Motor cortex inhibition induced by acoustic stimulation

The influence of the brainstem motor system on cerebral motor areas may play an important role in motor control in health and disease. A new approach to investigate this interaction in man is combining acoustic stimulation activating the startle system with transcranial magnetic stimulation (TMS) over the motor cortex. However, it is unclear whether the inhibition of TMS responses following acoustic stimulation occurs at the level of the motor cortex through reticulo-cortical projections or subcortically, perhaps through reticulo-spinal projections. We compared the influence of acoustic stimulation on motor effects elicited by TMS over motor cortical areas to those evoked with subcortical electrical stimulation (SES) through depth electrodes in five patients treated with deep brain stimulation for Parkinsons disease. SES bypasses the motor cortex, demonstrating any interaction with acoustic stimuli at the subcortical level. EMG was recorded from the contralateral biceps brachii muscle. Acoustic stimulation was delivered binaurally through headphones and used as a conditioning stimulus at an interstimulus interval of 50 ms. When TMS was used as the test stimulus, the area and amplitude of the conditioned motor response was significantly inhibited (area: 57.5±12.9%, amplitude: 47.9±7.4%, as percentage of unconditioned response) whereas facilitation occurred with SES (area: 110.1±4.3%, amplitude: 116.9±6.9%). We conclude that a startle-evoked activation of reticulo-cortical projections transiently inhibits the motor cortex.     

Effects of combined cortical and acoustic stimuli on muscle activity

Hitherto, it has proven difficult to investigate interactions between cerebral and brainstem motor systems in the human. We hypothesised that transcranial magnetic stimulation (TMS) centred over the dorsal premotor and primary motor cortices might elicit net facilitatory cortico-reticular effects that could interact at the level of the brainstem with a habituated startle to give a reticulospinal discharge and electromyographic (EMG) response with a longer latency than the direct corticospinal response. Conversely, any reticulo-cortical activity evoked by a habituated startle should influence the size of the direct response to cortical TMS. EMG was recorded from active left deltoid muscle in nine healthy volunteers. Acoustic stimulation was delivered binaurally through headphones and repeated until the startle response was habituated. When TMS was centred over the right dorsal premotor or primary motor cortices and delivered 50 ms after the habituated acoustic stimulus, the contralateral direct motor evoked potential was inhibited, compared with the response elicited by TMS alone. The contralateral silent period was shortened and associated with less of a decrease in EMG levels relative to TMS alone. Indeed, an actual increase in EMG over baseline levels occurred in the later half of the silent period in all subjects. We conclude that both cortico-reticular and reticular-cortical effects could be elicited in deltoid through the combination of acoustic stimulation and TMS at short interstimulus intervals. Effects were similar with TMS over premotor and primary motor cortex.     

Localization of diaphragm motor cortical representation and determination of corticodiaphragmatic latencies by using magnetic stimulation in normal adult human subjects

The aims of this study were to identify the motor cortical representation of the diaphragm and to assess the corticodiaphragmatic pathway from both hemispheres. Specially designed bipolar surface electrodes were used to record the ipsilateral and contralateral compound motor evoked potentials (CMEPs) of the diaphragm after transcranial magnetic stimulation (TMS) of the motor cortex. In addition, the response to cervical magnetic stimulation of the phrenic nerve roots, effected using a figure-of-eight magnetic coil, was also recorded. The study involved 30 normal adult male volunteers. The average point of optimal excitability (POE) was determined to be 3.7 cm lateral to the mid-sagittal plane and 0.89 cm anterior to the preauricular plane. The largest response was obtained at a stimulus coil orientation of 0–90°. The TMS of either hemisphere produced CMEPs in the contralateral and ipsilateral diaphragm muscles. TMS of either hemisphere elicited CMEPs that had significantly greater amplitudes and shorter latencies from the contralateral muscles compared with the ipsilateral response (P<0.0001). The central motor conduction time of the crossed tract (8.8 ms) was significantly shorter than that of the uncrossed tract (12.2 ms). No significant interhemispheric differences were recorded. The recorded CMEPs recorded in response to TMS were facilitated during volitional inspiration. Phrenic nerve latency was 5.7 ms and 5.6 ms for the right and left phrenic nerves, respectively, with no significant difference between these values. Both bilateral crossed and uncrossed corticospinal connections to the diaphragm were usually present, with the crossed tract predominating. The technique used in this study may be useful for investigations into the function and integrity of central and peripheral pathway of the diaphragm muscles in various neurological disorders. Electronic Publication     

