Plasticity In Human Motor Cortex Research Articles

Influence of BDNF Val66Met polymorphism on excitatory-inhibitory balance and plasticity in human motor cortex

ObjectiveWhile previous studies showed that the single nucleotide polymorphism (Val66Met) of brain-derived neurotrophic factor (BDNF) can impact neuroplasticity, the influence of BDNF genotype on cortical circuitry and relationship to neuroplasticity remain relatively unexplored in human. MethodsUsing individualised transcranial magnetic stimulation (TMS) parameters, we explored the influence of the BDNF Val66Met polymorphism on excitatory and inhibitory neural circuitry, its relation to I-wave TMS (ITMS) plasticity and effect on the excitatory/inhibitory (E/I) balance in 18 healthy individuals. ResultsExcitatory and inhibitory indexes of neurotransmission were reduced in Met allele carriers. An E/I balance was evident, which was influenced by BDNF with higher E/I ratios in Val/Val homozygotes. Both long-term potentiation (LTP-) and depression (LTD-) like ITMS plasticity were greater in Val/Val homozygotes. LTP- but not LTD-like effects were restored in Met allele carriers by increasing stimulus intensity to compensate for reduced excitatory transmission. ConclusionsThe influence of BDNF genotype may extend beyond neuroplasticity to neurotransmission. The E/I balance was evident in human motor cortex, modulated by BDNF and measurable using TMS. Given the limited sample, these preliminary findings warrant further investigation. SignificanceThese novel findings suggest a broader role of BDNF genotype on neurocircuitry in human motor cortex.

Extremely Low Frequency Magnetic Fields Do Not Affect LTP-Like Plasticity in Healthy Humans

IntroductionSeveral studies explored the biological effects of extremely low-frequency magnetic fields (ELF-MFs) in vitro, reporting the induction of functional changes in neuronal activity. In particular, ELF-MFs can influence synaptic plasticity both in vitro and in animal models but some studies reported an increase in long-term potentiation (LTP) whereas others suggested its reduction. However, no specific study has investigated such effect on humans.AimsTo evaluate whether ELF-MFs affect the propensity of the human cortex to undergo LTP-like plasticity.MethodsWe designed a randomized, single-blind, sham-controlled, cross-over study on 10 healthy subjects. Cortical plasticity was induced by intermittent theta burst stimulation (iTBS) before and after 45-min ELF-MFs (75 Hz; 1.8 mT) or sham exposure and was estimated by measuring the changes of motor evoked potentials (MEP) amplitude before and after each iTBS.ResultsNo adverse events were reported. No significant effects of ELF-MFs on cortical plasticity were found.ConclusionWhole-brain exposure to ELF-MFs (75 Hz; 1.8 mT) is safe and does not seem to significantly affect LTP-like plasticity in human motor cortex.

Real-time EEG-defined excitability states determine efficacy of TMS-induced plasticity in human motor cortex

BackgroundRapidly changing excitability states in an oscillating neuronal network can explain response variability to external stimulation, but if repetitive stimulation of always the same high- or low-excitability state results in long-term plasticity of opposite direction has never been explored in vivo. Objective/hypothesisDifferent phases of the endogenous sensorimotor μ-rhythm represent different states of corticospinal excitability, and repetitive transcranial magnetic stimulation (rTMS) of always the same high- vs. low-excitability state results in long-term plasticity of different direction. MethodsState-dependent electroencephalography-triggered transcranial magnetic stimulation (EEG-TMS) was applied to target the EEG negative vs. positive peak of the sensorimotor μ-rhythm in healthy subjects using a millisecond resolution real-time digital signal processing system. Corticospinal excitability was indexed by motor evoked potential amplitude in a hand muscle. ResultsEEG negative vs. positive peak of the endogenous sensorimotor μ-rhythm represent high- vs. low-excitability states of corticospinal neurons. More importantly, otherwise identical rTMS (200 triple-pulses at 100 Hz burst frequency and ∼1 Hz repetition rate), triggered consistently at this high-excitability vs. low-excitability state, leads to long-term potentiation (LTP)-like vs. no change in corticospinal excitability. ConclusionsFindings raise the intriguing possibility that real-time information of instantaneous brain state can be utilized to control efficacy of plasticity induction in humans.

