Changes In Cortical Excitability Research Articles

Older Adults Differentially Modulate Transcranial Magnetic Stimulation–Electroencephalography Measures of Cortical Inhibition during Maximal Single-joint Exercise

The effects of muscle fatigue are known to be altered in older adults, and age-related changes in the brain are likely to be a contributing factor. However, the neural mechanisms underlying these changes are not known. The aim of the current study was to use transcranial magnetic stimulation combined with electroencephalography (TMS–EEG) to investigate age-related changes in cortical excitability with muscle fatigue. In 23 young (mean age ± SD: 22 ± 2 years) and 17 older (mean age ± SD: 68.3 ± 5.6 years) adults, single-pulse TMS–EEG was applied before, during and after the performance of fatiguing, intermittent isometric abduction of the index finger. Motor-evoked potential (MEP) measures of cortical excitability were increased during (estimated mean difference, 123.3%; P < 0.0001) and after (estimated mean difference, 117.5%; P = 0.001) fatigue and this was not different between groups (P > 0.5). For TMS–EEG, the amplitude of the P30 and P180 potentials were unaffected by fatigue in older participants (P > 0.05). In contrast, the amplitude of the N45 potential in older adults was significantly reduced both during (positive cluster: mean voltage difference = 0.7 µV, P < 0.005; negative cluster: mean voltage difference = 0.9 µV, P < 0.0005) and after (mean voltage difference = 0.5 µV, P < 0.005) fatiguing exercise, whereas this response was absent in young participants. These results suggest that performance of maximal intermittent isometric exercise in old but not young adults is associated with modulation of cortical inhibition likely mediated by activation of gamma-aminobutyric acid type A receptors.

The Task at Hand: Fatigue-Associated Changes in Cortical Excitability during Writing.

Measures of corticospinal excitability (CSE) made via transcranial magnetic stimulation (TMS) depend on the task performed during stimulation. Our purpose was to determine whether fatigue-induced changes in CSE made during a conventional laboratory task (isometric finger abduction) reflect the changes measured during a natural motor task (writing). We assessed single-and paired-pulse motor evoked potentials (MEPs) recorded from the first dorsal interosseous (FDI) of 19 participants before and after a fatigue protocol (submaximal isometric contractions) on two randomized days. The fatigue protocol was identical on the two days, but the tasks used to assess CSE before and after fatigue differed. Specifically, MEPs were evoked during a writing task on one day and during isometric finger abduction to a low-level target that matched muscle activation during writing on the other day. There was greater variability in MEP amplitude (F (1,18) = 13.55, p < 0.01) during writing compared to abduction. When participants were divided into groups according to writing style (printers, n = 8; cursive writers, n = 8), a task x fatigue x style interaction was revealed for intracortical facilitation (F (1,14) = 9.90, p < 0.01), which increased by 28% after fatigue in printers but did not change in cursive writers nor during the abduction task. This study is the first to assess CSE during hand-writing. Our finding that fatigue-induced changes in intracortical facilitation depend on the motor task used during TMS, highlights the need to consider the task-dependent nature of CSE when applying results to movement outside of the laboratory.

Modulation of I-wave generating pathways by theta-burst stimulation: a model of plasticity induction.

