Reduction Of Intracortical Inhibition Research Articles

Reduction of intracortical inhibition (ICI) correlates with cognitive performance and psychopathology symptoms in schizophrenia

Cognitive impairment is a core symptom of schizophrenia (SZ), with GABAergic dysfunction in the brain potentially serving as a critical pathological mechanism underlying this condition. Intracortical inhibition (ICI), which includes short-interval intracortical inhibition (SICI) and long-interval intracortical inhibition (LICI), can be used to assess the inhibitory function of cortical GABAergic neurons. The aim of this study was to investigate the relationship between ICI and cognitive function, as well as psychopathological symptoms, in SZ patients. We recruited 130 SZ patients and 105 healthy controls (HCs). All subjects underwent paired-pulse transcranial magnetic stimulation (ppTMS) measurements, which included resting motor threshold (RMT), SICI and LICI. The cognitive function of all subjects was assessed using the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery (MCCB). The psychopathological symptoms of the SZ group were assessed using the Positive and Negative Syndrome Scale (PANSS). We examined group differences in MCCB scores, RMT, SICI, and LICI. Within the SZ group, we assessed the relationship between ICI and cognitive function, as well as psychopathological symptoms. Two-way ANOVA, Mann–Whitney U test, Receiver operating characteristic (ROC) curves, and partial Spearman correlation analysis were performed. The SZ group showed a worse cognitive score in all 6 cognitive dimensions of the MCCB compared to the HC group (all p < 0.05). The SZ group had lower degree of SICI and LICI compared to the HC group (both p < 0.05). ROC curves analysis showed that SICI and LICI all displayed good performance in differentiating SZ patients and HCs (both p < 0.05), and SICI exhibited a better performance, yielding an area under the curve (AUC) of 0.856 (95% CI 0.807–0.904). Furthermore, in the SZ group, SICI demonstrated a significant negative correlation with PANSS positive score, negative score, general psychopathology score, and total score (all pBonferroni < 0.05), and LICI demonstrated a significant negative correlation with PANSS positive score, general psychopathology score and total score (all pBonferroni < 0.05). Additionally, in the SZ group, SICI demonstrated a significant positive correlation with speed of processing score, working memory score, verbal learning score, visual learning score, and reasoning and problem-solving score of the MCCB (all pBonferroni < 0.05), while LICI was only weakly positive correlated with speed of processing score of the MCCB (r = 0.247, p = 0.005, pBonferroni = 0.03). Our results demonstrate that the reduction of ICI could serve as a trait-dependent in-vivo biomarker of GABAergic deficits for SZ and related cognitive impairments.

Pairing with Enriched Sound Exposure Restores Auditory Processing Degraded by an Antidepressant.

Antidepressants, while effective in treating depression and anxiety disorders, also induce deficits in sensory (particularly auditory) processing, which in turn may exacerbate psychiatric symptoms. How antidepressants cause auditory signature deficits remains largely unknown. Here, we found that fluoxetine-treated adult female rats were significantly less accurate when performing a tone-frequency discrimination task compared with age-matched control rats. Their cortical neurons also responded less selectively to sound frequencies. The degraded behavioral and cortical processing was accompanied by decreased cortical perineuronal nets, particularly those wrapped around parvalbumin-expressing inhibitory interneurons. Furthermore, fluoxetine induced critical period-like plasticity in their already mature auditory cortices; therefore, a brief rearing of these drug-treated rats under an enriched acoustic environment renormalized auditory processing degraded by fluoxetine. The altered cortical expression of perineuronal nets was also reversed as a result of enriched sound exposure. These findings suggest that the adverse effects of antidepressants on auditory processing, possibly because of a reduction in intracortical inhibition, can be substantially alleviated by simply pairing drug treatment with passive, enriched sound exposure. They have important implications for understanding the neurobiological basis of antidepressant effects on hearing and for designing novel pharmacological treatment strategies for psychiatric disorders.SIGNIFICANCE STATEMENT Clinical experience suggests that antidepressants adversely affect sensory (particularly auditory) processing, which can exacerbate patients' psychiatric symptoms. Here, we show that the antidepressant fluoxetine reduces cortical inhibition in adult rats, leading to degraded behavioral and cortical spectral processing of sound. Importantly, fluoxetine induces a critical period-like state of plasticity in the mature cortex; therefore, a brief rearing under an enriched acoustic environment is sufficient to reverse the changes in auditory processing caused by the administration of fluoxetine. These results provide a putative neurobiological basis for the effects of antidepressants on hearing and indicate that antidepressant treatment combined with enriched sensory experiences could optimize clinical outcomes.