Provision of somatosensory inputs during motor imagery enhances learning-induced plasticity in human motor cortex

Motor learning via physical practice leads to long-term potentiation (LTP)-like plasticity in motor cortex (M1) and temporary occlusion of additional LTP-like plasticity. Motor learning can be achieved through simulation of movement, namely motor imagery (MI). When combined with electrical stimulation, MI influenced M1 excitability to a larger extent than MI itself. We explored whether a training based on the combination of MI and peripheral nerve stimulation (ESMI) modulates M1 LTP-like plasticity inducing retention of a new acquired skill. Twelve subjects mentally performed thumb-index movements, with synchronous electrical nerve stimulation, following an acoustic cue, in order to increase movement speed. Two control groups physically performed or imagined the same number of finger movements following the acoustic cue. After each training session, M1 LTP-like plasticity was assessed by using PAS25 (paired associative stimulation) technique. Performance was tested before and after training and 24 hours after training. Results showed that physical practice and ESMI training similarly increased movement speed, prevented the subsequent PAS25-induced LTP-like plasticity, and induced retention of motor skill the following day. Training with MI had significant, but minor effects. These findings suggest that a training combining MI with somatosensory input influences motor performance through M1 plasticity similarly to motor execution.

P1-27. Influence of stimulus direction on the efficacy of continuous theta burst stimulation

Continuous theta burst stimulation (cTBS) is a method commonly used to induce long term depression (LTD)-like plasticity in human motor cortex. However, its after-effects are likely to be highly variable between individuals. In this study, we hypothesized that the direction of stimulus current may have a role in the efficacy of cTBS, as cTBS is usually applied using a biphasic stimulus pulse which preferentially induces anterior-to-posterior (AP) current in the second depolarizing phase in the brain. To test this, we investigated changes of motor evoked potentials (MEPs) after cTBS carried out with rotating the stimulation coil 45° clockwise from the conventional position, which preferentially induces medial-to-lateral current in the brain. Nine healthy volunteers participated in the study and transcranial magnetic stimulation (TMS) was given to the M1 representation of the right first dorsal interosseous muscle. We found that the modified cTBS with rotated coil tented to show better responder rate compared with the conventional cTBS (66.7% vs. 33.3%) though there were no statistical differences. We concluded that the after-effects of cTBS were highly variable irrespective of direction of stimulus current.

Quadri-pulse theta burst stimulation using ultra-high frequency bursts at I-wave periodicity induces direction dependent bi-directional plasticity in human motor cortex

Quadri-pulse theta burst stimulation using ultra-high frequency bursts at I-wave periodicity induces direction dependent bi-directional plasticity in human motor cortex

Stimulus uncertainty enhances long-term potentiation-like plasticity in human motor cortex

Plasticity can be induced in human cortex using paired associative stimulation (PAS), which repeatedly and predictably pairs a peripheral electrical stimulus with transcranial magnetic stimulation (TMS) to the contralateral motor region. Many studies have reported small or inconsistent effects of PAS. Given that uncertain stimuli can promote learning, the predictable nature of the stimulation in conventional PAS paradigms might serve to attenuate plasticity induction. Here, we introduced stimulus uncertainty into the PAS paradigm to investigate if it can boost plasticity induction. Across two experimental sessions, participants (n = 28) received a modified PAS paradigm consisting of a random combination of 90 paired stimuli and 90 unpaired (TMS-only) stimuli. Prior to each of these stimuli, participants also received an auditory cue which either reliably predicted whether the upcoming stimulus was paired or unpaired (no uncertainty condition) or did not predict the upcoming stimulus (maximum uncertainty condition). Motor evoked potentials (MEPs) evoked from abductor pollicis brevis (APB) muscle quantified cortical excitability before and after PAS. MEP amplitude increased significantly 15 min following PAS in the maximum uncertainty condition. There was no reliable change in MEP amplitude in the no uncertainty condition, nor between post-PAS MEP amplitudes across the two conditions. These results suggest that stimulus uncertainty may provide a novel means to enhance plasticity induction with the PAS paradigm in human motor cortex. To provide further support to the notion that stimulus uncertainty and prediction error promote plasticity, future studies should further explore the time course of these changes, and investigate what aspects of stimulus uncertainty are critical in boosting plasticity.

Modulation of the Direction and Magnitude of Hebbian Plasticity in Human Motor Cortex by Stimulus Intensity and Concurrent Inhibition.

