Silent period in the mentalis muscle induced by facial nerve and cutaneous stimulation.

The aim of this study was to demonstrate that silent periods of the mentalis muscle are induced after facial nerve stimulation and cutaneous stimulation in normal subjects. When the marginal mandibular branch of the facial nerve and the cutaneous nerve in areas adjacent to the lower lip were stimulated during slight voluntary contraction of the mentalis muscle, silent periods were elicited with surface electrodes on the mentalis muscle. The early phase and the late phase of the silent period were elicited by marginal mandibular branch stimulation. The early phase of the silent period was recognized following the F waves and it disappeared at 36.3 msec. The average duration of the late phase of the silent period was 59.2 msec, with an average latency of 62.5 msec. Only the late phase of the silent period after cutaneous stimulation could be elicited, with a duration and latency of 55.9 msec and 54.0 msec respectively. The authors conclude that the silent period is able to be elicited in the mentalis muscle by peripheral nerve stimulation, and is one of the late responses in facial muscles.     

Inhibition of hand muscle motoneurones by peripheral nerve stimulation in the relaxed human subject. Antidromic versus orthodromic input

In active muscle, a supramaximal conditioning stimulus to peripheral nerve produces a classic silent period in the EMG. The present experiments examined the effect of this type of conditioning stimulus on motoneurone excitability in relaxed muscle.EMG responses evoked by transcranial magnetic stimulation of the brain were recorded from the first dorsal interosseus muscle (FDI) in 10 healthy subjects and 5 patients with sensory neuropathy. These responses (motor evoked potentials) were conditioned by supramaximal peripheral nerve stimuli given 0–150 msec beforehand. In the normal subjects, the classic silent period in the FDI lasted about 100 msec. The same conditioning stimulus only abolished motor evoked potentials when the conditioning-test interval was so short that the antidromic peripheral nerve volley collided with the orthodromic volley set up by magnetic brain stimulation. At longer conditioning-test intervals, although remarkably inhibited (65% mean suppression between 10 and 40 msec), the test motor potential was never completely abolished and gradually recovered by 100 msec.Inhibition of cortically evoked motor potentials did not depend upon activity set up by the conditioning stimulus in peripheral nerve sensory fibres. The patients with complete peripheral sensory neuropathy had the same extent and time-course of inhibition as the normal subjects. We conclude that in relaxed subjects the inhibitory effect of peripheral conditioning results almost exclusively from the motoneuronal inhibitory mechanisms consequent to antidromic invasion.     

The electromyographic silent period produced by supramaximal electrical stimulation in normal man

The electromyographic silent period produced by supramaximal electrical stimulation of the median nerve was recorded in the abductor pollicis brevis muscle of four normal subjects during maximal isometric voluntary contraction. Except for an inconstant F response, electrical silence could usually be induced in the muscle from the twitch potential until the reappearance of uninterrupted voluntary activity. The silent period produced by stimulation at the wrist was approximately 25 msec longer than that produced by stimulation at the elbow and was independent of muscle tension. Further shortening of the muscle during the twitch contraction did not significantly alter the length of the silent period. A silent period in the abductor pollicis brevis muscle was also obtained after stimulation of the ulnar nerve, at the wrist and at the elbow. The onset of this period of silence was delayed, but it ended at the same time after the stimulus as the corresponding silent periods produced by median nerve stimulation. It is concluded that the end point of the silent period produced by supramaximal electrical stimulation of a mixed peripheral nerve is determined by an inhibitory spinal reflex, afferent impulses travelling in slowly-conducting fibres that are directly activated by the stimulus. Under these conditions the length of the silent period gives no indication of spindle activity in the muscle.     

An exteroceptive reflex in the sternocleidomastoid muscle produced by electrical stimulation of the supraorbital nerve in normal subjects and patients with spasmodic torticollis

