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The diversity in electromyography (EMG) techniques and their reporting present significant challenges across multiple disciplines in research and clinical practice, where EMG is commonly used. To address these challenges and augment the reproducibility and interpretation of studies using EMG, the Consensus for Experimental Design in Electromyography (CEDE) project has developed a checklist (CEDE-Check) to assist researchers to thoroughly report their EMG methodologies. Development involved a multi-stage Delphi process with seventeen EMG experts from various disciplines. After two rounds, consensus was achieved. The final CEDE-Check consists of forty items that address four critical areas that demand precise reporting when EMG is employed: the task investigated, electrode placement, recording electrode characteristics, and acquisition and pre-processing of EMG signals. This checklist aims to guide researchers to accurately report and critically appraise EMG studies, thereby promoting a standardised critical evaluation, and greater scientific rigor in research that uses EMG signals. This approach not only aims to facilitate interpretation of study results and comparisons between studies, but it is also expected to contribute to advancing research quality and facilitate clinical and other practical applications of knowledge generated through the use of EMG., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Introduction: Transcranial magnetic stimulation (TMS) is widely used to explore cortical physiology in health and disease. Surface electromyography (sEMG) is appropriate for superficial muscles, but cannot be applied easily to less accessible muscles. Muscle ultrasound (mUS) may provide an elegant solution to this problem, but fundamental questions remain. We explore the relationship between TMS evoked muscle potentials and TMS evoked muscle contractions measured with mUS., Methods: In 10 participants, we performed a TMS recruitment curve, simultaneously measuring motor evoked potentials (MEPs) and mUS in biceps (BI), first dorsal interosseous (FDI), tibialis anterior (TA), and the tongue (TO)., Results: Resting motor threshold (RMT) measurements and recruitment curves were found to be consistent across sEMG and mUS., Discussion: This work supports the use of TMS-US to study less accessible muscles. The implications are broad but could include the study of a new range of muscles in disorders such as amyotrophic lateral sclerosis., (© 2021 The Authors. Muscle & Nerve published by Wiley Periodicals LLC.)

Advances in genetics may enable a deeper understanding of disease mechanisms and promote a shift to more personalised medicine in the epilepsies. At present, understanding of consequences of genetic variants mainly relies on preclinical functional work; tools for acquiring similar data from the living human brain are needed. Transcranial magnetic stimulation (TMS), in particular paired-pulse TMS protocols which depend on the function of cortical GABAergic interneuron networks, has the potential to become such a tool. For this report, we identified and reviewed 23 publications on TMS studies of cortical excitability and inhibition in 15 different genes or conditions relevant to epilepsy. Reduced short-interval intracortical inhibition (SICI) and reduced cortical silent period (CSP) duration were the most commonly reported findings, suggesting abnormal GABA A - (SICI) or GABA B ergic (CSP) signalling. For several conditions, these findings are plausible based on established evidence of involvement of the GABAergic system; for some others, they may inform future research around such mechanisms. Challenges of TMS include lack of complete understanding of the neural underpinnings of the measures used: hypotheses and analyses should be based on existing clinical and preclinical data. Further pitfalls include gathering sufficient numbers of participants, and the effect of confounding factors, especially medications. TMS-EEG is a unique perturbational technique to study the intrinsic properties of the cortex with excellent temporal resolution; while it has the potential to provide further information of use in interpreting effects of genetic variants, currently the links between measures and neurophysiology are less established. Despite these challenges, TMS is a tool with potential for elucidating the system-level in vivo functional consequences of genetic variants in people carrying genetic changes of interest, providing unique insights., (© 2020 The Authors. Epilepsia published by Wiley Periodicals LLC on behalf of International League Against Epilepsy.)

The general purpose of normalization of EMG amplitude is to enable comparisons between participants, muscles, measurement sessions or electrode positions. Normalization is necessary to reduce the impact of differences in physiological and anatomical characteristics of muscles and surrounding tissues. Normalization of the EMG amplitude provides information about the magnitude of muscle activation relative to a reference value. It is essential to select an appropriate method for normalization with specific reference to how the EMG signal will be interpreted, and to consider how the normalized EMG amplitude may change when interpreting it under specific conditions. This matrix, developed by the Consensus for Experimental Design in Electromyography (CEDE) project, presents six approaches to EMG normalization: (1) Maximal voluntary contraction (MVC) in same task/context as the task of interest, (2) Standardized isometric MVC (which is not necessarily matched to the contraction type in the task of interest), (3) Standardized submaximal task (isometric/dynamic) that can be task-specific, (4) Peak/mean EMG amplitude in task, (5) Non-normalized, and (6) Maximal M-wave. General considerations for normalization, features that should be reported, definitions, and "pros and cons" of each normalization approach are presented first. This information is followed by recommendations for specific experimental contexts, along with an explanation of the factors that determine the suitability of a method, and frequently asked questions. This matrix is intended to help researchers when selecting, reporting and interpreting EMG amplitude data., Competing Interests: Declaration of Competing Interest None declared., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

