Effect of antagonistic voluntary contraction on motor responses in the forearm.

OBJECTIVE: We investigated the effects of voluntary contraction of agonist and antagonist muscles on motor evoked potentials (MEP) and on myoelectric activities in the target (agonist) muscle following transcranial magnetic stimulation (TMS). METHODS: The left extensor carpi radialis (ECR) and flexor carpi radialis (FCR) muscles were studied in 16 healthy subjects. H reflexes, MEP induced by TMS, and background electromyographic (EMG) activity were recorded using surface electrodes at rest and during voluntary contraction of either agonist or antagonist muscles. RESULTS: Voluntary contraction of antagonist muscles (at 10% of maximum contraction) enhanced the amplitudes of MEP for both muscles. The H reflex of the FCR muscle was inhibited by contraction (10% of maximum) of the ECR muscle. Background EMG activity did not differ between H-reflex trials and TMS trials. Enhancement of MEP amplitudes and background EMG activity during voluntary antagonist contraction was comparable in the two muscles. Appearance rate of MEP recorded by needle electrodes in response to subthreshold TMS was increased by antagonistic voluntary contraction. CONCLUSION: Facilitation occurs during voluntary contraction of antagonist muscles. Differences between the effects of voluntary contraction of the ECR muscle for the MEP and the H reflex of the FCR suggest that cortical facilitatory spread occurs between agonist and antagonist muscles.     

Mechanomyographic response to transcranial magnetic stimulation from biceps brachii and during transcutaneous electrical nerve stimulation on extensor carpi radialis

Transcranial magnetic stimulation (TMS) elicits short latency excitatory responses in the target muscles, termed motor evoked potential (MEP). When TMS is delivered during a voluntary contraction, the MEP is followed by a period of silence called silent period (SP). These MEP parameters are in general recordable by electromyography (EMG). Mechanomyography (MMG) on the other hand is the mechanical counterpart of EMG. Thus, this study has been conducted to observe whether the MEP parameters from MMG signals showed similar trait of EMG recordings. Five normal healthy male subjects were included in this study. The subjects were required to perform right biceps brachii muscles contraction at diverse graded of load level at 5, 10, 20, 30, 40, 60, and 100% maximum voluntary contraction (MVC). MEPs by single pulse TMS on left hemisphere were obtained from both EMG electrode and MMG accelerometer at rest and at different levels of predetermined load level. MEP amplitude and area obtained both from EMG and MMG record were increased with the increase of muscle contraction with a maximum of 60% MVC. With increasing the level of contraction there was a shortening of onset latency and decreasing in the length of silent period in both EMG and MMG signals. We also recorded the EMG- and MMG-MEP from the right extensor carpi radialis muscle during transcutaneous electric nerve stimulation in order to observe neural changes in sensory stimulation from both EMG and MMG responses. The EMG-MEP was not visible in electrical artifact whereas it was obvious in MMG responses. In accordance with other study, this study showed that the voluntary contraction of biceps brachii muscle influenced the MEP parameter which are moreover obtainable by MMG even in electrical noise may provide insight for future study.     

Reciprocal change of motor-evoked potentials preceding voluntary movement in humans

Reciprocal change of motor-evoked potentials (MEPs) recorded from the agonist and antagonist muscles of the forearm was studied in 10 normal subjects in whom transcranial magnetic stimulation (TMS) was applied to the hand motor area before voluntary wrist movements. MEP recorded from the agonist muscles, that is, radial extensor muscles for wrist extension and ulnar flexor muscle for wrist flexion, were gradually facilitated with shortening of the interval between the magnetic stimulation and the voluntary muscle contraction. In contrast, MEP recorded from the antagonist muscles, that is, ulnar flexor muscle for wrist extension and radial extensor muscles for wrist flexion, were gradually suppressed as the interval shortened. The reciprocal change of MEP was recognized when TMS was applied within 60 ms prior to the voluntary movements. The present data confirmed that reciprocal change of MEP was recognized before voluntary movements; they further suggest that cortically originated reciprocal control of the corticospinal pathway may exist and that it may be generated just before the voluntary movement. © 1996 John Wiley & Sons, Inc.     

Different patterns of excitation and inhibition of the small hand and forearm muscles from magnetic brain stimulation in humans.

