age. For NIBS-induced plasticity in M1, some protocols show more convincing differences with advancing age than others. Therefore, our view from the NIBS literature is that it should not be automatically assumed that M1 plasticity declines with age. Instead, the effects of age are likely to depend on how M1 plasticity is measured, and the characteristics of the elderly population tested. We also suggest that NIBS performed concurrently with motor training is likely to be most effective at producing improvements in M1 plasticity and motor skill learning in older adults. Proposed NIBS techniques for future studies include combining multiple NIBS protocols in a co-stimulation approach, or NIBS strategies to modulate intracortical inhibitory mechanisms, in an effort to more effectively boost M1 plasticity and improve motor skill learning in older adults.

Contribution of the brain-derived neurotrophic factor and neurometabolites to the motor performance.

Individual motor performance ability is affected by various factors. Although the key factor has not yet completely been elucidated, the brain-derived neurotrophic factor (BDNF) genotype as well as neurometabolites may become contibuting factors depending on the learning stage. We investigated the effects of the Met allele of the BDNF gene and those of the neurometabolites on visuomotor learning. In total, 43 healthy participants performed a visuomotor learning task consisting of 10 blocks using the right index finger (Val66Val, n = 15; Val66Met, n = 15; and Met66Met, n = 13). Glutamate plus glutamine (Glx) concentrations in the primary motor cortex, primary somatosensory cortex (S1), and cerebellum were evaluated using 3-T magnetic resonance spectroscopy in 19 participants who participated in the visuomotor learning task. For the learning stage, the task error (i.e., learning ability) was significantly smaller in the Met66Met group compared with that observed in the remaining groups, irrespective of the learning stage (all p values < 0.003). A significant difference was observed between the Val66Val and Met66Met groups in the learning slope (i.e., learning speed) in the early learning stage (p = 0.048) but not in the late learning stage (all p values> 0.54). Moreover, positive correlations were detected between the learning slope and Glx concentrations in S1 only in the early learning stage (r = 0.579, p = 0.009). The BDNF genotype and Glx concentrations in S1 partially contribute to interindividual variability on learning speed in the early learning stage.

Influence of Brain-Derived Neurotrophic Factor Genotype on Short-Latency Afferent Inhibition and Motor Cortex Metabolites.

The Met allele of the brain-derived neurotrophic factor (BDNF) gene confers reduced cortical BDNF expression and associated neurobehavioral changes. BDNF signaling influences the survival, development, and synaptic function of cortical networks. Here, we compared gamma-aminobutyric acid (GABA)ergic network activity in the human primary motor cortex (M1) between the Met (Val/Met and Met/Met) and non-Met (Val/Val) genotype groups. Short- and long-interval intracortical inhibition, short-latency afferent inhibition (SAI), and long-latency afferent inhibition were measured using transcranial magnetic stimulation (TMS) as indices of GABAergic activity. Furthermore, the considerable inter-individual variability in inhibitory network activity typically measured by TMS may be affected not only by GABA but also by other pathways, including glutamatergic and cholinergic activities; therefore, we used 3-T magnetic resonance spectroscopy (MRS) to measure the dynamics of glutamate plus glutamine (Glx) and choline concentrations in the left M1, left somatosensory cortex, and right cerebellum. All inhibitory TMS conditions produced significantly smaller motor-evoked potentials than single-pulses. SAI was significantly stronger in the Met group than in the Val/Val group. Only the M1 Glx concentration was significantly lower in the Met group, while the BDNF genotype did not affect choline concentration in any region. Further, a positive correlation was observed between SAI and Glx concentrations only in M1. Our findings provide evidence that the BDNF genotype regulates both the inhibitory and excitatory circuits in human M1. In addition, lower Glx concentration in the M1 of Met carriers may alter specific inhibitory network on M1, thereby influencing the cortical signal processing required for neurobehavioral functions.

Modulation of Motor Cortex Plasticity by Repetitive Paired-Pulse TMS at Late I-Wave Intervals Is Influenced by Intracortical Excitability.

