Cortical magnetic stimulation in amyotrophic lateral sclerosis

Forty patients with ALS underwent cortical magnetic stimulation. Twelve had marked pseudobulbar signs; in these motor evoked potentials (MEPs) could not be elicited. Mean MEP latencies in the others, who had predominantly lower motor neuron signs, measured 23.3 +/- 2.1 msec (thenar), 18.7 +/- 5.3 msec (EDC), and 13.4 +/- 2.9 msec (biceps), respectively. These values were significantly longer (P greater than 0.001) compared with normal values (n = 35), which measured 20.2 +/- 1.6, 14.2 +/- 1.7, and 9.4 +/- 1.7 msec, respectively. MEP amplitude was often markedly reduced (less than 15% of the M wave) compared with a normal mean of 39.5 +/- 13.0%. Overall abnormal MEPs (delayed, absent, or reduced in amplitude) approached 100%. It is argued that measuring central motor delay, which was not significantly different in the patients compared with normals, is subject to error in ALS.     

Motor evoked potentials and central motor conduction: studies of transcranial magnetic stimulation with recording from the leg.

To determine central conduction times in the corticospinal pathways of humans using magnetic stimulation, we have developed a method for consistently recording conduction times between the motor cortex and the L4-5 level of the spinal cord. In 30 subjects, motor evoked potentials (MEPs) were recorded from the tibialis anterior muscle following contralateral motor cortex and peroneal nerve stimulation. In 18 of these subjects, the L4-5 intervertebral space was stimulated. The stimuli consisted of single, painless, short-duration magnetic pulses. In 12 subjects, measurements were made during voluntary ankle dorsiflexion, and during vibration of the TA tendon at rest. All subjects had measureable MEP latencies of 30.3 +/- 2.2 msec (mean +/- S.D.). The central motor conduction time (CMCT) was calculated using both a direct as well as an indirect method. The direct method in 18 subjects had a mean value of 16.2 +/- 1.7 msec, while the indirect method in all 30 subjects was 13.8 +/- 1.8 msec. No significant correlation of the CMCT was found with either age or height in these subjects. Ankle dorsiflexion significantly reduced the MEP latency and increased the amplitude, whereas vibration of the TA tendon significantly increased the amplitude alone. We conclude that MEPs may be consistently and painlessly measured in the lower extremity using magnetic stimulation in adults. Facilitation of the MEPs was produced more consistently by voluntary contraction than by vibratory stimulation of the tibialis anterior muscle tendon. Finally, CMCT was independent of both age and height in our study population.     

AAEM minimonograph #35: Clinical experience with transcranial magnetic stimulation

We elicited motor evoked potentials (MEPs) using transcortical magnetic stimulation in 150 control subjects aged 14 to 85 years and 275 patients with a variety of diseases. There were no significant side effects. Cortex-to-target muscle latencies measured 20.2 +/- 1.6 ms (thenar), 14.2 +/- 1.7 ms (extensor digitorum communis), 9.4 +/- 1.7 ms (biceps), and 27.2 +/- 2.9 ms (tibialis anterior). Central motor delay between the cortex and the C-7 and L-5 measured 6.7 +/- 1.2 ms and 13.1 +/- 3.8 ms, respectively. Mean spinal cord motor conduction velocity measured 65.4 m/s. MEP amplitude expressed as a percentage of the maximum M wave was never less than 20% of the M wave. A value of less than 10% is considered abnormal. MEP latency increases linearly with age and central motor delay is longer in older subjects. Compound muscle action potentials and absolute MEP amplitudes decreased linearly with age. In multiple sclerosis (MS), MEP latency and central delay were often very prolonged. The MEP was more sensitive than the SEP in MS. In amyotrophic lateral sclerosis, MEP latencies were only modestly prolonged; the characteristic abnormality was reduced amplitude. When pseudobulbar features predominated MEPs were often absent. The MEP was of normal latency in Parkinson's disease, but age-related amplitude was often increased. MEP latency and amplitude were normal in Huntington's disease. Abnormal MEPs persisted several months after stroke despite good functional recovery. The MEP could be used to advantage to demonstrate proximal conduction slowing and block in demyelinating neuropathies. In plexopathy, ability to elicit an MEP several days after onset of paresis was good evidence of neuronal continuity in motor fibers.     