We examined suppression of EMG activity in the contracting sternocleidomastoid muscles, produced by electrical stimulation of the supraorbital nerve in 10 normal subjects and 9 patients with spasmodic torticollis. This exteroceptive reflex in the sternocleidomastoid muscle consisted of 2 or 3 phases: (1) an early, small, and unstable phase of facilitation, followed by (2) a period of suppression beginning 35 msec after the stimulus, lasting for 35 msec with a reduction in EMG activity to approximately 40% of the prestimulus level, and (3) a further phase of facilitation at a latency of 70 msec, with duration 35 msec and an increase in EMG activity to approximately 35% above prestimulus levels. The latency and duration of the suppressive phase of this reflex were similar to the exteroceptive suppression of EMG activity in the masseter muscle after supraorbital nerve stimulation (masseter silent period). In patients with spasmodic torticollis, the depth of this exteroceptive suppression in the sternocleidomastoid muscles was less than that observed in an age-matched cohort of normal subjects, although the latency and duration were normal. In contrast, exteroceptive suppression in the masseter muscle was normal. These findings suggest abnormal function of inhibitory interneuronal networks between the 5th cranial nerve and the motor neurons of the spinal accessory and upper cervical nerves which mediate exteroceptive suppression in the sternocleidomastoid muscle in patients with spasmodic torticollis.     

Absence of transcallosal inhibition following focal mangnetic stimulation in preschool children

Focal transcranial magnetic stimulation of the hand-associated motor cortex was used to study normal healthy preschool children (n = 7; mean age, 4.6 years) and adults (n = 7; mean age, 29.4 years) under the conditions of standardized tonic voluntary contraction of small hand muscles. Callosally mediated inhibitory as well as corticospinally mediated inhibitory and excitatory motor effects were investigated. Although children had no detectable transcallosal inhibition, their corticospinally mediated postexcitatory silent period was present (mean, 140.8 ± 30.2 msec). It was significantly shorter then in adults (mean, 192.5 ± 32.0 msec). The motor thresholds of the cortically elicited muscle responses, measured as the lowest stimulus intensity, were significantly higher in children (mean, 89 ± 5%) than in adults (mean, 46 ± 6%). The corticomuscular latency of transcranially elicited motor responses revealed no difference between children and adults. These observations may reflect maturation processes in the motor system. Maturation of at least some direct corticospinal fibers occurs early in life and is followed by that of intracortical excitatory and inhibitory connections. The maturation of functionally competent callosal connections appears to occur after the age of 5 years.     

Afferent excitation of human motor cortex as revealed by enhancement of direct cortico-spinal actions on motoneurones

Changes in motor cortex excitability induced by somatosensory afferences were evaluated in 5 subjects by testing how the short-latency cortico-spinal effects evoked by transcranial magnetic stimulation in flexor carpi radialis (FCR) motoneurones were influenced by volleys in median nerve afferent fibres. Transcranial magnetic stimulation induced two facilitatory peaks on FCR H reflex, the first at a conditioning-test interval of about −3 msec and the second at 0 msec, separated by a phase of inhibition. If an electric shock to the median nerve at the wrist, 0.8-1 × motor threshold (MT) for thenar muscles, preceded the cortical stimulus by 18–25 msec, an increase in size of both facilitatory peaks was observed. The increase was partly due to a direct action of the median nerve volley on motoneurones. When this contribution was subtracted, two peaks of additional facilitation resulted as the effect of combined conditioning. Additional facilitation was present even during the short-lasting phase ascribed to monosynaptic cortico-spinal excitation of motoneurones, i.e., the first millisecond of the earliest facilitatory peak. This result indicates that cortical responsiveness to magnetic stimulation had been enhanced by the peripheral stimulus. The time course of the excitability changes in motor cortex was compared with the cortical somatosensory evoked potentials (SEPs) induced by the same peripheral stimulus. Additional facilitation was present immediately after the N20 peak of SEPs and lasted 8–10 msec. Additional facilitation had the same threshold as N20 (0.6 × MT) and grew in parallel with it when grading the afferent stimulus up to 1 MT.     

Different short-term modulation of cortical motor output to distal and proximal upper-limb muscles during painful sensory nerve stimulation

The pattern of upper-limb muscle activation following painful stimulation has not been clarified in detail. We investigated the short-term inhibitory and excitatory effects of painful electrical digital stimulation on the motoneuron pools of distal and proximal upper-limb muscles. Transcranial magnetic stimulation (TMS) was used as test stimulus, and painful digital nerve stimulation as conditioning stimulus for motor evoked potential (MEP) recordings over the abductor digiti minimi (ADM), abductor pollicis brevis (APB), biceps brachii (BB), and deltoid muscles. Inhibition of the conditioned MEP response was most prominent in the distal muscles, whereas BB and deltoid muscles were only weakly inhibited. The mean MEP response over APB decreased with painful cutaneous stimuli, showing maximum inhibition (by 82%) at interstimulus intervals (ISIs) of 50 ms. Inhibition in the ADM was maximal (49%) but less pronounced at an ISI of 40 ms. The BB and deltoid muscles showed inhibition by 25% and 29%, respectively. Significant facilitation was present in BB and deltoid muscles by 43% and 41% at an ISI of 100 ms, but not in the smaller hand muscles. The observed pattern of upper-limb muscle activation corresponds to the protective withdrawal reflex and the neuronal basis of the observed short-term modulation of motor activity is compatible with a spinal or brainstem pathway.     