The late indirect (I)-waves recruited by transcranial magnetic stimulation (TMS) over primary motor cortex (M1) can be modulated using I-wave periodicity repetitive TMS (iTMS). The purpose of this study was to determine if the response to iTMS is influenced by different interstimulus intervals (ISIs) targeting late I-waves, and whether these responses were associated with individual variations in intracortical excitability. Seventeen young (27.2 ± 6.4 years, 12 females) healthy adults received iTMS at late I-wave intervals (4.0, 4.5, and 5.0 ms) in three separate sessions. Changes due to each intervention were examined with motor evoked potential (MEP) amplitudes and short-interval intracortical facilitation (SICF) using both posterior-anterior (PA) and anterior-posterior (AP) TMS current directions. Changes in MEP amplitude and SICF were influenced by iTMS ISI, with the greatest facilitation for ISIs at 4 and 5 ms with PA TMS, and 4 ms with AP TMS. Maximum SICF at baseline (irrespective of ISI) was associated with increased iTMS response, but only for PA stimulation. These results suggest that modifying iTMS parameters targeting late I-waves can influence M1 plasticity. They also suggest that maximum SICF may be a means by which responders to iTMS targeting the late I-waves could be identified.

The effects of mechanical tactile stimulation on corticospinal excitability and motor function depend on pin protrusion patterns.

Somatosensory stimulation modulates corticospinal excitability. Mechanical tactile stimulation (MS) activates cortical activity depending on tactile stimulation patterns. In this study, we examined whether the effects of mechanical tactile stimulation on corticospinal excitability and motor function depend on different pin protrusions patterns. This single-blind study included 18 healthy subjects. Two types of MS interventions were used: repetitive global stimulus (RGS) intervention was used to stimulate the finger by using 24 pins installed on a finger pad, and sequential stepwise displacement stimulus (SSDS) intervention was used to stimulate the finger by moving a row of 6 pins between the left and right sides on the finger pad. MS interventions were applied to the right index finger for 20 min (stim on/stim off, 1 s/5 s) at a frequency of 20 Hz. After RGS intervention, motor evoked potentials (MEPs) by transcranial magnetic stimulation were observed to be significantly smaller than pre-intervention MEPs; however, motor function using the grooved pegboard task remained unchanged. After SSDS intervention, MEPs were significantly larger and motor function significantly improved compared with pre-intervention values. Our results demonstrated that MS intervention can modulate corticospinal excitability and motor function and that the effects of MS intervention depend on MS intervention patterns.

Comparison of transcranial electrical stimulation regimens for effects on inhibitory circuit activity in primary somatosensory cortex and tactile spatial discrimination performance.

Transcranial electrical stimulation (tES) can be used to modulate inhibitory circuits in primary somatosensory cortex, resulting in improved somatosensory function. However, efficacy may depend on the specific stimulus modality and patterns. For instance, transcranial alternating current stimulation (tACS), transcranial random noise stimulation (tRNS), and transcranial pulsed current stimulation (tPCS) were found to stably and effectively modulate neuronal excitability, while anodal transcranial direct current stimulation (tDCS) appeared less effective overall but with substantial response heterogeneity among subjects. Therefore, we compared the effects of tES applied to primary somatosensory cortex on somatosensory evoked potential paired-pulse depression (SEP-PPD) and tactile discrimination performance in 17 neurologically healthy subjects. In Experiment 1, somatosensory evoked potential N20/P25_SEP-PPD, N20_SEP-PPD, and P25_SEP-PPD responses were assessed before and immediately after anodal tDCS, tACS (stimulation frequency, 140 Hz), tRNS (stimulation frequency, 0.1-640 Hz), anodal tPCS (pulse width, 50 ms; inter-pulse interval, 5 ms), and sham stimulation applied to primary somatosensory cortex. In Experiment 2, a grating orientation task (GOT) was performed before and immediately after the same anodal tDCS, tRNS, anodal tPCS, and sham stimulation regimens. Anodal tDCS and anodal tPCS decreased N20_SEP-PPD, and tRNS increased the first N20 SEP amplitude. Furthermore, tRNS and anodal tPCS decreased GOT discrimination threshold (improved performance). These results suggest that tRNS and anodal tPCS can improve sensory perception by modulating neuronal activity in primary somatosensory cortex.

The effect of combined transcranial direct current stimulation and peripheral nerve electrical stimulation on corticospinal excitability.