The Consensus for Experimental Design in Electromyography (CEDE) project is an international initiative which aims to guide decision-making in recording, analysis, and interpretation of electromyographic (EMG) data. The quality of the EMG recording, and validity of its interpretation depend on many characteristics of the recording set-up and analysis procedures. Different electrode types (i.e., surface and intramuscular) will influence the recorded signal and its interpretation. This report presents a matrix to consider the best electrode type selection for recording EMG, and the process undertaken to achieve consensus. Four electrode types were considered: (1) conventional surface electrode, (2) surface matrix or array electrode, (3) fine-wire electrode, and (4) needle electrode. General features, pros, and cons of each electrode type are presented first. This information is followed by recommendations for specific types of muscles, the information that can be estimated, the typical representativeness of the recording and the types of contractions for which the electrode is best suited. This matrix is intended to help researchers when selecting and reporting the electrode type in EMG studies., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Background: Previous research suggested that anterior-posterior (AP) directed currents induced by TMS in motor cortex (M1) activate interneuron circuits different from those activated by posterior-anterior currents (PA). The present experiments provide evidence that pulse duration also determines the activation of specific interneuron circuits., Objective: To use single motor unit (SMU) recordings to confirm the difference in onset latencies of motor-evoked potentials (MEPs) evoked by different current directions and pulse durations: AP 30 , AP 120 , PA 30 and PA 120 . To test whether the amplitude of the MEPs is differentially influenced by somatosensory inputs from the hand (short-latency afferent inhibition, SAI), and examine the sensitivity of SAI to changes in cerebellar excitability produced by direct current stimulation (tDCS Cb )., Methods: Surface electromyograms and SMUs were recorded from the first dorsal interosseous muscle. SAI was tested with an electrical stimulus to median or digital nerves ~20-25 ms prior to TMS delivered over the M1 hand area via a controllable pulse parameter TMS (cTMS) device. SAI was also tested during the application of anodal or sham tDCS Cb . Because TMS pulse specificity is greatest at low stimulus intensities, most experiments were conducted with weak voluntary contraction to reduce stimulus threshold., Results: AP 30 currents recruited the longest latency SMU and surface MEP responses. During contraction SAI was greater for AP 30 responses versus all other pulses. Online anodal tDCS Cb reduced SAI for the AP 30 currents only., Conclusions: AP 30 currents activate an interneuron circuit with functional properties different from those activated by other pulse types. Pulse duration and current direction determine what is activated in M1 with TMS., (Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: In a small group of patients, we have previously shown that a combination of electrophysiological tests was able to distinguish functional (psychogenic) tremor and organic tremor with excellent sensitivity and specificity., Objectives: This study aims to validate an electrophysiological test battery as a tool to diagnose patients with functional tremor with a "laboratory-supported" level of certainty., Methods: For this prospective data collection study, we recruited 38 new patients with functional tremor (mean age 37.9 ± 24.5 years; mean disease duration 5.9 ± 9.0 years) and 73 new patients with organic tremor (mean age 55.4 ± 25.4 years; mean disease duration 15.8 ± 17.7 years). Tremor was recorded at rest, posture (with and without loading), action, while performing tapping tasks (1, 3, and 5 Hz), and while performing ballistic movements with the less-affected hand. Electrophysiological tests were performed by raters blinded to the clinical diagnosis. We calculated a sum score for all performed tests (maximum of 10 points) and used a previously suggested cut-off score of 3 points for a diagnosis of laboratory-supported functional tremor., Results: We demonstrated good interrater reliability and test-retest reliability. Patients with functional tremor had a higher average score on the test battery when compared with patients with organic tremor (3.6 ± 1.4 points vs 1.0 ± 0.8 points; P < .001), and the predefined cut-off score for laboratory-supported functional tremor yielded a test sensitivity of 89.5% and a specificity of 95.9%., Conclusion: We now propose this test battery as the basis of laboratory-supported criteria for the diagnosis of functional tremor, and we encourage its use in clinical and research practice., (© 2016 International Parkinson and Movement Disorder Society.)