Upper motor neuron involvement in X-linked recessive bulbospinal muscular atrophy.

OBJECTIVE: Clinicopathological findings of X-linked recessive bulbospinal muscular atrophy (SBMA) are indicative of lower motor neuron and primary sensory neuron involvement. The aim of our study was to investigate the presence of subclinical upper motor neuron (UMN) dysfunction in this disease. METHODS: Two siblings with clinical presentation, routine electrophysiological tests, histopathological features of muscle and nerve biopsies and genetic testing consistent with diagnosis of SBMA underwent transcranial magnetic stimulation (TMS). The analysed parameters were motor evoked potential (MEP) threshold, silent period (SP) and central motor conduction time. Intracortical inhibition with paired pulses from 1 to 6ms interstimulus intervals (ISIs) was evaluated in the older brother. RESULTS: MEP parameters were significantly altered in limb and cranial muscles and MEP suppression after paired stimulation significantly reduced in the older brother. MEP abnormalities were present in one lower limb, but SP abolished in all limbs, in the younger brother. CONCLUSIONS: Subclinical involvement of UMNs may be present in patients affected by SBMA. This finding suggests that the array of neuronal systems whose function may be affected by the pathogenic process of SBMA is larger than it was considered so far. SIGNIFICANCE: TMS is a sensitive diagnostic tool for the identification of UMN dysfunction and should be included in the diagnostic evaluation of patients with SBMA.     

Initial positive deflection of the compound muscle action potential in the median nerve conduction studies can be originated from lumbrical muscles in patients with carpal tunnel syndrome]

In motor nerve conduction studies we sometimes encounter a small initial positive deflection (IPD) of the compound muscle action potential (CMAP). This potential represents a volume conduction from nearby muscles other than the objective muscle. We demonstrated recordings of motor nerve conduction studies from two patients with carpal tunnel syndrome (CTS). In patients with CTS IPDs can be recorded from a surface electrode above the abductor pollicis brevis when intense stimuli to the median nerve provoked a stimulus spread to the ulnar nerve. However, without this stimulus spread to the ulnar nerve, IPDs can be observed by contraction of median nerve innervated muscles. In the CTS thenar branch of the median nerve is apt to be more severely damaged than lumbrical branch. In such an occasion volume conduction from the lumbrical muscles is relatively large, which gives rise to the IPD in the CMAP recorded from abductor pollicis brevis. We reported two cases of IDPs originated from lumbrical muscles. The peak latencies were identical between IDP of abductor pollicis brevis recording and negative potential of lumbrical recording. These potentials didn't change by median nerve stimulation at the elbow 3 msec after the ulnar nerve stimulation at the wrist (collision technique). Finally, we repeat that IPDs in the median nerve conduction studies can be originated from not only the stimulus spread to the ulnar nerve but also the median nerve innervated lumbrical muscles in patients with CTS.     

The clinical diagnostic utility of transcranial magnetic stimulation: report of an IFCN committee.