Human handedness and asymmetry of the motor cortical silent period

We performed transcranial magnetic stimulation of the motor cortex in 22 left-handed and 25 right-handed subjects during active contraction of a small hand muscle. Motor evoked potentials had the same latency, amplitude and threshold on both sides of the body, whilst the silent period duration was shorter in the dominant hand. Silent periods elicited by nerve and brainstem stimulation were the same in both hands. Since the latter part of the cortical silent period is due mainly to withdrawal of corticospinal input to spinal motoneurones, we speculate that the results are compatible with the suggestion that tonic contractions of the non-dominant hand are associated with a greater involvement of the corticospinal tract than those of the dominant hand. It also seems likely that there is an asymmetry in the excitability of cortical inhibitory mechanisms with those responsible for the cortical silent period being less excitable in the dominant motor cortex. Received: 29 July 1998 / Accepted: 21 April 1999     

Ipsilateral and contralateral motor inhibitory control in musical and vocalization tasks

The inhibitory motor control mechanisms in human singing and vocalization are not well understood. Using transcranial magnetic stimulation (TMS), we show that singing resulted in right-sided prolongation of ipsilateral silent period and bilateral reduction in contralateral silent period. Reading led to reduced contralateral silent period duration with right-sided TMS only, but no significant inhibitory changes, both ipsilateral and contralateral, were evident with humming. The findings support the presence of enhanced interhemispheric inhibitory motor interaction during singing, as opposed to reading tasks, in dynamic word generation coupled with production of melody.     

Suppression of the transcallosal motor output: a transcranial magnetic stimulation study in healthy subjects

We tested the hypothesis that transcranial magnetic stimulation (TMS), in addition to its inhibitory action on the corticospinal output, can also exert some inhibitory effect on the transcallosal system connecting the two motor cortices. In seven normal subjects, instructed to keep their right opponens pollicis (OP) muscle fully relaxed and their left OP muscle voluntarily contracted, we used a paired-pulse TMS protocol, to stimulate the left motor cortex. We evaluated the effect of low-intensity conditioning stimulation on the ipsilateral silent period (iSP) elicited by the subsequent test stimulus. Compelling evidence exists to support that this iSP is mediated by the activation of transcallosal motor fibres. Simultaneously, the inhibition of the motor evoked potential (MEP) in the right OP muscle was also investigated. At the interstimulus interval (ISI) of 3 ms, the iSP was significantly (P<0.0001, repeated-measures ANOVA) suppressed by conditioning intensities ranging from 1.2 to 0.6 of MEP threshold. The assessment of the time-course showed that iSP inhibition was present in all the tested subjects only at ISIs of 2 and 3 ms (for each subject P<0.05, repeated-measures ANOVA). Several findings suggest that the suppression of iSP is brought about by the activation of inhibitory mechanisms operating in the stimulated (left) motor cortex. We propose that the assessment of iSP suppression could be a method to study the excitability of intracortical inhibitory circuits in the affected hemisphere of patients with unilateral damage of the corticospinal tract.     

Organization of ipsilateral excitatory and inhibitory pathways in the human motor cortex