Fast ballistic flexion movements of the wrist are produced by a triphasic pattern of electromyographic (EMG) activity in flexor and extensor muscle. Whereas it is generally accepted that the primary motor cortex generates the first agonist burst (AG1), its contribution to the following antagonist burst (ANT) and second agonist burst (AG2) is unresolved. We applied single pulses of suprathreshold transcranial magnetic stimulation (TMS) at different times to the motor cortex ipsilateral to wrist flexion. This produced interhemispheric inhibition of the opposite motor cortex and a silent period in the ballistic EMG pattern that started about 30 ms after the stimulus and lasted for a further 30 ms. If the silence was timed to start within the first 30 ms of AG1, then timing of the subsequent ANT and AG2 bursts was delayed. However, if the silence began later, then the timing of the ANT burst was not changed. A similar effect on the onset latency of the AG2 was seen if the silence began in the first part of the ANT burst. The results are compatible with a model in which the triphasic pattern is not triggered as a single entity. Instead we suggest that each burst has its own trigger that occurs about 30-40 ms after the start of AG1 (or ANT). If AG1 (or ANT) is interrupted within this time period then this trigger, and hence later bursts, are delayed. If the interruption occurs after 30-40 ms it has no effect on the onset of later bursts since they have already been triggered.

Transcranial alternating current stimulation (TACS) is commonly used to synchronize a cortical area and its outputs to the stimulus waveform, but gathering evidence for this based on brain recordings in humans is challenging. The corticospinal tract transmits beta oscillations (∼21 Hz) from the motor cortex to tonically contracted limb muscles linearly. Therefore, muscle activity may be used to measure the level of beta entrainment in the corticospinal tract due to TACS over the motor cortex. Here, we assessed whether TACS is able to modulate the neural inputs to muscles, which would provide indirect evidence for TACS‐driven neural entrainment. In the first part of the study, we ran simulations of motor neuron (MN) pools receiving inputs from corticospinal neurons with different levels of beta entrainment. Results suggest that MNs are highly sensitive to changes in corticospinal beta activity. Then, we ran experiments on healthy human subjects (N = 10) in which TACS (at 1 mA) was delivered over the motor cortex at 21 Hz (beta stimulation), or at 7 Hz or 40 Hz (control conditions) while the abductor digiti minimi or the tibialis anterior muscle were tonically contracted. Muscle activity was measured using high‐density electromyography, which allowed us to decompose the activity of pools of motor units innervating the muscles. By analysing motor unit pool activity, we observed that none of the TACS conditions could consistently alter the spectral contents of the common neural inputs received by the muscles. These results suggest that 1 mA TACS over the motor cortex given at beta frequencies does not entrain corticospinal activity. Key points: Transcranial alternating current stimulation (TACS) is commonly used to entrain the communication between brain regions.It is challenging to find direct evidence supporting TACS‐driven neural entrainment due to the technical difficulties in recording brain activity during stimulation.Computational simulations of motor neuron pools receiving common inputs in the beta (∼21 Hz) band indicate that motor neurons are highly sensitive to corticospinal beta entrainment.Motor unit activity from human muscles does not support TACS‐driven corticospinal entrainment. [ABSTRACT FROM AUTHOR]

Background: Volitional control of involuntary movements has so far been considered a hallmark of tic disorders. However, modulation of involuntary movements can also be observed in other hyperkinesias. Cases Here, we present 6 patients with chorea able to suppress their involuntary movements, on demand. In 3 of them, surface electromyography was used to quantify degree of suppression and confirmed a reduction of muscle activity up to 68%, during volitional control. Conclusion: This observation represents a first step toward a description of a new clinical feature in choreic syndromes and an opportunity to redefine the role of volitional inhibition in hyperkinetic movement disorders. View Supplementary Video [ABSTRACT FROM AUTHOR]

