Increased Motor Cortical Excitability Research Articles

Imagining Speeds up the Effect of Motor Imagery on Central Motor Conduction Time.

Although motor imagery (MI) has been reported to increase motor cortical excitability, its effect on central motor conduction time (CMCT), a widely used neurophysiological diagnostic method, has not been investigated. In this study, we sought to determine the effect of MI on CMCT. In this cross-sectional study, 21 healthy volunteers (11 females, 10 males) aged 24 to 67 years (mean age: 38.8 years) were recruited between April 2022 and June 2023.CMCT was calculated during MI from the abductor digiti minimi (ADM) and tibialis anterior (TA) muscles. Measurements were also performed with conventional measurement methods, such as resting and voluntary contraction, to compare the effect of MI on CMCT. The ANOVAtest revealed that the CMCT session (rest, MI, and voluntary contraction) was a significant factor (p < 0.05). In both muscles, CMCT was shorter in the imagery state than in the resting state but longer than in the voluntary contraction state (p < 0.05). Similarly, motor-evoked potential (MEP) latencies obtained during imagery were shorter for both muscles than the resting state but longer for the voluntary contraction state. The study's findings suggest that MI is a mental activity that modulates CMCT measurement.MI shows a voluntary contraction-like effect on CMCT and MEP latency, although the effect is more uncertain.

Repeated spaced cortical paired associative stimulation promotes additive plasticity in the human parietal-motor circuit

ObjectiveRepeated spaced sessions of repetitive transcranial magnetic stimulation (TMS) to the human primary motor cortex can lead to dose-dependent increases in motor cortical excitability. However, this has yet to be demonstrated in a defined cortical circuit. We aimed to examine the effects of repeated spaced cortical paired associative stimulation (cPAS) on excitability in the motor cortex. MethodscPAS was delivered to the primary motor cortex (M1) and posterior parietal cortex (PPC) with two coils. In the multi-dose condition, three sessions of cPAS were delivered 50-min apart. The single-dose condition had one session of cPAS, followed by two sessions of a control cPAS protocol. Motor-evoked potentials were evaluated before and up to 40 min after each cPAS session as a measure of cortical excitability. ResultsCompared to a single dose of cPAS, motor cortical excitability significantly increased after multi-dose cPAS. Increasing the number of cPAS sessions resulted in a cumulative, dose-dependent effect on excitability in the motor cortex, with each successive cPAS session leading to notable increases in potentiation. ConclusionRepeated spaced cPAS sessions summate to increase motor cortical excitability induced by single cPAS. SignificanceRepeated spaced cPAS could potentially restore abilities lost due to disorders like stroke.

Excitability of somatosensory cortex is increased in ALS: A SEP recovery function study

ObjectiveNeuronal loss in the somatosensory, as well as the motor cortex in amyotrophic lateral sclerosis (ALS), indicative of a structural abnormality has been reported. Previously we have shown that afferent inhibition was impaired in ALS, suggestive of sensory involvement. In this study, we aimed to evaluate excitability changes in the somatosensory cortex of ALS patients. MethodsALS patients underwent a paired pulse somatosensory evoked potential (SEP) paradigm at various interstimulus intervals (ISI). The amplitude ratio obtained by dividing the amplitude of paired pulse SEP stimulation S2 (paired pulse stimulation) to S1 (the single pulse stimulation) was considered the somatosensory cortex excitability parameter. Findings were compared to the results obtained from healthy controls. Resting motor threshold (RMT) was also assessed in the ALS group. ResultsAn increased S2/S1 ratio was found in the ALS group in every ISI examined. Additionally, the reduced inhibition correlated negatively with forced vital capacity, Medical Research Council sum score, median nerve compound muscle action potential amplitude, while there was a positive association with Penn upper motor neuron score and sural nerve conduction velocity. No correlation existed with RMT. ConclusionsOur findings demonstrated increased somatosensory cortical excitability in ALS, which was associated with clinical parameters such as reduced pulmonary function and motor strength. SignificanceSomatosensory cortical excitability is impaired in ALS. Whether this is associated with increased motor cortical excitability requires further studies.