Motor cortex stimulation has both excitatory and inhibitory effects on ipsilateral muscles. Excitatory effects can be assessed by ipsilateral motor-evoked potentials (iMEPs). Inhibitory effects include an interruption of ipsilateral voluntary muscle activity known as the silent period (iSP) and a reduction in corticospinal excitability evoked by conditioning stimulation of the contralateral motor cortex (interhemispheric inhibition, IHI). Both iSP and IHI may be mediated by transcallosal pathways. Their relationship to the contralateral corticospinal projection and whether iSP and IHI represent the same phenomenon remain unclear. The neuronal population activated by transcranial magnetic stimulation (TMS) is highly dependent on the direction of the induced current in the brain. We examined the relationship among iMEP, iSP, IHI, and the contralateral corticospinal system by examining the effects of different stimulus intensities and current directions. Surface electromyography (EMG) was recorded from both first dorsal interosseous (FDI) muscles. The iSP in the right FDI muscle was obtained by right motor cortex stimulation during voluntary muscle contraction. IHI was examined by conditioning stimulation of the right motor cortex followed by test stimulation of the left motor cortex at interstimulus intervals (ISIs) of 2-80 ms. The induced current directions tested in the right motor cortex were anterior medial (AM), posterior medial (PM), posterior lateral, and anterior lateral (AL). Contralateral MEPs (cMEPs) had the lowest threshold with the AM direction and the shortest latency with the PM direction. iMEPs were present in 8 of 10 subjects. Both iMEP and IHI did not show significant directional preference. iSP was observed in all subjects with the highest threshold for the AL direction and the longest duration for the AM direction. cMEP, iSP, and IHI all increased with stimulus intensity up to approximately 75% stimulator output. Target muscle activation decreased IHI at 8-ms ISI but had little effect on IHI at 40-ms ISI. iSP and IHI at 8-ms ISI did not correlate at any stimulus intensities and current directions tested, and factor analysis showed that they are explained by different factors. However, active IHI at 40-ms ISI was explained by the same factor as iSP. The different directional preference for cMEP compared with iMEP and IHI suggests that these ipsilateral effects are mediated by populations of cortical neurons that are different from those activating the corticospinal neurons. iSP and IHI do not represent the same phenomenon and should be considered complementary measures of ipsilateral inhibition.     

On the origin of the postexcitatory inhibition seen after transcranial magnetic brain stimulation in awake human subjects

Non-invasive transcranial magnetic stimulation (TMS) of motor cortex induces motor evoked potentials in contralateral muscles which are thought to be conducted by the corticospinal tract. Furthermore, inhibitory actions can be elicited by TMS which appear directly after the motor evoked potential (postexcitatory inhibition, PI) and can be visualized by blockade of tonic voluntary EMG activity. It was the aim of the present study to answer the questions of whether this inhibitory action is mainly of cortical or of spinal origin, which brain area generates this inhibition, and whether the duration of PI differs between proximal and distal muscles. Experiments were performed on a total of 34 healthy volunteers. Brain stimuli were delivered with a Novametrix Magstim 200HP with a maximum output of 2.0 T, and stimulation was performed during tonic voluntary activation of the muscle under study. Stimulation strength was 1.5 times threshold level. Duration of PI was defined as the time from the onset of the motor evoked potential to the reoccurrence of the EMG background activity. PI was found more pronounced in distal hand muscles than in proximal arm and leg muscles. The largest PI values were observed when the primary motor cortex was stimulated. To test the excitability of the spinal motoneurones during PI, cortical double stimulation at various intervals was performed and the soleus H-reflex was evoked at different intervals after cortical stimulation. Neither test revealed a decrease in the excitability of the spinal motoneurones during PI. These findings imply that spinal segmental inhibitory action cannot account for PI and that, most probably, inhibitory actions within the motor cortex play a major role in the genesis of PI.Dedicated to the memory of Prof. Dr. O. Creutzfeldt     

The origin of activity in the biceps brachii muscle during voluntary contractions of the contralateral elbow flexor muscles

During strong voluntary contractions, activity is not restricted to the target muscles. Other muscles, including contralateral muscles, often contract. We used transcranial magnetic stimulation (TMS) to analyse the origin of these unintended contralateral contractions (termed “associated” contractions). Subjects (n = 9) performed maximal voluntary contractions (MVCs) with their right elbow-flexor muscles followed by submaximal contractions with their left elbow flexors. Electromyographic activity (EMG) during the submaximal contractions was matched to the associated EMG in the left biceps brachii during the right MVC. During contractions, TMS was delivered to the motor cortex of the right or left hemisphere and excitatory motor evoked potentials (MEPs) and inhibitory (silent period) responses recorded from left biceps. Changes at a spinal level were investigated using cervicomedullary stimulation to activate corticospinal paths (n = 5). Stimulation of the right hemisphere produced silent periods of comparable duration in associated and voluntary contractions (218 vs 217 ms, respectively), whereas left hemisphere stimulation caused a depression of EMG but no EMG silence in either contraction. Despite matched EMG, MEPs elicited by right hemisphere stimulation were ∼1.5–2.5 times larger during associated compared to voluntary contractions (P < 0.005). Similar inhibition of the associated and matched voluntary activity during the silent period suggests that associated activity comes from the contralateral hemisphere and that motor areas in this (right) hemisphere are activated concomitantly with the motor areas in the left hemisphere. Comparison of the MEPs and subcortically evoked potentials implies that cortical excitability was greater in associated contractions than in the matched voluntary efforts.     