Mechanisms underlying plasticity induction by repetitive transcranial magnetic stimulation protocols such as intermittent theta-burst stimulation (iTBS) remain poorly understood. Individual response to iTBS is associated with recruitment of late indirect wave (I-wave) generating pathways that can be probed by the onset latency of transcranial magnetic stimulation applied to primary motor cortex (M1) at different coil orientations. We found an association between late I-wave recruitment [reflected by anterior-posterior (AP)-lateromedial (LM) latency; i.e. the excess latency of motor-evoked potentials generated by transcranial magnetic stimulation with an AP orientation over the latency of motor-evoked potentials evoked by direct activation of corticospinal axons using LM stimulation] and changes in cortical excitability following iTBS, confirming previous studies. AP-LM latency significantly decreased following iTBS, and this decrease correlated with the iTBS-induced increase in cortical excitability across subjects. Plasticity in the motor network may in part derive from a modulation of excitability and the recruitment of late I-wave generating cortical pathways. Plasticity-induction following theta burst transcranial stimulation (TBS) varies considerably across subjects, and the underlying neurophysiological mechanisms remain poorly understood, representing a challenge for scientific and clinical applications. In human motor cortex (M1), recruitment of indirect waves (I-waves) can be probed by the excess latency of motor-evoked potentials elicited by transcranial magnetic stimulation with an anterior-posterior (AP) orientation over the latency of motor-evoked potentials evoked by direct activation of corticospinal axons using lateromedial (LM) stimulation, referred to as the 'AP-LM latency' difference. Importantly, AP-LM latency has been shown to predict individual responses to TBS across subjects. We, therefore, hypothesized that the plastic changes in corticospinal excitability induced by TBS are the result, at least in part, of changes in excitability of these same I-wave generating pathways. In 20 healthy subjects, we investigated whether intermittent TBS (iTBS) modulates I-wave recruitment as reflected by changes in the AP-LM latency. As expected, we found that AP-LM latencies before iTBS were associated with iTBS-induced excitability changes. A novel finding was that iTBS reduced AP-LM latency, and that this reduction significantly correlated with changes in cortical excitability observed following iTBS: subjects with larger reductions in AP-LM latencies featured larger increases in cortical excitability following iTBS. Our findings suggest that plasticity-induction by iTBS may derive from the modulation of I-wave generating pathways projecting onto M1, accounting for the predictive potential of I-wave recruitment. The excitability of I-wave generating pathways may serve a critical role in modulating motor cortical excitability and hence represent a promising target for novel repetitive transcranial magnetic stimulation protocols.

Sustained Maximal Voluntary Contractions Elicit Different Neurophysiological Responses in Upper- and Lower-Limb Muscles in Men

This study compared the effects of fatigue on corticospinal responsiveness in the upper- and lower-limb muscles of the same participants. Seven healthy males performed a 2-min maximal voluntary isometric contraction of the elbow flexors or knee extensors on four separate days. Electromyographic responses were elicited by nerve stimulation (maximal M-wave) in all sessions and by transcranial magnetic stimulation (motor-evoked potential; silent period) and spinal tract stimulation (cervicomedullary or thoracic motor-evoked potentials; silent period) in one session each per limb. During sustained maximal voluntary contractions, motor-evoked potential area normalised to M-waves increased from baseline in biceps brachii (155 ± 55%) and rectus femoris (151 ± 44%) (both p ≤ 0.045). At the end of maximal voluntary contractions, spinal tract motor-evoked potential area normalised to M-waves was smaller than baseline in biceps brachii (74 ± 23%; p = 0.012) but not rectus femoris (108 ± 40%; p = 0.999). The ratio of motor-evoked potential to spinal tract-evoked potential areas increased dramatically from 90 to 115 s in biceps brachii (p = 0.001) but not in rectus femoris (p = 0.999). Silent period durations increased similarly in both muscles (p ≤ 0.008) after transcranial and spinal stimulation. Sustained maximal contractions elicit different neurophysiological adjustments in upper- and lower-limb muscles. Specifically, motoneuronal excitability was reduced in biceps brachii, but not in rectus femoris, and this reduction required greater compensatory adjustments from the motor cortex. Therefore, changes in cortical and spinal excitability during sustained maximal exercise are likely specific to the muscle performing the task.

MRI-based visualization of rTMS-induced cortical plasticity in the primary motor cortex.

