Human cortical potentials evoked by stimulation of the median nerve. II. Cytoarchitectonic areas generating long-latency activity

1. The anatomic generators of human median nerve somatosensory evoked potentials (SEPs) in the 40 to 250-ms latency range were investigated in 54 patients by means of cortical-surface and transcortical recordings obtained during neurosurgery. 2. Contralateral stimulation evoked three groups of SEPs recorded from the hand representation area of sensorimotor cortex: P45-N80-P180, recorded anterior to the central sulcus (CS) and maximal on the precentral gyrus; N45-P80-N180, recorded posterior to the CS and maximal on the postcentral gyrus; and P50-N90-P190, recorded near and on either side of the CS. 3. P45-N80-P180 inverted in polarity to N45-P80-N180 across the CS but was similar in polarity from the cortical surface and white matter in transcortical recordings. These spatial distributions were similar to those of the short-latency P20-N30 and N20-P30 potentials described in the preceding paper, suggesting that these long-latency potentials are generated in area 3b of somatosensory cortex. 4. P50-N90-P190 was largest over the anterior one-half of somatosensory cortex and did not show polarity inversion across the CS. This spatial distribution was similar to that of the short-latency P25-N35 potentials described in the preceding paper and, together with our and Goldring et al. 1970; Stohr and Goldring 1969 transcortical recordings, suggest that these long-latency potentials are generated in area 1 of somatosensory cortex. 5. SEPs of apparently local origin were recorded from several regions of sensorimotor cortex to stimulation of the ipsilateral median nerve. Surface and transcortical recordings suggest that the ipsilateral potentials are generated not in area 3b, but rather in other regions of sensorimotor cortex perhaps including areas 4, 1, 2, and 7. This spatial distribution suggests that the ipsilateral potentials are generated by transcallosal input from the contralateral hemisphere. 6. Recordings from the periSylvian region were characterized by P100 and N100, recorded above and below the Sylvian sulcus (SS) respectively. This distribution suggests a tangential generator located in the upper wall of the SS in the second somatosensory area (SII). In addition, N125 and P200, recorded near and on either side of the SS, suggest a radial generator in a portion of SII located in surface cortex above the SS. 7. In comparison with the short-latency SEPs described in the preceding paper, the long-latency potentials were more variable and were more affected by intraoperative conditions.     

Human cortical potentials evoked by stimulation of the median nerve. II. Cytoarchitectonic areas generating short-latency activity

1. The anatomic generators of human median nerve somatosensory evoked potentials (SEPs) in the 40 to 250-ms latency range were investigated in 54 patients by means of cortical-surface and transcortical recordings obtained during neurosurgery. 2. Contralateral stimulation evoked three groups of SEPs recorded from the hand representation area of sensorimotor cortex: P45-N80-P180, recorded anterior to the central sulcus (CS) and maximal on the precentral gyrus; N45-P80-N180, recorded posterior to the CS and maximal on the postcentral gyrus; and P50-N90-P190, recorded near and on either side of the CS. 3. P45-N80-P180 inverted in polarity to N45-P80-N180 across the CS but was similar in polarity from the cortical surface and white matter in transcortical recordings. These spatial distributions were similar to those of the short-latency P20-N30 and N20-P30 potentials described in the preceding paper, suggesting that these long-latency potentials are generated in area 3b of somatosensory cortex. 4. P50-N90-P190 was largest over the anterior one-half of somatosensory cortex and did not show polarity inversion across the CS. This spatial distribution was similar to that of the short-latency P25-N35 potentials described in the preceding paper and, together with our and Goldring et al. 1970; Stohr and Goldring 1969 transcortical recordings, suggest that these long-latency potentials are generated in area 1 of somatosensory cortex. 5. SEPs of apparently local origin were recorded from several regions of sensorimotor cortex to stimulation of the ipsilateral median nerve. Surface and transcortical recordings suggest that the ipsilateral potentials are generated not in area 3b, but rather in other regions of sensorimotor cortex perhaps including areas 4, 1, 2, and 7. This spatial distribution suggests that the ipsilateral potentials are generated by transcallosal input from the contralateral hemisphere. 6. Recordings from the periSylvian region were characterized by P100 and N100, recorded above and below the Sylvian sulcus (SS) respectively. This distribution suggests a tangential generator located in the upper wall of the SS in the second somatosensory area (SII). In addition, N125 and P200, recorded near and on either side of the SS, suggest a radial generator in a portion of SII located in surface cortex above the SS. 7. In comparison with the short-latency SEPs described in the preceding paper, the long-latency potentials were more variable and were more affected by intraoperative conditions.(ABSTRACT TRUNCATED AT 400 WORDS)     