The physiological basis of the effects of intermittent theta burst stimulation of the human motor cortex

Theta burst stimulation (TBS) is a form of repetitive transcranial magnetic stimulation (TMS). When applied to motor cortex it leads to after-effects on corticospinal and corticocortical excitability that may reflect LTP/LTD-like synaptic effects. An inhibitory form of TBS (continuous, cTBS) suppresses MEPs, and spinal epidural recordings show this is due to suppression of the I1 volley evoked by TMS. Here we investigate whether the excitatory form of TBS (intermittent, iTBS) affects the same I-wave circuitry. We recorded corticospinal volleys evoked by single pulse TMS of the motor cortex before and after iTBS in three conscious patients who had an electrode implanted in the cervical epidural space for the control of pain. As in healthy subjects, iTBS increased MEPs, and this was accompanied by a significant increase in the amplitude of later I-waves, but not the I1 wave. In two of the patients we tested the excitability of the contralateral cortex and found a significant suppression of the late I-waves. The extent of the changes varied between the three patients, as did their age. To investigate whether age might be a significant contributor to the variability we examined the effect of iTBS on MEPs in 18 healthy subjects. iTBS facilitated MEPs evoked by TMS of the conditioned hemisphere and suppressed MEPs evoked by stimulation of the contralateral hemisphere. There was a slight but non-significant decline in MEP facilitation with age, suggesting that interindividual variability was more important than age in explaining our data. In a subgroup of 10 subjects we found that iTBS had no effect on the duration of the ipsilateral silent period suggesting that the reduction in contralateral MEPs was not due to an increase in ongoing transcallosal inhibition. In conclusion, iTBS affects the excitability of excitatory synaptic inputs to pyramidal tract neurones that are recruited by a TMS pulse, both in the stimulated hemisphere and in the contralateral hemisphere. However the circuits affected differ from those influenced by the inhibitory, cTBS, protocol. The implication is that cTBS and iTBS may have different therapeutic targets.     

LTD-like plasticity induced by paired associative stimulation: direct evidence in humans

Paired associative stimulation (PAS), in which peripheral nerve stimuli are followed by transcranial magnetic stimulation (TMS) of the motor cortex, may produce a long lasting change in cortical excitability. At an interstimulus interval slightly shorter than the time needed for the afferent inputs to reach cerebral cortex (10 ms), motor cortex excitability decreases. Indirect data support the hypothesis that PAS at this interval (PAS10) involves LTD like-changes in cortical synapses. The aim of present paper was to investigate more directly PAS10 effects. We recorded corticospinal descending volleys evoked by single pulse TMS before and after PAS10 in two conscious subjects who had a high cervical epidural electrode implanted for pain control. These synchronous volleys provide a measure of cortical synaptic activity. PAS10 significantly reduced the amplitude of later descending waves while the earliest descending wave was not modified. Present results confirm the cortical origin of the effect of PAS10.     

Task-dependent modulation of excitatory and inhibitory functions within the human primary motor cortex

We evaluated motor evoked potentials (MEPs) and duration of the cortical silent period (CSP) from the right first dorsal interosseous (FDI) muscle to transcranial magnetic stimulation (TMS) of the left motor cortex in ten healthy subjects performing different manual tasks. They abducted the index finger alone, pressed a strain gauge with the thumb and index finger in a pincer grip, and squeezed a 4-cm brass cylinder with all digits in a power grip. The level of FDI EMG activity across tasks was kept constant by providing subjects with acoustic-visual feedback of their muscle activity. The TMS elicited larger amplitude FDI MEPs during pincer and power grip than during the index finger abduction task, and larger amplitude MEPs during pincer gripping than during power gripping. The CSP was shorter during pincer and power grip than during the index finger abduction task and shorter during power gripping than during pincer gripping. These results suggest excitatory and inhibitory task-dependent changes in the motor cortex. Complex manual tasks (pincer and power gripping) elicit greater motor cortical excitation than a simple task (index finger abduction) presumably because they activate multiple synergistic muscles thus facilitating corticomotoneurons. The finger abduction task probably yielded greater motor cortical inhibition than the pincer and power tasks because muscles uninvolved in the task activated the cortical inhibitory circuit. Increased cortical excitatory and inhibitory functions during precision tasks (pincer gripping) probably explain why MEPs have larger amplitudes and CSPs have longer durations during pincer gripping than during power gripping. Electronic Publication     