Transcranial direct current stimulation (tDCS) and peripheral nerve electrical stimulation (PES) can change corticospinal excitability. tDCS can be used to non-invasively modulate the cerebral cortex's excitability by applying weak current to an electrode attached to the head, and the effect varies with the electrode's polarity. Previous studies have reported the effect of combined tDCS and PES on corticospinal excitability; when compared to single stimulation, combined stimulation increases cortical excitability. In contrast, another study reported that the effect of tDCS is attenuated by PES; hence, there is no consensus opinion on the effect on combined stimulation. Therefore, this study aimed to clarify the effect of combined tDCS and PES on corticospinal excitability. In Experiment 1, the combined stimulation of anodal tDCS and PES (anodal tDCS + PES) was performed, and in Experiment 2, a combined stimulation with PES, after cathodal tDCS (PES after cathodal tDCS), was performed using a homeostatic metaplasticity theoretical model. In Experiment 1, anodal tDCS produced a significant increase from baseline in motor-evoked potential (MEP) amplitude 10 min after stimulation, but no significant changes in MEP amplitude were observed with PES or the anodal tDCS + PES condition. Experiment 2 showed a significant decrease in MEP amplitude immediately after cathodal tDCS, and a significant increase in MEP amplitude 15 min after PES, but no significant change in MEP amplitude was observed with sequential PES following cathodal tDCS. In conclusion, our data indicate that PES with anodal tDCS suppressed the effect of tDCS. Also, PES after cathodal tDCS did not induce homeostatic metaplasticity and increase corticospinal excitability.

Repetitive Passive Movement Modulates Corticospinal Excitability: Effect of Movement and Rest Cycles and Subject Attention.

Repetitive passive movement (PM) affects corticospinal excitability; however, it is unknown whether a duty cycle which repeats movement and rest, or subjects' conscious attention to movements, affects corticospinal excitability. We aimed to clarify the effect of the presence or absence of a duty cycle and subjects' attention on corticospinal excitability. Three experiments were conducted. In Experiment 1, PM of the right index finger was performed for 10 min. Three conditions were used: (1) continuous PM (cPM) at a rate of 40°/s; (2) intermittent PM (iPM) with a duty cycle at 40°/s; and (3) iPM at 100°/s. In conditions 1 and 3, motor evoked potential (MEP) amplitude was significantly reduced. In Experiment 2, PM was performed for 30 min: condition 1 comprised cPM at a rate of 40°/s and Condition 2 comprised iPM at 40°/s. MEP amplitude significantly decreased in both conditions. In Experiment 3, PM was performed for 10 min: condition 1 comprised paying attention to the moving finger during iPM and Condition 2 was similar to Condition 1 but while counting images on a monitor without looking at the movement finger, and Condition 3 comprised counting images on a monitor without performing PM. MEP amplitude significantly increased only under Condition 1. Thus, afferent input from movements above a certain threshold may affect corticospinal excitability reduction. Furthermore, corticospinal excitability increases when paying attention to passive finger movement.

Repetitive Passive Finger Movement Modulates Primary Somatosensory Cortex Excitability.

Somatosensory inputs induced by repetitive passive movement (RPM) modulate primary motor cortex (M1) excitability; however, it is unclear whether RPM affects primary somatosensory cortex (S1) excitability. In this study, we investigated whether RPM affects somatosensory evoked potentials (SEPs) and resting state brain oscillation, including alpha and beta bands, depend on RPM frequency. Nineteen healthy subjects participated in this study, and SEPs elicited by peripheral nerve electrical stimulation were recorded from the C3' area in order to assess S1 excitability (Exp. 1: n = 15). We focused on prominent SEP components such as N20, P25 and P45-reflecting S1 activities. In addition, resting electroencephalograms (EEGs) were recorded from C3' area to assess the internal state of the brain network at rest (Exp. 2: n = 15). Passive abduction/adduction of the right index finger was applied for 10 min at frequencies of 0.5, 1.0, 3.0, and 5.0 Hz in Exp. 1, and 1.0, 3.0, and 5.0 Hz in Exp. 2. No changes in N20 or P25 components were observed following RPM. The 3.0 Hz-RPM decreased the P45 component for 20 min (p < 0.05), but otherwise did not affect the P45 component. There was no difference in the alpha and beta bands before and after any RPM; however, a negative correlation was observed between the rate of change of beta power and P45 component at 3.0 Hz-RPM. Our findings indicated that the P45 component changes depending on the RPM frequency, suggesting that somatosensory inputs induced by RPM influences S1 excitability. Additionally, beta power enhancement appears to contribute to the P45 component depression in 3.0 Hz-RPM.