Non-invasive evaluation of central motor tract excitability changes following peripheral nerve stimulation in healthy humans.

The interval between muscle stretch and the onset of the long latency electromyographic responses (LLRs) has been theoretically fragmented into an afferent time (AT), taken at the peak of wave N20 of somatosensory evoked potentials and an efferent time (ET), calculated by means of magnetic transcranial stimulation (TCS), the two being separated by a cortical interval (CI). If this were the case, the afferent input should progressively 'energize' the sensorimotor cortex during the CI and change the excitability of cortico-spinal tracts. To investigate this, motor evoked potentials (MEPs) from thumb flexor muscles were recorded, whilst a conditioning stimulation of median or ulnar nerve randomly preceded (10-48 msec intervals) magnetic brain TCS. Nerve stimulation was adjusted to motor threshold and amplitudes of conditioned and test MEPs at different nerve-TCS interstimulus intervals were evaluated. Conditioned MEPs were significantly attenuated with nerve-TCS intervals between 16 and 20 msec for elbow and 20 and 22 msec for wrist stimulation. This was followed by MEP potentiation with nerve-TCS intervals corresponding to the sum of AT + CI (mean 23.2 msec, range 21.7-24.8). The onset latency of facilitated conditioned MEPs was about 1 msec briefer than that of test MEPs, but invariably longer than the latency of MEPs facilitated by a voluntary contraction. This protocol did not demonstrate amplitude facilitation of the segmental H reflex, corroborating the idea that the facilitated part of the conditioning nerve-TCS curve receives a transcortical loop contribution.     

Effect of exercise on motor evoked potentials elicited by transcranial magnetic stimulation in psychiatric patients.

SUMMARY: Under normal conditions, motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation increase in amplitude if the subject exercises the examined muscle immediately before recording. The authors examined the effect of nonfatiguing exercise on the amplitude of MEPs on 42 psychiatric, medicated inpatients (14 with depression, 14 with schizophrenia, and 14 with mania) compared with 14 healthy control subjects. For each subject, a total of 50 baseline and 50 postexercise MEPs were recorded. The mean (+/- standard deviation) postexercise MEP facilitation, expressed as a percentage of mean baseline values, was significantly lower (p 相似文献   

脊髓型颈椎病病人经颅磁电刺激运动诱发电位的对比研究

目的探讨磁电刺激运动诱发电位（ＭＥＰ）在脊髓型颈椎病（ＣＳＭ）的应用价值，并对其临床相关性进行分析。方法采用经颅磁、电刺激对３０例脊髓型颈椎病病人以及年龄性别等相配匹的３０名健康成人分别于外展小指肌、肱二头肌及下肢展短肌表面进行ＭＥＰ的检测。结果全部病人的ＭＥＰ都出现异常，表现为潜伏期、中枢传导时间（ＣＭＣＴ）延长，时限增宽，波辐降低或不能引出。磁刺激ＭＥＰ的ＣＭＣＴ和皮层刺激潜伏期与脊髓型颈椎病临床日本整形外科协会（ＪＯＡ）评分间有密切相关性，能较好地反映ＣＳＭ病人的病情。结论ＭＥＰ在检测ＣＳＭ病人运动功能方面具有定量评价作用。与电刺激相比，磁刺激ＭＥＰ能更好地反映ＣＳＭ病人的病情。     

Cricopharyngeal sphincter muscle responses to transcranial magnetic stimulation in normal subjects and in patients with dysphagia.