OBJECTIVES: The objective of the present study is to quantify the effects of voluntary muscle contraction of the small hand (abductor pollicis brevis, first dorsal interosseus (FDI)) and forearm muscles (extensor carpi radialis (ECR), extensor carpi ulnaris (ECU), flexor carpi radialis (FCR) and flexor carpi ulnaris (FCU)) on motor evoked potentials (MEPs). METHODS: MEPs were recorded in 12 healthy subjects by a circular coil placed over the vertex at 1.2 times the resting motor threshold at different levels of the muscle contraction (0-100% of maximum voluntary contraction (MVC)). The effects of transcranial magnetic stimulation (TMS) on the onset latency, MEP area and silent period (SP) as a function of the %MVC were evaluated using a piecewise linear regression analysis. RESULTS: The MEP areas for the small hand muscles were almost completely saturated at 20% of MVC. In contrast, the MEP areas for radial muscles (ECR, FCR) had a dual increase at 40% of MVC while the ulnar muscles (ECU, FCU) had a dual increase at 20% of MVC. A uniform latency shift (1.5-3 ms reduction) was observed in all muscles with a changing point at 10% of MVC. The SPs were the longest for FDI and were not significantly influenced by MVC for any muscles. CONCLUSIONS: The excitatory and inhibitory effects of TMS on the MEPs differed for the small hand and forearm muscles and also between the ulnar and radial muscles. These results probably resulted from the different degrees of direct corticomotoneuronal inputs to each muscle and the inherent properties of the spinal motoneurons.     

Inhibition in the human motor cortex is reduced just before a voluntary contraction.

OBJECTIVE: To examine inhibition in the human motor cortex before and during voluntary movements. METHODS: The balance between the excitation and inhibition of corticospinal neurons in the human motor cortex was tested by conditioning the motor evoked potentials (MEP) evoked in forearm muscles by transcranial magnetic stimulation with a preceding subthreshold stimulus delivered through the same coil. RESULTS: When normal individuals (n = 9) made a tonic wrist extension, inhibition of the forearm extensor MEP decreased, whereas that of the forearm flexors was unchanged. When these individuals made a tonic wrist flexion, inhibition of the forearm flexor MEP diminished, whereas that of the forearm extensors was unchanged. When normal individuals (n = 10) made a phasic wrist extension in response to an auditory signal, inhibition of the extensor MEP began to decline about 95 msec before the onset of the agonist EMG activity. CONCLUSIONS: The changes in balance of excitation and inhibition of corticospinal neurons associated with a voluntary movement precede the movement and are directed at the corticospinal neurons projecting to the agonists. These changes may help to select the population of cortical neurons responsible for the movement.     

Modulation of motor activity by cutaneous input: inhibition of the magnetic motor evoked potential by digital electrical stimulation

We examined the inhibitory effect of a brief train of digital (D2) electrical stimuli at 4 times perception threshold on transcranial magnetic motor evoked potentials (MEPs) recorded from abductor pollicis brevis (APB) and flexor carpi radialis (FCR) muscles ipsilateral to the side of D2 stimulation. We compared this to the inhibitory effect of ipsilateral D2 stimulation on averaged rectified EMG recorded at 10% maximum voluntary contraction and on F-responses and H-reflexes recorded from these same muscles. We also compared MEPs recorded following D2 stimulation just above perception threshold to MEPs following higher intensity D2 stimulation. As well, we assessed the effect of preceding D2 stimulation on MEPs recorded from a relaxed versus tonically contracted hand muscle. D2 stimulation elicited a triphasic response of modest MEP facilitation followed by inhibition and further facilitation. The duration and onset of MEP inhibition correlated with those of the initial period of rectified EMG inhibition, however, the magnitude of MEP inhibition was generally less than the magnitude of EMG inhibition, consistent with a greater inhibitory effect of digital afferents on smaller motor neurons. MEN were not facilitated during the rebound of EMG activity (the E2 period) that usually followed the initial period of EMG inhibition (I1 period). The behavior of H-reflexes and F-responses following ipsilateral D2 stimulation suggested that inhibition of both EMG and MEPs is not mediated via presynaptic inhibition of la afferents, and that inhibition is augmented by descending rather than segmental input to spinal motor neurons. Tonic contraction of the target muscle during D2 stimulation decreased the inhibitory effect of the preceding digital stimulus possibly due to recruitment of larger spinal motor neurons less likely to be inhibited by cutaneous input.     

Motor evoked potentials of the first dorsal interosseous muscle in step and ramp index finger abduction.