Focal depression of cortical excitability induced by fatiguing muscle contraction: a transcranial magnetic stimulation study

Motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) and transcranial electrical stimulation (TES) of the motor cortex were recorded in separate sessions to assess changes in motor cortex excitability after a fatiguing isometric maximal voluntary contraction (MVC) of the right ankle dorsal flexor muscles. Five healthy male subjects, aged 37.4±4.2 years (mean±SE), were seated in a chair equipped with a load cell to measure dorsiflexion force. TMS or TES was delivered over the scalp vertex before and after a fatiguing MVC, which was maintained until force decreased by 50%. MEPs were recorded by surface electrodes placed over quadriceps, hamstrings, tibialis anterior (TA), and soleus muscles bilaterally. M-waves were elicited from the exercised TA by supramaximal electrical stimulation of the peroneal nerve. H-reflex and MVC recovery after fatiguing, sustained MVC were also studied independently in additional sessions. TMS-induced MEPs were significantly reduced for 20 min following MVC, but only in the exercised TA muscle. Comparing TMS and TES mean MEP amplitudes, we found that, over the first 5 min following the fatiguing MVC, they were decreased by about 55% for each. M-wave responses were unchanged. H-reflex amplitude and MVC force recovered within the 1st min following the fatiguing MVC. When neuromuscular fatigue was induced by tetanic motor point stimulation of the TA, TMS-induced MEP amplitudes remained unchanged. These findings suggest that the observed decrease in MEP amplitude represents a focal reduction of cortical excitability following a fatiguing motor task and may be caused by intracortical and/or subcortical inhibitory mechanisms.     

经颅磁刺激对部位相关癫癎患者运动皮质功能的评估

目的:采用经颅磁刺激技术(TMS)探讨症状性运动部位相关癫癎患者发作间期运动皮质的兴奋性.方法:对诊断明确的34例癫癎患者(分治疗组和未治疗组)及20例年龄、性别匹配的正常对照组进行单脉冲经颅磁刺激,刺激部位头颅相应的运动手区和颈7棘突外侧,并于对侧小指外展肌记录运动诱发电位(MEP),分析其阈强度(TI)、周围潜伏期(PL)及皮质潜伏期(CL)、中枢传导时间(CCT)和静息期(SP).结果:所有癫癎患者PL、CL及CCT均在正常范围内,但TI和SP明显低于正常对照组(P< 0.01).在癫癎患者中,未治疗组TI及SP明显低于治疗组(P< 0.01),致癎灶侧TI及SP低于非致癎灶侧(P< 0.05),但非致癎灶侧SP亦缩短.结论:单脉冲低频TMS能有效地反映中枢运动皮质的功能状态,用于症状性运动部位相关癫癎患者发作间期运动皮质兴奋性研究具有重要的实用价值.     

Effects of transcranial direct current stimulation over the human motor cortex on corticospinal and transcallosal excitability

Weak transcranial direct current stimulation (tDCS) can induce long lasting changes in cortical excitability. In the present study we asked whether tDCS applied to the left primary motor cortex (M1) also produces aftereffects distant from the site of the stimulating electrodes. We therefore tested corticospinal excitability in the left and the right M1 and transcallosal excitability between the two cortices using transcranial magnetic stimulation (TMS) before and after applying tDCS. Eight healthy subjects received 10 min of anodal or cathodal tDCS (1 mA) to the left M1. We examined the amplitude of contralateral motor evoked potentials (MEPs) and the onset latency and duration of transcallosal inhibition with single pulse TMS. MEPs evoked from the tDCS stimulated (left) M1 were increased by 32% after anodal and decreased by 27% after cathodal tDCS, while transcallosal inhibition evoked from the left M1 remained unchanged. The effect on MEPs evoked from the left M1 lasted longer for cathodal than for anodal tDCS. MEPs evoked from the right M1 were unchanged whilst the duration of transcallosal inhibition evoked from the right M1 was shortened after cathodal tDCS and prolonged after anodal tDCS. The duration of transcallosal inhibition returned to control values before the effect on the MEPs from the left M1 had recovered. These findings are compatible with the idea that tDCS-induced aftereffects in the cortical motor system are limited to the stimulated hemisphere, and that tDCS not only affects corticospinal circuits involved in producing MEPs but also inhibitory interneurons mediating transcallosal inhibition from the contralateral hemisphere.     