Background: Demographic and clinical studies imply that female sex may be protective for PD, but pathophysiological evidence to support these observations is missing. In early PD, functional changes may be detected in primary motor cortex using transcranial magnetic stimulation.Objective: We hypothesised that if pathophysiology differs between sexes in PD, this will be reflected in differences of motor cortex measurements.Methods: Forty-one newly diagnosed PD patients (22 males, 19 females) were clinically assessed using MDS-UPDRS part III, and various measures of cortical excitability and sensorimotor cortex plasticity were measured over both hemispheres, corresponding to the less and more affected side, using transcranial magnetic stimulation. Twenty-three healthy (10 men, 13 women) participants were studied for comparison.Results: Among patients, no significant differences between sexes were found in age, age of diagnosis, symptom duration, and total or lateralized motor score. However, male patients had disturbed interhemispheric balance of motor thresholds, caused by decreased resting and active motor thresholds in the more affected hemisphere. Short interval intracortical inhibition was more effective in female compared to male patients in both hemispheres. Female patients had a preserved physiological focal response to sensorimotor plasticity protocol, whereas male patients showed an abnormal spread of the protocol effect.Conclusion: The study provides one of the first neurophysiological evidences of sex differences in early PD. Female patients have a more favorable profile of transcranial magnetic stimulation measures, possibly reflecting a more successful cortical compensation or delayed maladaptive changes in the sensorimotor cortex. © 2019 International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Pallidal deep brain stimulation is an established treatment in patients with dystonia. However, evidence from case series or uncontrolled studies suggests that it may lead in some patients to specific parkinsonian symptoms such as freezing of gait, micrographia, and bradykinesia. We investigated parkinsonian signs using the Movement Disorder Society Unified Parkinson's Disease Rating Scale motor score by means of observer-blinded video ratings in a group of 29 patients treated with pallidal stimulation and a non-surgical control group of 22 patients, both with predominant cervical dystonia. Additional assessments included MRI-based models of volume of neural tissue activated to investigate areas of stimulation related to dystonic symptom control and those likely to induce parkinsonian signs as well as an EMG analysis to investigate functional vicinity of stimulation fields to the pyramidal tract. Compared with controls, stimulated patients had significantly higher motor scores (median, 25th-75th percentile: 14.0, 8.0-19.5 versus 3.0, 2.0-8.0; P < 0.0001), as well as bradykinesia (8.0, 6.0-14.0 versus 2.0, 0.0-3.0; P < 0.0001) and axial motor subscores (2.0, 1.0-4.0 versus 0.0, 0.0-1.0; P = 0.0002), while rigidity and tremor subscores were not different between groups. Parkinsonian signs were partially reversible upon switching stimulation off for a median of 90 min in a subset of 19 patients tolerating this condition. Furthermore, the stimulation group reported more features of freezing of gait on a questionnaire basis. Quality of life was better in stimulated patients compared with control patients, but parkinsonian signs were negatively associated with quality of life. In the descriptive imaging analysis maximum efficacy for dystonia improvement projected to the posteroventrolateral internal pallidum with overlapping clusters driving severity of bradykinesia and axial motor symptoms. The severities of parkinsonian signs were not correlated with functional vicinity to the pyramidal tract as assessed by EMG. In conclusion, parkinsonian signs, particularly bradykinesia and axial motor signs, due to pallidal stimulation in dystonic patients are frequent and negatively impact on motor functioning and quality of life. Therefore, patients with pallidal stimulation should be monitored closely for such signs both in clinical routine and future clinical trials. Spread of current outside the internal pallidum is an unlikely explanation for this phenomenon, which seems to be caused by stimulation of neural elements within the stimulation target volume. [ABSTRACT FROM AUTHOR]

Background: In Huntington's disease there is evidence of structural damage in the motor system, but it is still unclear how to link this to the behavioral disorder of movement. One feature of choreic movement is variable timing and coordination between sequences of actions. We postulate this results from desynchronization of neural activity in cortical motor areas.Objectives: The objective of this study was to explore the ability to synchronize activity in a motor network using transcranial magnetic stimulation and to relate this to timing of motor performance.Methods: We examined synchronization in oscillatory activity of cortical motor areas in response to an external input produced by a pulse of transcranial magnetic stimulation. We combined this with EEG to compare the response of 16 presymptomatic Huntington's disease participants with 16 age-matched healthy volunteers to test whether the strength of synchronization relates to the variability of motor performance at the following 2 tasks: a grip force task and a speeded-tapping task.Results: Phase synchronization in response to M1 stimulation was lower in Huntington's disease than healthy volunteers (P < .01), resulting in a reduced cortical activity at global (P < .02) and local levels (P < .01). Participants who showed better timed motor performance also showed stronger oscillatory synchronization (r = -0.356; P < .05) and higher cortical activity (r = -0.393; P < .05).Conclusions: Our data may model the ability of the motor command to respond to more subtle, physiological inputs from other brain areas. This novel insight indicates that impairments of the timing accuracy of synchronization and desynchronization could be a physiological basis for some key clinical features of Huntington's disease. © 2018 International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Cortical excitability, as measured by transcranial magnetic stimulation combined with electromyography, is a potential biomarker for the diagnosis and follow-up of epilepsy. We report on long-interval intracortical inhibition data measured in four different centres in healthy controls (n = 95), subjects with refractory genetic generalized epilepsy (n = 40) and with refractory focal epilepsy (n = 69). Long-interval intracortical inhibition was measured by applying two supra-threshold stimuli with an interstimulus interval of 50, 100, 150, 200 and 250 ms and calculating the ratio between the response to the second (test stimulus) and to the first (conditioning stimulus). In all subjects, the median response ratio showed inhibition at all interstimulus intervals. Using a mixed linear-effects model, we compared the long-interval intracortical inhibition response ratios between the different subject types. We conducted two analyses; one including data from the four centres and one excluding data from Centre 2, as the methods in this centre differed from the others. In the first analysis, we found no differences in long-interval intracortical inhibition between the different subject types. In all subjects, the response ratios at interstimulus intervals 100 and 150 ms showed significantly more inhibition than the response ratios at 50, 200 and 250 ms. Our second analysis showed a significant interaction between interstimulus interval and subject type (P = 0.0003). Post hoc testing showed significant differences between controls and refractory focal epilepsy at interstimulus intervals of 100 ms (P = 0.02) and 200 ms (P = 0.04). There were no significant differences between controls and refractory generalized epilepsy groups or between the refractory generalized and focal epilepsy groups. Our results do not support the body of previous work that suggests that long-interval intracortical inhibition is significantly reduced in refractory focal and genetic generalized epilepsy. Results from the second analysis are even in sharper contrast with previous work, showing inhibition in refractory focal epilepsy at 200 ms instead of facilitation previously reported. Methodological differences, especially shorter intervals between the pulse pairs, may have contributed to our inability to reproduce previous findings. Based on our results, we suggest that long-interval intracortical inhibition as measured by transcranial magnetic stimulation and electromyography is unlikely to have clinical use as a biomarker of epilepsy. [ABSTRACT FROM AUTHOR]