Repetitive transcranial magnetic stimulation (rTMS) induces changes in cortical excitability for minutes to hours after the end of intervention. However, it has not been precisely determined to what extent cortical plasticity prevails spatially in the cortex. Recent studies have shown that rTMS induces changes in “interhemispheric” functional connectivity, the resting-state functional connectivity between the stimulated region and the symmetrically corresponding region in the contralateral hemisphere. In the present study, quadripulse stimulation (QPS) was applied to the index finger representation in the left primary motor cortex (M1), while the position of the stimulation coil was constantly monitored by an online navigator. After QPS application, resting-state functional magnetic resonance imaging was performed, and the interhemispheric functional connectivity was compared with that before QPS. A cluster of connectivity changes was observed in the stimulated region in the central sulcus. The cluster was spatially extended approximately 10 mm from the center [half width at half maximum (HWHM): approximately 3 mm] and was extended approximately 20 mm long in depth (HWHM: approximately 7 mm). A localizer scan of the index finger motion confirmed that the cluster of interhemispheric connectivity changes overlapped spatially with the activation related to the index finger motion. These results indicate that cortical plasticity in M1 induced by rTMS was relatively restricted in space and suggest that rTMS can reveal functional dissociation associated with adjacent small areas by inducing neural plasticity in restricted cortical regions.

Transcranial random noise stimulation (tRNS): a wide range of frequencies is needed for increasing cortical excitability

Transcranial random noise stimulation (tRNS) is a recent neuromodulation protocol. The high-frequency band (hf-tRNS) has shown to be the most effective in enhancing neural excitability. The frequency band of hf-tRNS typically spans from 100 to 640 Hz. Here we asked whether both the lower and the higher half of the high-frequency band are needed for increasing neural excitability. Three frequency ranges (100–400 Hz, 400–700 Hz, 100–700 Hz) and Sham conditions were delivered for 10 minutes at an intensity of 1.5 mA over the primary motor cortex (M1). Single-pulse transcranial magnetic stimulation (TMS) was delivered over the same area at baseline, 0, 10, 20, 30, 45 and 60 minutes after stimulation, while motor evoked potentials (MEPs) were recorded to evaluate changes in cortical excitability. Only the full-band condition (100–700 Hz) was able to modulate excitability by enhancing MEPs at 10 and 20 minutes after stimulation: neither the higher nor the lower sub-range of the high-frequency band significantly modulated cortical excitability. These results show that the efficacy of tRNS is strictly related to the width of the selected frequency range.

Dissociation between cortical and spinal excitability of the antagonist muscle during combined motor imagery and action observation

Inhibitory neural control of antagonist muscle is one of the fundamental neural mechanism of coordinated human limb movement. Previous studies have revealed that motor execution (ME) and motor imagery (MI) share many common neural substrates; however, whether inhibitory neural activity occurs during MI remains unknown. In addition, recent studies have demonstrated that a combined MI and action observation (MI + AO) produces strong neurophysiological changes compared with MI or AO alone. Therefore, we investigated inhibitory changes in cortical and spinal excitability of the antagonist muscle during MI + AO and ME. Single-pulse transcranial magnetic stimulation (TMS) experiments revealed that corticospinal excitability of the antagonist muscle was decreased during MI + AO. Conversely, F-wave experiments showed that F-wave persistence of the antagonist muscle increased. Paired-pulse TMS experiment also demonstrated that short-interval intracortical inhibition (SICI) did not contribute to this inhibition. Therefore, cortical mediated inhibition, except for SICI, may be related to this inhibition. Conversely, such clear inhibition of the antagonist muscle was not observed during ME, presumably owing to the effects of muscle contraction to decelerate the movements and/or sensory input accompanying the joint movements. These findings provide important insights into the neurophysiological differences between MI + AO and ME.