Facilitatory effect on the motor cortex by electrical stimulation over the cerebellum in humans

Electrical stimulation over the cerebellum is known to transiently suppress the contralateral motor cortex in humans. However, projections from the cerebellar nuclei to the primary motor cortex are disynaptic excitatory pathways through the ventral thalamus. In the present investigation we studied facilitatory effects on the motor cortical excitability elicited by electrical stimulation over the cerebellum by recording surface electromyographic (EMG) responses from the first dorsal interosseous (FDI) muscle in nine normal volunteers. For primary motor cortical activation magnetic stimuli were given over the contralateral hand motor area with a figure-of-eight shaped coil with a current to preferentially elicit I3-waves (test stimulus). For cerebellar stimulation high-voltage electric stimuli were given with an anode on the ipsilateral mastoid process and a cathode over the contralateral process as previously described (conditioning stimulus). The effect of conditioning-test interstimulus intervals was investigated. Anodal cerebellar stimuli increased the size of EMG responses to magnetic cortical stimulation at an interstimulus interval of 3 ms. Reversing the current of conditioning stimulus abolished the facilitation. The same (anodal) conditioning stimuli did not affect electrically evoked cortical responses. Based on the effective polarity of the conditioning stimulus and the time course of facilitation we consider that this effect is due to motor cortical facilitation elicited by activation of the excitatory dentatothalamocortical pathway at the deep cerebellar nuclei or superior cerebellar peduncle. We conclude that the motor cortical facilitation is evoked by cerebellar stimulation in humans     

Cathodal transcranial direct current stimulation suppresses ipsilateral projections to presumed propriospinal neurons of the proximal upper limb

This study investigated whether cathodal transcranial direct current stimulation (c-tDCS) of left primary motor cortex (M1) modulates excitability of ipsilateral propriospinal premotoneurons (PNs) in healthy humans. Transcranial magnetic stimulation (TMS) of the right motor cortex was used to obtain motor evoked potentials (MEPs) from the left biceps brachii (BB) while participants maintained contraction of the left BB. To examine presumed PN excitability, left BB MEPs were compared with those conditioned by median nerve stimulation (MNS) at the left elbow. Interstimulus intervals between TMS and MNS were set to produce summation at the C3-C4 level of the spinal cord. MNS facilitated BB MEPs elicited at TMS intensities near active motor threshold but inhibited BB MEPs at slightly higher intensities, indicative of putative PN modulation. c-tDCS suppressed the facilitatory and inhibitory effects of MNS. Sham tDCS did not alter either component. There was no effect of c-tDCS and sham tDCS on nonconditioned left BB MEPs or on the ipsilateral silent period of left BB. Right first dorsal interosseous MEPs were suppressed by c-tDCS. These results indicate that M1 c-tDCS can be used to modulate excitability of ipsilateral projections to presumed PNs controlling the proximal arm muscle BB. This technique may hold promise for promoting motor recovery of proximal upper limb function after stroke.     

Electrical stimulation of the human common peroneal nerve elicits lasting facilitation of cortical motor-evoked potentials