Background: Subthalamic deep brain stimulation (STN-DBS) is an effective treatment for Parkinson's disease (PD), but can have side effects caused by stimulus spread to structures outside the target volume such as the pyramidal tract.Objectives: To assess the relevance of pyramidal tract activation with STN-DBS in PD.Methods: In a multimodal, blinded study in 20 STN-DBS patients, we measured stimulation thresholds for evoking electromyographic activity in orbicularis oris and first dorsal interosseous muscles at each of 150 electrode sites. We also modeled the electric field spread and calculated its overlap with the estimated anatomical location of corticospinal and corticobulbar tracts from primary motor cortex using 3 Tesla MRI probabilistic tractography.Results: Mean resting motor thresholds were significantly lower for the contralateral orbicularis oris (3.5 ± 1.0 mA) compared with ipsilaterally (4.1 ± 1.1 mA) and with the contralateral first dorsal interosseous (4.0 ± 1.2 mA). The modeled volumes of corticobulbar and corticospinal tract activated correlated inversely with the resting motor threshold of the contralateral orbicularis oris and first dorsal interosseous, respectively. Active motor thresholds were significantly lower compared with resting motor thresholds by around 30% to 35% and correlated with the clinically used stimulation amplitude. Backward multiple regression in 12 individuals with a "lateral-type" speech showed that stimulation amplitude, levodopa equivalent dose reduction postsurgery, preoperative speech intelligibility, and first dorsal interosseous resting motor thresholds explained 79.9% of the variance in postoperative speech intelligibility.Conclusions: Direct pyramidal tract activation can occur at stimulation thresholds that are within the range used in clinical routine. This spread of current compromises increase in stimulation strengths and is related to the development of side effects such as speech disturbances with chronic stimulation. © 2017 International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Background: Alternating hemiplegia of childhood is a very rare and serious neurodevelopmental syndrome; its genetic basis has recently been established. Its characteristic features include typically-unprovoked episodes of hemiplegia and other transient or more persistent neurological abnormalities. Methods: We used transcranial magnetic stimulation to assess the effect of the condition on motor cortex neurophysiology both during and between attacks of hemiplegia. Nine people with alternating hemiplegia of childhood were recruited; eight were successfully tested using transcranial magnetic stimulation to study motor cortex excitability, using single and paired pulse paradigms. For comparison, data from ten people with epilepsy but not alternating hemiplegia, and ten healthy controls, were used. Results: One person with alternating hemiplegia tested during the onset of a hemiplegic attack showed progressively diminishing motor cortex excitability until no response could be evoked; a second person tested during a prolonged bilateral hemiplegic attack showed unusually low excitability. Three people tested between attacks showed asymptomatic variation in cortical excitability, not seen in controls. Paired pulse paradigms, which probe intracortical inhibitory and excitatory circuits, gave results similar to controls. Conclusions: We report symptomatic and asymptomatic fluctuations in motor cortex excitability in people with alternating hemiplegia of childhood, not seen in controls. We propose that such fluctuations underlie hemiplegic attacks, and speculate that the asymptomatic fluctuation we detected may be useful as a biomarker for disease activity. [ABSTRACT FROM AUTHOR]