Cortical somatosensory evoked potentials. II. Effects of excision of somatosensory or motor cortex in humans and monkeys

1. To clarify the generators of human short-latency somatosensory evoked potentials (SEPs) thought to arise in sensorimotor cortex, we studied the effects on SEPs of surgical excision of somatosensory or motor cortex in humans and monkeys. 2. Normal median nerve SEPs (P20-N30, N20-P30, and P25-N35) were recorded from the cortical surface of a patient (G13) undergoing a cortical excision for relief of focal seizures. All SEPs were abolished both acutely and chronically after excision of the hand area of somatosensory cortex. Similarly, excision of the hand area of somatosensory cortex abolished corresponding SEPs (P10-N20, N10-P20, and P12-N25) in monkeys. Excision of the crown of monkey somatosensory cortex abolished P12-N25 while leaving P10-N20 and N10-P20 relatively unaffected. 3. After excision of the hand area of motor cortex, all SEPs were present when recorded from the cortical surface of a patient (W1) undergoing a cortical excision for relief of focal seizures. Similarly, all SEPs were present in monkeys after excision of the hand area of motor cortex. 4. Although all SEPs were present after excision of motor cortex in monkeys, variable changes were observed in SEPs after the excisions. However, these changes were not larger than the changes observed after excision of parietal cortex posterior to somatosensory cortex. We concluded that the changes were not specific to motor cortex excision. 5. These results support two major conclusions. 1) Median nerve SEPs recorded from sensorimotor cortex are produced by generators in two adjacent regions of somatosensory cortex: a tangentially oriented generator in area 3b, which produces P20-N30 (human) and P10-N20 (monkey) [recorded anterior to the central sulcus (CS)] and N20-P30 (human) and N10-P20 (monkey) posterior to the CS; and a radially oriented generator in area 1, which produces P25-N35 (human) and P12-N25 (monkey) recorded from the postcentral gyrus near the CS. 2) Motor cortex makes little or no contribution to these potentials.     

Somatosensory evoked potentials/fields--exploration of brain function

We have summarized the history of electroencephalography(EEG) since 1875, when a paper by Richard Caton was published describing the first EEG recordings in animals. Somatosensory evoked potentials (SEPs) were recorded by George Dawson in 1951. Thereafter, SEPs were developed for clinical use with other evoked potentials such as auditory evoked potentials(VEPs). To understand evoked potentials, related mechanism of induction of far-fields-potentials(FFP) following stimulation of the median nerve has been discussed. SEPs consisted of P9, N9, N10, P11, N11, N13, P13, P14, N18, N20 and P20/P22. Scalp recorded P9 FFP arises from the distal portion of the branchial plexus as reflected by N9 stationary negative potential recorded over the stimulated arm. Cervical N11 and N13 arise from the root entry zone and dorsal horn, respectively. Scalp recorded P13, P14 and N18 FFP originate from the brainstem. In this communication, magnetoencephalography(MEG) and results of one of our recent studies on somatosensory evoked fields(SEFs) are also discussed. One of the important features of MEG is that magnetic signals detected outside the head arise mainly from cortical currents tangential to the skull. Since the net postsynaptic current follows the orientation of cortical pyramidal cells, the MEG signals mainly reflect activity of the fissural cortex, whereas radial current may remain undetected. In our study, we demonstrated SEFs elicited by compression and decompression of a subject's glabrous skin by a human operator. Their dipoles were tangentially oriented from the frontal lobe to parietal lobe.     