Motor-evoked potentials (MEP) in the tibialis anterior (TA) muscle were shown to be facilitated by repetitive electrical stimulation of the common peroneal (CP) nerve at intensities above motor threshold. The TA electromyogram (EMG) and ankle flexion force were recorded in response to transcranial magnetic stimulation (TMS) of the leg area of the motor cortex to evaluate the excitability of cortico-spinal-muscular pathways. Repetitive stimulation of the CP nerve at 25 Hz for 30 min increased the MEP by 50.3 ± 13.6% (mean ± S.E.) at a TMS intensity that initially gave a half-maximum MEP (MEP_h). In contrast the maximum MEP (MEP_max) did not change. Ankle flexion force (103 ± 21.9%) and silent period duration (75.3 ± 12.9%) also increased. These results suggest an increase in corticospinal excitability, rather than total connectivity due to repetitive CP stimulation. Facilitation was evident after as little as 10 min of stimulation and persisted without significant decrement for at least 30 min after stimulation. The long duration of silent period following CP stimulation (99.2 ± 14.8 ms) suggests that this form of stimulation may have effects on the motor cortex. To exclude the possibility that MEP_h facilitation was primarily due to sensory fibre activation, we performed several control experiments. Preferentially activating Ia muscle afferents by vibration in the absence of motor activity had no significant effect. Cutaneous afferent activation via stimulation of the superficial peroneal nerve increased the amplitude of responses at MEP_max rather than MEP_h. Concurrent tendon vibration and superficial peroneal nerve stimulation failed to facilitate TA MEP responses. In summary, repetitive electrical stimulation of the CP nerve elicits lasting changes in corticospinal excitability, possibly as a result of co-activating motor and sensory fibres.Due to an error in the citation line, this revised PDF (published in December 2003) deviates from the printed version, and is the correct and authoritative version of the paper.     

Effects of motor cortical stimulation on the excitability of contralateral motor and sensory cortices

Single pulses of transcranial magnetic stimulation (TMS) were applied to the right hemisphere over either the hand sensory area, the hand motor area (M1), ventral premotor area (vPM), dorsolateral prefrontal cortex, or 10 cm away from head (sham stimulation) in order to test the effect on motor evoked potentials (MEPs) elicited by single pulse TMS or transcranial electrical stimulus (TES) over the left M1 or the somatosensory evoked potential (SEP) elicited by an electrical stimulus to the right median nerve. The interstimulus intervals (ISIs) for MEP experiments were 50, 100, 150, 200, 300 and 400 ms, with those for SEP experiments being adjusted for the impulse conduction time from the wrist to the cortex. TMS over the right M1 reduced MEPs elicited by TMS of the left motor cortex at ISIs of 50–150 ms, whereas MEPs produced by TES were unaffected. TMS over M1 and vPM facilitated the contralateral cortical median nerve SEPs at an ISI of 100–200 ms, whereas it had no effect on tibial nerve SEPs or paired median nerve stimulation SEP. Based on these results, we conclude that at around 150-ms intervals, TMS over the motor areas (M1 and vPM) reduces the excitability of the contralateral motor area. This has a secondary effect of enhancing the responsiveness of the sensory cortex through cortico-cortical connections.     

Modulation of motor cortex excitability by median nerve and digit stimulation

We investigated the time course of changes in motor cortex excitability after median nerve and digit stimulation. Although previous studies showed periods of increased and decreased corticospinal excitability following nerve stimulation, changes in cortical excitability beyond 200 ms after peripheral nerve stimulation have not been reported. Magnetoencephalographic studies have shown an increase in the 20-Hz rolandic rhythm from 200 to 1000 ms after median nerve stimulation. We tested the hypothesis that this increase is associated with reduced motor cortex excitability. The right or left median nerve was stimulated and transcranial magnetic stimulation (TMS) was applied to left motor cortex at different conditioning-test (C-T) intervals. Motor-evoked potentials (MEPs) were recorded from the right abductor pollicis brevis (APB), first dorsal interosseous (FDI), and extensor carpi radialis (ECR) muscles. Right median nerve stimulation reduced test MEP amplitude at C-T intervals from 400 to 1000 ms for APB, at C-T intervals from 200 to 1000 ms for FDI, and at C-T intervals of 200 and 600 ms for ECR, but had no effect on FDI F-wave amplitude at a C-T interval of 200 ms. Left median nerve (ipsilateral to TMS) stimulation resulted in less inhibition than right median nerve stimulation, but test MEP amplitude was significantly reduced at a C-T interval of 200 ms for all three muscles. Digit stimulation also reduced test MEP amplitude at C-T intervals of 200–600 ms. The time course for decreased motor cortex excitability following median nerve stimulation corresponds well to rebound of the 20-Hz cortical rhythm and supports the hypothesis that this increased power represents cortical deactivation. Received: 11 December 1998 / Accepted: 30 April 1999