Corticospinal excitability following repetitive voluntary movement.

Post-exercise cortical depression (PED) is induced by non-fatiguing finger movement. Because the type of exercise that causes PED remains unclear, we conducted two experiments to clarify which exercise factors induce PED. Fifteen healthy participants performed repetitive abduction movements of the right index finger at 2.0 Hz (simple rhythmic task) and 0.2 Hz (adjustment task) for 6 min each in experiment 1. Twelve healthy participants performed repetitive and isometric abduction contractions of the right index finger at 1.0 Hz with visuomotor tracking (visuomotor task) and without visuomotor tracking (simple isometric task) for 5 min each in experiment 2. Muscle contraction levels were 10% of the maximum voluntary contraction in all tasks. Motor evoked potentials (MEPs) evoked by transcranial magnetic stimulation were recorded from the right first dorsal interosseous muscle before and after the movement tasks. The simple rhythmic task transiently reduced MEP amplitudes when compared with baseline in experiment 1. In contrast, the visuomotor task increased MEP amplitudes in experiment 2. No MEP changes were observed following the adjustment task in experiment 1 and the simple isometric task in experiment 2. This study suggests that PED is induced by simple rhythmic movement.

Somatosensory Inputs Induced by Passive Movement Facilitate Primary Motor Cortex Excitability Depending on the Interstimulus Interval, Movement Velocity, and Joint Angle.

Somatosensory inputs affect primary motor cortex (M1) excitability; however, the effect of movement-induced somatosensory inputs on M1 excitability is unknown. This study examined whether M1 excitability is modulated by somatosensory inputs with passive movement in 29 healthy subjects. Motor-evoked potentials (MEPs), elicited by transcranial magnetic stimulation (TMS) were recorded from the first dorsal interosseous (FDI) muscle (Experiment 1). M- and F-waves were measured from the FDI muscle (Experiment 2). Passive movements of the index finger were performed in the adduction direction. TMS pulses were preceded by starting passive movements with interstimulus intervals (ISIs) of 30, 60, 90, 120, 150, 180, and 210 ms. TMS or electrical stimulation was performed in the midrange of the metacarpophalangeal joint during passive movements. MEPs were significantly facilitated at 90, 120, and 150 ms (p < 0.05). No M- or F-wave changes were observed for any ISI. In addition, we investigated whether MEP changes were dependent on passive movement velocity and joint angle. Passive movement was performed at two movement velocities (Experiment 3) or joint angles (Experiment 4). MEP facilitation was observed depending on the movement velocities or joint angles. These experiments demonstrated that somatosensory inputs induced by passive movements facilitated M1 excitability depending on the ISIs, passive movement velocity, and joint angle.

Modulation of Corticospinal Excitability Depends on the Pattern of Mechanical Tactile Stimulation.

We investigated the effects of different patterns of mechanical tactile stimulation (MS) on corticospinal excitability by measuring the motor-evoked potential (MEP). This was a single-blind study that included nineteen healthy subjects. MS was applied for 20 min to the right index finger. MS intervention was defined as simple, lateral, rubbing, vertical, or random. Simple intervention stimulated the entire finger pad at the same time. Lateral intervention stimulated with moving between left and right on the finger pad. Rubbing intervention stimulated with moving the stimulus probe, fixed by protrusion pins. Vertical intervention stimulated with moving in the forward and backward directions on the finger pad. Random intervention stimulated to finger pad with either row protrudes. MEPs were measured in the first dorsal interosseous muscle to transcranial magnetic stimulation of the left motor cortex before, immediately after, and 5-20 min after intervention. Following simple intervention, MEP amplitudes were significantly smaller than preintervention, indicating depression of corticospinal excitability. Following lateral, rubbing, and vertical intervention, MEP amplitudes were significantly larger than preintervention, indicating facilitation of corticospinal excitability. The modulation of corticospinal excitability depends on MS patterns. These results contribute to knowledge regarding the use of MS as a neurorehabilitation tool to neurological disorder.