Changes in somatosensory-evoked potentials and high-frequency oscillations after paired-associative stimulation

Paired-associative stimulation (PAS), combining electrical median nerve stimulation with transcranial magnetic stimulation (TMS) with a variable delay, causes long-term potentiation or depression (LTP/LTD)-like cortical plasticity. In the present study, we examined how PAS over the motor cortex affected a distant site, the somatosensory cortex. Furthermore, the influences of PAS on high-frequency oscillations (HFOs) were investigated to clarify the origin of HFOs. Interstimulus intervals between median nerve stimulation and TMS were 25 ms (PAS₂₅) and 10 ms (PAS₁₀). PAS was performed over the motor and somatosensory cortices. SEPs following median nerve stimulation were recorded before and after PAS. HFOs were isolated by 400–800 Hz band-pass filtering. PAS₂₅ over the motor cortex increased the N20–P25 and P25–N33 amplitudes and the HFOs significantly. The enhancement of the P25–N33 amplitude and the late HFOs lasted more than 60 min. After PAS₁₀ over the motor cortex, the N20–P25 and P25–N33 amplitudes decreased for 40 min, and the HFOs decreased for 60 min. Frontal SEPs were not affected after PAS over the motor cortex. PAS_25/10 over the somatosensory cortex did not affect SEPs and HFOs. PAS_25/10 over the motor cortex caused the LTP/LTD-like phenomena in a distant site, the somatosensory cortex. The PAS paradigms over the motor cortex can modify both the neural generators of SEPs and HFOs. HFOs may reflect the activation of GABAergic inhibitory interneurons regulating pyramidal neurons in the somatosensory cortex.     

Source analysis of median nerve and finger stimulated somatosensory evoked potentials: Multichannel simultaneous recording of electric and magnetic fields combined with 3d-MR tomography

Summary At the current state of technology, multichannel simultaneous recording of combined electric potentials and magnetic fields should constitute the most powerful tool for separation and localization of focal brain activity. We performed an explorative study of multichannel simultaneous electric SEPs and magnetically recorded SEFs. MEG only sees tangentially oriented sources, while EEG signals include the entire activity of the brain. These characteristics were found to be very useful in separating multiple sources with overlap of activity in time. The electrically recorded SEPs were adequately modelled by three equivalent dipoles located: (1) in the region of the brainstem, modelling the P14 peak at the scalp, (2) a tangentially oriented dipole, modelling the N20-P20 and N30-P30 peaks, and part of the P45, and (3) a radially oriented dipole, modelling the P22 peak and part of the P45, both located in the region of the somatosensory cortex. Magnetically recorded SEFs were adequately modelled by a single equivalent dipole, modelling the N20-P20 and N30-P30 peaks, located close to the posterior bank of the central sulcus, in area 3b (mean deviation: 3 mm). The tangential sources in the electrical data were located 6 mm on average from the area 3b. MEG and EEG was able to locate the sources of finger stimulated SEFs in accordance with the somatotopic arrangement along the central fissure. A combined analysis demonstrated that MEG can provide constraints to the orientation and location of sources and helps to stabilize the inverse solution in a multiple-source model of the EEG.     

兔水中毒时体感诱发电位

应用水负荷附加抗利尿激素,复制水中毒模型。当水负荷增加兔体重10%后,体感诱发电位(SEP)成份P7、N9、P12和N15峰值潜伏期随体重增加而逐渐延长。体重增加10%及15%时,P12和N15成份振幅均增大,但当增加体重15%以上时,两成份振幅减小或消失。水负荷后SEP峰间潜伏期的延长以P12—N15最显著。各种程度水负荷时,P7和N9的振幅均无显著变化。结果说明,水负荷增加体重10%后,可使神经元的传导发生延缓及皮层神经元兴奋性改变;不同程度的水负荷对神经元兴奋性的影响并不相同,此外水负荷对大脑皮层功能的影响较低位脑干严重。     

皮层运动诱发电位监测在脑中央区术中的应用

目的:探讨在全凭静脉麻醉下,使用皮层运动诱发电位(MEP)对脑中央区手术进行术中监测的方法。方法:使用皮层电极对12例中央区肿瘤患者进行诱发电位术中监测,在中央后回感觉皮层区相应部位记录皮层体感诱发电位(SEP)的N20-P25波,沿中央后回功能区皮层向前移动电极,直至记录到一个波型相反(位相倒置)、波幅相近的波型P20-N25,将其定为运动中枢刺激点。使用高频串刺激(TS)直接刺激该点,在上肢肌肉记录MEP。结果:12例患者均能成功地记录到MEP。术中注意保护此区,术后患者症状无明显加重,被监测的上肢肌力无明显减退。结论:对于脑中央区手术,在全凭静脉麻醉下找出运动中枢刺激点并作MEP监测(术中注意保护此区)是一种优良的术中监测手段。     