Cortical disinhibition in Parkinson's disease.

In Parkinson's disease, striatal dopamine depletion produces profound alterations in the neural activity of the cortico-basal ganglia motor loop, leading to dysfunctional motor output and parkinsonism. A key regulator of motor output is the balance between excitation and inhibition in the primary motor cortex, which can be assessed in humans with transcranial magnetic stimulation techniques. Despite decades of research, the functional state of cortical inhibition in Parkinson's disease remains uncertain. Towards resolving this issue, we applied paired-pulse transcranial magnetic stimulation protocols in 166 patients with Parkinson's disease (57 levodopa-naïve, 50 non-dyskinetic, 59 dyskinetic) and 40 healthy controls (age-matched with the levodopa-naïve group). All patients were studied OFF medication. All analyses were performed with fully automatic procedures to avoid confirmation bias, and we systematically considered and excluded several potential confounding factors such as age, gender, resting motor threshold, EMG background activity and amplitude of the motor evoked potential elicited by the single-pulse test stimuli. Our results show that short-interval intracortical inhibition is decreased in Parkinson's disease compared to controls. This reduction of intracortical inhibition was obtained with relatively low-intensity conditioning stimuli (80% of the resting motor threshold) and was not associated with any significant increase in short-interval intracortical facilitation or intracortical facilitation with the same low-intensity conditioning stimuli, supporting the involvement of cortical inhibitory circuits. Short-interval intracortical inhibition was similarly reduced in levodopa-naïve, non-dyskinetic and dyskinetic patients. Importantly, intracortical inhibition was reduced compared to control subjects also on the less affected side (n = 145), even in de novo drug-naïve patients in whom the less affected side was minimally symptomatic (lateralized Unified Parkinson's Disease Rating Scale part III = 0 or 1, n = 23). These results suggest that cortical disinhibition is a very early, possibly prodromal feature of Parkinson's disease.

P78-T Intracortical inhibition and facilitation after arm and face transplantation

Background Facial tissue and hand area are among the most specific regions of the cortex. The intracortical inhibition (ICI) and facilitation (ICF) of the human motor cortex is seen as a marker of brain plasticity. Material and methods In this study, ICI and ICF changes in the motor cortex were compared between six arm and face transplantation patients (3 arms/3 faces) and seven healthy volunteers. Paired-pulse transcranial magnetic stimulation was used to examine the presentation of Abductor Pollicis Brevis (APB) muscle in the brain. The MEP responses were recorded with surface EMG electrodes. The hot spot, subthreshold and supramaximal amplitude values of APB muscle were determined by single pulse TIntracortical inhibition and facilitation was examined by 1,2,3,4,5,6,7,8,9,10 ms interstimulus interval (ISI) double stimulation for ICI and 10,12,14,16,18,20,22,24,26,28,30 ms ISI for ICF. Results In normal cases, there was an inhibition of 76 ± 21% in 1–10 ms ISI double stimulation and there was 111 ± 14% facilitation in 10–30 ms ISI. No significant ICI (94 ± 4%) and ICF (81 ± 26%) was observed in the patients with face transplantation. However, ICI was more prominent in arm transplant cases (68 ± 46%) than normal cases and inhibition is continued to 10–30 ms ISI (64 ± 23%). Conclusions We found different cortical excitability pattern in arm and face transplantation patients; there is an intracortical inhibition in arm transplants but a reduction of intracortical inhibition and intracortical facilitation. We conclude that after transplantation there are dissimilar changes in the activity of intracortical interneuronal circuits of APB area in arm and face patients. This Project (215e012) was supported by TUBITAK.

Cortical contributions to anticipatory postural adjustments in the trunk.

