Radial Nerve Stimulation Research Articles

Trigeminal integration of vestibular and forelimb nerve inputs.

Experiments were carried out on anaesthetized guinea pigs to evaluate whether vestibular and somatosensory informations converge upon the same trigeminal motoneurones and, if so, how they interact in the modulation of their activity. It was found that excitatory responses occurred in these motoneurones when an appropriate electrical stimulation was applied to the common radial nerve. The same was true if the electrical stimulus was applied to the vestibular ampullae. In another set of experiments the stimulation was applied both to the vestibular ampullae and to the common radial nerve at various time-intervals. The amplitude of the motoneuronal responses to common radial nerve stimulation was reduced when preceded by a vestibular stimulation. The same was true when the sequence of stimulations was reversed: in this case there was a decrease in amplitude of the testing response to vestibular stimulation. The degree of these reductions depended upon the time-interval elapsed between the afferent stimulations. The maximal degree of depression was observed at 4-6 ms time-interval for conditioning vestibular stimulation and at 10-12 ms time-interval for conditioning radial nerve stimulation. It appears, therefore, that somatosensory and vestibular signals may modulate the activity of trigeminal motor units innervating masticatory muscles, suggesting that extratrigeminal afferents may control the contraction of these muscles.

Inhibitory action of forearm flexor muscle afferents on corticospinal outputs to antagonist muscles in humans.

1. To find out whether muscle afferents influence the excitability of corticospinal projections to antagonist muscles, we studied sixteen healthy subjects and one patient with a focal brain lesion. 2. Using transcranial magnetic and electrical brain stimulation we tested the excitability of corticomotoneuronal connections to right forearm muscles at rest after conditioning stimulation of the median nerve at the elbow. Somatosensory potentials evoked by median nerve stimulation were also recorded in each subject. 3. Test stimuli delivered at 13-19 ms after median nerve stimulation significantly inhibited EMG responses elicited in forearm extensor muscles by transcranial magnetic stimulation, but did not inhibit responses to electrical stimulation. In contrast, magnetically and electrically elicited responses in forearm flexor muscles were suppressed to the same extent. 4. The higher the intensity of the test shocks, the smaller was the amount of median nerve-elicited inhibition. Inhibition in extensor muscles was also smaller during tonic wrist extension, or if the induced electrical stimulating current in the brain flowed from posterior to anterior over the motor strip rather than vice versa. Test responses evoked by magnetic transcranial stimulation in the first dorsal interosseous and in brachioradialis muscles were not inhibited after median nerve stimulation at the elbow. Stimulation of digital nerves failed to inhibit motor potentials in extensor muscles. 5. Test stimuli delivered at 15 and 17 ms after radial nerve stimulation significantly inhibited EMG responses elicited in forearm flexor muscles by magnetic transcranial stimulation. 6. In the patient with a focal thalamic lesion, who had dystonic postures and an absent N20 component of the somatosensory-evoked potentials but normal strength, median nerve stimulation failed to inhibit magnetically evoked responses in forearm extensor muscles. 7. We propose that activation of median nerve muscle afferents can suppress the excitability of cortical areas controlling the antagonist forearm extensor muscles acting on the hand. The inhibitory effect occurs at short latency and might assist spinal pathways mediating reciprocal inhibition by contrasting the co-activation of antagonistic pools of corticospinal cells.

Synergism Between Sevoflurane and Intravenous Fentanyl on A delta and C Somatosympathetic Reflexes in Dogs

