Analysis of motor pathway involvement in konzo using transcranial electrical and magnetic stimulation

To elucidate the involvement of motor pathways in konzo, 21 konzo subjects (mean age 22 years) underwent transcranial electrical stimulation (TES) in 1998. Fourteen konzo subjects (mean age 21 years) underwent transcranial magnetic stimulation (TMS) in 2000. Three subjects underwent both TES and TMS. Motor evoked potentials (MEPs) were recorded in the abductor pollicis brevis (APB) muscle with TES, and in the abductor digiti minimi (ADM) and tibialis anterior (TA) muscles with TMS. APB-MEPs were normal in 2 of 21 subjects and absent in 9; central conduction time (CCT) was prolonged in 10. Resting ADM-MEPs were absent in 9 of 14 subjects with clinically preserved upper limbs. Among these nine, seven subjects responded after facilitation. Most subjects (13 of 14) failed to show TA-MEPs. Of the subjects who underwent both types of stimulation, one had normal TES-MEP but abnormal ADM-MEP with TMS. These findings suggest involvement of both corticomotoneurons and motor descending pathways in konzo.     

Effect of fatiguing maximal voluntary contraction on excitatory and inhibitory responses elicited by transcranial magnetic motor cortex stimulation

Vertex transcranial magnetic stimulation (TMS) elicited tibialis anterior motor evoked potentials (MEPs) and silent periods (SPs) that were recorded during and following isometric maximal volitional contraction (MVC). During MVC in 6 healthy subjects, MEP amplitudes in the exercised muscle showed an increasing trend from an initial value of 4539 ± 809 μV (mean ± SE) to 550 ± 908 μV (P < 0.13) while force and EMG decreased (P < 0.01). Also, SP duration increased from 165 ± 37 ms to 231 ± 32 ms (P < 0.01). Thus, during a fatiguing MVC both excitatory and inhibitory TMS-induced responses increased. TMS delivered during repeated brief 10% MVC contractions before and after a fatiguing MVC in 5 subjects, showed no change in MEP amplitude but SP duration was prolonged after MVC. This SP prolongation was focal to the exercised muscle. Silent periods recorded after pyramidal tract stimulation were unchanged following the MVC. These results suggest that MEP and SP might have common sources of facilitation during an MVC and that inhibitory mechanisms remain focally augmented following a fatiguing MVC. © 1996 John Wiley & Sons, Inc.     

Cortical mechanisms mediating the inhibitory period after magnetic stimulation of the facial motor area

We studied the silent period (SP) that interrupts voluntary electromyographic activity (EMG) in facial muscles, after transcranial magnetic stimulation (TMS), in normal subjects. High-intensity magnetic stimulation with a 12-cm round coil centered at the vertex induced a long-lasting SP (215 ms), whereas supramaximal stimulation of the facial nerve only induced a short (< 20 ms) and incomplete EMG suppression, and cutaneous stimuli had no inhibitory effect at all. Cutaneous trigeminal stimulation delivered after TMS evoked blink-like reflexes, showing that facial motoneurons were not inhibited during the SP. Simultaneous recordings from perioral muscles (large cortical representation) and from orbicularis oculi and masseter muscles (small cortical representation) showed SPs of identical duration. Focal stimuli with a figure-of-eight coil showed that positioning of the coil was critical and that the optimal scalp sites for evoking the largest motor potentials and longest SPs coincided. Low-intensity stimulation occasionally elicited short SPs without a preceding motor potential. We conclude that the SP induced in facial muscles by TMS results from the excitation of cortical inhibitory interneurons surrounding the upper motoneurons. © 1997 John Wiley & Sons, Inc. Muscle Nerve, 20, 418–424, 1997.     

Modification of the silent period by double transcranial magnetic stimulation.

OBJECTIVES: To study the time course of the changes of the inhibitory network of the human motor system, we investigated the silent period (SP) in 7 healthy subjects by double suprathreshold transcranial magnetic stimulation (TMS). METHODS: SPs and motor evoked potentials (MEPs) were recorded from the voluntarily activated right abductor digiti minimi muscle. Conditioning and test stimuli were delivered with equal intensity, which was set to yield a baseline SP duration of 130 ms by a single pulse, and with various interstimulus intervals (ISIs). In addition, a control experiment with adjustment of the intensity of single stimuli was performed. RESULTS: At ISIs of 20 and 30 ms the test pulse SP duration was prolonged, without increasing the MEP amplitude. The SP duration shortened at longer ISIs and showed a significant depression between ISIs of 60-110 ms. The shortened SP was accompanied by a diminished MEP. The control experiment revealed that the SPs evoked by the adjusted pulses were significantly shorter than the test pulse SPs. CONCLUSIONS: A conditioning stimulus can prolong and shorten the test pulse SP duration at different ISIs. The prolongation is probably cortically generated, whereas the shortening is likely to occur at a cortical and spinal level.     