Increases in activity of trunk muscles that occur prior to, or concurrent with, a voluntary limb movement are termed anticipatory postural adjustments (APAs). APAs are important for maintaining postural stability in response to perturbations but the neural mechanisms underlying APAs remain unclear. Our results showed that corticospinal excitability of erector spinae (ES) muscle increased at 40ms prior to rapid shoulder flexion, with a reduction in intracortical inhibition and no change in spinal excitability. Changes in corticospinal excitability were observed in ES, with similar excitability profiles between standing and lying positions, but were not observed in rectus abdominis. We suggest that the neural control of postural adjustments involves changes at a cortical level, which in part are due to reduced inhibition. Voluntary limb movements are associated with increases in trunk muscle activity, some of which occur within a time window considered too fast to be induced by sensory feedback; these increases are termed anticipatory postural adjustments (APAs). Although it is known that the function of APAs is to maintain postural stability in response to perturbations, excitability of the corticospinal projections to the trunk muscles during the APAs remains unclear. Thirty-four healthy subjects performed rapid shoulder flexion in response to a visual cue in standing and lying positions. Transcranial magnetic stimulation (TMS) was delivered over the trunk motor cortex to examine motor evoked potentials (MEPs) in erector spinae (ES) and in rectus abdominis (RA) muscles at several time points prior to the rise in electromyographic activity (EMG) of anterior deltoid (AD) muscle. TMS was also used to assess short-interval intracortical inhibition (SICI) and cervicomedullary MEPs (CMEPs) in ES in the standing position. MEPs in ES were larger at time points closer to the rise in AD EMG in both standing and lying positions, whereas MEPs in RA did not differ over the time course examined. Notably, SICI was reduced at time points closer to the rise in AD EMG, with no change in CMEPs. Our results demonstrate that increasing excitability of corticospinal projections to the trunk muscles prior to a voluntary limb movement is likely to be cortical in origin and is muscle specific.

Metaplasticity in human primary somatosensory cortex: effects on physiology and tactile perception.

Theta-burst stimulation (TBS) over human primary motor cortex evokes plasticity and metaplasticity, the latter contributing to the homeostatic balance of excitation and inhibition. Our knowledge of TBS-induced effects on primary somatosensory cortex (SI) is limited, and it is unknown whether TBS induces metaplasticity within human SI. Sixteen right-handed participants (6 females, mean age 23 yr) received two TBS protocols [continuous TBS (cTBS) and intermittent TBS (iTBS)] delivered in six different combinations over SI in separate sessions. TBS protocols were delivered at 30 Hz and were as follows: a single cTBS protocol, a single iTBS protocol, cTBS followed by cTBS, iTBS followed by iTBS, cTBS followed by iTBS, and iTBS followed by cTBS. Measures included the amplitudes of the first and second somatosensory evoked potentials (SEPs) via median nerve stimulation, their paired-pulse ratio (PPR), and temporal order judgment (TOJ). Dependent measures were obtained before TBS and at 5, 25, 50, and 90 min following stimulation. Results indicate similar effects following cTBS and iTBS; increased amplitudes of the second SEP and PPR without amplitude changes to SEP 1, and impairments in TOJ. Metaplasticity was observed such that TOJ impairments following a single cTBS protocol were abolished following consecutive cTBS protocols. Additionally, consecutive iTBS protocols altered the time course of effects when compared with a single iTBS protocol. In conclusion, 30-Hz cTBS and iTBS protocols delivered in isolation induce effects consistent with a TBS-induced reduction in intracortical inhibition within SI. Furthermore, cTBS- and iTBS-induced metaplasticity appear to follow homeostatic and nonhomeostatic rules, respectively.

Modulation of cortical and spinal inhibition with functional recovery of upper extremity motor function among patients with chronic stroke.

We hypothesized that recovery of upper extremity motor function is associated with reduction of intracortical inhibition and improved reciprocal inhibition. This study examines the relationships of functional recovery in chronic stroke with the intracortical inhibition and spinal reciprocal inhibition. Participants were 61 patients with chronic hemiparetic stroke. The participants were applied hybrid assistive neuromuscular dynamic stimulation (HANDS) therapy for 3 weeks. The Fugl-Meyer test upper extremity motor score (FM) and modified Ashworth scale (MAS) were assessed before (T0), immediately after (T1) and 3 months after (T2) the end of HANDS therapy. A paired pulse TMS paradigm was applied to assess short intracortical inhibition (SICI). Reciprocal inhibition (RI) was assessed with H reflex conditioning-test paradigm. FM and MAS were improved until T2. The change of FM from T0 to T2 was positively correlated with the change in affected SICI from T0 toT1. The change of wrist MAS from T0 to T1 was positively correlated with the change of RI. In chronic stroke patients with moderate or severe hemiparesis, well-recovered patients showed disinhibition of ipsilesional hemisphere and increased resiprocal inhibition of forearm.