Mechanisms of theta burst transcranial ultrasound induced plasticity in the human motor cortex

BackgroundTranscranial ultrasound stimulation (TUS) is a novel non-invasive brain stimulation technique with high depth penetrance and spatial resolution. Theta-burst TUS (tbTUS) is a plasticity-inducing protocol which increases motor cortical excitability for up to 30 min following 80s of sonication. While this protocol may have therapeutic potential for the treatment of psychiatric and neurological disorders, the mechanisms of action of TUS remain unclear. ObjectiveWe conducted the first pharmacological study to examine the mechanisms of TUS in human primary motor cortex. By administering brain-active drugs with known mechanisms of action, we aimed to elucidate the mechanisms of tbTUS. MethodsFourteen healthy subjects participated in a within-subjects randomized, double-blind, cross-over study with five visits. At each visit, one of four study drugs (carbamazepine – Na+ channel blocker, nimodipine – L-type Ca2+ channel blocker, lorazepam – positive allosteric modulator of gamma-aminobutyric acid (GABA) type A receptor, dextromethorphan – N-methyl-d-aspartate receptor antagonist) or placebo was administered in random order, followed by tbTUS. ResultsThe plasticity effects of tbTUS on motor cortex excitability measured by motor-evoked potential amplitudes elicited by transcranial magnetic stimulation were reduced by all study drugs compared to placebo. ConclusiontbTUS may induce NMDA-dependent synaptic plasticity since the effects are blocked by increased GABAA receptor activities and voltage-gated Na+ and Ca2+ channels blockers. These results are consistent with the hypotheses that tbTUS induced long-term potentiation-like mechanisms and that TUS involves activation of mechanosensitive Na+ and Ca2+ channels. Alternatively, non-specific pharmacologically induced changes in excitatory/inhibitory balance might have interfered with the effects of tbTUS.

Dual-hemispheric transcranial direct current stimulation (tDCS) over primary motor cortex does not affect movement selection.

Volition and sense of agency are two primary components of a voluntary or internally generated movement. It has been shown that movement selection cannot be altered without interfering with the sense of volition using single pulse transcranial magnetic stimulation over the primary motor cortex. In the current study, we aimed at examining whether modulating the cortical excitability of the final effector in the voluntary motor pathway—the primary motor cortex, using transcranial direct current stimulation (tDCS) would alter movement selection. Our hypothesis was that anodal tDCS would increase motor cortical excitability and thereby decrease the threshold for movement execution, which could favor selection of the contralateral hand. We recruited 13 healthy adults to perform a movement selection task involving free-choice and externally-cued trials while applying real/sham tDCS in a C3-C4 dual-hemispheric electrode montage. Contrary to our hypothesis, we did not observe any effect of tDCS on movement selection either at the individual or group level. However, our data confirms the strong preference of right-handed individuals for the dominant right hand. We also found higher reaction time for internally generated movement compared to externally triggered movement. We therefore conclude that movement selection cannot be influenced at the level of primary motor cortex and that brain areas upstream of the primary motor cortex in the voluntary motor pathway may be possible targets for influencing movement selection.

Impaired Motor Skill Acquisition Using Mirror Visual Feedback Improved by Transcranial Direct Current Stimulation (tDCS) in Patients With Parkinson's Disease.