The review focuses on the clinical diagnostic utility of transcranial magnetic stimulation (TMS). The central motor conduction time (CMCT) is a sensitive method to detect myelopathy and abnormalities may be detected in the absence of radiological changes. CMCT may also detect upper motor neuron involvement in amyotrophic lateral sclerosis. The diagnostic sensitivity may be increased by using the triple stimulation technique (TST), by combining several parameters such as CMCT, motor threshold and silent period, or by studying multiple muscles. In peripheral facial nerve palsies, TMS may be used to localize the site of nerve dysfunction and clarify the etiology. TMS measures also have high sensitivity in detecting lesions in multiple sclerosis and abnormalities in CMCT or TST may correlate with motor impairment and disability. Cerebellar stimulation may detect lesions in the cerebellum or the cerebellar output pathway. TMS may detect upper motor neuron involvement in patients with atypical parkinsonism and equivocal signs. The ipsilateral silent period that measures transcallosal inhibition is a potential method to distinguish between different parkinsonian syndromes. Short latency afferent inhibition (SAI), which is related to central cholinergic transmission, is reduced in Alzheimer's disease. Changes in SAI following administration of cholinesterase inhibitor may be related to the long-term efficacy of this treatment. The results of MEP measurement in the first week after stroke correlate with functional outcome. We conclude that TMS measures have demonstrated diagnostic utility in myelopathy, amyotrophic lateral sclerosis and multiple sclerosis. TMS measures have potential clinical utility in cerebellar disease, dementia, facial nerve disorders, movement disorders, stroke, epilepsy, migraine and chronic pain.     

Cortical projection to erector spinae muscles in man as assessed by focal transcranial magnetic stimulation.

We stimulated the motor cortex in 9 subjects using focal transcranial magnetic stimulation with a figure of 8 coil in order to examine the cortical representation of the erector spinae muscles. Recordings were made from the erector spinae 3.5 cm lateral to the third lumbar vertebra. In 5 subjects clearly reproducible responses could be obtained which had a latency compatible with transmission via fast conducting fibers in a mono- or oligosynaptic pathway. In the remaining 4 subjects responses were poorly defined. Latencies in surface recordings varied between 13 and 24 msec but were longer when needle recordings were used. Mapping of the motor cortex was performed by moving the coil in 2 cm steps on either side of Cz. Different patterns of hemispheric representation were found ranging from a contralateral projection in either hemisphere to a representation of both back muscles in one hemisphere (2 subjects). Responses were followed by a silent period. The latter was interrupted or terminated by a response between 52 and 85 msec post stimulus which was found predominantly in the muscle ipsilateral to the side of stimulation.     

The silent period induced by transcranial magnetic stimulation in muscles supplied by cranial nerves: normal data and changes in patients.

The silent period induced by transcranial magnetic stimulation of the sensorimotor cortex (Magstim 200, figure of eight coil, loop diameter 7 cm) in active muscles supplied by cranial nerves (mentalis, sternocleidomastoid, and genioglossus) was studied in 14 control subjects and nine patients with localised lesions of the sensorimotor cortex. In the patients, measurements of the silent period were also made in the first dorsal interosseus and tibialis anterior muscles. In the controls, there was a silent period in contralateral as well as ipsilateral cranial muscle and the duration of the silent period increased with increasing stimulus intensities. The mean duration of the silent period was around 140 ms in contralateral mentalis muscle and around 90 ms in contralateral sternocleidomastoid muscle at 1.2 x threshold stimulation strengths. Whereas the duration of the silent period in ipsilateral mentalis muscle was shorter than on the contralateral side it was similar on both sides in sternocleidomastoid muscle. In patients with focal lesions of the face associated primary motor cortex and corresponding central facial paresis, the silent period in mentalis muscle was shortened whereas it was unchanged or prolonged in limb muscles (first dorsal interosseus, tibialis anterior) with stimulation over the affected hemisphere. By contrast, in a patient with a lesion within the parietal cortex, the silent period in mentalis muscle was prolonged with stimulation of the affected side.     

Spinal motor neuron excitability during the cutaneous silent period

The physiologic mechanisms generating the cutaneous silent period (CSP) remain uncertain. It is not known whether the CSP occurs because of inexcitability of the spinal motor neuron. We, therefore, assessed excitability of the motor neuron during the CSP using F-wave responses. H-reflexes were also elicited during the CSP. Electrical stimulation to the fifth digit produced the CSP in the voluntarily contracting abductor pollicis brevis muscle (APB). Median nerve stimulation at the wrist elicited control F or H responses during isometric APB contraction (condition 1) and in resting muscle (condition 2). Control amplitudes were compared to those elicited in the midst of the CSP. In Condition 1, F-wave amplitudes and frequency during the CSP were unchanged compared with controls. However, F-waves were increased in amplitude and frequency during the CSP (P < 0.001) relative to responses elicited in resting muscle (condition 2). H-reflexes during the CSP were suppressed (P < 0.001) compared with controls elicited during contraction (condition 1), but facilitated relative to the resting state (condition 2) in which no H-reflexes were elicitable. We conclude that spinal motor neurons remain excitable to antidromic volleys at the same time that the corticospinal volley is inhibited to produce the CSP. Moreover, motor neuron excitability appears to be increased during the CSP compared to the relaxed state. © 1995 John Wiley & Sons, Inc.     