Increased cortical excitability after selective REM sleep deprivation in healthy humans: A transcranial magnetic stimulation study

REM sleep has antiepileptogenic properties whereas, its loss is known to have a proconvulsive role. However, the mechanisms underlying the proepileptogenic effects of REM sleep deprivation are yet not fully understood. The aim of our study was to evaluate the effects of selective REM sleep deprivation (SRD) on cortical excitability in healthy subjects by means of transcranial magnetic stimulation (TMS). Ten normal subjects underwent three TMS sessions: (1) in baseline condition (BL), (2) after SRD by awakening them at each REM sleep onset and (3) after non-rapid eye movement sleep awakenings (NREM-A) as control for potential non-specific effects of interruptions. The TMS investigation included two protocols: (a) the evaluation of motor evoked potentials (MEPs) and silent period (SP) parameters, recorded in response to single pulse magnetic stimulation; (b) the evaluation of the time course of intracortical motor activity tested with paired-pulse TMS applied at inter-stimulus intervals of 1-10 ms. After SRD the principal finding observed using single pulse TMS was a significant reduction in the duration of SP whereas, a reduction of intracortical inhibition was found, using the paired-pulse TMS. TMS parameters did not show significant changes after NREM-A with respect to BL. SRD may influence cortical excitability with a reduction of inhibitory intracortical mechanisms, thus supporting the proconvulsant role of REM loss.

Enriched experience and recovery from amblyopia in adult rats: Impact of motor, social and sensory components

Amblyopia is one of the most common forms of visual impairment, arising from an early functional imbalance between the two eyes. It is currently accepted that, due to a lack of neural plasticity, amblyopia is an untreatable pathology in adults. Environmental enrichment (EE) emerged as a strategy highly effective in restoring plasticity in adult animals, eliciting recovery from amblyopia through a reduction of intracortical inhibition. It is unknown whether single EE components are able to promote plasticity in the adult brain, crucial information for designing new protocols of environmental stimulation suitable for amblyopic human subjects. Here, we assessed the effects of enhanced physical exercise, increased social interaction, visual enrichment or perceptual learning on visual function recovery in adult amblyopic rats. We report a complete rescue of both visual acuity and ocular dominance in exercised rats, in animals exposed to visual enrichment and in animals engaged in perceptual learning. These effects were accompanied by a reduced inhibition/excitation balance in the visual cortex. In contrast, we did not detect any sign of recovery in socially enriched rats or in animals practicing a purely associative visual task. These findings could have a bearing in orienting clinical research in the field of amblyopia therapy.

OP Brain and environment: towards an endogenous pharmacology

Experience-dependent plasticity in the visual cortex declines after the critical period. This limits the capacity of the adult visual system to recover from pathological conditions due to developmental defects or damage. Therefore, one outstanding challenge is to find strategies enhancing plasticity in the adult. Here we report that environmental enrichment (EE) or fluoxetine treatment restore plasticity in the adult visual cortex of the rat. In addition we present results on the effects of enrichment of prenatal babies or of babies soon after birth. We evaluated recovery of visual functions in adult Long-Evans hooded rats rendered amblyopic by long-term monocular deprivation and then subjected to reverse eye-lid suture (RS) under two different experimental conditions: (1) They were reared in an EE setting for 3 weeks, or (2) They were chronically treated with fluoxetine for 4 weeks (in this case, RS was performed during the last 2 weeks of antidepressant treatment). Visual acuity and ocular dominance were assessed in both groups using electrophysiological recordings or behavioural methods. We found that either EE and fluoxetine administration promoted a full recovery of visual functions in adult amblyopic animals. These effects were accompanied by reduced intracortical inhibition and increased expression of BDNF in the visual cortex. Cortical administration of diazepam totally prevented amblyopia recovery, indicating that the reduction of intracortical inhibition directly promotes visual cortical plasticity in the adult. Our results highlight a potential clinical application for EE and antidepressants in neurological disorders in which neuronal plasticity is compromised because of excessive intracortical inhibition.

Food restriction enhances visual cortex plasticity in adulthood

Neural circuits display a heightened sensitivity to external stimuli during well-established windows in early postnatal life. After the end of these critical periods, brain plasticity dramatically wanes. The visual system is one of the paradigmatic models for studying experience-dependent plasticity. Here we show that food restriction can be used as a strategy to restore plasticity in the adult visual cortex of rats. A short period of food restriction in adulthood is able both to reinstate ocular dominance plasticity and promote recovery from amblyopia. These effects are accompanied by a reduction of intracortical inhibition without modulation of brain-derived neurotrophic factor expression or extracellular matrix structure. Our results suggest that food restriction could be investigated as a potential way of modulating plasticity.