Recent non-invasive brain stimulation techniques in combination with motor training can enhance neuroplasticity and learning. It is reasonable to assume that such neuroplasticity-based interventions constitute a useful rehabilitative tool for patients with Parkinson’s Disease (PD). Regarding motor skill training, many kinds of tasks that do not involve real motor movements have been applied to PD patients. The purpose of this study is to elucidate whether motor skill training using mirror visual feedback (MVF) is useful to patients with PD in order to improve untrained hand performance dependent on the time course of training; and whether MVF combined with anodal transcranial direct current stimulation (tDCS) over primary motor cortex (M1) causes an additional effect based on increased motor cortical excitability. Eighteen right-handed patients with PD in the off-medication state and 10 age-matched healthy subjects (HS) performed four sessions of right-hand ball rotation using MVF (intervention) on two separate days, 1 week apart (day 1 and day 2). HS subjects received only sham stimulation. The intervention included four sessions of motor-skill training using MVF for 20 min comprised of four sets of training for 30 s each. PD patients were randomly divided into two intervention groups without or with anodal tDCS over the right M1 contralateral to the untrained hand. As the behavior evaluation, the number of ball rotations of the left hand was counted before (pre) and immediately after (post) intervention on both days (pre day 1, post day 1, pre day 2, and post day 2). Motor evoked potential (MEP), input-output function, and cortical silent period were recorded to evaluate the motor cortical excitatory and inhibitory system in M1 pre day 1 and post day 2. The number of ball rotations of the left hand and the facilitation of MEP by intervention were significantly impaired in patients with PD compared to HS. In contrast, if anodal tDCS was applied to right M1 of patients with PD, the number of ball rotations in accordance with I-O function at 150% intensity was significantly increased after day 1 and retained until day 2. This finding may help provide a new strategy for neurorehabilitation improving task-specific motor memory without real motor movements in PD.

A short bout of high-intensity exercise alters ipsilesional motor cortical excitability post-stroke

ABSTRACT Background: Acute exercise can increase motor cortical excitability and enhance motor learning in healthy individuals, an effect known as exercise priming. Whether it has the same effects in people with stroke is unclear. Objectives: The objective of this study was to investigate whether a short, clinically-feasible high-intensity exercise protocol can increase motor cortical excitability in non-exercised muscles of chronic stroke survivors. Methods: Thirteen participants with chronic, unilateral stroke participated in two sessions, at least one week apart, in a crossover design. In each session, they underwent either high-intensity lower extremity exercise or quiet rest. Motor cortical excitability of the extensor carpi radialis muscles was measured bilaterally with transcranial magnetic stimulation before and immediately after either exercise or rest. Motor cortical excitability changes (post-exercise or rest measures normalized to pre-test measures) were compared between exercise vs. rest conditions. Results: All participants were able to reach the target high-intensity exercise level. Blood lactate levels increased significantly after exercise (p < .001, d = 2.85). Resting motor evoked potentials from the lesioned hemisphere increased after exercise (mean 1.66; 95% CI: 1.19, 2.13) compared to the rest condition (mean 1.23; 95% CI: 0.64, 1.82), p = .046, d = 2.76, but this was not the case for the non-lesioned hemisphere (p = .406, d = 0.25). Conclusions: High-intensity exercise can increase lesioned hemisphere motor cortical excitability in a non-exercised muscle post-stroke. Our short and clinically-advantageous exercise protocol shows promise as a potential priming method in stroke rehabilitation.

Learning from Goal and Action Based Observations Differentially Modulates Functional Motor Cortical Plasticity

Action observation can facilitate motor skill learning and lead to a memory trace in motor representations of action. However, it remains unclear whether the action itself or the goal of the action drive changes in motor representations after learning by observation. We performed two experiments. In Experiment 1, using serial reaction time task and transcranial magnetic stimulation, we showed that observation of right-hand actions during skill learning only increased left motor cortical excitability, leading to behavioral gains in the same hand as the observed hand. In contrast, observing a sequence of visual cue positions devoid of hand action increases motor cortical excitability in both hemispheres and facilitates motor skill learning in the right hand (Experiment 1) and left hand for a mirror-symmetric sequence (Experiment 2). We propose that the encoding of observed movements maps onto motor representations of the same action to form a limb-specific motor memory, whereas the learning of spatial goals forms memory traces in the motor representations in both hemispheres to prepare for potential action in either hand.

Impaired Sensorimotor Integration in Restless Legs Syndrome.