The present experiment was undertaken to study the change in motor cortex excitability as a function of muscle contraction speed during ramp and step abduction by the index finger. Motor evoked potentials (MEPs) of the first dorsal interosseous muscle elicited by transcranial magnetic stimulation (TMS) were modulated by different muscle contraction speeds. When TMS was delivered at 10% maximum voluntary contraction (MVC), MEP amplitudes were always significantly larger in step than in ramp contractions. These differences were dependent on the amount of background electromyographic activity (EMG), which was significantly larger in step than in ramp contractions. However, using maximum output of TMS (100%) with a trigger level at 10% MVC, these differences disappeared. With a trigger level at 30% MVC, these differences also disappeared in spite of differences in the amount of background EMG between them. These results are attributed to different central motor commands. Motor evoked potential amplitudes are dependent not only on the level of background EMG activity but also on the nature of descending motor commands.     

Facilitation of motor evoked potentials by postcontraction response (Kohnstamm phenomenon)

We have applied repeated transcranial magnetic stimuli during the involuntary postcontraction muscle activity (Kohnstamm phenomenon) or during a tonic vibration reflex, both presumably arising from subcortical levels. The motor evoked potentials (MEPs) were compared with the MEPs evoked during a comparable voluntary contraction (cortical origin). The MEP amplitudes from the deltoid muscle appeared linearly related to the mean amplitude of the smoothed rectified background EMG preceding the stimulus. No differences in the facilitatory effect between voluntary and involuntary preinnervation manoeuvres were founf. If we accept the hypothesis of a subcortical origin of the involuntary muscle activity in the Kohnstamm phenomenon, the similar facilitatory effect of involuntary and voluntary background EMG supports a predominantly spinal localisation of the facilitatory mechanism in this proximal muscle both during involuntary and during voluntary activity, at least under the present conditions of rather low stimulus strengths. In about 20–30% of all the trials an extra facilitatory effect on the MEP amplitude was observed during the shortening contraction compared to an MEP elicited during the lengthening contraction, in spite of a similar background EMG. This extra facilitatory effect of the shortening contraction was observed during involuntary and voluntary preactivation, suggesting an elevated excitatory state at the spinal level.     

Corticospinal drive during painful voluntary contractions at constant force output

In the voluntary contractions, output force can be maintained constant although the inhibitory influences exerted by pain on muscle activity. We investigated changes in the spontaneous and evoked activity of the abductor digiti minimi muscle (ADM) and the biceps brachii muscle (BIC) in healthy volunteers during constant force noxious contraction, resulting from chemically activated nociceptive afferents. EMG-force relationship, motor-evoked response (MEP) to transcranial magnetic stimulation and determinism (DET) of surface EMG signals during constant force contraction was analyzed before, during and after chemically induced tonic activation of their nociceptive afferents. Under constant force contraction, amplitude of surface EMG signal decreased in BIC and increased in ADM during pain with respect to control condition. In both muscles, the size of motor-evoked potential (MEP) induced by transcranial magnetic stimulation (TMS) of the primary motor cortex was significantly higher during pain than in control. Level of determinism extracted from surface EMG signal by non-linear method was similarly and significantly increased in both muscles during pain stimulation. Finally, nociceptive stimulation caused a decline in steadiness of the force exerted by ADM and BIC. These results are interpreted in terms of increased corticospinal synchronizing inputs. The possibility that it may play a role in governing force production to counteract pain inhibitory influences on motor system is considered.     

Differential modulation of motor evoked potential and silent period by activation of intracortical inhibitory circuits.

OBJECTIVES: To investigate the effect of activation of intracortical inhibitory circuits, as tested by short interval (3 ms) paired-pulse transcranial magnetic stimulation (TMS) with a conditioning-test paradigm, on the electromyographic (EMG) pause (silent period, SP) following the motor evoked potential (MEP) in normal subjects. METHODS: SPs and MEPs were recorded from the right first dorsal interosseous (FDI) muscle during a tonic voluntary contraction (from 70 to 90% of the maximum). Using a focal coil, we compared the SP duration after single-pulse TMS, paired-pulse TMS and single-pulse TMS of reduced intensity such as to evoke MEPs matched in size to the conditioned ones after paired-pulse TMS. In addition, we compared in a control experiment the duration of the SP following matched size MEPs evoked, respectively, by focal TMS with preferential activation of indirect I1- or I3-waves. RESULTS: SP duration after paired-pulse TMS was significantly longer than after single-pulse TMS evoking MEPs of a similar size. In no case the SP duration was longer when focal TMS preferentially activated I1-waves. CONCLUSIONS: The conditioning sub-threshold stimulus is more powerful in reducing the MEP size than in cutting down the subsequent EMG silence, suggesting that the neural circuits underlying MEP and SP are, at least in part, different.     