Reduced intra-cortical inhibition after sleep deprivation: A transcranial magnetic stimulation study

Sleep deprivation has multiple effects on brain function. It increases the risk for epileptic seizures both in healthy individuals and in patients with epilepsy. Furthermore it represents an effective antidepressive intervention with rapid onset. However, the mechanisms underlying these effects are still largely unknown [2]. Transcranial magnetic stimulation (TMS) can be used as a non-invasive method for the measurement of motor cortex excitability. Here we used TMS for assessing sleep deprivation effects on cortical excitability in healthy individuals. Before and after 24 h of sleep deprivation, parameters of cortical excitability (resting motor threshold, short intracortical inhibition, intracortical facilitation, cortical silent period) were measured in a sample of 15 healthy volunteers (11 women, 4 men, aged between 21 and 30 years with a mean of 24.3 ± 2.7 years). We detected a significant ( p = 0.042) reduction of short intracortical inhibition (SICI) after sleep deprivation. Motor threshold, intracortical facilitation and contralateral silent period remained unchanged. Our results confirm previous studies which have demonstrated changes of SICI after sleep deprivation. Our findings further suggest that the increased risk for epileptic seizures after sleep deprivation is mediated by a reduction of intracortical inhibition. Whether this mechanism is also involved in mediating the antidepressant effect of sleep deprivation has to be addressed by further studies in depressive patients.

L-dopa modulates motor cortex excitability in Alzheimer’s disease patients

In Alzheimer's disease (AD), transcranial magnetic stimulation (TMS) studies have shown abnormalities of motor cortical excitability, such as a decreased intra-cortical inhibition (ICI) and changes in resting motor threshold (rMT). We studied the effects of L-dopa on rMT and ICI in a cohort of moderate AD patients after paired-pulse TMS. Results were compared with a control group of healthy subjects. As expected, AD patients showed a significant reduction in ICI and a lower rMT. L-dopa administration (soluble form, melevodopa 200 mg) promptly reversed the ICI impairment up to normalization. This effect was specific, since it was not mimicked in control subjects. These results indicate a possible role of dopamine in modulating AD cortical excitability, thus suggesting an interaction between dopaminergic ascending pathways and endogenous intracortical transmitters. In addition, considering that L-dopa showed a pharmacological profile similar to the one of cholinomimetics, L-dopa might represent a reliable tool to study new therapeutic perspective and strategies for AD.

Environmental enrichment in adulthood promotes amblyopia recovery through a reduction of intracortical inhibition

Loss of visual acuity caused by abnormal visual experience during development (amblyopia) is an untreatable pathology in adults. We report that environmental enrichment in adult amblyopic rats restored normal visual acuity and ocular dominance. These effects were due to reduced GABAergic inhibition in the visual cortex, accompanied by increased expression of BDNF and reduced density of extracellular-matrix perineuronal nets, and were prevented by enhancement of inhibition through benzodiazepine cortical infusion.

Reduction of Intracortical Inhibition in Soleus Muscle During Postural Activity

Short-interval intracortical inhibition (SICI) decreases during voluntary contraction of the target muscle. It is unknown whether this effect also occurs with postural contractions. We have compared the effects of voluntary and postural contractions on SICI in the soleus (SOL) muscle. We applied transcranial magnetic stimuli (TMS) in subjects under three tasks: sitting at rest (Rest), sitting while activating the SOL muscle (Voluntary), or standing quietly (Postural). In control trials, we applied suprathreshold TMS to obtain unconditioned motor-evoked potentials (MEPs). In test trials, the same TMS was preceded by a subthreshold TMS at different interstimulus intervals (ISIs), to obtain a conditioned MEP. SICI and intracortical facilitation (ICF) were expressed as the decrease or increase in MEP size relative to unconditioned MEPs. There was significant effect of task in mean SICI or mean ICF in SOL. Mean SICI in SOL was 52% in Rest and decreased to 21% in Voluntary and 15% in Postural. Mean ICF in SOL was 132% and decreased to 113% in Voluntary and to 108% in Postural. Mean SICI in SOL was not different in Voluntary and Postural tasks. There was no effect of task in mean SICI or mean ICF in TA. Our results indicate that decrease of SICI with muscle contraction occurs to a similar extent with tonic voluntary and postural activation, suggesting that those contractions require a similar type of cortical involvement. However, it cannot be excluded that some part of the SICI reduction with muscle contraction depends on changes in segmental excitability.

Abnormal cortical excitability in sporadic but not homozygous D90A SOD1 ALS

Background: Excitotoxicity is one pathogenic mechanism proposed in amyotrophic lateral sclerosis (ALS), and loss of cortical inhibitory influence may be contributory. Patients with ALS who are homozygous for the D90A...