Objective: Restless legs syndrome (RLS) is a complicated sensorimotor syndrome that may be linked to changes in sensorimotor integration. The mechanism of such changes is unclear. The aim of this study was to investigate sensorimotor integration in patients with RLS through transcranial magnetic stimulation-motor evoked potentials (TMS-MEPs) preceded by peripheral electric stimulation.Methods: Fourteen RLS patients and 12 healthy, age-matched controls were investigated. The clinical severity of RLS was evaluated based on the International Criteria of the International Restless Legs Syndrome Study Group (IRLSSG) severity scores. The tibial and median H-reflexes and the resting motor threshold (RMT) of the abductor pollicis brevis (APB) were tested in all 26 subjects. The RMT of the tibialis anterior (TA) was tested in 8 patients and 7 controls. All 26 subjects underwent measurement of unconditioned MEPs of the APB. Electric pulses were applied to the right median nerve, followed by TMS pulses over the left motor cortex at interstimulus intervals (ISIs) of 20, 25, 30, 50, 100, 150, and 200 ms. Unconditioned MEPs of the TA were measured in 8 patients and 7 controls. Electric pulses were applied to the right peroneal nerve, followed by TMS pulses over the left motor cortex at ISIs of 30, 35, 45, 60, 100, and 200 ms. The degree of modulation of MEPs by electric stimulation was expressed as the ratio of the conditioned MEP amplitude to the unconditioned MEP amplitude. Ratios <1 indicated inhibition, and ratios >1 indicated facilitation.Results: No significant differences in RMT or H-reflex latencies or amplitudes were found between RLS patients and controls. A significant increase in unconditioned MEP amplitudes of the TA was observed in patients compared to controls (p = 0.03). Long-latency afferent inhibition (LAI) of the median nerve in RLS patients was decreased significantly at ISIs of 150 (p = 0.000) and 200 ms (p = 0.004). Upon peroneal nerve stimulation, no significant difference was observed between the two groups at any ISI.Conclusions: Our results suggest increased motor cortical excitability of the legs and disturbed sensorimotor integration in RLS patients; this disturbance might originate at the cortical level.

Fear-conditioned alterations of motor cortex excitability: The role of amygdala.

We hypothesized that fear-conditioning may increase motor cortical excitability in preparation for response to fear. We tested our hypothesis in healthy subjects and in the second step, to determine the role of amygdala in alterations of motor cortex excitability, we included a group of patients who previously underwent unilateral amygdalo-hippocampectomy for temporal lobe epilepsy. In the first step, we included 16 healthy volunteers. In the second step, 14 patients who previously underwent unilateral amygdalo-hippocampectomy for temporal lobe epilepsy and who were seizure-free were included in the study. Motor evoked potentials (MEPs) recorded over right hand were recorded twice before and after the observation of fearful faces (fear-conditioning). Auditory startle response (ASR) was also recorded. Comparisons of before and after fear-conditioning MEP parameters within the healthy subjects group showed MEP amplitude was higher after fear-conditioning (p=0.019). Same comparison in patients with unilateral amygdalo-hippocampectomy demonstrated shorter MEP latency (p=0.036) and higher MEP amplitudes after fear-conditioning (p=0.046). CSPs did not show any change after this paradigm in both groups. Comparisons of ASR findings before and after fear-conditioning demonstrated enhanced responses after fear-conditioning in both healthy subjects and in patients with unilateral amygdalo-hippocampectomy. For MEPs or ASRs, there was a similar enhancement in patients with left- or right-sided operation. Fear-potentiation of both corticospinal and reticulospinal pathways occurs in healthy humans and bilateral potentiation of ASR and potentiation of MEPs are maintained even after resection of unilateral amygdala regardless of its side.

S84 Subthalamic and GPI stimulation and cortical plasticity

Objectives Review the effects of subthalamic (STN) and internal globus pallidus (GPi) stimulation on cortical plasticity. Methods Several relevant studies are reviewed. Results Using paired associative stimulation, most studies found decreased plasticity in Parkinson’s disease (PD). Dopaminergic medications restored plasticity in patients without levodopa-induced dyskinesia but not in patients with dyskinesia. Early, drug naive PD patients had decreased plasticity on the more affected side but had exaggerated plasticity on the less affected side. This asymmetry in plastsicity decreased over 12 months, which may reflect reduced compensation. In dyskinetic PD patients treated with STN deep brain stimulation (DBS), cortical plasticity was deficient in the off medication state but was restored in the medication on state with the stimulator turned on. STN DBS increases motor cortical excitability at about 3 ms likely through antidromic activation of the hyperdirect pathway, and at 23 ms likely through the indirect pathway. Repeated pairing STN DBS and cortical magnetic stimulation at these specific intervals induced motor cortical plasticity in PD patients. Similarly, repeated pairing of GPi stimulation and cortical magnetic stimulation at specific intervals induced cortical plasticity in dystonia patients. Discussion Cortical plasticity appears to be decreased in PD patients and is partially restored in some patients on medications while increased plasticity may be a compensatory mechanism in early PD. Cortical plasticity is strongly influenced by the basal ganglia. Conclusion DBS can modulate and induce cortical plasticity in PD and dystonia. Significance Modulation of cortical plasticity may be involved in mediating the effects of DBS.