Central changes in muscle fatigue during sustained submaximal isometric voluntary contraction as revealed by transcranial magnetic stimulation

Changes in responses to transcranial magnetic stimulation (TMS) during submaximal isometric voluntary contraction (60% of maximal voluntary contraction (MVC) of the adductor pollicis muscle and the subsequent recovery period have been studied in healthy volunteers. TMS at twice the motor threshold was applied during the sustained contraction, as well as at rest and during short-lasting (2 s) 60% MVCs before and immediately after the sustained contraction, and at 5 min intervals during the recovery period. Both motor evoked potential (MEP) magnitude (peak and area) and silent period (SP) duration in electromyographic activity (EMG) of the adductor pollicis muscle showed a gradual decrease up to the endurance point and an increase thereafter. MEPs elicited at rest immediately after the fatiguing contraction were larger, whereas those elicited later on during the recovery period did not differ significantly from the controls. It is suggested that the changes in responses to TMS, divergent from those in ongoing voluntary EMG during the sustained 60% MVC, indicate complex processes at levels preceding the motor cortex output cells in an attempt to maintain a submaximal contraction of the fatigued muscle. The increase in MEP magnitude after the sustained 60% MVC may indicate residual changes in cortical activity after fatiguing contraction.     

An investigation of the late excitatory potential in the hand following magnetic stimulation of the motor cortex

Magnetic stimulation of the motor cortex gives rise to a motor evoked potential (MEP) followed by a silent period (SP) during which a late excitatory potential (LEP) may occur in the surface EMG. To elucidate the mechanism of the LEP we investigated the effect of muscle contraction, stimulus intensity and stimulation site on the LEP recorded from the abductor pollicis brevis muscle. The amplitude of the LEP increased with increasing levels of muscle contraction and decreased with increasing stimulus intensity. There was no direct relationship between the amplitude of the LEP and the MEP, but there was an inverse relationship between LEP amplitude and SP duration. The latency of the LEP was unaffected by the level of muscle contraction, but increased with increasing stimulus intensity. Topographic mapping with stimulation at multiple scalp sites yielded a LEP at sites partially encircling but not including the centre of the APB motor area. These results are consistent with the LEP being due to reflex alpha motoneurone firing as a result of gamma motoneurone activation or with a period of disinhibition at cortical level allowing breakthrough of voluntary activity.     

Motor inhibition and excitation are independent effects of magnetic cortical stimulation.

We administered magnetic cortical stimulation (MCS) during voluntary contraction of intrinsic hand muscles to 8 patients with motor neuron disease (MND), 5 patients with pure lower motor neuron syndromes (LMN), a patient with severe subacute sensory neuropathy (SSN), and 10 healthy volunteers. Patients with MND had clinical evidence of upper MND and elevated thresholds for (3 patients) or absence of (5 patients) motor evoked potentials (MEPs). MCS during sustained contraction inhibited electromyographic activity in 6 of 8 patients with MND, without preceding MEPs. MCS had no effect on the electromyogram (EMG) of the other 2 patients with MND. In normal subjects and patients with LMN, inhibition of EMG was never seen without a preceding MEP, regardless of stimulus intensity. In the patient with SSN, MCS elicited normal MEPs and inhibited the EMG in a pattern similar to normal subjects, whereas supramaximal electrical stimulation of median and ulnar nerves failed to inhibit the EMG despite normal M and F responses. Our findings indicate that the inhibitory effects of MCS on EMG are not dependent solely on changes in afferent feedback caused by the muscle twitch produced by the MEP, or on Renshaw cell inhibition. We suggest that some of the inhibitory and excitatory effects of MCS on the motor system are mediated by distinct cortical elements, which may have different susceptibilities to pathophysiological processes in MND.     