Mechanisms underlying mirror movements in Parkinson's disease: a transcranial magnetic stimulation study.

The neural mechanisms underlying unintended mirror movements (MMs) of one hand during unimanual movements of the other hand in patients with Parkinson's disease (PD) are largely unexplored. Here we used surface electromyographic (EMG) analysis and focal transcranial magnetic stimulation (TMS) to investigate the pathophysiological substrate of MMs in four PD patients. Surface EMG was recorded from both abductor pollicis brevis (APB) and first dorsal interosseous (FDI) muscles. Cross-correlation EMG analysis revealed no common motor drive to the two APBs during intended unimanual tasks. Focal TMS of either primary motor cortex (M1) elicited normal motor-evoked potentials (MEPs) in the contralateral APB, whereas MEPs were not seen in the ipsilateral hand. During either mirror or voluntary APB contraction, focal TMS of the contralateral M1 produced a long-lasting silent period (SP), whereas stimulation of the ipsilateral M1 produced a short-lasting SP. During either mirror or voluntary finger tapping, 5 Hz repetitive TMS (rTMS) of the contralateral M1 disrupted EMG activity in the target FDI, whereas the effects of rTMS of the ipsilateral M1 were by far slighter. During either mirror or voluntary APB contraction, paired-pulse TMS showed a reduction of short-interval intracortical inhibition in the contralateral M1. These findings provide converging evidence that, in PD, MMs do not depend on unmasking of ipsilateral projections but are explained by motor output along the crossed corticospinal projection from the mirror M1.     

Conditioning effect on the long latency potentials in the lower limb to transcranial magnetic stimulation

Objectives – We used an electrical conditioning stimulation followed by transcranial magnetic stimulation (TMS) to facilitate the occurrence of long latency potentials (LLPs) in order to study the relationship between primary motor evoked potentials (MEPs) and LLPs in the lower limbs. Materials and methods – The study group included 6 healthy subjects, 1 patient with right thalamic infarction, and 3 patients with spinal cord injuries. The subjects were subjected to electrical conditioning (C) stimulation delivered to the left big toe at 250 Hz in a train of pulses of 20 ms duration prior to TMS (T) from 0 to 150 ms at an increment of 10 ms. The surface electromyographic signals were recorded at the tibialis anterior and gastrocnemius medialis for 400 ms. Results – The C-T test facilitated both primary MEPs and LLPs with a pattern similar to the primary MEPs of its antagonist. There was no facilitation of the primary MEPs or LLPs in the affected limb of patients with thalamic or spinal cord lesions. Conclusion – At appropriate C-T interval, LLPs could be consistently provoked by TMS. The LLPs were absent in the patients with thalamic infarction and spinal cord injuries. It suggests that LLPs might be provoked through a supraspinal control.     

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.     

Excitability Profile of Motor Evoked Potentials and Silent Periods

The aim of this study was to confirm the excitability profile of human cortical circuits on the motor evoked potential (MEP) and the silent period (SP) after paired transcranial magnetic stimulation (TMS) with variable interstimulus intervals (ISI), and to compare the time courses of MEP and SP after paired TMS at variable ISIs. MEPs were elicited at the hypothenar muscles at rest, and during tonic muscle contraction by applying paired TMS to the motor cortex. The authors measured the MEP amplitude during rest and the duration of SP during tonic muscle contraction at various ISIs. The response to paired stimuli was inhibited by an ISI of 1–5 ms and facilitated by an ISI of 10–20 ms. The SP at an ISI of 1–5 ms was shorter than that at the single suprathreshold stimulus, but the SP at an ISI of 15–25 ms was longer than this. A significant correlation was observed between the MEP amplitude and the duration of SP at ISIs of 1–20 ms and for a CS of 80% of threshold. These results may provide useful data for the study of the function of cortical excitability in disease states and suggest that the neural circuits underlying MEP and SP differ partly.     