A Framework for Understanding the Relationship between Descending Pain Modulation, Motor Corticospinal, and Neuroplasticity Regulation Systems in Chronic Myofascial Pain.

Myofascial pain syndrome (MPS) is a leading cause of chronic musculoskeletal pain. However, its neurobiological mechanisms are not entirely elucidated. Given the complex interaction between the networks involved in pain process, our approach, to providing insights into the neural mechanisms of pain, was to investigate the relationship between neurophysiological, neurochemical and clinical outcomes such as corticospinal excitability. Recent evidence has demonstrated that three neural systems are affected in chronic pain: (i) motor corticospinal system; (ii) internal descending pain modulation system; and (iii) the system regulating neuroplasticity. In this cross-sectional study, we aimed to examine the relationship between these three central systems in patients with chronic MPS of whom do/do not respond to the Conditioned Pain Modulation Task (CPM-task). The CPM-task was to immerse her non-dominant hand in cold water (0−1°C) to produce a heterotopic nociceptive stimulus. Corticospinal excitability was the primary outcome; specifically, the motor evoked potential (MEP) and intracortical facilitation (ICF) as assessed by transcranial magnetic stimulation (TMS). Secondary outcomes were the cortical excitability parameters [current silent period (CSP) and short intracortical inhibition (SICI)], serum brain-derived neurotrophic factor (BDNF), heat pain threshold (HPT), and the disability related to pain (DRP). We included 33 women, (18–65 years old). The MANCOVA model using Bonferroni's Multiple Comparison Test revealed that non-responders (n = 10) compared to responders (n = 23) presented increased intracortical facilitation (ICF; mean ± SD) 1.43 (0.3) vs. 1.11 (0.12), greater motor-evoked potential amplitude (μV) 1.93 (0.54) vs. 1.40 (0.27), as well a higher serum BDNF (pg/Ml) 32.56 (9.95) vs. 25.59 (10.24), (P < 0.05 for all). Also, non-responders presented a higher level of DRP and decreased HPT (P < 0.05 for all). These findings suggest that the loss of net descending pain inhibition was associated with an increase in ICF, serum BDNF levels, and DRP. We propose a framework to explain the relationship and potential directionality of these factors. In this framework we hypothesize that increased central sensitization leads to a loss of descending pain inhibition that triggers compensatory mechanisms as shown by increased motor cortical excitability.

Whole body heat stress increases motor cortical excitability and skill acquisition in humans

ObjectiveVigorous systemic exercise stimulates a cascade of molecular and cellular processes that enhance central nervous system (CNS) plasticity and performance. The influence of heat stress on CNS performance and learning is novel. We designed two experiments to determine whether passive heat stress (1) facilitated motor cortex excitability and (2) improved motor task acquisition compared to no heat stress. MethodsMotor evoked potentials (MEPs) from the first dorsal interosseus (FDI) were collected before and after 30min of heat stress at 73°C. A second cohort of subjects performed a motor learning task using the FDI either following heat or the no heat condition. ResultsHeat stress increased heart rate to 65% of age-predicted maximum. After heat, mean resting MEP amplitude increased 48% (p<0.05). MEP stimulus–response amplitudes did not differ according to stimulus intensity. In the second experiment, heat stress caused a significant decrease in absolute and variable error (p<0.05) during a novel movement task using the FDI. ConclusionsPassive environmental heat stress (1) increases motor cortical excitability, and (2) enhances performance in a motor skill acquisition task. SignificanceControlled heat stress may prime the CNS to enhance motor skill acquisition during rehabilitation.