Factors influencing cortical silent period: optimized stimulus location, intensity and muscle contraction

Inhibitory silent period (SP) is a transient suppression of voluntary muscle activity after depolarization of representative motor neuronal populations following transcranial magnetic stimulation (TMS). Our aim was to evaluate and present an optimal protocol for the measurement of SP by (1) determining the impact of muscle activation level and stimulus intensity (SI) on the duration of SP, and, (2) studying the relationship between motor evoked potential (MEP) and SP, using targeted stimulus delivery. Single magnetic pulses were focused on the optimal representation area of the thenar musculature on primary motor cortex. We utilized real-time 3D-positioning of TMS-evoked electric field on anatomical structures derived from individual MR-images. The SI varied from 80% to 120% of individual resting motor threshold (MT). Muscle activation levels varied from 20% to 80% of the maximal voluntary contraction (MVC). Contralateral SP lengthened significantly with increasing SI independent of target muscle activation. The peak amplitude of the MEP was affected by SI and force. Latency and duration of the MEP were practically unaffected by SI or force. Focal stimulation at 110-120% MT and approximately 50% MVC (with only negligible need for control) provides most stable and informative SP. MEP should be included in SP as the error from marking the onset diminishes. This study provides a guideline for the consistent measurement of SP, which is applicable when using navigated or traditional TMS.     

Postexercise facilitation of motor evoked potentials following transcranial magnetic stimulation: a study in normal subjects

The size of the motor evoked potential (MEP) elicited by transcranial magnetic stimulation increases soon after a nonexhaustive voluntary contraction of the target muscle (postexercise facilitation). Our aim was to determine whether the duration or intensity of voluntary muscle contraction influenced postexercise facilitation in normal subjects. We recorded the MEP from the thenar muscles following contractions of different durations (5, 15, and 30 s) and intensities (10%, 25%, and 50% of maximal voluntary contraction). We found that every combination of the tested intensities and durations of physical effort could induce postexercise MEP facilitation. Although the degree of postexercise MEP facilitation was comparable across the different durations and intensities, the maximal facilitation was observed with the shortest and strongest muscle contraction. Our study thus defines the optimal setting to study postexercise facilitation for clinical purposes.     

Effect of discharge desynchronization on the size of motor evoked potentials: an analysis.

OBJECTIVE: Motor evoked potentials (MEPs) after transcranial magnetic brain stimulation (TMS) are smaller than CMAPs after peripheral nerve stimulation, because desynchronization of the TMS-induced motor neurone discharges occurs (i.e. MEP desynchronization). This desynchronization effect can be eliminated by use of the triple stimulation technique (TST; Brain 121 (1998) 437). The objective of this paper is to study the effect of discharge desynchronization on MEPs by comparing the size of MEP and TST responses. METHODS: MEP and TST responses were obtained in 10 healthy subjects during isometric contractions of the abductor digiti minimi, during voluntary background contractions between 0% and 20% of maximal force, and using 3 different stimulus intensities. Additional data from other normals and from multiple sclerosis (MS) patients were obtained from previous studies. RESULTS: MEPs were smaller than TST responses in all subjects and under all stimulating conditions, confirming the marked influence of desynchronization on MEPs. There was a linear relation between the amplitudes of MEPs vs. TST responses, independent of the degree of voluntary contraction and stimulus intensity. The slope of the regression equation was 0.66 on average, indicating that desynchronization reduced the MEP amplitude on average by one third, with marked inter-individual variations. A similar average proportion was found in MS patients. CONCLUSIONS: The MEP size reduction induced by desynchronization is not influenced by the intensity of TMS and by the level of facilitatory voluntary background contractions. It is similar in healthy subjects and in MS patients, in whom increased desynchronization of central conduction was previously suggested to occur. Thus, the MEP size reduction observed may not parallel the actual amount of desynchronization.     

Task-dependent differences in corticobulbar excitability of the submental motor projections: Implications for neural control of swallowing

It has been suggested that the primary motor cortex plays a substantial role in the neural circuitry that controls swallowing. Although its role in the voluntary oral phase of swallowing is undisputed, its precise role in motor control of the more reflexive, pharyngeal phase of swallowing is unclear. The contribution of the primary motor cortex to the pharyngeal phase of swallowing was examined using transcranial magnetic stimulation (TMS) to evoke motor evoked potentials (MEPs) in the anterior hyomandibular muscle group during either volitional submental muscle contraction or contraction during the pharyngeal phase of both volitionally, and reflexively, initiated swallowing. For each subject, in all three conditions, TMS was triggered when submental surface EMG (sEMG) reached 75% of the mean maximal submental sEMG amplitude measured during 10 volitional swallows. MEPs recorded during volitional submental muscle contraction were elicited in 22 of the 35 healthy subjects examined (63%). Only 16 of these 22 subjects (45.7%) also displayed MEPs recorded during volitional swallowing, but their MEP amplitudes were larger when triggered by submental muscle contraction than when triggered by volitional swallowing. Additionally, only 7 subjects (of 19 tested) showed MEPs triggered by submental muscle contraction during a reflexively triggered pharyngeal swallow. These differences indicate differing levels of net M1 excitability during execution of the investigated tasks, possibly brought about by task-dependent changes in the balance of excitatory and inhibitory neural activity.     