65例颈椎型脊髓病体感诱发电位分析

目的研究颈椎型脊髓病皮质体感诱发电位（ＳＥＰ）变化。方法对６５例颈椎型脊髓病患者和２６例正常人进行正中神经和胫后神经刺激的ＳＥＰ对照研究，并对１０例患者作治疗前后对照观察。结果本组异常率为４５％，主要表现为各波替伏期和波间期（Ｎ２０—Ｐ２５，Ｐ２５—Ｎ３５，Ｐ４０—Ｎ４５）延长，且下肢的延长更加明显，部分患者出现波形分化不良。经保守治疗后６例正常，２例好转，且ＳＥＰ的好转先于临床的改善。结论ＳＥＰ对评判颈椎型脊髓病的脊髓传导功能具有重要的意义，且有助于临床预后的评价。     

糖尿病患者的体感诱发电位

应用电子计算机迭加平均技术,记录了23名正常人和25例糖尿病患者的电刺激正中神经和胫后神经的体感诱发电位(somatosensory evoked potentials,SEPs)。结果发现,大部分患者均有SEPs成份峰值潜伏期的延长,以及正中神经和胫后神经传入纤维传导速度的减慢;部分患者有中枢传导时间(N13-N20传导时间和P40-N80传导时间)的延长。此外,外周神经三相电位的波形也出现异常变化。这些结果提示,糖尿病患者不仅可出现外周神经传导功能障碍,而且也可出现中枢神经传导功能异常。     

Mechanisms of differences in gating effects on short-and long-latency somatosensory evoked potentials relating to movement

We investigated the mechanisms underlying the differences in gating effects on short- and long-latency somatosensory evoked potentials (SEPs) relating to movement. SEPs were recorded in normal subjects for 6 different tasks in Experiment 1: Control, Movement, Distraction, Attention, Movement during Distraction and Movement during Attention, and for 4 different tasks in Experiment 2: Control, Passive Movement, Contralateral Movement and Movement Imagery. The amplitudes of short-latency SEPs were significantly reduced by active and passive movement of the stimulated hand, but long-latency SEPs (N140-P200) were significantly enhanced by active movement of the stimulated hand. Attention, Distraction, Contralateral Movement and Movement Imagery did not affect the amplitudes of SEPs. The degree of enhancement of long-latency SEPs by active Movement was greater than that by active movement with Attention or Distraction. Gating effects on long-latency SEPs were different from those on short-latency SEPs. Since this effect was not related to Attention/Distraction, Passive Movement, Movement Imagery or Movement of another site, it is probably due to specific centrifugal effects, which are different from more direct gating effects on short-latency components. This study showed the difference in gating effects on somatosensory perception depending on time periods following stimulation, which may indicate an interaction between motor and somatosensory cortex.     

Dipolar sources of the early scalp somatosensory evoked potentials to upper limb stimulation Effect of increasing stimulus rates

Brain electrical source analysis (BESA) of the scalp electroencephalographic activity is well adapted to distinguish neighbouring cerebral generators precisely. Therefore, we performed dipolar source modelling in scalp medium nerve somatosensory evoked potentials (SEPs) recorded at 1.5-Hz stimulation rate, where all the early components should be identifiable. We built a four-dipole model, which was issued from the grand average, and applied it also to recordings from single individuals. Our model included a dipole at the base of the skull and three other perirolandic dipoles. The first of the latter dipoles was tangentially oriented and was active at the same latencies as the N20/P20 potential and, with opposite polarity, the P24/N24 response. The second perirolandic dipole showed an initial peak of activity slightly earlier than that of the N20/P20 dipolar source and, later, it was active at the same latency as the central P22 potential. Lastly, the third perirolandic dipole exaplaining the fronto-central N30 potential scalp distribution was constantly more posterior than the first one. In order to evaluate the effect of an increasing repetition frequency on the activity of SEP dipolar sources, we applied the model built from 1.5-Hz SEPs to traces recorded at 3-Hz and 10-Hz repetition rates. We found that the 10-Hz stimulus frequency reduced selectively the later of the two activity phases of the first perirolandic dipole. The decrement in strength of this dipolar source can be explained if we assume that: (a) the later activity of the first perirolandic dipole can represent the inhibitory phase of a “primary response”; (b) two different clusters of cells generate the opposite activities of the tangential perirolandic dipole. An additional finding in our model was that two different perirolandic dipoles contribute to the centro-parietal N20 potential generation. Received: 5 August 1997 / Accepted: 26 November 1997     