Effects of single-session cathodal transcranial direct current stimulation on tic symptoms in Tourette\u2019s syndrome

Tourette syndrome is a neurodevelopmental disorder characterised by motor and phonic tics. For some, tics can be managed using medication and/or forms of behavioural therapy; however, adverse side effects and access to specialist resources can be barriers to treatment. In this sham-controlled brain stimulation study, we investigated the effects of transcranial direct current stimulation (tDCS) on the occurrence of tics and motor cortical excitability in individuals aged 16–33 years with Tourette syndrome. Changes in tics were measured using video recordings scored using the RUSH method (Goetz et al. in Mov Disord 14:502–506, 1999) and changes in cortical excitability were measured using single-pulse transcranial magnetic stimulation (spTMS) over the primary motor cortex (M1). Video recordings and spTMS measures were taken before and after 20 min of sham or active tDCS: during which cathodal current was delivered to an electrode placed above the supplementary motor area (SMA). Tic impairment scores, calculated from the video data, were significantly lower post-cathodal stimulation in comparison with post-sham stimulation; however, the interaction between time (pre/post) and stimulation (cathodal/sham) was not significant. There was no indication of a statistically significant change in M1 cortical excitability following SMA stimulation. This study presents tentative evidence that tDCS may be helpful in reducing tics for some individuals, and provides a foundation for larger scale explorations of the use of tDCS as a treatment for reducing tics.

Effects of L-DOPA on quadripulse magnetic stimulation–induced long-term potentiation in older adults

Reduced cortical plasticity has been previously reported in older adult as compared with young adults. However, the effects of dopamine on this plasticity reduction remain unknown. Here, we assessed the effects of high-dose (200 mg) and medium-dose (100 mg) L-3,4-dihydroxyphenylalanine (L-DOPA) intake on the long-term potentiation (LTP)-like effect induced by quadripulse magnetic stimulation (QPS) in older adults (aged ∼65 years). The subjects were 32 (200 mg) and 20 (100 mg) healthy older adult volunteers. This study was designed as a double-blind, crossover and placebo-controlled trial on one dose of L-dopa. Two hours after taking L-DOPA or placebo-drug, QPS was applied over the motor cortex. Motor evoked potentials were recorded to evaluate the motor cortical excitability changes. We found that both doses of L-DOPA enhanced LTP after QPS in older adults as one group. We classified subjects into QPS responders and QPS nonresponders. Both L-DOPA doses produced significant LTP enhancement in QPS nonresponders, whereas either of doses did not produce significant LTP enhancement in QPS responders. Collectively, our findings suggest that the neural plasticity reductions observed in older adults could be partly improved by dopamine.

Somatosensory cortical excitability changes precede those in motor cortex during human motor learning.

Motor learning is associated with plasticity in both motor and somatosensory cortex. It is known from animal studies that tetanic stimulation to each of these areas individually induces long-term potentiation in its counterpart. In this context it is possible that changes in motor cortex contribute to somatosensory change and that changes in somatosensory cortex are involved in changes in motor areas of the brain. It is also possible that learning-related plasticity occurs in these areas independently. To better understand the relative contribution to human motor learning of motor cortical and somatosensory plasticity, we assessed the time course of changes in primary somatosensory and motor cortex excitability during motor skill learning. Learning was assessed using a force production task in which a target force profile varied from one trial to the next. The excitability of primary somatosensory cortex was measured using somatosensory evoked potentials in response to median nerve stimulation. The excitability of primary motor cortex was measured using motor evoked potentials elicited by single-pulse transcranial magnetic stimulation. These two measures were interleaved with blocks of motor learning trials. We found that the earliest changes in cortical excitability during learning occurred in somatosensory cortical responses, and these changes preceded changes in motor cortical excitability. Changes in somatosensory evoked potentials were correlated with behavioral measures of learning. Changes in motor evoked potentials were not. These findings indicate that plasticity in somatosensory cortex occurs as a part of the earliest stages of motor learning, before changes in motor cortex are observed.NEW & NOTEWORTHY We tracked somatosensory and motor cortical excitability during motor skill acquisition. Changes in both motor cortical and somatosensory excitability were observed during learning; however, the earliest changes were in somatosensory cortex, not motor cortex. Moreover, the earliest changes in somatosensory cortical excitability predict the extent of subsequent learning; those in motor cortex do not. This is consistent with the idea that plasticity in somatosensory cortex coincides with the earliest stages of human motor learning.