Facilitation of motor evoked potentials by somatosensory afferent stimulation.

The effect of an electrically induced peripheral afferent volley upon electrical and magnetic motor evoked potentials (MEPs) from muscles of the upper and lower extremities was studied in 16 healthy volunteers. A standard conditioning-test (C-T) paradigm was employed whereby the test stimulus (transcranial electric or magnetic) was applied at random time intervals, from 10 msec prior to 90 msec after the conditioning stimulus (peripheral nerve stimulus). MEP amplitude facilitation was observed for the majority of the upper extremity muscles tested at two distinct periods, one occurring at short, and the other at long C-T intervals. This bimodal trend of MEP facilitation was found to be equally as prominent in the lower extremity muscles tested. The period of short C-T interval facilitation is consistent with modifications in the spinal excitability of the segmental motoneuron pool. On the other hand, the period of long C-T interval facilitation is suggested to be due to alterations in excitability of the motor cortex as a result of the arrival of the orthodromic sensory volley. Although most pronounced in muscles innervated by the nerve to which the conditioning stimulus was applied, this bimodal facilitatory effect was also observed in adjacent muscles not innervated by the stimulated nerve. Qualitatively, the conditioned MEPs from the upper and lower extremities responded similarly to both electrical and magnetic trans-cranial stimulation. In addition, our study demonstrates that the C-T paradigm has potential for use in the assessment of spinal and cortical sensorimotor integration by providing quantitative information which cannot be obtained through isolated assessment of sensory and/or motor pathways.(ABSTRACT TRUNCATED AT 250 WORDS)     

Crossed and direct effects of digital nerves stimulation on motor evoked potential: a study with magnetic brain stimulation

We studied the influence of contralateral and ipsilateral cutaneous digital nerve stimulation on motor evoked potentials (MEPs) elicited in hand muscles by transcranial magnetic stimulation (TMS). We tested the effect of different magnetic stimulus intensities on MEPs recorded from the thenar eminence (TE) muscles of the right hand while an electrical conditioning stimulus was delivered to the second finger of the same hand with an intensity four times above the sensory threshold. Amplitude decrement of conditioned MEPs as a function of magnetic stimulus intensity was observed. The lowest TMS stimulus intensity produced the largest decrease in conditioned MEPs. Moreover, we investigated the effects of ipsilateral and contralateral electrical digital stimulation on MEPs elicited in the right TE and biceps muscle using an intensity 10% above the threshold. Marked MEP inhibition in TE muscles following both ipsilateral and contralateral digital stimulation is the main finding of this study. The decrease in conditioned MEP amplitude to ipsilateral stimulation reached a level of 50% of unconditioned MEP amplitude with the circular coil and 30% with the focal coil. The amplitude of conditioned MEPs to contralateral digital stimulation showed a decrease of 60% with the circular coil and more than 50% with the focal coil. The onset of the inhibitory effect of contralateral stimulation using the focal coil occurred at a mean of 15 ms later than that of ipsilateral stimulation. No MEP inhibition was observed when recording from proximal muscles. Ipsilateral and contralateral digital stimulation had no effect on F wave at appropriate interstimulus intervals, where the main MEP suppression was noted. We stress the importance of selecting an appropriate test stimulus intensity to evaluate MEP inhibition by digital nerves stimulation. Spinal and cortical sites of sensorimotor integration are adduced to explain the direct and crossed MEP inhibition following digital nerves stimulation.     

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.     

Analysis of stimuli triggering attacks of paroxysmal dystonia induced by exertion

In a patient with a familial form of paroxysmal exertion induced dyskinesia (PED), the efficacy of different stimuli and manoeuvres in triggering dystonic attacks in the arm was studied. As a new approach, transcranial magnetic stimulation (TMS) of the motor cortex was used to trigger motor paroxysms and to monitor cortical excitability during attacks. Motor paroxysms could be provoked by muscle vibration, passive movements, TMS, magnetic stimulation of the brachial plexus, and electrical nerve stimulation. Sham stimulation over the motor cortex and thermal and tactile cutaneous stimuli were ineffective in triggering attacks. It is concluded that dystonic attacks are triggered by proprioceptive afferents rather than cutaneous stimuli or the descending motor command itself. Outside the attacks, motor cortical excitatory and inhibitory neuronal mechanisms as assessed by TMS (response threshold and amplitudes, duration of the contralateral and ipsilateral silent period, corticocortical inhibition, and facilitation) were normal, which underlines the paroxysmal character of the disorder.     