We recently showed that subcortical circuits contribute to control the gain of motor cortical inputs to spinal motoneurons during precision grip of a small object. Here, we examine whether the involvement of the motor cortex could be revealed by grasping with different hand postures. Using noninvasive cortical, cervicomedullary, and peripheral nerve stimulation we examined in humans motorevoked potentials (MEPs) and the activity in intracortical circuits (suppression of voluntary electromyography) and spinal motoneurons (F-waves) in intrinsic hand muscles when graspinga6mm cylinder with the index finger and thumb while the hand was held in the neutral position or during full pronation and supination. We demonstrate that the size of cortically evoked MEPs in the first dorsal interosseous, but not in the abductor pollicis brevis and abductor digit minimi muscles, was reduced to a similar extent during grasping with the hand pronated or supinated compared with the neutralposition. Notably, the suppression of MEPs was present from the MEP onset, suggesting that indirect corticospinal pathways were less likely to be involved than direct connections. There was less intracortical inhibition targeting the first dorsal interosseous during hand pronation and supination compared with neutral and this negatively correlated with changes in MEP size. In contrast, cervicomedullary MEPs and F-waves remained unchanged across conditions, as did MEPs evoked during unopposed weak flexion of the index finger. Our findings reveal a distinct influence of the posture of the hand on the activity of cortical pathways controlling different hand muscles during grasping. [ABSTRACT FROM AUTHOR]

Surround inhibition ( SI) is a neural process that has been extensively investigated in the sensory system and has been recently probed in the motor system. Muscle-specific modulation of corticospinal excitability at the onset of an isolated finger movement has been assumed to reflect the presence of SI in the motor system. This study attempted to characterise this phenomenon in a large cohort of normal volunteers and investigate its relationship with muscle activity in the hand. Corticospinal excitability of the pathways projecting to three hand muscles [first dorsal interosseus ( FDI), abductor pollicis brevis (APB) and abductor digiti minimi ( ADM)] and electromyographic ( EMG) activity of the same muscles were assessed in 31 healthy volunteers during an isolated index finger movement. In the agonist FDI muscle both corticospinal excitability and EMG activity were found to be increased at the onset of the movement ( P < 0.001 and P < 0.001, respectively). On the contrary, in the surround ADM, there was dissociation between the corticospinal excitability (decreased: P < 0.001) and EMG activity (increased: P < 0.001). Cross-correlation analysis of the EMG activity showed that neuronal signals driving the agonist and surround muscles are not synchronised when SI is present. The results suggest a distinctive origin of the neuronal signals driving the agonist and surround muscles. In addition, they indicate that cortical output might be simultaneously modulated by voluntary and non-voluntary activity, generated in cortical and subcortical structures, respectively. [ABSTRACT FROM AUTHOR]

Paired-pulse transcranial magnetic stimulation ( TMS) is used to measure the excitability of interhemispheric inhibition ( IHI) between the hand areas of the two motor cortices. It varies from person to person, and is highly predictive of individual differences in callosal anatomy (fractional anisotropy) and even motor behaviour, e.g. the amount of involuntary electromyographic ( EMG) 'mirroring' in one hand during rapid contraction of the other. The present experiments tested whether it also predicts how well individuals can improve motor performance in a task involving the two hands. Healthy participants were given 100 trials to maximize the initial acceleration of a ballistic finger movement made with one hand while trying to maintain a tonic low level of EMG activity in the other hand. Initially, each movement was accompanied by additional unwanted EMG mirroring in the other hand. However, after practice, participants had on average increased acceleration by approximately one-third without changing the amount of EMG mirroring in the contralateral hand; indeed, in some individuals EMG mirroring activity declined. TMS measures showed that there was an increase in corticospinal excitability in the trained hemisphere, but there was no change in the excitability of short- or long-latency IHI from the trained to non-trained hemisphere. Nevertheless, in each individual, the baseline (pre-practice) excitability of short-latency IHI was highly predictive ( r = 0.65; P = 0.0019) of the change in EMG mirroring. The implication is that a physiological measure of brain excitability at rest can predict behaviour in response to training. [ABSTRACT FROM AUTHOR]

Background Cognition is affected early in Huntington disease (HD), and in HD animal models there is evidence that this reflects abnormal synaptic plasticity. The authors investigated whether there is any evidence for abnormal synaptic plasticity using the human motor cortex-rTMS model and, if so, if there is any difference between premanifest HD gene carriers and very early manifest HD patients or any relationship with ratings of the severity of motor signs. Methods Fifteen HD gene carriers (seven premanifest, eight very early manifest) and 14 control participants were given a continuous train of 100 bursts of theta burst stimulation (cTBS: three pulses at 50 Hz and 80% AMT repeated every 200 ms). The size of the motorevoked potential was measured at regular intervals until 21 min after cTBS. Results HD gene carriers and controls responded differently to theta burst stimulation (F4.9,131.9¼1.37, p¼0.048) with controls having more inhibition than HD gene carriers (F1,27¼13.3, p¼0.001). Across all time points, mean inhibition differed between the groups (F2,26¼6.32, p¼0.006); controls had more inhibition than either HD gene carrier subgroup (p¼0.006 for premanifest and p¼0.009 for early symptomatic), whereas there was no difference between premanifest and early symptomatic HD gene carriers. The measure of cortical plasticity was not associated with any clinical ratings (Unified Huntington Disease Rating Scale motor score, estimate of age at onset). Conclusions Motor cortex plasticity is abnormal in HD gene carriers but is not closely linked to the development of motor signs of HD. [ABSTRACT FROM AUTHOR]