OBJECTIVE: Cricopharyngeal (CP) muscle of the upper oesophageal sphincter (UES) has a significant role in the pharyngo-esophageal phase of deglutition. The linkage between the CP muscle of UES and the motor cortex has not been previously studied electrophysiologically in healthy humans and in patients with neurogenic dysphagia. METHODS: Needle recordings of EMG responses were carried out from the CP sphincter muscle following transcranial magnetic stimulation (TMS) over the vertex around the Cz electrode position (cortical MEP), and on the parieto-occipital skull and the occiput ipsilaterally (peripheral MEP) in 14 healthy control subjects and in 26 patients with and without neurogenic dysphagia. Needle recordings obtained from the cricothyroid muscle of the larynx were also evaluated in six healthy subjects. RESULTS: The cortical motor latency of CP sphincter muscle was 10.7+/-0.5 ms with an amplitude of 0.8+/-0.2 mV in healthy subjects. Both the latency and amplitude of CP-MEP were facilitated during swallowing. The peripheral MEP of the CP muscle was very stable in all normal subjects (5.1+/-0.3 ms; 1.3+/-0.3 mV) and swallowing did not influence these parameters. The cortically elicited CP-MEP was significantly longer than the cortical MEPs obtained from the cricothyroid muscle of the larynx. In 10 dysphagic patients with corticobulbar tract involvement (6 ALS and 4 pseudobulbar palsy) and with pathologic and hyperreflexic EMG of the CP-sphincter muscle, the cortical MEP of CP muscle of the upper esophageal sphincter could not be elicited, although the peripheral CP-MEPs were obtained. TMS never produced a swallowing movement in neither healthy subjects nor patients. CONCLUSION: The CP muscle of the upper esophageal sphincter can produce MEPs by cortical TMS and by stimulation at the root/nerve levels of vagus nerve. The MEP latency values and central motor delay suggest that there is an oligosynaptic corticobulbar pathway to the motoneurons of CP muscles. When the pathway is affected by a pathology (i.e. ALS or pseudobulbar palsy) the CP sphincter becomes hyperreflexic due to disinhibition and the cortical MEP of the CP muscle disappears due to degeneration of the corticobulbar pathway. These mechanisms appear to be responsible for the pathogenesis of dysphagia.     

Enhancement of motor cortical excitability in humans by non-invasive electrical stimulation appears prior to voluntary movement

The time course of facilitation of motor evoked potentials (MEPs) to transcranial electrical stimulation delivered at varying intervals near the onset of a voluntary ballistic movement was studied in 4 normal subjects. MEPs were recorded from the left thenar muscles to unifocal anodal stimulation of the right scalp overlying the hand motor area delivered every 8-10 sec. A click, occasionally associated with the scalp stimulation (P = 0.3-0.6), was the signal for the subject to make a brief thumb press on a piston at short latency. The timing of the scalp stimulus and the click was adjusted so that the former occurred approximately between 100 msec before and 100 msec after the onset of the voluntary movement signaled by the EMG in the thenar muscles. MEPs were not detected when the scalp was stimulated 80 msec or more before onset of voluntary movement and then appeared with increasing probability as the time interval before movement shortened. The amplitudes of MEPs in the 80-40 msec period preceding movement onset were small (less than 20% of maximum) and achieved maximum values 20 msec after movement onset.     

磁刺激运动诱发肌电位对运动机能评价的临床应用

目的：观察磁刺激运动诱发肌电位对运动机能的评价。方法：用磁刺激装置对正常人１２例，运动障碍患者３１例进行了经颅脑刺激，记录运动诱发肌电位。结果：受检测的４３例，无一例引起头痛和感觉异常，也无癫痫及意识障碍等副作用。正常人中，诱发肌电位的潜伏期相对恒定，振幅在个体间虽存有差异，但同一例左右侧几乎相同。对２０例单侧肢体功能障碍的肌力按体征分级，比较患侧和健侧的诱发肌电位，发现患侧振幅较健侧明显减低。对肌力０～２级的病例，不能诱发出肌电位。结论：磁刺激运动诱发肌电位，在临床上可在数量上正确评价肢体的运动机能，并且经颅磁刺激法是安全的。     

Facilitation and reciprocal inhibition by imagining thumb abduction.

It is well known that motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) of the motor cortex are facilitated by voluntary muscle contraction. We evaluated the effects of imagination of movements on MEP latencies of agonist and antagonist muscles in the hand using TMS. Twenty-two healthy volunteers were studied. TMS delivered at rest and while imagining tonic abduction of the right thumb. MEPs were recorded in response to magnetic stimulation over the scalp and cervical spine (C7-T1), and central motor conduction times (CMCT) were calculated. MEPs were recorded from right abductor pollicis brevis muscle (APB) and adductor pollicis muscle (AP) simultaneously. Imagination of abduction resulted in a shortened latency of MEPs in the APB muscle, and a prolonged latency in the AP muscle. But the imagination caused no significant change in the latency of MEPs elicited by stimulation over the cervical spine. The changes of the CMCT may account for these latency changes with imagination of movement. These findings indicate that imagination of thumb abduction facilitates motoneurons of agonist muscle and has an inhibitory effect on those of antagonist muscle (reciprocal inhibition).     