In this study, we defined the nature of the interactions between sevoflurane and fentanyl on spontaneous and reflex-evoked sympathetic activity, resting heart rate (HR), and mean arterial pressure (MAP). Spontaneous renal sympathetic nerve activity (RSNA) and A delta- and C-fiber-mediated somatosympathetic reflexes, evoked by electrical stimulation of radial nerves, and HR and MAP were recorded in anesthetized dogs. In one group, the effects of incremental doses of 2-64 micrograms/kg fentanyl i.v. were observed. It had a greater inhibitory effect on C than on A delta reflexes, which were abolished by mean cumulative doses of 64 micrograms/kg and approximately 128 micrograms/kg, respectively. Although 1.5% sevoflurane reduced C reflexes by 28% and A delta reflexes by only 12%, it reduced the total doses of fentanyl required for their abolition to 32 micrograms/kg and 64 micrograms/kg, respectively. Mean RSNA, HR, and MAP values were reduced by 46%, 54%, and 30%, respectively, by fentanyl alone and by 23%, 11%, and 17%, respectively, in response to 1.5% sevoflurane. The combination of fentanyl and sevoflurane caused reductions of 44%, 54%, and 41%, respectively, which indicates a less than additive effect. These results indicate that sevoflurane interacts synergistically with fentanyl to depress A delta and C somatosympathetic reflexes, whereas for RSNA, HR, and MAP, their effects were less than the additive. Although fentanyl caused a greater depression of C than of A delta reflexes to the point of abolition, the maximal depression of spontaneous sympathetic activity, heart rate, and arterial pressure occurred at smaller doses. The combined depressant effects of sevoflurane and fentanyl were synergistic on somatosympathetic reflexes but were less than additive on spontaneous sympathetic activity, heart rate, and arterial pressure.

Dissociation between the effect of nitrous oxide on spontaneous and reflexly evoked sympathetic activity in dogs

We have examined the effect of nitrous oxide on spontaneous sympathetic activity and A delta- and C-fibre mediated somatosympathetic reflexes in renal nerves, evoked by supramaximal electrical stimulation of radial nerves in anaesthetized, paralysed dogs undergoing mechanical ventilation. In six preparations, nitrous oxide was administered at end-tidal concentrations of 10%, 30%, 50% and 70%, each for 20 min. Spontaneous renal sympathetic activity increased significantly to 147.8% and 151.2% of control values with 50% and 70% nitrous oxide, respectively (P < 0.05), but there were no significant changes in A delta and C reflexes. We conclude that the large increase in spontaneous sympathetic activity was dissociated from somatosympathetic reflexes which remained unchanged at these concentrations of nitrous oxide.

Median and tibial nerve somatosensory evoked potentials: middle-latency components from the vicinity of the secondary somatosensory cortex in humans

The topography of the middle-latency N110 after radial nerve stimulation suggested a generator in SII. To support this hypothesis, we have tried to identify a homologous component in the tibial nerve SEP (somatosensory evoked potential). Evoked potentials following tibial nerve stimulation (motor+sensory threshold) were recorded with 29 electrodes (bandpass 0.5–500 Hz, sampling rate 1000 Hz). For comparison, the median nerve was stimulated at the wrist. Components were identified as peaks in the global field power (GFP). Map series were generated around GFP peaks and amplitudes were measured from electrodes near map maxima. With median nerve stimulation, we recorded a negativity with a maximum in temporal electrode positions and 106±12 ms peak latency (mean±SD), comparable to the N110 following radial nerve stimulation. After tibial nerve stimulation the latency of a component with the same topography was 131±11 ms (N130). Both N110 and N130 were present ipsi- as well as contralaterally. Amplitudes were significantly higher on the contralateral than the ipsilateral scalp for both median (3.1±2.4 μV vs. 1.7±1.6 μV) and tibial nerve (1.9±1.2 μV vs. 0.6+1 μV). The topography of the N130 can be explained by a generator in the vicinity of SII. The latency difference between median and tibial nerve stimulation is related to the longer conduction distance (cf. N20 and P40). The smaller ipsilateral N130 is consistent with the bilateral body representation in SII.

Cutaneous reflex activity of the cat forelimb during fictive locomotion

To investigate mechanisms of rhythmic modulation of cutaneous reflex by the central pattern generator for locomotion, we made intracellular recordings from elbow flexor motoneurons, biceps brachii (Bi) and brachialis (Br), and quantitatively analyzed excitatory postsynaptic potentials (EPSPs) evoked by stimulation of superficial radial (SR) nerves during forelimb fictive locomotion, which was evoked in immobilized, decerebrate cats with the low thoracic spinal cord transected. We found that (1) in both Br and Bi, SR stimulation evoked trisynaptic EPSPs (segmental latencies were 2.10±0.39 ms for Br and 2.07±0.93 ms for Bi), (2) the SR-EPSPs of Br and Bi were rhythmically modulated with a similar pattern; the maximal and minimal EPSPs appeared in the flexor and extensor phase, respectively, (3) however, there were differences as follows. In the control state where fictive locomotion was absent, the mean amplitude of SR-EPSPs of Br (4.65±2.76 mV, n=14) was much larger than that of Bi (1.25±1.22 mV, n=10). During fictive locomotion, the maximum amplitude of SR-EPSPs of Br was 5.63±1.79 mV ( n=18), and the minimum was 3.82±1.69 mV ( n=18); that is, the maximum during fictive locomotion was larger or smaller than that of the control, while the minimal were always smaller. In contrast, SR-EPSPs of Bi were modulated over the control level; the maximum was 3.97±1.71 mV ( n=16) and the minimum was 2.24±1.11 mV ( n=16), both the maximum and the minimum during locomotion being larger than that of the control. These results may suggest that two mechanisms are involved in the rhythmic modulation, first, cyclic facilitation in the flexor phase, and secondly, cyclic inhibition in the extensor phase. The former was involved in both cases of Bi and Br motoneurons, while the latter would be involved only in the case of Br motoneurons. © 1997 Elsevier Science B.V. All rights reserved.