Changes of motor cortical excitability and response inhibition in patients with obsessive–compulsive disorder

Deficits in cortical inhibitory processes have been suggested as underlying pathophysiological mechanisms of obsessive–compulsive disorder (OCD). We examined whether patients with OCD have altered cortical excitability using paired-pulse transcranial magnetic stimulation (TMS). We also tested associations between TMS indices and OCD-related characteristics, including age of onset and response inhibition in the go/no-go paradigm, to examine whether altered cortical excitability contributes to symptom formation and behavioural inhibition deficit in patients with OCD. We assessed motor cortex excitability using paired-pulse TMS in 51 patients with OCD and 39 age-matched healthy controls. We also assessed clinical symptoms and response inhibition in the go/nogo task. All patients were undergoing treatment with serotonin reuptake inhibitors. We performed repeated-measures multivariate analysis of covariance to compare TMS indices between patients with OCD and controls. Compared to controls, patients with OCD showed a shorter cortical silent period and decreased intracortical facilitation. However, we found no significant difference between groups for resting motor threshold or short-interval intracortical inhibition. In the OCD group, the shortened cortical silent period was associated with a prompt reaction time in the go/no-go task and with early onset of OCD. We could not exclude the influence of medications on motor cortex excitability. These findings suggest abnormal cortical excitability in patients with OCD. The associations between cortical silent period and response inhibition and age of onset further indicate that altered cortical excitability may play an important role in the development of OCD.

A ketogenic diet normalizes interictal cortical but not subcortical responsivity in migraineurs

BackgroundA short ketogenic diet (KD) treatment can prevent migraine attacks and correct excessive cortical response. Here, we aim to prove if the KD-related changes of cortical excitability are primarily due to cerebral cortex activity or are modulated by the brainstem.MethodsThrough the stimulation of the right supraorbital division of the trigeminal nerve, we concurrently interictally recorded the nociceptive blink reflex (nBR) and the pain-related evoked potentials (PREP) in 18 migraineurs patients without aura before and after 1-month on KD, while in metabolic ketosis. nBR and PREP reflect distinct brain structures activation: the brainstem and the cerebral cortex respectively. We estimated nBR R2 component area-under-the-curve as well as PREP amplitude habituation as the slope pof the linear regression between the 1st and the 2nd block of 5 averaged responses.ResultsFollowing 1-month on KD, the mean number of attacks and headache duration reduced significantly. Moreover, KD significantly normalized the interictal PREP habituation (pre: + 1.8, post: − 9.1, p = 0.012), while nBR deficit of habituation did not change.ConclusionsThe positive clinical effects we observed in a population of migraineurs by a 1-month KD treatment coexists with a normalization at the cortical level, not in the brainstem, of the typical interictal deficit of habituation. These findings suggest that the cerebral cortex may be the primary site of KD-related modulation.Trial registrationClinicalTrials.gov NCT03775252 (retrospectively registered, December 09, 2018).

Transcranial Magnetic Stimulation-Electroencephalography Measures of Cortical Neuroplasticity Are Altered after Mild Traumatic Brain Injury.

While the potential long-term side effects of mild traumatic brain injury (mTBI) are becoming increasingly recognized, the associated neurophysiological mechanisms remain poorly understood. However, changes in cortical inhibitory function and neuroplasticity have been suggested as possible contributing factors. The current study applied transcranial magnetic stimulation (TMS) in conjunction with electroencephalography (combined TMS-EEG) to investigate further the effects of mTBI on these processes. In 17 patients with a history of mTBI and 15 healthy control subjects with no mTBI history, paired-pulse TMS-EEG measures of short- (SICI) and long-interval intracortical inhibition (LICI) were used to assess intracortical inhibitory function. Single-pulse TMS-EEG was used to assess neuroplastic changes in cortical excitability after application of continuous theta burst stimulation (cTBS, a plasticity inducing TMS paradigm). Inhibition of the TMS-evoked EEG potential after application of SICI and LICI was not different between groups. In contrast, the inhibitory effects of cTBS on both P30 (p < 0.05) and N45 (p = 0.04) TEP components was significantly increased in patients, with the modulation of N45 in patients significantly related to the time since injury (p = 0.04). While these results provide further evidence that inhibitory circuits involving γ-aminobutyric acid (GABA) are modified after mTBI, they place greater emphasis on the plasticity of inhibitory networks involving the GABAA receptor subtype.