Effect of different approaches to target force on transcranial magnetic stimulation responses

Introduction: The aim of this study was to determine whether the manner in which a target force is approached can influence the electromyographic (EMG) and mechanical parameters evoked by transcranial magnetic stimulation (TMS) during brief muscle contractions. Methods: The amplitude of motor‐evoked potentials (MEP) and superimposed twitch and the duration of the silent period were recorded in 8 healthy participants in response to TMS delivered during brief isometric voluntary contractions of the quadriceps maintaining a target force (10% and 50% of maximal voluntary force) or gradually increasing or decreasing to reach this point. Results: MEP and superimposed twitch, unlike the silent period, are influenced by the manner of reaching a low force. Conclusions: Clear instructions must be provided to research participants and patients. Rapidly increasing to a target force without exceeding it and maintaining the force before the delivery of TMS results in stable, representative MEP amplitudes. Muscle Nerve 48 : 430–432, 2013     

Trigeminal sensory input elicited by electric or magnetic stimulation interferes with the central motor drive to the intrinsic hand muscles.

In 6 normal subjects, unilateral supraorbital magnetic or electric stimulation resulted in a consistent symmetrical inhibition of the motor evoked potentials (MEPs) of the relaxed and preactivated first dorsal interosseus (FDI) muscle. A supraorbital stimulus caused a significant reduction in amplitude when the trigeminal CS was given 30 to 65 ms before transcranial magnetic stimulation (TMS). In addition, supraorbital magnetic stimulation induced a bilateral EMG suppression of the isometrically contracting FDI muscles, starting about 40 to 50 ms after the magnetic stimulus. In 4 subjects, MEPs evoked by transcranial electric stimulation or by TMS during slight muscle contraction showed a comparable trigeminomotor inhibition. These findings demonstrate that electromagnetic stimulation of trigeminal afferents interferes with the motor output to the intrinsic hand muscles inducing a bilateral inhibition which is probably mediated by a multisynaptic subcortical network. In all 6 subjects, TMS over the motor hand area or the cerebellum elicited a reproducible blink reflex. Since the blink reflex is a sensitive indicator of trigeminal excitation, one has to assume that TMS is associated with a significant excitation of trigeminal afferents. Therefore, trigeminomotor inhibition has to be considered in all TMS studies that use a conditioning-test design.     

Investigation of paroxysmal dystonia in a patient with multiple sclerosis: a transcranial magnetic stimulation study.

OBJECTIVE: To study the pathogenesis of paroxysmal dystonia affecting the right body side in a patient with a demyelinating lesion in the descending motor pathways, also involving the basal ganglia. METHODS: Single-pulse transcranial magnetic stimulation (TMS) was applied to study motor evoked potentials (MEPs) and the following silent periods (SPs) in the first dorsal interosseous muscle (FDI) of both sides and in the right extensor carpi radialis muscle (ECR) during voluntary contractions performed outside the dystonic attacks. During the dystonic paroxysms, single-pulse TMS was used to investigate the time course of MEPs and SPs in both FDI and ECR of the right side. Furthermore, paired-pulse TMS was applied at rest to investigate short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF) in both FDI muscles. RESULTS: At rest SICI and ICF were normal in both motor cortices. During voluntary contraction the MEP was smaller and the SP was longer in the affected FDI than in the contralateral. During the paroxysms, the MEPs and SPs were suppressed in comparison with the responses elicited during voluntary contraction. CONCLUSIONS: These results fit well with the theory of ephaptic excitement of corticospinal axons for the pathogenesis of paroxysmal dystonia due to a demyelinating lesion. SIGNIFICANCE: Identification of the mechanisms underlying paroxysmal dystonia in demyelinating disorders extends our knowledge on the pathophysiology of dystonia.