Predominant activation of I1-waves from the leg motor area by transcranial magnetic stimulation

We performed transcranial magnetic stimulation (TMS) to elucidate the D- and I-wave components comprising the motor evoked potentials (MEPs) elicited from the leg motor area, especially at near-threshold intensity. Recordings were made from the tibialis anterior muscle using needle electrodes. A figure-of-eight coil was placed so as to induce current in the brain in eight different directions, starting from the posterior-to-anterior direction and rotating it in 45 degrees steps. The latencies were compared with those evoked by transcranial electrical stimulation (TES) and TMS using a double cone coil. Although the latencies of MEPs ranged from D to I3 waves, the most prominent component evoked by TMS at near-threshold intensity represented the I1 wave. With the double cone coil, the elicited peaks always represented I1 waves, and D waves were evoked only at very high stimulus intensities, suggesting a high effectiveness of this coil in inducing I1 waves. Using the figure-of-eight coil, current flowing anteriorly or toward the hemisphere contralateral to the recorded muscle was more effective in eliciting large responses than current flowing posteriorly or toward the ipsilateral hemisphere. The effective directions induced I1 waves with the lowest threshold, whereas the less effective directions elicited I1 and I2 waves with a similar frequency. Higher stimulus intensities resulted in concomitant activation of D through I3 waves with increasing amount of D waves, but still the predominance of I1 waves was apparent. The amount of I waves, especially of I1 waves, was greater than predicted by the hypothesis that TMS over the leg motor area activates the output cells directly, but rather suggests predominant transsynaptic activation. The results accord with those of recent human epidural recordings.     

Transcranial magnetic and electrical stimulation compared: Does TES activate intracortical neuronal circuits?

OBJECTIVE: To determine whether, and under which conditions, transcranial electrical stimulation (TES) and transcranial magnetic stimulation (TMS) can activate similar neuronal structures of the human motor cortex, as indicated by electromyographic recordings. METHODS: Focal TMS was performed on three subjects inducing a postero-anterior directed current (p-a), TES with postero-anteriorly (p-a) and latero-medially (l-m) oriented electrodes. We analyzed the onset latencies and amplitudes (single-pulse) and intracortical inhibition and excitation (paired-pulse). RESULTS: TMS p-a and TES p-a produced muscle responses with the same onset latency, while TES l-m led to 1.4-1.9 ms shorter latencies. Paired-pulse TMS p-a and TES p-a induced inhibition at short inter-stimulus intervals (ISI) (maximum: 2-3 ms) and facilitation at longer ISIs (maximum: 10 ms). No inhibition but a strong facilitation was obtained from paired-pulse TES l-m (ISIs 1-5 ms). CONCLUSIONS: Our findings support the hypothesis, that current direction is the most relevant factor in determining the mode of activation for both TMS and TES: TMS p-a and TES p-a are likely to activate the corticospinal neurons indirectly. In contrast, TES l-m may preferentially activate the corticospinal fibres directly, distant of the neuronal body. SIGNIFICANCE: TES is a suitable tool to induce intracortical inhibition and excitation.     

Muscle vibration: different effects on transcranial magnetic and electrical stimulation.

Transcranial magnetic stimulation (TMS) and transcranial electrical stimulation (TES) were applied before and 3 s after onset of vibration (0.5 mm, 80 Hz) of the right extensor carpi radialis muscle in 5 healthy subjects. Vibration induced significant augmentation and latency shortening of motor evoked potentials elicited by TMS, but not TES. This provides evidence for an involvement of cortical mechanisms by muscle vibration in the augmentation of MEPs following TMS.     

Differences between the effects of three plasticity inducing protocols on the organization of the human motor cortex

Several experimental protocols induce lasting changes in the excitability of motor cortex. Some involve direct cortical stimulation, others activate the somatosensory system and some combine motor and sensory stimulation. The effects usually are measured as changes in amplitude of the motor-evoked-potential (MEP) or short-interval intracortical inhibition (SICI) elicited by a single or paired pulses of transcranial magnetic stimulation (TMS). Recent work has also tested sensorimotor organization within the motor cortex by recording MEPs and SICI during short periods of vibration applied to single intrinsic hand muscles. Here sensorimotor organization is focal: MEPs increase and SICI decreases in the vibrated muscle, whilst the opposite occurs in neighbouring muscles. In six volunteers we compared the after effects of three protocols that lead to lasting changes in cortical excitability: (i) paired associative stimulation (PAS) between a TMS pulse and an electrical stimulus to the median nerve; (ii) motor practice of rapid thumb abduction; and (iii) sensory input produced by semicontinuous muscle vibration, on MEPs and SICI at rest and on the sensorimotor organization. PAS increased MEP amplitudes, whereas vibration changed sensorimotor organization. Motor practice had a dual effect and increased MEPs as well as affecting sensorimotor organization. The implication is that different protocols target different sets of cortical circuits. We speculate that protocols that involve repeated activation of motor cortical output lead to lasting changes in efficacy of synaptic connections in output circuits, whereas protocols that emphasize sensory inputs affect the strength of sensory inputs to motor circuits.     