Optimization of facilitation related to threshold in transcranial magnetic stimulation.

OBJECTIVES: To attain the standardized procedure for optimal facilitation, we analyzed motor-evoked potential (MEP) responses to the degree of voluntary contraction and stimulus intensity. METHODS: Fifteen normal subjects were included. MEPs were elicited at thenar muscles during rest and at gradual voluntary contraction (MVC), using 10, 30, and 50% of MVC. During rest and each contraction, the excitability threshold at rest (RET) and at contraction (CET) were determined. Consecutive stimuli were applied, with the intensity of ratio increments (110-150% of ET). RESULTS: The RET showed a remarkable decrease after contraction. Shortening of latency reached a saturation level at 10% of MVC. Amplitude reached a saturation level at 30% of MVC with 62.7+/-8.5% of the maximum output, which is equal to 140% intensity of CET, and 110% of RET. The MEP amplitudes at rest and at 10% MVC were influenced by their ETs, but those measured above 30% of MVC were not related. CONCLUSIONS: The procedure recommended for optimal facilitation is as follows: to achieve minimal latency of MEPs, a minimal contraction (10% of MVC) with RET intensity is sufficient and for maximal amplitude, a moderate contraction (30% of MVC) with 110% of RET intensity is adequate.     

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.     

Topographic mapping of the human motor cortex with magnetic stimulation: factors affecting accuracy and reproducibility.

We recorded motor evoked potentials (MEPs) from deltoid, biceps brachii, abductor pollicis brevis and flexor carpi radialis muscles of 5 normal volunteers during transcranial magnetic stimulation. With the subjects at rest, an 8-shaped magnetic coil was used to deliver 30 stimuli to different scalp positions 0.5 or 1.0 cm apart. The variability in amplitude and latency of MEPs was studied as a function of the scalp position stimulated, the number of stimuli at each position, and the percentage of maximal peripheral M responses (%M) elicited. The results were used to estimate the optimal number of stimuli at each position and the optimal spacing of scalp positions for topographic mapping of the human motor cortex. The amplitude and latency variability of MEPs were higher when suboptimal scalp positions were stimulated. Consequently, a larger number of stimuli were required to determine representative MEP amplitudes at suboptimal positions. In addition, there was an inverse relationship between %M recruited by transcranial magnetic stimuli in different subjects and the variability in MEP amplitude and latency. Latency variability was less pronounced than amplitude variability. Optimal sampling conditions are required to produce the best topographic maps, particularly to show subtle reorganization patterns in the human motor cortex.     

Influence of isoflurane anesthesia on motor evoked potentials elicited by transcortical,brainstem, and spinal root stimulation

Abstract

Electrical stimulation over the motor cortexl base ofthe skulll and cervical spine motor roots was performed in 9 male rats (41 0 ± 86 g) before and after induction with isoflurane at 7 MAC concentration. The mean latency and amplitude of descending spinal evoked potential (OSEP) from spinal cord and motor evoked potentials (MEPs) from forearm muscles obtained after motor cortexl brainsteml and cervical root stimulations were calculated and compared. The electrical current intensity to elicit the MEPs after corticall brainsteml and spinal roots stimulation were 23.4 ± 7.61 7.0 ± 3.71 and 7.4 ± 0.8 mAl respectively. The brainstem stimulation activated descending motor pathways with a latency midway between that produced by electrical stimulation over the motor cOrtexI and by electrical stimulation over the cervical enlargements. The latency difference between cortical (8.8 ± 3.2 msec) and brainstem (5.7 ± 7.2 msec) stimulation was 3.7 ± 2.3 msec in all forearm extensor muscles. The latency difference between cervical (3.6 ± 0.9 msec) and brainstem stimulation (5.7 ± 7.2 msec) was 2.3 ± 7.7 msec for the same musclesl suggesting the brainstem stimulation activates the descending motor neurons at the level of cervicalmedullary junction. The amplitudes were 789 ± 7471 672 ± 3541 and 765 ± 389 µV for corticall brainsteml and cervical root stimulations. The inhalation anesthesia isoflurane at 7MAC (7.2%) completely abolished the cortical and brainstem MEPs within minutesl while the MEPs elicited by direct stimulation of the cervical spinal roots remained unchanged. Our results indicate synaptic-dependent MEPs elicited at motor cortex or brainstem levels are highly sensitive to isoflurane anesthesia. [Neural Res 1998; 20: 555-558]     

Afferent conditioning of motor evoked potentials following transcranial magnetic stimulation of motor cortex in normal subjects.