O047. The sound-induced flash illusions reveal visual cortex hyperexcitability in cluster headache.

Objectives Pathophysiology of cluster headache (CH) is not wellknown. Although posterior hypothalamus has been suggested to play a pivotal role, evidence exists of a more diffuse involvement of the central nervous system including brainstem and cerebral cortex. In this regard, we recently observed increased motor cortical excitability in episodic CH patients both outside and inside bout [1]. The sound-induced flash illusions (SIFI) represent an example of multisensory integration, and provide a tool to indirectly explore the excitability state of the visual cortex [2]. SIFI are classified as “fission” and “fusion” illusions. When one visual stimulus (flash) is accompanied by two or more auditory stimuli (beeps), it is often perceived as multiple flashes (fission illusion). Conversely, fusion illusion occurs when subjects perceive less number of flashes when these are presented with only one beep. On such bases, here we used SIFI to explore excitability of visual cortex in CH patients.

Spinal cord injury affects I-wave facilitation in human motor cortex.

Transcranial magnetic stimulation (TMS) is a useful non-invasive approach for studying cortical physiology. To further clarify the mechanisms of cortical reorganization after spinal cord injury (SCI), we used a non-invasive paired TMS protocol for the investigation of the corticospinal I-waves, the so-called I-wave facilitation, in eight patients with cervical SCI. We found that the pattern of I-wave facilitation significantly differs between SCI patients with normal and abnormal central motor conduction (CMCT), and healthy controls. The group with normal CMCT showed increased I-wave facilitation, while the group with abnormal CMCT showed lower I-wave facilitation compared to a control group. The facilitatory I-wave interaction occurs at the level of the motor cortex, and the mechanisms responsible for the production of I-waves are under control of GABA-related inhibition. Therefore, the findings of our small sample preliminary study provide further physiological evidence of increased motor cortical excitability in patients with preserved corticospinal projections. This is possibly due to decreased GABAergic intracortical inhibition. The excitability of networks producing short-interval intracortical facilitation could increase after SCI as a mechanism to enhance activation of residual corticospinal tract pathways and thus compensate for the impaired ability of the motor cortex to generate appropriate voluntary movements. Finally, the I-wave facilitation technique could be used in clinical neurorehabilitation as an additional method of assessing and monitoring function in SCI.

Sensorimotor event-related desynchronization represents the excitability of human spinal motoneurons

Amplitudes of mu and beta (7–26Hz) oscillations measured by electroencephalography over the sensorimotor areas are suppressed during motor imagery as well as during voluntary movements. This phenomenon is referred to as event-related desynchronization (ERD) and is known to reflect motor cortical excitability. The increased motor cortical excitability associated with ERD during hand motor imagery would induce a descending cortical volley to spinal motoneurons, resulting in facilitation of spinal motoneuronal excitability. Therefore, in the present study, we tested the association of ERD during motor imagery with the excitability of spinal motoneurons in 15 healthy participants. Spinal excitability was tested using the F-wave recorded from the right abductor pollicis brevis muscle. The F-wave results from antidromic activation of spinal motoneurons and is induced by peripheral nerve stimulation. Participants performed 5s of motor imagery of right thumb abduction following 7s of rest. The right median nerve was stimulated at wrist level when the ERD magnitude of the contralateral hand sensorimotor area exceeded predetermined thresholds during motor imagery. The results showed ERD magnitude during hand motor imagery was associated with an increase in F-wave persistence, but not with the response average of F-wave amplitude or F-wave latency. These findings suggest that the ERD magnitude may be a biomarker representing increases in the excitability of both cortical and spinal levels.

Enhanced motor cortex excitability after spinal cord injury.

Enhanced motor cortex excitability after spinal cord injury.

Whole-hand water flow stimulation increases motor cortical excitability: a study of transcranial magnetic stimulation and movement-related cortical potentials.