Central fatigue as revealed by postexercise decrement of motor evoked potentials

We have previously shown that the amplitudes of motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) were transiently decreased after exercise, indicating fatigue of motor pathways in the central nervous system. The responsible mechanism is apparently decreased efficiency in the generation of the descending volleys in the motor cortex. We also noted a progressive decrement inamplitude from the first to the fourth MEP. To further clarify the mechanism of this phenomenon, 5 subjects were studied with TMS deliveredat the rates of 0.1, 0.15, 0.3, 1, 3, and 6 Hz. The effect was best demonstrated at 0.3 Hz, and occurred after both isometric and isotonic exercise. Three of the subjects also had 0.3-Hz percutaneous electrical stimulation of the brainstem, and a decrement in MEP amplitude did not occur. Further, the delivery of TMS during muscle contraction after muscle fatigue failed to produce a decrement. The results are similar to those found at the neuromuscular junction in myasthenia gravis and are consistent with a reduced safety factor of cortical synaptic transmission in central nervous system fatigue. © 1994 John Wiley & Sons, Inc.     

Pre-movement motor excitability is reduced ipsilateral to low force pinch grips

Motor excitability ipsilateral to pinch grips was investigated during the pre-movement period. Subjects performed right-handed phasic pinch grips with 2% or 20% maximum voluntary contraction (MVC) in response to a visual go-signal. Transcranial magnetic stimulation (TMS) was applied over the right motor cortex at various intervals before the go-signal and 100 msec after movement onset. Motor evoked potentials were recorded from the relaxed left first dorsal interosseous muscle. Immediately prior to and during 2% MVC pinch grips, MEP amplitudes were reduced. In contrast, MEPs obtained by transcranial electrical stimulation tended to be increased, indicating that MEP decreases are mediated at a cortical level. Before and during 20% MVC pinch grips MEP amplitudes were enhanced. TMS delayed reaction time if applied close to the go-signal. We conclude that the motor cortex ipsilateral to low force movements is inhibited prior to and during movement.     

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.     

Facilitation of corticospinal excitability in the tibialis anterior muscle during robot-assisted passive stepping in humans

Although phasic modulation of the corticospinal tract excitability to the lower limb muscles has been observed during normal walking, it is unclear to what extent afferent information induced by walking is related to the modulation. The purpose of this study was to test the corticospinal excitability to the lower limb muscles by using transcranial magnetic stimulation (TMS) and transcranial electrical stimulation of the motor cortex while 13 healthy subjects passively stepped in a robotic driven-gait orthosis. Specifically, to investigate the effect of load-related afferent inputs on the corticospinal excitability during passive stepping, motor evoked potentials (MEPs) in response to the stimulation were compared between two passive stepping conditions: 40% body weight unloading on a treadmill (ground stepping) and 100% body weight unloading in the air (air stepping). In the rectus femoris, biceps femoris and tibialis anterior (TA) muscles, electromyographic activity was not observed throughout the step cycle in either stepping condition. However, the TMS-evoked MEPs of the TA muscle at the early- and late-swing phases as well as at the early-stance phase during ground stepping were significantly larger than those observed during air stepping. The modulation pattern of the transcranial electrical stimulation-evoked MEPs was similar to that of the TMS-evoked MEPs. These results suggest that corticospinal excitability to the TA is facilitated by load-related afferent inputs. Thus, these results might be consistent with the notion that load-related afferent inputs play a significant role during locomotor training for gait disorders.     

Motor evoked potentials from masseter muscle induced by transcranial magnetic stimulation of the pyramidal tract: the importance of coil orientation

BACKGROUND: Reliable recording of motor evoked potentials (MEPs) of the masseter muscle by transcranial magnetic stimulation (TMS) has proved more difficult than from facial or intrinsic hand muscles. Up to now it was unclear whether this difficulty was due to methodological and/or anatomical reasons. METHODS: The mechanism of pyramidal cell activation in masseter MEPs was investigated by using magnetic and electric transcranial stimulation. Analysing the effect of magnetic coil positioning and orientation over the scalp, and scrutinizing the masseter recording technique to avoid compound motor action potential (CMAP) contamination from facial muscles, an optimized method of masseter MEPs was developed. RESULTS: In particular, an antero-lateral inducing current orientation in the stimulating coil, approximately paralleling the central sulcus, proved clearly more effective for the masseter muscles than the postero-lateral orientation (P=0.005) found optimal for intrinsic hand muscles. The thus evoked masseter MEPs by transcranial magnetic stimulation (TMS) were found to be identical in shape, amplitude and latency as those evoked by transcranial electric stimulation (TES), evidencing a direct rather than trans-synaptic activation of the pyramidal cells. CONCLUSIONS: We conclude that in TMS evoked MEPs of masseter muscles, the direct stimulation of the pyramidal tract is more easily achieved than the trans-synaptic activation, which is in contrast to the intrinsic hand muscles. We hypothesize that the presynaptic projections to pyramidal cells of the masticatory muscles are less abundant than in hand muscles, and are therefore less accessible to trans-synaptic stimulation.     