Emergence of radial nerve dominance in median nerve cortex after median nerve transection in an adult squirrel monkey.

Throughout the glabrous representation in Area 3b, electrical stimulation of the dominant (median or ulnar) input produces robust, short-latency excitation, evident as a net extracellular "sink" in the Lamina 4 current source density (CSD) accompanied by action potentials. Stimulation of the collocated nondominant (radial nerve) input produces a subtle short-latency response in the Lamina 4 CSD unaccompanied by action potentials and followed by a clear excitatory response 12-15 ms later. Laminar response profiles for both inputs have a "feedforward" pattern, with initial activation in Lamina 4, followed by extragranular laminae. Such corepresentation of nondominant radial nerve inputs with the dominant (median or ulnar nerve) inputs in the glabrous hand surface representation provides a likely mechanism for reorganization after median nerve section in adult primates. To investigate this, we conducted repeated recordings using an implanted linear multi-electrode array straddling the cortical laminae at a site in "median nerve cortex" (i.e., at a site with a cutaneous receptive field on the volar surface of D2 and thus with its dominant afferent input conveyed by the median nerve) in an adult squirrel monkey. We characterized the baseline responses to median, radial, and ulnar nerve stimulation. We then cut the median nerve and semichronically monitored radial nerve, ulnar nerve and median nerve (proximal stump) evoked responses. The radial nerve response in median nerve cortex changed progressively during the weeks after median nerve transection, ultimately assuming the characteristics of the dominant nerve profile. During this time, median, and ulnar nerve profiles displayed little or no change.

Long-lasting potentiation in the secondary somatosensory cortex affects motor control: assessment by H-reflex.

We investigated descending projections from the secondary somatosensory cortex to the feline spinal cord and the effects of long-lasting potentiation in secondary somatosensory cortex on the activities of motoneurons of the cat. Electrophysiological examinations revealed that the low-intensity subthreshold secondary somatosensory cortex stimulation could change the H-Reflex induced by radial nerve stimulation. The H-wave amplitudes, recorded in wrist flexor muscles, were enhanced when the intervals from secondary somatosensory cortex to radial nerve stimuli were altered from 0 to 30 ms (initial excitation, 146 +/- 11% (mean +/- S.E.M.) of the control value). In contrast, the H-waves were suppressed with intervals longer than 30 ms (80 +/- 3%). The descending pathways from secondary somatosensory cortex to the spinal cord were assessed using an immunohistochemical technique. c-Fos and Zif268 proteins, induced by stimulation of the hand-represented secondary somatosensory cortex areas, could thus express in activated cervical neurons. The density of labeled cells was significantly higher in the seventh and eighth cervical segments than in other levels. The great majority of positive cells were distributed in the lateral part of the contralateral ventral horn and their somas ranged from 10 to 50 microns in size. Finally, we examined the effects of long-lasting potentiation, induced by high-frequency stimulation of the ventral posterolateral thalamic nucleus, on the activities of spinal motoneurons. Long-lasting potentiation altered the previously observed effects of secondary somatosensory cortex stimulation on the H-wave amplitude. The secondary somatosensory cortex-conditioned initial excitation of the H-reflex was enhanced (from 139 to 175%, P < 0.05), while late suppression was completely blocked (from 74 to 112%, P < 0.01). In conclusion, the descending pathways from secondary somatosensory cortex to the spinal cord modulated the H-reflex, and long-lasting potentiation in secondary somatosensory cortex affected this modulation. We have previously reported that corticocortical inputs from primary to secondary somatosensory cortex is required for induction of long-lasting potentiation in secondary somatosensory cortex. Taken together, the present study suggests that cortical plasticity in secondary somatosensory cortex amplifies somatic inputs from primary somatosensory cortex as a means of adaptive motor control by the sensory system.