Different TMS patterns of intracortical inhibition in early onset Alzheimer dementia and frontotemporal dementia

Objective: To investigate putative changes in cortical excitability of patients affected by early-onset mild dementia by means of transcranial magnetic stimulation (TMS) and to verify whether a peculiar neurophysiological profile may contribute to characterise Alzheimer's disease (AD) vs frontotemporal dementia (FTD). Methods: Motor threshold and intracortical inhibition (ICI) and facilitation (ICF) after paired-pulse TMS (inter-stimulus intervals from 1 to 20 ms) were studied in two groups of early-onset demented patients with a neuropsychological profile suggestive of AD ( n=12) and FTD ( n=8). Twelve age-matched healthy subjects were considered as control group. In both patient groups, recordings were performed before and after a single oral dose of 4 mg galantamine. Results: No significant difference in motor threshold was observed among the three studied groups. On the contrary, early-onset AD showed a significant reduction of ICI compared to control group, no changes were detected in FTD patients. No significant changes in ICF were found between both patient groups and healthy subjects. The acute administration of galantamine reversed the modified ICI in AD group. Conclusions: The differential pattern of ICI exhibited by early-onset AD vs FTD in the early stage of disease may represent a non-invasive, reproducible electrophysiological tool, which may contribute to early differential diagnosis and, possibly, to monitor therapeutic effectiveness. Significance: The present results support the possibility that subtle, early modifications in intracortical circuitry features AD, but not FTD patients.

Changes in motor cortical excitability in humans following orally administered theophylline

The effects of theophylline on human corticospinal excitability were studied using transcranial magnetic stimulation (TMS) before and after double-blind oral administration of theophylline or placebo in 20 healthy volunteers. TMS measurements included resting and active motor threshold, silent period, intracortical inhibition (ICI), and intracortical facilitation. F-wave and compound muscle action potential (CMAP) were also measured. Theophylline produces a reduction in ICI, while other parameters of corticospinal excitability remained unaffected. Since ICI is thought to depend on GABA A intracortical inhibitory mechanisms, our data suggest that the increase of human motor cortex excitability is the result of a decrease in GABAergic transmission. Our results further support the hypothesis that theophylline might induce convulsions by inhibiting GABA A receptor binding.

Focal reduction of intracortical inhibition in the motor cortex by selective proprioceptive stimulation

The influence of proprioception on motorcortical excitability was assessed by muscle vibration (MV; 80 Hz, 0.5 mm amplitude) of the flexor carpi radialis muscle (FCR) and compared to voluntary contraction and relaxation conditions. Motor thresholds, motor-evoked potentials (MEPs) in response to single pulses of transcranial magnetic stimulation (TMS) and the intracortical inhibition (ICI) and facilitation (ICF) after paired magnetic stimuli were studied. A control experiment using TMS inducing posteriorly directed current was performed. MEPs were recorded simultaneously from the FCR, the extensor carpi radialis, the abductor pollicis brevis and the first dorsal interosseus. In the FCR, MV led to an increase of excitability shown by a decrease of motor threshold, a facilitation of MEPs in response to single-pulse TMS, a reduction of ICI and an increase of ICF. Since especially the ICI and ICF remain unchanged in other recorded muscles, this increase of excitability is specific for the vibrated muscle. With posteriorly directed current the ICI in the FCR was reduced as well, showing an involvement of later I-waves. We suggest that MV induces a focused motorcortical activation which relies on a reduced activity of intracortical inhibitory interneuronal circuits targeting selectively the motorcortical representation of the vibrated muscle.

Modulation of motor cortex excitability in the left hemisphere during action observation: a single- and paired-pulse transcranial magnetic stimulation study of self- and non-self-action observation

Motor system excitability was tested by transcranial magnetic stimulation (TMS), and F-wave and H-reflex evaluation in different action observation tasks. Our aim was to investigate the effects produced by self- versus non-self-hand movement observation (MO). No significant differences were found between the self- and non-self-conditions. Movement observation significantly modulated motor cortex excitability, producing an increase in the amplitude of motor evoked potentials (MEPs) with a single magnetic pulse and a reduction in intracortical inhibition (ICI) with paired-pulse stimulation. No significant changes were found in motor cortex excitability during the observation of geometric objects. Motor imagery produced similar effects to those of action observation; no significant differences in modulation of motor system excitability between motor imagery and action observation were found in those muscles involved in actual motor execution. No significant effect on spinal excitability was found in any of the test conditions.