Transcranial magnetic stimulation of motor pathways directed to muscles supplied by cranial nerves in amyotrophic lateral sclerosis.

OBJECTIVES: In amyotrophic lateral sclerosis (ALS), transcranial magnetic stimulation (TMS) detects remarkable abnormalities of central motor circuits: cortical excitability threshold, silent period (SP) duration and intra-cortical inhibition. TMS directed to cranio-facial musculature was performed in ALS patients in order: (1) to document the neurophysiological involvement of motor central and peripheral cranial pathways by evaluating changes of threshold and SP; (2) to discover a possible correlation between the clinical picture and abnormal excitability properties. METHODS: Motor evoked potentials (MEPs) were recorded from masseter, genioglossus and orbicularis oris muscles of both sides in 25 ALS patients and 25 controls, in response to TMS delivered over the face M1 area and the vertex. RESULTS: TMS gave rise to two orders of responses: bilateral MEPs during contraction represented the central responses, and motor action potentials (MAPs) during rest represented the peripheral responses. MEPs were followed by SPs, which increased linearly with increasing TMS intensity (r=0.8). At least one of the analyzed parameters was abnormal in all patients: central abnormalities (increased active threshold, delayed MEPs, reduced SP) were found in 96% of patients, alone or combined with abnormalities of the MAPs (reduced area and/or prolonged latency). The reduction of SP was linearly related to the Norris score (r=0.95). CONCLUSIONS: Our study shows that TMS is able to detect the involvement of multiple cranial muscles in ALS. This finding offers often pre-clinical information about the disease picture. Therefore, it can be employed as a valuable means for early diagnosis.     

Quadro-pulse stimulation is more effective than paired-pulse stimulation for plasticity induction of the human motor cortex

OBJECTIVE: Repetitive paired-pulse transcranial magnetic stimulation (TMS) at I-wave periodicity has been shown to induce a motor-evoked potential (MEP) facilitation. We hypothesized that a greater enhancement of motor cortical excitability is provoked by increasing the number of pulses per train beyond those by paired-pulse stimulation (PPS). METHODS: We explored motor cortical excitability changes induced by repetitive application of trains of four monophasic magnetic pulses (quadro-pulse stimulation: QPS) at 1.5-ms intervals, repeated every 5s over the motor cortex projecting to the hand muscles. The aftereffects of QPS were evaluated with MEPs to a single-pulse TMS, motor threshold (MT), and responses to brain-stem stimulation. These effects were compared to those after PPS. To evaluate the QPS safety, we also studied the spread of excitation and after discharge using surface electromyograms (EMGs) of hand and arm muscles. RESULTS: Sizes of MEPs from the hand muscle were enhanced for longer than 75min after QPS; they reverted to the baseline at 90min. Responses to brain-stem stimulation from the hand muscle and cortical MEPs from the forearm muscle were unchanged after QPS over the hand motor area. MT was unaffected by QPS. No spreads of excitation were detected after QPS. The appearance rate of after discharges during QPS was not different from that during sham stimulation. CONCLUSIONS: Results show that QPS can safely induce long-lasting, topographically specific enhancement of motor cortical excitability. SIGNIFICANCE: QPS is more effective than PPS for inducing motor cortical plasticity.     

INTRA-RATER RELIABILITY OF A TRANSCRANIAL MAGNETIC STIMULATION TECHNIQUE TO OBTAIN MOTOR EVOKED POTENTIALS

The purpose of this study was to determine the intra-rater reliability of motor evoked potentials (MEP) obtained through transcranial magnetic stimulation (TMS). TMS was applied over the primary motor cortex of 16 healthy subjects. Motor thresholds, MEP latencies, and amplitudes were recorded from the contralateral upper limb on 6 occasions over 15 days. An intraclass correlation coefficient (ICC 2,1) was used to estimate reliability. The ICCs ranged from 0.60 to 0.92 for all MEP measures except amplitude (ICC = 0.01 to 0.34). MEPs obtained with the TMS technique described are generally reliable, although MEP amplitudes demonstrated less consistency.