Attenuation of somatosensory evoked potentials immediately following rapid reaction movement

We investigated the changes in the somatosensory evoked potentials (SEPs) and particularly which components of the SEPs altered immediately after rapid reaction movements. N20, P23, N35, and P45 components measured over the scalp were all attenuated except for the P45 component measured at CZ. Particularly, the N20 and P23 components were markedly attenuated at both C3' and CZ immediately following rapid reaction movements. N18 and N20 components are thought to represent thalamocortical and primary sensory cortex activities. Therefore, the present results suggest that following rapid reaction movements, the thalamocortical and primary sensory activities are significantly attenuated. Moreover, following rapid reaction movements, the onset of EMG activity preceded the afferent discharge of the muscle spindle. Therefore, it may be concluded that central factors were principally responsible for the attenuation of the SEPs immediately following rapid reaction movements.     

体感诱发电位和磁共振弥散加权成像在急性脑梗死中的应用研究

目的：探讨弥散加权成像（diffusion weighted imaging，DWI）和躯体感觉诱发电位（somatosensory evoked potentials，SEPs）在急性脑梗死患者早期诊断、评估预后中的应用价值。方法：对71例发病2小时～7天的急性脑梗死患者进行MRI／DWI和SEPs检查，并分析其变化。结果：71例患者中，70例出现了DWI高信号改变（证实为责任病灶），其阳性率明显高于常规MPI（P〈0．01）；46例出现SEPs异常，主要表现为N20、P25缺失，（N13-N20）IPL延长，并与神经功能受损程度及预后相关。结论：DWI结合SEPs检查，能够准确早期诊断脑梗死，并早期评估预后。     

Changes in muscle and cutaneous cerebral potentials during standing

Summary The cerebral potentials produced by electrical stimulation of mechanoreceptive afferents from the foot were recorded in the sitting and standing postures to determine whether transmission to cortex was altered by the postural change. The latencies of the early components of the cerebral potentials produced by muscle afferents (posterior tibial nerve) and cutaneous afferents (sural nerve) did not change with posture. Standing was associated with an approximately 25–35% decline in amplitude of the earliest components of the posterior tibial cerebral potential (N38-P40, P40-N50) for a stimulus intensity associated with a submaximal afferent volley. The amplitude of the equivalent N38-P40 and P40-N50 components produced by sural afferents also declined during quiet stance. In most experiments the subcortical component (P32-N38) was not reduced by stance so that the amplitude attenuation probably occurs in part at cortical level. Qualitatively similar changes in the cerebral potentials were documented for a range of stimulus intensities, including those which evoked a maximal initial component in the nerve volley. For a similar reduction in the initial (N38-P40) component of the cerebral potential, voluntary plantar flexion in the sitting position produced less attenuation in subsequent components than did standing. Thus, attenuation of the cerebral potential during standing may involve specific posture-related factors in addition to those related to volition.     

Modulation of somatosensory evoked potentials during wake-sleep states and spike-wave discharges in the rat

STUDY OBJECTIVE: To clarify the cortical evoked responses in the primary somatosensory cortex of the rat under states of waking, slow-wave sleep (SWS), paradoxical sleep (PS), and spike-wave discharges (SWDs), which are associated with absence seizure. DESIGN: Somatosensory evoked potentials (SEPs) in response to single- and paired-pulse stimulations under waking, SWS, PS, and SWDs were compared. SEPs to a single-pulse stimulus with regard to cortical spikes of sleep spindles and SWDs were also evaluated. PARTICIPANTS: Twenty Long Evans rats. INTERVENTIONS: Single- and paired-pulse innocuous electrical stimulations were applied to the tail of rats with chronically implanted electrodes in the primary somatosensory cortex and neck muscle under waking, SWS, PS, and SWDs. MEASUREMENTS AND RESULTS: SEPs displayed distinct patterns under waking/PS and SWS/SWDs. The short-latency P1-N1 wave of the SEP was severely impeded during SWDs but not in other states. Reduction of the P1-N1 magnitude to the second stimulus of the paired-pulse stimulus for interstimulus intervals of < or = 300 milliseconds appeared in waking and PS states, but the decrease occurred only at particular interstimulus intervals under SWS. Interestingly, augmentation was found under SWDs. Moreover, cyclic augmentation of the P1-N1 magnitude was associated with spindle spikes, but cyclic reduction was observed with SWD spikes. CONCLUSION: Changes in SEPs are not only behavior dependent, but also phase locked onto ongoing brain activity. Distinct short-term plasticity of SEPs during sleep spindles or SWDs may merit further studies for seizure control and tactile information processing.     