Previous studies examining the influence of afferent stimulation on corticospinal excitability have demonstrated that the intensity of afferent stimulation and the nature of the afferents targeted (cutaneous/proprioceptive) determine the effects. In this study, we assessed the effects of whole-hand water immersion (WI) and water flow stimulation (WF) on corticospinal excitability and intracortical circuits by measuring motor evoked potential (MEP) recruitment curves and conditioned MEP amplitudes. We further investigated whether whole-hand WF modulated movement-related cortical activity. Ten healthy subjects participated in three experiments, comprising the immersion of participants' right hands with (whole-hand WF) or without (whole-hand WI) water flow, and no immersion (control). We evaluated MEP recruitment curves produced by a single transcranial magnetic stimulation (TMS) pulse at increasing stimulus intensities, short-interval intracortical inhibition (SICI), and intracortical facilitation (ICF) using the paired TMS technique before and after 15 min of intervention. Movement-related cortical potentials (MRCPs) were evaluated to examine primary motor cortex, supplementary motor area, and somatosensory cortex excitability upon movement before and after whole-hand WF. After whole-hand WF, the slope of the MEP recruitment curve significantly increased, whereas SICI decreased and ICF increased in the contralateral motor cortex. The amplitude of the Bereitschaftspotential, negative slope, and motor potential of MRCPs significantly increased after whole-hand WF. We demonstrated that whole-hand WF increased corticospinal excitability, decreased SICI, and increased ICF, although whole-hand WI did not change corticospinal excitability and intracortical circuits. Whole-hand WF modulated movement-related cortical activity, increasing motor cortex activation for the planning and execution of voluntary movements.

Training in a ballistic task but not a visuomotor task increases responses to stimulation of human corticospinal axons

Short periods of training in motor tasks can increase motor cortical excitability. This study investigated whether changes also occur at a subcortical level. Subjects trained in ballistic finger abduction or visuomotor tracking. The right index finger rotated around the metacarpophalangeal (MCP) joint in a splint. Surface EMG was recorded from the first dorsal interosseous. Transcranial magnetic stimulation over the back of the head (double-cone coil) elicited cervicomedullary motor evoked potentials (CMEPs) by stimulation of corticospinal axons. Responses were recorded from the relaxed muscle before, between, and after two sets of training. In study 1 (n = 7), training comprised two sets of 150 maximal finger abductions. Feedback of acceleration was provided. With training, acceleration increased significantly. CMEPs increased to 248 ± 152% (± SD) of baseline immediately after training (P = 0.007) but returned to control level (155 ± 141%) 10 min later. In study 2 (n = 7), subjects matched MCP joint angle to a target path on a computer screen. After ∼30 min of training, tracking improved as shown by increased correlation between joint angle and the target pathway, reduced time lag, and reduced EMG(rms). However, CMEPs remained unchanged. These results show that transmission through the corticospinal pathway at a spinal level increased after repeated ballistic movements but not after training in a visuomotor task. Thus, changes at a spinal level may contribute to improved performance in some motor tasks.

Increased motor cortical excitability after whole-hand electrical stimulation: A TMS study

To examine the neuromodulatory effect of whole-hand mesh-glove (MG) stimulation on motor cortical pathways, we explored motor cortical excitability before and after suprathreshold whole-hand MG stimulation using transcranial magnetic stimulation (TMS). Twenty-eight healthy volunteers (14 controls) were studied at baseline, immediately post and 1h post-MG stimulation for 30 min. Motor thresholds (MTs), motor evoked potentials (MEPs) recruitment curve, short intracortical inhibition (SICI) and intracortical facilitation (ICF) after paired magnetic stimuli were evaluated. After MG stimulation the MTs were significantly reduced and slope of MEP recruitment curve significantly increased; furthermore, the stimulation led to a sustained decrease of SICI and increase of ICF in the contralateral motor cortex. These effects lasted for at least 60 min and were stronger 1h post-stimulation compared with testing immediately after stimulation. A sham group did not show any differences before and after MG stimulation. We provide a first demonstration that MG whole-hand stimulation induces increases in motor cortical excitability lasting at least 1h. Both the strength of the corticospinal projections and the inhibitory and facilitatory intracortical mechanisms are involved. Synaptic modifications such as long-term potentiation mechanisms may underlie this stimulation-induced cortical plasticity changes. Present results prove the MG stimulation to be a promising tool in neurorehabilitation.