The mechanisms mediating the efficacy and variability of paired associative stimulation (PAS), thought to be mediated by Hebbian plasticity, remain incompletely understood. The magnitude and direction of Hebbian plasticity may be modulated by the level of neural depolarisation, which is influenced by stimulation intensity and interactions with cortical circuits. PAS effects would be influenced by the intensity of transcranial magnetic stimulation (TMS) and interaction with other circuits. In particular, PAS would be inhibited by concurrent inhibitory input following median nerve stimulation, known as short latency afferent inhibition (SAI). PAS was tested at an interstimulus interval (ISI) 2 ms or 6 ms longer than the N20 peak of the median nerve somatosensory-evoked potential (PASN20+2, PASN20+6). PASN20+2 was tested at three different TMS intensities. Short interval intracortical facilitation and inhibition were tested in the presence of SAI (SICFSAI, SICISAI). The propensity for long term potentiation like effects increased with higher PASN20+2 TMS stimulus intensity, whereas long term depression like effects ensued at subthreshold intensity. Stronger SAI correlated with weaker PAS LTP-like effects across individuals. PASN20+2 (maximal SAI) was less effective than PASN20+6 (weak SAI). SICFSAI or SICISAI did not influence PAS response. Inter-individual differences in SAI contribute to the variability in PAS efficacy. The magnitude and direction of PAS effects is modulated by TMS intensity. Together, these findings indicate that the level of neural activity induced by stimulation likely plays a crucial role in determining the direction and magnitude of Hebbian plastic effects evoked by PAS in human cortex.

Augmenting LTP-Like Plasticity in Human Motor Cortex by Spaced Paired Associative Stimulation

Paired associative stimulation (PASLTP) of the human primary motor cortex (M1) can induce LTP-like plasticity by increasing corticospinal excitability beyond the stimulation period. Previous studies showed that two consecutive PASLTP protocols interact by homeostatic metaplasticity, but animal experiments provided evidence that LTP can be augmented by repeated stimulation protocols spaced by ~30min. Here we tested in twelve healthy selected PASLTP responders the possibility that LTP-like plasticity can be augmented in the human M1 by systematically varying the interval between two consecutive PASLTP protocols. The first PASLTP protocol (PAS1) induced strong LTP-like plasticity lasting for 30-60min. The effect of a second identical PASLTP protocol (PAS2) critically depended on the time between PAS1 and PAS2. At 10min, PAS2 prolonged the PAS1-induced LTP-like plasticity. At 30min, PAS2 augmented the LTP-like plasticity induced by PAS1, by increasing both magnitude and duration. At 60min and 180min, PAS2 had no effect on corticospinal excitability. The cumulative LTP-like plasticity after PAS1 and PAS2 at 30min exceeded significantly the effect of PAS1 alone, and the cumulative PAS1 and PAS2 effects at 60min and 180min. In summary, consecutive PASLTP protocols interact in human M1 in a time-dependent manner. If spaced by 30min, two consecutive PASLTP sessions can augment LTP-like plasticity in human M1. Findings may inspire further research on optimized therapeutic applications of non-invasive brain stimulation in neurological and psychiatric diseases.

Brain-derived neurotrophic factor and human motor cortex plasticity

Brain-derived neurotrophic factor and human motor cortex plasticity

Observing and perceiving: A combined approach to induce plasticity in human motor cortex

ObjectiveTo test whether action observation combined with peripheral nerve electrical stimulation was able to evoke plasticity in the primary motor cortex (M1). MethodsThe stimulation protocol consisted in the observation of a video showing repetitive thumb-index tapping movements (AO) combined with peripheral electrical nerve stimulation (PNS) delivered on the median nerve (AO–PNS). M1 excitability, measured by means of transcranial magnetic stimulation, was compared with that assessed after AO and PNS alone. ResultsM1 excitability increased after AO–PNS, whilst no modifications occurred after AO and PNS alone. The increased M1 excitability after AO–PNS was long-lasting (45min) and specific for the stimulated muscle. ConclusionsThis study described an innovative stimulation paradigm that exploited the mirror neuron system to induce plasticity in M1. However, this occurred only when action observation was combined with afferent signals coming from periphery. SignificanceThis study supports the literature proposing the mirror neuron system as neural substrate for rehabilitation and opens a debate on the rehabilitative treatments that employ AO to improve patients’ motor functions. Indeed, these results suggest that AO has to be combined with afferent inputs from periphery to evoke plasticity in the human motor system.

Inter-subject variability of LTD-like plasticity in human motor cortex: a matter of preceding motor activation.