We explored interhemispheric facilitation (IHF) between (a) left and right primary motor cortex (M1) and (b) left dorsal premotor (dPM) and right M1 in 20 right-handed healthy human subjects using a paired pulse transcranial magnetic stimulation (TMS) protocol. A conditioning TMS pulse (CP) applied to left M1 or dPM with an intensity of 80% and 60% active motor threshold (CP80%AMT and CP60%AMT, respectively) was followed by a test pulse (TP) over right M1 induced by anterior–posterior- or posterior–anterior- (TPAP, TPPA) directed currents in the brain at interstimulus intervals (ISIs) of 3–8 and 10 ms. EMG was recorded from left first dorsal interosseous muscle. In the main experimental condition IHF was evoked by CP80%AMT over left M1 and TPAP at ISIs of 6 and 8 ms. The same CP80%AMT produced IHF at an ISI of 8 ms when applied over left dPM but only with TPPA. In addition, when CP60%AMT was given to M1, IHF was present at an ISI of 6 ms (but not 8 ms) when followed by TPPA, indicating that IHF elicited over dPM was not caused by current spread of the conditioning pulse to M1. We conclude that IHF can be induced differentially by conditioning M1 and dPM using subthreshold CP. These facilitatory interactions depended on the intensity and ISI of the CP as well as the current flow direction of the TP. We suggest that not only do the CPs activate separate anatomical pathways but also that these pathways project to different populations of interneurons in the receiving M1. These may correspond to elements involved in the generation of I3 and I1 waves, respectively. [ABSTRACT FROM AUTHOR]

Background & Aims: Excitatory brain stimulation with repetitive transcranial magnetic stimulation (rTMS) has been proposed as a treatment for dysphagia after stroke. Moreover, 1-Hz rTMS can induce a “virtual lesion” in the human pharyngeal motor cortex that suppresses brain activity and temporarily disrupts swallowing. We thus examined if rTMS could reverse the disrupted brain and swallowing functions following a unilateral virtual lesion in the pharyngeal motor cortex, such that rTMS might be developed as a therapy. Methods: Healthy subjects (n = 23) were given varying conditions of 5-Hz rTMS over the pharyngeal motor cortex to determine the most effective excitatory parameters. Thereafter, a unilateral virtual lesion was made in the pharyngeal motor cortex using 1-Hz rTMS, followed by contralateral active or sham 5-Hz rTMS. Motor evoked potentials and serial swallowing reaction times were recorded before and for 60 minutes postlesion to assess reversibility of the disruption to the brain and swallowing. Results: The greatest increase in pharyngeal motor cortex excitability was seen following 250 pulses of 5-Hz rTMS (F(1,11) = 10.3, P = .008), an effect that lasted over 2 hours. In contrast to sham rTMS, active contralateral 5-Hz rTMS completely abolished the cortical suppression induced by the virtual lesion, with effects occurring for up to 50 minutes in both unlesioned (F(1,11) = 6, P = .03) and lesioned (F(1,11) = 67, P < .001) hemispheres. Active rTMS also reversed the changes in swallowing behavior (F(1,8) = 9, P = .018), restoring function to prelesional levels. Conclusions: Contralesional-targeted neurostimulation modulates brain activity and swallowing motor behavior after experimental disruption and might be usefully applied in stroke-affected patients as a therapy for dysphagia. [Copyright &y& Elsevier]

Abstract: Acoustic stimuli can evoke reflex EMG responses (acoustic jaw reflex) in the masseter muscle. Although these were previously ascribed to activation of cochlear receptors, high intensity sound can also activate vestibular receptors. Since anatomical and physiological studies, both in animals and humans, have shown that masseter muscles are a target for vestibular inputs we have recently reassessed the vestibular contribution to masseter reflexes. We found that high intensity sound evokes two bilateral and symmetrical short-latency responses in active unrectified masseter EMG of healthy subjects: a high threshold, early p11/n15 wave and a lower threshold, later p16/n21 wave. Both of these reflexes are inhibitory but differ in their threshold, latency and appearance in the rectified EMG average. Experiments in healthy subjects and in patients with selective lesions showed that vestibular receptors were responsible for the p11/n15 wave (vestibulo-masseteric reflex) whereas cochlear receptors were responsible for the p16/n21 wave (acoustic masseteric reflex). The possible functional significance of the double vestibular control over masseter muscles is discussed. [ABSTRACT FROM AUTHOR]