A propriospinal-like contribution to electromyographic responses evoked in wrist extensor muscles by transcranial stimulation of the motor cortex in man.

We tested the hypothesis that some of the electromyographic (EMG) responses elicited in preactivated forearm muscles by transcranial stimulation of the human motor cortex are produced by activity in a disynaptic corticospinal linkage involving propriospinal-like interneurones with cell bodies in the spinal C3-4 segments. The experimental design incorporated a previous observation that stimulation of afferents in the superficial radial nerve inhibits propriospinal-like neurones projecting to the extensor carpi radialis (ECR) muscle. Surface EMG responses were recorded from the active ECR muscle after transcranial electrical or magnetic stimulation over the motor cortex. In random trials, single conditioning stimuli at twice perceptual threshold were given to the superficial radial nerve at the wrist at different times before a cortical shock. When the cortex was stimulated electrically, the conditioning stimulus suppressed the EMG responses when the interval between the shocks was 11 ms or more. This was about 3.5 ms longer than the minimum time calculated for a possible direct cutaneous effect on spinal motoneurones. The time course of suppression began earlier and was more complex during magnetic stimulation of the cortex. It is argued that this difference is due to the repetitive I waves generated by the magnetic shock. Whether electrical or magnetic stimulation was used, the first 1-3 ms of the EMG response was relatively unaffected by superficial radial nerve stimulation at any interstimulus interval, whereas clear suppression was seen in the later portion of the response. In contrast, if the EMG response in ECR was suppressed by a conditioning stimulus to the median nerve at the elbow, then all portions of the EMG response were inhibited including the first 1-3 ms. The median nerve effect is thought to be due to direct reciprocal inhibition of the extensor motoneurones. Thus sparing of the initial part of the cortically evoked response with superficial radial stimulation suggests that the latter type of inhibition occurs at a premotoneuronal level. The timing of the effect is compatible with the explanation that corticospinal excitation is produced in ECR motoneurones through both monosynaptic and disynaptic (including propriospinal premotoneuronal) pathways, with superficial radial nerve inhibition being exerted at the propriospinal level.

Electrophysiological evidence for overlapping dominant and latent inputs to somatosensory cortex in squirrel monkeys.

1. The pattern of reorganization in area 3b of adult primates after median or ulnar nerve section suggests that somatic afferents from the dorsum of the hand, carried by the radial nerve, have preferential access to the cortical territories normally expressing glabrous inputs carried by the median and ulnar nerves. A likely mechanism underlying preferential access is preexisting, but silent, radial nerve inputs to the glabrous region of cortex. 2. We tested this by comparing the effects of electrical stimulation of median or ulnar versus radial nerves, on responses in the hand representation of area 3b. Laminar current source density and multiunit activity profiles were sampled with the use of linear array multicontact electrodes spanning the laminae of area 3b. Data were obtained from three squirrel monkeys anesthetized during recording. 3. Compared with colocated median or ulnar nerve responses, the radial nerve response had 1) an initial short-latency response in the middle laminae that was subtle; there was a small transmembrane current flow component without a discernable multiunit activity correlate; and 2) a laminar sequence and distribution of activity that was similar to those of the median or ulnar nerve responses (i.e., initial activation of the middle, followed by upper and lower laminae), but the significant current flow and multiunit response to radial nerve stimulation occurs 12-15 ms later. 4. Normal corepresentation of nondominant dorsum hand (radial) inputs with the dominant (median or ulnar) inputs in the glabrous hand surface representation provides a clear vehicle for the biased patterns of reorganization occurring after peripheral nerve section. The initial, "subtle" activity phase in the nondominant response is believed to reflect intracortical inhibition, and the later "significant" response phase, a rebound excitation, possibly compounded by an indirect or extralemniscal input. The spatiotemporal pattern of nondominant input is proposed to play a role in normal somatosensory perception.

Middle-latency somatosensory evoked potentials after stimulation of the radial and median nerves: component structure and scalp topography.