Continuous theta burst stimulation (cTBS) of the human primary motor cortex (M1) induces long-term depression (LTD)-like plastic changes in corticospinal excitability, but several studies have reported high inter-subject variability of this effect. Most studies use a tonic voluntary contraction of the target muscle before cTBS to set stimulation intensity; however, it is unclear how this might affect response variability. To examine the influence of pre-activation of the target hand muscle on inter-subject response variability to cTBS of the human M1. The response to cTBS was assessed by changes in motor evoked potential (MEP) amplitude in the right first dorsal interosseous (FDI) muscle. For Study 1, ten healthy subjects attended two sessions. They were instructed in one session to keep their FDI relaxed for the entire testing period (pre-relax), and in the other to perform a 2-min 10% of maximal voluntary tonic contraction 15 min before cTBS (pre-active). For Study 2, data from our previous study were re-analyzed to extend the pre-relax condition to an additional 26 subjects (total n = 36). cTBS-induced highly consistent LTD-like MEP depression in the pre-relax condition, but not in the pre-active condition. Inter-subject response variability increased in the pre-active condition. cTBS induces consistent LTD-like plasticity with low inter-subject variability if pre-activation of the stimulated motor cortex is avoided. This affirms a translational potential of cTBS in clinical applications that aim at reducing cortical excitability.

LP38: A new paradigm to induce plasticity in human motor cortex: action observation combined with peripheral electrical nerve stimulation

LP38: A new paradigm to induce plasticity in human motor cortex: action observation combined with peripheral electrical nerve stimulation

Deleterious Effects of a Low Amount of Ethanol on LTP-Like Plasticity in Human Cortex

Ingesting ethanol (EtOH) at low doses during social drinking is a common human behavior for its facilitating effects on social interactions. However, low-dose EtOH may have also detrimental effects that so far are underexplored. Here we sought to test the effects of low-dose EtOH on long-term potentiation (LTP)-like plasticity in human motor cortex. Previous cellular experiments showed that low-dose EtOH potentiates extrasynaptic GABAAR and reduces NMDAR-mediated currents, processes that would limit the expression of LTP. Paired associative transcranial magnetic stimulation (PASLTP) was employed in nine healthy subjects for induction of LTP-like plasticity, indexed by a long-term increase in motor-evoked potential input-output curves. Synaptic α1-GABAAR function was measured by saccadic peak velocity (SPV). Very low doses of EtOH (resulting in blood concentrations of <5 mM) suppressed LTP-like plasticity but did not affect SPV when compared with a placebo condition. In contrast, 1 mg of alprazolam, a classical benzodiazepine, or 10 mg of zolpidem, a non-benzodiazepine hypnotic, decreased SPV but did not significantly affect LTP-like plasticity when compared with placebo. This double dissociation of low-dose EtOH vs alprazolam/zolpidem effects is best explained by the putatively high affinity of EtOH but not alprazolam/zolpidem to extrasynaptic GABAARs and to NMDARs. Findings suggest that enhancement of extrasynaptic GABAAR-mediated tonic inhibition and/or reduction of NMDAR-mediated neurotransmission by EtOH blocks LTP-like plasticity in human cortex at very low doses that are easily reached during social drinking. Therefore, low-dose EtOH may jeopardize LTP-dependent processes, such as learning and memory formation.

Dose-response curve of associative plasticity in human motor cortex and interactions with motor practice

Associative plasticity is hypothesized to be an important neurophysiological correlate of memory formation and learning with potentials for applications in neurorehabilitation and for the development of new electrophysiological measures to study disorders of cortical plasticity. We hypothesized that the magnitude of the paired associative stimulation (PAS)-induced long-term potentiation (LTP)-like effect depends on the number of pairs in the PAS protocol. We also hypothesized that homeostatic interaction of PAS with subsequent motor learning is related to the magnitude of the PAS-induced LTP-like effect. We studied 10 healthy subjects. In experiment 1a, subjects received 90 (PAS90), 180 (PAS180), or 270 (PAS270) pairs of stimuli, followed by a dynamic motor practice (DMP) 1 h after the end of the PAS protocols. In experiment 1b, the DMP preceded the PAS protocol. In experiment 2, the time course of PAS270 was studied. We found that PAS270 resulted in greater increase in motor evoked potential (MEP) amplitude compared with protocols with fewer pairs of stimuli. Moreover, the interaction between PAS protocols with motor learning differed depending on the number of stimulus pairs used to induce PAS. While DMP alone increased MEP amplitudes, DMP during the LTP-like effects induced by PAS270 led to a long-term depression (LTD)-like effect (homeostatic interaction). This homeostatic interaction did not occur after PAS90 and PAS180. In conclusion, we found a dose-dependent effect of the number of stimulus pairs used in the PAS protocol on cortical plasticity. Homeostatic interaction between PAS and DMP was observed only after PAS270.