The present study determined the effects of percutaneous electrical stimulation of the plantar surface on motor evoked potentials (MEPs) in tibialis anterior (TA) and soleus (SOL) of normal subjects following transcranial magnetic stimulation of motor cortex. The conditioning stimulation consisted of a 20 msec train of electrical pulses (500 Hz; 0.1 msec rectangular) delivered to the medial border of the sole of the foot at an intensity just subthreshold for evoking a flexion reflex. The conditioning (C) stimulation preceded the test (T) cortical stimulation by intervals of 20-130 msec. Magnetic stimulation of motor cortex (Cadwell MES-10) was delivered through a 9.5 cm focal point coil positioned tangential to the scalp and located with the rim over vertex. Five healthy adults served as subjects and each was investigated on at least 2 occasions. At C-T intervals 20-50 msec there was a mild inhibition of MEPs in both TA and SOL. This was followed by marked facilitation (greater than 300%) of MEPs at C-T intervals 50-85 msec in both TA and SOL in all subjects. At longer C-T intervals greater than 110 msec, there was an inhibition of MEPs in TA but not in SOL. Based on the time course of these 3 phases of MEP amplitude modulation, and different stimulation thresholds for each phase, it appears that separate neurophysiological processes underlie each phase of MEP modulation. These observations also suggest that percutaneous electrical stimulation may be useful as a means of enhancing low amplitude or subliminal MEPs in normal subjects or patients with myelopathy.     

Post-exercise facilitation and depression of motor evoked potentials to transcranial magnetic stimulation: a study in multiple sclerosis.

OBJECTIVE: To evaluate motor cortex excitability changes by transcranial magnetic stimulation (TMS) following repetitive muscle contractions in patients with multiple sclerosis (MS); to state whether a typical pattern of post-exercise motor evoked potentials (MEPs) is related to clinical fatigue in MS. METHODS: In 41 patients with definite MS (32 with fatigue and 9 without fatigue according to Fatigue Severity Scale) and 13 controls, MEPs were recorded at rest: at baseline condition, following repetitive contractions until fatigue, and after fatigue, to evaluate post-exercise MEP facilitation (PEF) and depression (PED). RESULTS: After exercise, MEP amplitude significantly increased both in patients and controls (PEF). When fatigue set in, MEP amplitude was significantly reduced in normal subjects (PED), but not in patients. Post-exercise MEP findings were similar both in patients with and without fatigue. CONCLUSIONS: Our findings suggest an intracortical motor dysfunction following a voluntary contraction in MS patients, possibly due to failure of depression of facilitatory cortical circuits, or alternatively of inhibitory mechanisms.     

Inhibitory period following motor potentials evoked by magnetic cortical stimulation.

Following motor potentials evoked (MEPs) by magnetic cortical stimulation, there is a transient suppression of muscle action potentials (inhibitory period). We recorded MEPs, the inhibitory period, V1 waves and F waves from the abductor pollicis brevis muscle in 20 normal subjects and in 17 patients with spastic hyperreflexia due to cerebral infarction. The duration of the inhibitory period increased in correspondence with increasing stimulus intensity and did not necessarily depend on the amplitude of the MEPs. The duration of the inhibitory period elicited by a twin coil, which can stimulate the motor cortex locally, was shorter than by a single coil. The mean duration of the inhibitory period was significantly shorter in patients with spastic hyperreflexia than in normal subjects, and it correlated with the amplitude of F waves. The effects of the inhibitory period on V1 waves were different from its effects on F waves in one patient with large V1 and F waves. The amplitudes of V1 waves recorded during the inhibitory period were approximately 30-50% of the maximal amplitude of V1 waves, but F waves were not smaller. The inhibitory period is probably caused primarily by central inhibitory mechanisms.     

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.     

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.     

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.