Somatosensory evoked potentials (SEPs) after radial nerve stimulation are studied less frequently than those after median nerve stimulation. Therefore, little is known about their component structure and scalp topography. We investigated radial nerve SEPs after electrical stimulation at the left wrist. For comparison, the median nerve was also stimulated at the wrist. SEPs were recorded with 15 scalp electrodes (bandpass 0.5-200 Hz) in 27 healthy subjects. The waveform of the radial nerve SEP at a contralateral parietal lead was comparable to that of the median nerve SEP, consisting of P14, N20, P30, and N60. In spite of comparable stimulus intensities, SEP amplitudes were smaller after radial than after median nerve stimulation. Significant latency differences were found only for N20 (earlier for median nerve) and P30 (earlier for radial nerve). The duration of the primary complex N20-P30 thus was significantly shorter for the radial nerve. Whereas N20 and P30 were present with either earlobe or frontal reference, N60 had a prerolandic maximum and was best recorded with a bipolar transverse derivation. In addition, another middle-latency negativity (N110) was found near the secondary somatosensory cortex, which had previously been described only for radial nerve stimulation. In standard SEP derivations, the N110 is riding on the ascending limb of the vertex negativity. It could best be recorded in low temporal leads versus a midline reference. The scalp topographies of P30, N60, and N110 were similar for radial and median nerve stimulation.

Clonidine Has Comparable Effects on Spontaneous Sympathetic Activity and Afferent Aδ– and C-Fiber-mediated Somatosympathetic Reflexes in Dogs

Clonidine, an alpha 2-adrenergic agonist, has been studied as an adjunct or alternative to spinal opioids in the management of moderate to severe pain. This study examined the relative effects of clonidine on efferent spontaneous sympathetic activity and afferent A delta and C fiber-mediated somatosympathetic responses. Spontaneous and evoked sympathetic activity in renal sympathetic nerves, mediated by A delta and C fibers by means of supramaximal electrical stimulation of the radial and tibial nerves, were observed in anesthetized dogs. Incremental doses of clonidine were administered intrathecally or intravenously in each of five preparations followed by intravenous naloxone 2 mg and yohimbine 5 mg. Both spontaneous sympathetic outflow and afferent A delta- and C fiber-mediated somatosympathetic responses evoked by tibial nerve stimulation were depressed in a similar dose dependent manner by clonidine administered intrathecally or intravenously in a dose ratio of approximately 1:4. Intrathecal clonidine inhibited and eliminated both local spontaneous sympathetic outflow and tibial nerve evoked sympathetic responses but had no significant depressant effect on the radial nerve evoked sympathetic reflexes. When administered intravenously clonidine had a similar depressant effect on both radial and tibial nerve elicited reflexes and spontaneous sympathetic activity. Clonidine, administered intrathecally or intravenously, has a similar depressant effect on both spontaneous sympathetic outflow and afferent A delta- and C fiber-mediated somatosympathetic reflexes. When administered intrathecally it has little effect on reflexes evoked via the descending pathway by radial nerve stimulation.

Bilateral reciprocal organisation in man: focus on IA interneurone.

The H reflex of flexor carpi radialis and radial-induced reciprocal inhibition were recorded in normal subjects during conditioning stimulation of the contralateral median or radial nerves. It was found that stimulation of the contralateral median nerve enhanced the degree of reciprocal inhibition exerted by the radial nerve on the median nerve, while contralateral radial nerve stimulation reduced the reciprocal inhibition exerted by the extensor on the flexor. In two subjects in which a pure extensor H reflex was recorded specular features were observed following contralateral median and radial stimulation. These findings are considered to be the electrophysiological manifestation of contralateral modulation of reciprocal inhibition, which is likely to act at the level of the IA interneurone.