痉挛性斜颈体感诱发电位的研究

目的：探讨痉挛性斜颈患者大脑皮层功能的变化。方法：对30例痉挛性斜颈患者刺激正中神经后体感诱发电位（SEP）的P22、N30波潜伏期及P22、N30波幅进行比较分析,30例正常对照组仅在颈部主动向右侧扭转时对双侧P22、N30波幅进行比较分析。结果：病例组SEPP22、N30潜伏期正常,双侧比较差异无统计学意义,头部扭转方向的对侧大脑半球前中央区的P22-N30波幅比明显高于对侧,差异有统计学意义。正常对照组前中央区记录的双侧P22N30波幅比较差异无统计学意义。结论：SEP P22、N30潜伏期正常提示传导通路结构完整,头部扭转方向的对侧大脑半球前中央区的P22-N30波幅比明显高于对侧,提示患者对侧大脑皮层前中央区电活动存在异常的兴奋及抑制,即抑制性减弱,兴奋性增高,N30记录的是刺激正中神经SEP中长潜伏成分,可能来源于运动辅助区,进一步提示患者存在感觉一运动整合功能异常。     

Component-specific effects of physostigmine on the cat visual evoked potential

Pattern visual evoked potentials (VEPs) were recorded from the pial surface of the cat primary visual cortex prior to and following the intravenous administration of physostigmine, an agent which blocks the enzyme responsible for the breakdown of synaptically released acetylcholine. The control VEP was composed of a small initial positive deflection (P1), a subsequent large negative wave (N1) and a second large positive wave (P2). Following physostigmine, the amplitude of P1-N1 was diminished whereas that of N1-P2 increased. These effects were long lasting and were blocked by prior treatment with scopolamine, a result consistent with mediation by a muscarinic cholinergic pathway. Waveform subtraction revealed that the physostigmine-sensitive component had a slow, negative polarity waveform while the physostigmine-insensitive component was also slow, but positive in polarity. The fundamental nature of these components remains to be assessed. Nevertheless, the results indicate that waveforms of different polarity combine algebraically to yield the conventional VEP.     

Altered cortical integration of dual somatosensory input following the cessation of a 20 min period of repetitive muscle activity

The adult human central nervous system (CNS) retains its ability to reorganize itself in response to altered afferent input. Intracortical inhibition is thought to play an important role in central motor reorganization. However, the mechanisms responsible for altered cortical sensory maps remain more elusive. The aim of the current study was to investigate changes in the intrinsic inhibitory interactions within the somatosensory system subsequent to a period of repetitive contractions. To achieve this, the dual peripheral nerve stimulation somatosensory evoked potential (SEP) ratio technique was utilized in 14 subjects. SEPs were recorded following median and ulnar nerve stimulation at the wrist (1 ms square wave pulse, 2.47 Hz, 1× motor threshold). SEP ratios were calculated for the N9, N11, N13, P14–18, N20–P25 and P22–N30 peak complexes from SEP amplitudes obtained from simultaneous median and ulnar (MU) stimulation divided by the arithmetic sum of SEPs obtained from individual stimulation of the median (M) and ulnar (U) nerves. There was a significant increase in the MU/M + U ratio for both cortical SEP components following the 20 min repetitive contraction task, i.e. the N20–P25 complex, and the P22–N30 SEP complex. These cortical ratio changes appear to be due to a reduced ability to suppress the dual input, as there was also a significant increase in the amplitude of the MU recordings for the same two cortical SEP peaks (N20–P25 and P22–N30) following the typing task. No changes were observed following a control intervention. The N20 (S1) changes may reflect the mechanism responsible for altering the boundaries of cortical sensory maps, changing the way the CNS perceives and processes information from adjacent body parts. The N30 changes may be related to the intracortical inhibitory changes shown previously with both single and paired pulse TMS. These findings may have implications for understanding the role of the cortex in the initiation of overuse injuries.