Self-Paced Online vs. Cue-Based Offline Brain-Computer Interfaces for Inducing Neural Plasticity.

Brain–computer interfaces (BCIs), operated in a cue-based (offline) or self-paced (online) mode, can be used for inducing cortical plasticity for stroke rehabilitation by the pairing of movement-related brain activity with peripheral electrical stimulation. The aim of this study was to compare the difference in cortical plasticity induced by the two BCI modes. Fifteen healthy participants participated in two experimental sessions: cue-based BCI and self-paced BCI. In both sessions, imagined dorsiflexions were extracted from continuous electroencephalogram (EEG) and paired 50 times with the electrical stimulation of the common peroneal nerve. Before, immediately after, and 30 min after each intervention, the cortical excitability was measured through the motor-evoked potentials (MEPs) of tibialis anterior elicited through transcranial magnetic stimulation. Linear mixed regression models showed that the MEP amplitudes increased significantly (p < 0.05) from pre- to post- and 30-min post-intervention in terms of both the absolute and relative units, regardless of the intervention type. Compared to pre-interventions, the absolute MEP size increased by 79% in post- and 68% in 30-min post-intervention in the self-paced mode (with a true positive rate of ~75%), and by 37% in post- and 55% in 30-min post-intervention in the cue-based mode. The two modes were significantly different (p = 0.03) at post-intervention (relative units) but were similar at both post timepoints (absolute units). These findings suggest that immediate changes in cortical excitability may have implications for stroke rehabilitation, where it could be used as a priming protocol in conjunction with another intervention; however, the findings need to be validated in studies involving stroke patients.

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.

P83-T ONAMIG: Effect of BOTOX® over cortical excitability (measured by transcranial magnetic stimulation) in chronic migraine

Background Several transcranial magnetic stimulation (TMS) studies have demonstrated cortical excitability changes in patients with migraine. It has been suggested that central sensitization may be associated with poor response to treatment. The recognition of these phenomena and the effect of different treatments on them may have clinical relevance. The aim of the study is to evaluate changes in cortical excitability parameters in patients with chronic migraine (CM) after treatment with BOTOX®. Material and methods Patients with CM and candidates for treatment with BOTOX® were included. In addition, patients with episodic migraine (EM) were recruited as controls. Clinical data and disability scales were collected as well as cortical excitability parameters measured by TMS: motor threshold at rest (RMT), cortical silence period (CSP) and intracortical inhibition (SICI) ). A baseline clinical and neurophysiological study was performed and repeated after two cycles of botox treatment. Results We included 19 patients with CM and 16 with EM. After treatment with BOTOX® in CM the RMT was reduced (58.9 ± 13.3% vs 55.1 ± 11.9%, p = 0.004) approaching the values of controls (53.75 ± 9.88%, p = 0.019); increased CSP (85.6 ± 26.4 ms and 100.9 ± 33.0 ms, p = 0.004) approaching the values of controls (121.53 ± 39.92, p = 0003). In addition, parameters of greater inhibition in the SICI predicted an improvement in frequency and intensity >50%. Conclusions Treatment with BOTOX® is associated with changes in the cortical excitability of patients with CM who can translate mechanisms of central cortical modulation.