LACK OF A CEILING EFFECT FOR INTRATHECAL BUPRENORPHINE ON C FIBRE MEDIATED SOMATOSYMPATHETIC REFLEXES

We observed that buprenorphine 20 micrograms kg-1 i.v. in dogs caused an initial significant reduction in both A delta and C fibre mediated somatosympathetic reflexes evoked by tibial and radial nerve stimulation, to approximately 75% and 70% of control values. Larger doses (up to 100 micrograms kg-1 i.v.) had progressively less effect and the mean responses were depressed to only approximately 65% and 55% of control, indicating a ceiling effect. Buprenorphine 450 micrograms intrathecally (i.t.) completely abolished tibial C fibre reflexes, but 20% of A delta responses could not be eliminated with doses up to 1050 micrograms i.t. Fentanyl 100 micrograms kg-1 i.v. or 150 micrograms i.t. after buprenorphine i.v. or i.t., respectively, had little additional effect. This study confirms the limited ceiling effect of buprenorphine on nociceptive reflexes when administered systemically, and provides evidence that when administered i.t. in sufficient doses it abolishes the C responses (lack of ceiling effect for C responses), but the A delta responses show a plateau or ceiling effect.

Effects of electrical stimulation of motor and cutaneous nerves on spinal cord blood flow.

The effects of electrical stimulation of the motor and cutaneous branch of the radial nerve on spinal cord blood flow (SCBF) in the cervical region and the correlation between the changes in SCBF and the amplitudes of spinal cord evoked potentials were investigated in cats anesthetized with alpha-chloralose. When measured by the hydrogen clearance technique, with stimuli of the cutaneous branch, the SCBF significantly (P < 0.01) increased from 37 +/- 8 (mean +/- SD) to 59 +/- 27 ml.100 g-1.min-1 at 10 Hz and from 39 +/- 6 to 54 +/- 9 ml.100 g-1.min-1 at 30 Hz, but stimulation of the motor branch had no effect. When measured by laser Doppler flowmetry, stimulation of the motor branch caused a small, transient, and significant increase in SCBF ending within 2 minutes. Stimulation of the cutaneous branch produced a large, prolonged, and significant increase in SCBF. The increase in SCBF produced by stimulation of the cutaneous nerve was significantly greater than that by stimulation of the motor branch. The SCBF was correlated linearly with the amplitude of the spinal cord evoked potential (r = 0.504; P < 0.01). The increase in SCBF caused by radial nerve stimulation may arise from changes in neuronal metabolism via peripheral nerve activation.

EFFECT OF LOW AND HIGH CONCENTRATIONS OF ALFENTANIL ADMINISTERED INTRATHECALLY ON Aδ AND C FIBRE MEDIATED SOMATOSYMPATHETIC REFLEXES

We have studied the effects of alfentanil administered intrathecally on somatosympathetic reflexes evoked by stimulation of radial and tibial nerves in 10 anaesthetized and paralysed dogs. In five animals, alfentanil was administered in doses of 100, 100, 200 and 400 micrograms in 0.8 ml and 800 micrograms in 1.6 ml prepared from the formulation of 500 micrograms ml-1. Five others received alfentanil (high concentration formulation, 5 mg ml-1) in doses of 500 and 2000 micrograms in 0.5 ml and 5000 micrograms in 1 ml. C fibre tibial nerve reflexes were depressed by 100 micrograms and abolished with doses of 200-400 micrograms, but the A delta response remained unaffected. A delta responses were depressed also and abolished, respectively, by doses of alfentanil 2000 micrograms and 5000 micrograms. At the larger, but not the smaller, concentration there was evidence of baroreflex sensitization probably caused by systemic absorption of the drug.

Segmental dysfunction of the cervical cord revealed by abnormalities of the spinal N13 potential in cervical spondylotic myelopathy.

We studied somatosensory potentials (SEPs) evoked by stimulation of radial, median, and ulnar nerves in 11 patients with MRI evidence of cervical spondylosis. All patients presented with progressive spastic paraparesis that was either isolated or associated with lower motor neuron signs in the upper limbs, with preserved joint, touch, pain, and temperature sensations in the four limbs. In all patients, scalp SEPs reflecting the activity of the dorsal column system up to the parietal cortex were normal while segmental cervical cord dysfunction was manifested by an abnormal spinal N13 potential in 95% of radial, 90% of median, and 54% of ulnar nerve SEPs. These subclinical abnormalities of the spinal N13 SEP probably result from reduced blood supply due to compression of the anterior spinal artery in patients with cervical spondylotic myelopathy.

Changes in presynaptic inhibition of afferents to propriospinal-like neurones in man during voluntary contractions.