P 176. Evidence for high-fidelity timing dependent synaptic plasticity of human motor cortex

A single transcranial magnetic stimulation (TMS) pulse typically evokes a short series of spikes in corticospinal neurons (known as indirect (I)-waves) which are thought to arise from transynaptic input. Delivering a second pulse at inter-pulse intervals (IPIs) corresponding to the timing of these I-waves leads to a facilitation of the response, and if stimulus pairs are delivered repeatedly, a persistent LTP-like increase in excitability can occur. This has been demonstrated at an IPI of 1.5 ms, which corresponds to the first I-wave interval, in an intervention referred to as ITMS (I-wave TMS), and it has been argued that this may have similarities with timing dependent plasticity models. Consequently we hypothesised that if the second stimulus is delivered so as not to coincide with I-wave timing it should lead to Ltd. We performed a cross-over study in ten subjects in which TMS doublets were timed to coincide (1.5 ms IPI, ITMS 1.5 ) or not coincide (2 ms IPI, ITMS 2 ) with I-wave firing. Single pulse motor evoked potential (MEP) amplitude, resting motor threshold (RMT) and short-interval cortical inhibition (SICI) were measured from the first dorsal interosseous (FDI) muscle. After ITMS 1.5 corticomotor excitability was increased by around ∼170% for 15 min ( p < 0.05) and returned to baseline by 20 min. Increasing the IPI by just 500 μs–2 ms reversed the after-effect and MEP amplitude was significantly reduced (−35%, p < 0.05) for 15 min before returning to baseline. This reduction was not associated with an increase in SICI, suggesting a reduction in excitatory transmission rather than an increase in inhibitory efficacy. RMT also remained unchanged suggesting that these changes were not due to changes in membrane excitability. Amplitude-matching ITMS 2 did not modulate excitability. The results are consistent with timing-dependent synaptic LTP/D-like effects, and suggest that there are plasticity mechanisms operating in the human motor cortex with a temporal resolution of the order of a few hundreds of microseconds.

P 93. Induction of cortical plasticity by transcranial biphasic quadro-pulse stimulation

Long-term potentiation (LTP) and long-term depression (LTD) are forms of cortical plasticity and are considered to be synaptic processes underlying learning and memory. Transcranial magnetic stimulation (TMS) with monophasic quadro-pulses (QPS) demonstrated to be effective to induce LTD-and LTP-like plasticity in human motor cortex (M1). Here, we aimed to study whether biphasic QPS at different inter-stimulus-and inter-burst-intervals induces plastic changes in human M1. We investigated healthy volunteers ( n = 10 per protocol) with quadro-pulse stimulation (QPS) consisting of repeated bursts of four biphasic TMS pulses (duration: 160 μs) separated by inter-stimulus intervals of 1.5 ms and 50 ms and inter-burst intervals of 200 ms, 1 s and 5 s resulting in 6 different protocols (QPS 1.5−200 , QPS 1.5−1 , QPS 1.5−5 , QPS 50−200 , QPS 50−1 , QPS 50−5 ; 1440 total stimulus counts per protocol). TMS was applied by a custom-made magnetic stimulator (IMETUM, Munich). Resting motor threshold (rMT), and motor evoked potential (MEP) amplitudes with stimulus intensities to target amplitudes of 1mv and 0.4 mV (SI 1mV and SI 0.4mV ) were measured before (Pre) QPS directly after (Post1), after 15 min (Post2), after 30 min (Post3) and after 60 min (Post4). We found a significant increase of MEPs after QPS 1.5−5 at SI 0.4mV and a significant decrease after QPS 50−200 , QPS 50−5 and QPS 1.5−200 at SI 1 mV . QPS 1.5−1 and QPS 50−1 had no significant effect on MEPs, respectively. Significant changes in rMT, referring to a model of intrinsic plasticity, were observed for QPS 50−200 but not for QPS 50−5 . Biphasic QPS demonstrated to induce intensity and frequency dependent LTP-or LTD-like effects displayed by an increase or decrease in MEP amplitudes. This form of stimulation might offer new opportunities in investigations of cortical plasticity in humans.