The analysis of single motor unit (SMU) activity provides the foundation from which information about the neural strategies underlying the control of muscle force can be identified, due to the one-to-one association between the action potentials generated by an alpha motor neuron and those received by the innervated muscle fibers. Such a powerful assessment has been conventionally performed with invasive electrodes (i.e., intramuscular electromyography (EMG)), however, recent advances in signal processing techniques have enabled the identification of single motor unit (SMU) activity in high-density surface electromyography (HDsEMG) recordings. This matrix, developed by the Consensus for Experimental Design in Electromyography (CEDE) project, provides recommendations for the recording and analysis of SMU activity with both invasive (needle and fine-wire EMG) and non-invasive (HDsEMG) SMU identification methods, summarizing their advantages and disadvantages when used during different testing conditions. Recommendations for the analysis and reporting of discharge rate and peripheral (i.e., muscle fiber conduction velocity) SMU properties are also provided. The results of the Delphi process to reach consensus are contained in an appendix. This matrix is intended to help researchers to collect, report, and interpret SMU data in the context of both research and clinical applications. [ABSTRACT FROM AUTHOR]

Objectives Tremor in Charcot-Marie-Tooth disease (CMT) can be disabling. Cerebellar abnormalities are thought to underpin neuropathic tremor. Here, we aim to clarify the potential role of the cerebellum in CMT tremor. Methods We assessed prevalence of tremor by questionnaire in 84 patients with CMT. Of those, 23 patients with CMT with and without arm tremor and healthy controls underwent a clinical assessment, classical eyeblink conditioning, electro-oculography, visuomotor adaptation test, tremor recording with surface EMG and accelerometry, and retrospective correlation with nerve conduction studies to investigate the possible mechanisms of tremor generation. Results The prevalence study revealed tremor in 21% of patients and in 42% of those it caused impairment of function. Tremor recordings revealed a mild-to-moderate amplitude tremor with a weight load-invariant 7.7 Hz frequency component. Performance on classical eyeblink conditioning, visuomotor adaptation and electro-oculography were no different between tremulous and non-tremulous patients and healthy controls. Conclusions These results argue against a prominent role for an abnormal cerebellum in tremor generation in the patients studied with CMT. Rather, our results suggest an enhancement of the central neurogenic component of physiological tremor as a possible mechanism for tremor in the patients studied. Significance This study is the first to propose differing pathogenic mechanisms for subtypes of neuropathic tremor. [ABSTRACT FROM AUTHOR]

High-density surface electromyography (HDsEMG) can be used to measure the spatial distribution of electrical muscle activity over the skin. As this distribution is associated with the generation and propagation of muscle fiber action potentials, HDsEMG is processed to extract information on regional muscle activation, muscle fiber characteristics and behaviour of individual motor units. This matrix, developed by the Consensus for Experimental Design in Electromyography (CEDE) project, summarizes recommendations on the use of HDsEMG in experimental studies. For each application, recommendations are included regarding electrode montage, electrode type and configuration, electrode location and orientation, data analysis, and interpretation. Cautions and reporting standards are also included. The steps of the Delphi process to reach consensus are contained in an appendix. This matrix is intended to help researchers when collecting, reporting, and interpreting HDsEMG data. It is hoped that this document will be used to generate new empirical evidence to improve how HDsEMG is used in research and in clinical applications. [ABSTRACT FROM AUTHOR]

Abstract: Objective: To test whether inhibitory continuous Theta Burst (cTBS) transcranial magnetic stimulation (TMS) can alter neural activity involved in planning and execution of a self-paced movement. Methods: In seven subjects, cTBS was applied over either the left or right primary motor cortex (left M1 and right M1) and the left dorsal premotor cortex (left PMd) in different experimental sessions. Motor evoked potentials (MEP) at rest were measured as well as the two main components of the movement related cortical potential (MRCP), the Bereitschaftspotential (BP) and the negative slope (NS’), prior to self-paced right thumb opposition. Results: cTBS suppressed contralateral MEPs when it was applied over left M1, right M1 and left PMd. In addition, cTBS over left M1, but not at any other location, reduced the amplitude of the NS’ and tended to shorten the BP onset without changing EMG activity associated with voluntary muscular output. There was a significant correlation between the percent suppression of the MEP and the reduction in amplitude of the total MRCP (BP+NS’). Conclusions: cTBS can produce long-lasting effects on brain activity involved in the preparation and execution of a volitional movement. Significance: The fact that movement was not compromised while brain activity changed suggests that the motor system of healthy subjects operates with a safety factor that can adjust patterns of activation to compensate for the partial disruption caused by cTBS. [Copyright &y& Elsevier]