Parkinson's disease rigidity: magnetic motor evoked potentials in a small hand muscle

We studied the EMG potentials evoked in the bilateral first dorsal interosseus muscle by electromagnetic stimulation of the corticomotoneuronal descending system in 10 Parkinson's disease patients and in 10 age- and sex-matched normal controls. We selected patients who did not have tremor but had predominant rigidity with asymmetric body involvement. On the rigid side of the PD patients, the threshold to cortical stimulation was lower than on the contralateral side or than normal values. On average, patients had normal central conduction times, but their motor evoked potentials (MEPs) on the rigid side were larger than those of controls when the cortical stimulus was at rest or during slight tonic contraction of the target muscle. In the latter condition, a silent period shorter than that of controls followed MEPs, whereas the peripheral silent period following ulnar nerve stimulation at the wrist was prolonged. Alpha motor neuron excitability, tested by the F-wave method, was enhanced on the rigid side at rest. In rigidity, spinal motor nuclei may be more responsive than normal to descending inputs from motor cortex, or the entire corticomotoneuron system may prove hyperexcitable under given conditions.     

Ia presynaptic inhibition after muscle twitch in the arm

Contraction of upper limb muscles in healthy subjects was used to investigate presynaptic inhibition at spinal level. The H reflex recorded in the forearm flexor muscles in response to median nerve stimulation was depressed in amplitude from 400 ms to 1 s after a muscle twitch induced by transcranial stimulation, root stimulation, direct biceps stimulation, and triceps tendon tap. Stimulation of the cutaneous branch of musculocutaneous nerve, ipsilateral triceps and contralateral biceps, and biceps tendon tap did not alter H-reflex size. Forearm flexor H-reflex amplitude is therefore related to changes in proprioceptive inflow secondary to the biceps muscle twitch. Root and direct muscle stimulation both failed to reduce the size of the motor evoked potential (MEP) after transcranial magnetic stimulation, suggesting that the inhibition acts at presynaptic level. Attenuation of H-reflex amplitude was related to the size of the muscle twitch and was less pronounced during an isometric twitch than during free joint movement. Our results suggest that the biceps muscle twitch produces long-lasting inhibition of the Ia afferents from forearm flexor muscles. This is an important and a simple mechanism for suppressing proprioceptive input during movement.     

Modulation of upper extremity motor evoked potentials by cutaneous afferents in humans.

The excitability of motoneurons controlling upper limb muscles in humans may vary with cutaneous nerve stimulation. We investigated the effect of noxious and non-noxious conditioning stimuli applied to right and left digit II and right digit V on motor evoked potentials (MEPs) recorded from right thenar eminence, abductor digiti minimi, biceps and triceps brachii muscles in twelve healthy subjects. Transcranial magnetic stimulation (TMS) was applied at interstimulus intervals (ISI) ranging from 40 to 160 ms following conditioning distal digital stimulation. TMS and transcranial electrical stimulation (TES) were compared at ISI 80 ms. Painful digital stimulation caused differential MEP amplitude modulation with an early maximum inhibition in hand muscles and triceps brachii followed by a maximum facilitation in arm muscles. Stimulation of different digits elicited a similar pattern of MEP modulation, which largely paralleled the behavior of cutaneous silent periods in the same muscles. Contralateral digital stimulation was less effective. MEPs following TMS and TES did not differ in their response to noxious digital stimulation. MEP latencies were shortened by cutaneous stimuli. The observed effects were stimulus intensity dependent. We conclude that activation of A-alpha and A-delta fibers gives rise to complex modulatory effects on upper limb motoneuron pools. A-delta fibers initiate a spinal reflex resulting in MEP amplitude reduction in muscles involved in reaching and grasping, and MEP amplitude facilitation in muscles involved in withdrawal. These findings suggest a protective reflex mediated by A-delta fibers that protects the hand from harm. A-alpha fibers induce MEP latency shortening possibly via a transcortical excitatory loop.