1. The possibility was investigated that the facilitation of the transmission in the propriospinal-like system during voluntary contraction, documented in the companion paper (Burke, Gracies, Mazevet, Meunier & Pierrot-Deseilligny, 1992), is due to a decrease in presynaptic inhibition of afferents projecting to propriospinal-like neurones. 2. The radial nerve was stimulated to evoke presynaptic inhibition of the monosynaptic Ia projections to forearm flexor motoneurones (Berardelli, Day, Marsden & Rothwell, 1987) and, hopefully, of the afferent input to propriospinal-like neurones projecting to these motoneurones. 3. The propriospinal-like excitation of forearm motoneurones evoked from mixed afferent inputs was depressed by radial nerve stimulation, and this depression was long-lasting (200 ms). Despite the convergence of mixed nerve and cutaneous afferents onto common propriospinal-like neurones, the radial stimulation did not depress the cutaneous-induced excitation. This differential effect and the time course of the depression suggest that it results from presynaptic inhibition of mixed nerve afferents (presumably large muscle afferents) projecting to propriospinal-like neurones. 4. With voluntary contractions, phasic or tonic, the radial-induced depression of the propriospinal-like excitation evoked by mixed nerve afferents was much greater than at rest, but the cutaneous-evoked excitation was unchanged. Thus, with voluntary contractions, there was no evidence of decreased gating of the afferent input to propriospinal-like neurones whether the input was of muscle or cutaneous origin and it is concluded that changes in presynaptic inhibition cannot account for the facilitation of the transmission in the propriospinal-like system during voluntary contraction. 5. By contrast, presynaptic inhibition of the monosynaptic Ia projections to motoneurones was consistently reduced at the onset of contraction, and to a much lesser extent during a weak tonic contraction.

The influence of contralateral primary afferents on Ia inhibitory interneurones in humans.

1. Contralateral influences on short latency reciprocal inhibition between wrist extensor and flexor muscles were investigated in twenty-two healthy volunteers. Reciprocal inhibition, probably mediated through the Ia inhibitory interneurone, was measured by conditioning the flexor carpi radialis (FCR) H reflex by weak stimulation of the ipsilateral radial nerve. Maximum reciprocal inhibition occurring at a precise delay between conditioning and conditioned stimulations was taken as the test level of inhibition. 2. Contralateral median or radial nerves were stimulated at short intervals before the onset of reciprocal inhibition. The latter was increased by 8.6% after median nerve stimulation and decreased by 16.5% after radial nerve stimulation. 3. The contribution of sensory fibres in the two nerves to contralateral effects was investigated by stimulating purely sensory branches of the nerves. No clear modification of the contralateral reciprocal inhibition was observed. The effects produced by mixed nerve stimulation are thus likely to have been mediated by Ia fibres. 4. In three hemiplegic patients where reciprocal inhibition was reduced unilaterally, stimulation on the spastic side produced contralateral effects similar to those observed in normal subjects. This result indicates that contralateral effects are not mediated through the Ia inhibitory interneurone ipsilateral to the conditioning stimulus. 5. Since contralateral effects occur after short delays (2 ms, median nerve; 3 ms, radial nerve), we suggest a functional scheme in which the excitability of Ia inhibitory interneurones is modified by contralateral primary afferents via the interneurones activated by group I fibres, probably Ia fibres. The short delays indicate that the interneurone transmitting primary afferent influences to the contralateral side is probably excitatory.

Effects of electric and magnetic transcranial stimulation on long latency reflexes

The interaction of transcranial electric and magnetic brain stimulation with electrically elicited short- and long latency reflexes (LLR) of hand and forearm flexor muscles has been investigated in normal subjects. In the first paradigm, the motor potential evoked in thenar muscles by transcranial stimulation was conditioned by median nerve stimulation at various conditioning-test intervals. At short intervals (electric: 5-12.5 ms, magnetic: 0-7.5 ms) facilitation occurred that corresponded to the H-reflex and at longer intervals (electric: 25-40 ms, magnetic: 22.5-35 ms) there was a facilitation corresponding to the LLR. Electric and magnetic stimulation resulted in a similar degree of facilitation. A second paradigm investigated the facilitation of the forearm flexor H-reflex by a cutaneo-muscular LLR elicited by radial superficial nerve stimulation and transcranial stimulation used separately or together. When electric and magnetic brain stimulation were compared, magnetic brain stimulation was followed by significant extrafacilitation but electric stimulation was not. This result favours an interaction between the afferent volley eliciting the LLR and transcranial magnetic stimulation most likely at supraspinal level.