Transcranial magnetic stimulation relieves pain and improves cortical excitability after stroke

Objective To investigate the effect of repeatedly applying transcranial magnetic stimulation (rTMS) in treating post-stroke pain (CPSP). Methods Forty stroke survivors experiencing CPSP were randomly divided into a treatment group and a control group, each of 20. All of the patients received conventional rehabilitation. In the treatment group, 20 patients received 10 Hz rTMS at 80% of their resting motor threshold applied over the primary motor cortex on their affected side, while those in the control group received sham stimulation. Both groups were treated once a day, 6 times a week for 4 weeks. Before and after the treatment, both groups were assessed using a pain score self-assessed on a visual analogue scale (VAS). Their resting motor thresholds (RMTs), cortical silent periods (CSPs) and motor evoked potentials (MEPs) were also recorded. Results After the intervention, the average VAS score, RMT, CSP and MEP latency of the treatment group were (3.1±1.2), (51.3±4.8)%, (188.9±63.0)ms and (27.9±5.7)ms, all significantly better than those before the intervention [(5.1±1.3), (60.1±5.9)%, (239.7±43.5)ms and (35.5±4.4)ms] (P<0.05). They were also significantly better than those of the control group after the intervention [(4.7±1.0), (57.6±5.1)%, (241.7±33.9)ms and (31.7±5.2)ms] (P<0.05). Conclusion Transcranial magnetic stimulation can relieve post-stroke pain. The mechanisms might be related to positive changes in cortical excitability in the affected hemisphere. Key words: Repetitive transcranial magnetic stimulation; Stroke; Pain; Cortical excitability

Blinding is compromised for transcranial direct current stimulation at 1mA for 20min in young healthy adults.

Transcranial direct current stimulation (tDCS) is a non-invasive brain stimulation method that is frequently used to study cortical excitability changes and their impact on cognitive functions in humans. While most stimulators are capable of operating in double-blind mode, the amount of discomfort experienced during tDCS may break blinding. Therefore, specifically designed sham stimulation protocols are being used. The "fade-in, short-stimulation, fade-out" (FSF) protocol has been used in hundreds of studies and is commonly believed to be indistinguishable from real stimulation applied at 1 mA for 20min. We analysed subjective reports of 192 volunteers, who either received real tDCS (n=96) or FSF tDCS (n=96). Participants reported more discomfort for real tDCS and correctly guessed the condition above chance-level. These findings indicate that FSF does not ensure complete blinding and that better active sham protocols are needed.

Cortical and spinal excitability changes after repetitive transcranial magnetic stimulation combined to physiotherapy in stroke spastic patients.

Repetitive Transcranial Magnetic Stimulation (rTMS) has been used to treat post-stroke upper limb spasticity (ULS) in addition to physiotherapy (PT). To determine whether rTMS associated with PT modulates cortical and spinal cord excitability as well as decreases ULS of post-stroke patients. Twenty chronic patients were randomly assigned to either the intervention group-1Hz rTMS on the unaffected hemisphere and PT, or control group-sham stimulation and PT, for ten sessions. Before and after sessions, ULS was measured using the modified Ashworth scale and cortical excitability using the output intensity of the magnetic stimulator (MSO). The spinal excitability was measured by the Hmax/Mmax ratio of the median nerve at baseline, at the end of treatment, and at the 4-week follow-up. The experimental group showed at the end of treatment an enhancement of cortical excitability, i.e., lower values of MSO, compared to control group (p = 0.044) and to baseline (p = 0.028). The experimental group showed a decreased spinal cord excitability at the 4-week follow-up compared to control group (p = 0.021). ULS decreased by the sixth session in the experimental group (p < 0.05). One-hertz rTMS associated with PT increased the unaffected hemisphere excitability, decreased spinal excitability, and reduced post-stroke ULS.

Transcranial Direct Current Stimulation Modulates GABA Levels Beyond the Stimulated Region: Perspectives for Stroke Rehabilitation.

Transcranial direct current stimulation (tDCS) is a method of non-invasive brain stimulation that induces changes in cortical excitability by applying a weak electric current transcranially. The direction of tDCS-induced cortical excitability change depends on the stimulation polarity. In general,