P 29. BDNF val66met polymorphism influences the time course of changes in corticospinal excitability induced by paired associative and transcranial direct current stimulation

It is widely appreciated that brain-derived neurotrophic factor (BDNF) is released in an activity dependent manner within the brain, and that it plays a key role in regulating synaptic plasticity and long-term potentiation (LTP). A single nucleotide polymorphism (SNP) arises at nucleotide 196 of the eponymous gene in humans. This gives rise to a valine to methionine substitution at codon 66 of the precursor protein. When assessed in animal models, the presence of this substitution is associated with impaired intracellular transport and reduced capacity for LTP. Differences between met carriers and val homozygotes have been reported in studies investigating the plasticity of human motor cortex in response to various forms of brain stimulation. Those who are homozygous for the val allele show elevations in corticospinal excitability following paired associative stimulation (PAS) ( Cirillo et al., 2012 ) and “theta burst” repetitive transcranial magnetic stimulation (rTMS) ( Cheeran et al., 2008 ), that are larger than those exhibited by individuals with a met allele. In contrast, Antal et al. (2010) reported that met carriers show an accentuated response to transcranial direct current stimulation (tDCS). Given the clinical potential of brain stimulation techniques, there is a pressing need to establish the basis of these contrarieties, and the generality of effects attributable to BDNF genotype. In the present study, we focused on corticospinal projections to muscles of the forearm that are of particular significance in rehabilitation following stroke. Consideration was given to two forms of brain stimulation-PAS and tDCS that putatively have utility in this context. A total of 56 participants (29 Female) aged 19–32 (mean ± SD: 22.31 ± 3.42 years) underwent PAS. There were 53 participants (30 Female) aged between 18 and 32 (mean ± SD: 22.35 ± 3.44) who took part in the tDCS condition. PAS consisted of a train of electrical stimulation (1 ms pulse width, 10 Hz, 500 ms duration) delivered to the right Flexor Carpi Radialis (FCR) motor point, followed 25 ms later by a TMS pulse delivered to M1. This was repeated every 10 s for 30 min (total 180 pairs). Anodal 1 mA tDCS was delivered to M1 for 30 min. Motor evoked potentials (MEPs) in response to TMS of the target area were obtained on prior to the intervention, and at 0, 10, 20 and 30 min following the cessation of stimulation. With respect to FCR, val homozygotes exhibited increased corticospinal excitability following tDCS that emerged after 10 min and remained elevated thereafter. In met carriers there was a transient increase in MEP amplitude that peaked 10 min post-intervention. The val homozygotes exhibited a qualitatively similar pattern of response to PAS, whereby increases in corticospinal excitability were delayed. Although weaker overall, the elevations of MEP amplitude exhibited by met carriers were larger immediately following the cessation of stimulation than subsequently. In relation to ECR, the profile of response to tDCS was similar to that manifested in FCR. The val homozygotes exhibited an immediate and sustained elevation in ECR MEP amplitude following PAS. No such changes were present for met carriers. In summary, these findings suggest that met carriers respond transiently, albeit weakly, to brain stimulation. Responses to tDCS are more prominent than those to PAS. Val homozygotes exhibit responses to both forms of stimulation that tend to increase in magnitude over 30 min post-intervention.

P 75. Selective enhancement of motor cortical plasticity by observed mirror-matched actions

Question Watching others learn a motor task can enhance an observer’s own later performance when learning the same motor task. This is thought to be due to activation of the action observation (or mirror neuron) network. We investigated whether transcranial magnetic stimulation (TMS) induced plasticity in human motor cortex (M1) is also influenced by the nature of prior action observation. Methods In separate sessions, 17 participants watched a video showing repeated goal-directed movements (action observation) involving either the right hand (congruent condition) or the same video mirror-reversed to simulate the left hand (incongruent condition). Participants then received pulses of TMS over the hand area of left M1 paired with median nerve stimulation of the right hand (paired associative stimulation; PAS). Results The resting motor-evoked potential (MEP) in right abductor pollicis brevis (APB) increased significantly 20 min after PAS, but only when participants had previously watched the congruent video. In this condition, all participants showed an increase in MEP amplitude at 20 min post-PAS. There was no change in MEP amplitude following PAS when participants watched the incongruent video. Conclusions Prior action observation is a potent modulator of subsequent PAS-induced neuroplasticity, which may have important therapeutic applications.

Promoting endogenous associative plasticity in human primary motor cortex

Promoting endogenous associative plasticity in human primary motor cortex