The effect of changing stimulus intensities on median nerve somatosensory-evoked potentials

We investigated median nerve somatosensory-evoked potentials (SEP) in 31 healthy volunteers to test the hypothesis that 1) increasing stimulus intensity influences SEP components in both amplitude and latency 2) SEP components respond differently to changing intensities. Cluster analysis and analysis of variance were used for statistical testing. Three groups of components could be found according to latency changes in response to increasing stimulus intensities: N13, and P15, the primary cortical response (N19, P22) and the components over 30 ms. In general, SEP components below 30 ms significantly shortened in latency and increased in amplitude with subsequent saturation. In contrast, in components over 30 ms latencies decreased linearly and amplitudes changed inhomogeneously. The clear effect of stimulus intensity on most median nerve SEP components makes it necessary to maintain comparable stimulus intensities when comparing intra- and interindividual registrations.     

A thalamic component of the cervical evoked potential in man

Somatosensory evoked potentials (SEPs) were recorded simultaneously from scalp and neck locations following median nerve stimulation. By subtracting the latency of the major negative peak of the cervical SEP (N13) from that of the primary cortical response (N20), the central somatosensory conduction time was calculated (5.9 ms). On the descending slope of the cervical SEP was superimposed a positive potential of probable thalamic origin (P17). By subtracting the latency of N13 from that of P17 and P17 from that of N20 respectively, the transit time for the afferent volley both within the brainstem (3.9 ms) and the thalamo-cortical radiation (2.0 ms) was obtained.     

Reconsiderations about the abnormalities of somatosensory evoked potentials in motor neuron disease

The frequency of involvement of sensory pathways in motor neuron disease (MND) remains the matter of controversy. For this reason the purpose of the present work was to test how often sensory system involvement might be detected by somatosensory evoked potentials (SEP) studies and then to verify the presence of alteration of the sensory conduction and to detect the frequency of abnormalities of somatosensory peripheral, spinal, subcortical and cortical potentials in MND. SEP were tested after median nerve stimulation at the wrist, recorded from Erb's point, Ce2, Ce7 and scalp. Pearson's correlation coefficients test and Wilcoxon rank-sum test were used for statistical analysis. 74 patients (22 women and 52 men) were examined. Mean age of patients was 54.07 +/- 11.24 years; mean duration of the disease -19.25 +/- 15.87 months. SEP were abnormal in 39 of 74 patients (about 53%) whereas the sensory NCV in median nerve was abnormal in 14 of 74 patients (19%). The most frequent pattern of abnormalities consisted of the absence or delay of cortical responses. The mean values of SEP latencies (N9, N11, N13, N20 and P25) were significantly increased in MND patients (p < 0.05) as compared with controls. The N9 and N11 latencies correlated with the duration of the disease. The results of our study (concerning a large group of MND patients) suggest that the involvement of sensory pathways is not rare in MND.     

Median nerve somatosensory evoked potentials: recording with cephalic and noncephalic references

We performed both cephalic and noncephalic reference SEP recordings with median nerve stimulation in normals and compared the results obtained from both recordings. Median nerve SEP with non cephalic reference revealed four positive and three negative potentials on scalp, while median nerve SEP with cephalic reference showed only one negative potential on scalp. We conclude that potentials originated from subcortical regions can be recorded from scalp by using noncephalic reference, which is not possible by cephalic reference and potential N20 obtained from somatosensory cortex by using cephalic reference does not present a single potential, consisting of combination of a few potentials. To differentiate these potentials, noncephalic reference must be used.     

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.     

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。     

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.     

Proprioceptive sensory function in Parkinson's disease and Huntington's disease: evidence from proprioception-related EEG potentials

In both Parkinson's disease and Huntington's disease, proprioceptive sensory deficits have been suggested to contribute to the motor manifestations of the disease. Here, proprioceptive sensory function was investigated in Parkinson's disease patients, Huntington's disease patients, and healthy control subjects (each group n=8), using proprioception-related evoked potentials. Proprioception-related potentials were elicited by passive index finger movements and measured with high-density EEG. Conventional median nerve somatosensory evoked potentials (mnSEPs) were recorded in the same session. Analysis included amplitude and latency measures from selected scalp electrodes and dipole source reconstruction. We found a proprioception-related N90 component of normal latency in both Parkinson's disease and Huntington's disease. The source strength of the underlying cortical generator was normal in Parkinson's disease, but marginally reduced in Huntington's disease. Using the source location of the N20–P20 component of the mnSEP as a landmark for postcentral area 3b, the N90 was localized to the precentral motor cortex. At a latency around 170–180 ms proprioception-related potentials were explained by bilateral sensory cortex activation with an altered distribution in Parkinson's disease and a reduction of ipsilateral activation in Huntington's disease. Together, the results show largely normal early proprioception-related potentials, but changes in the cortical processing of kinaesthetic signals at longer latencies in both diseases. Electronic Publication     

Activation of respiratory afferents by resistive loaded breathing modifies somatosensory evoked potentials to median nerve stimulation in humans

The cortical projections of respiratory afferents (vagus and respiratory muscle nerves) are well documented in humans. It is also shown that their activation during loaded breathing modifies the perception of tactile sensation as well as the motor drive to skeletal muscles. The effects of expiratory or inspiratory loaded breathing on somatosensory evoked potentials (SEPs) elicited by median nerve stimulation were studied in eight healthy subjects. No significant changes occurred in latencies of N20, N30 and P40 throughout the expiratory loading period, except for a significant lengthening in P1 latency compared with unloaded breathing. However, inspiratory loading induced a significant increase in peak latency of N20, N30 and P40 components. We suggest that projections of inspiratory afferents from the diaphragm and the intercostal muscles, activated by inspiratory loading, could be responsible for the lengthened latency of median nerve SEP components. Thus, respiratory afferents very likely interact with pathways of the somatosensory system.     

Changes in P300 latency and amplitude in schizophrenic patients and healthy controls during the examination.

In 30 schizophrenic patients (sixteen of the paranoid subtype, 14 of the nonparanoid) and healthy controls (n = 30) event-related potentials were obtained with a somatosensory reaction-time (RT) version of the "oddball paradigm" by stimulating the right (first run) and the left (second run) median nerve. Variations of P300 amplitude and latency and of RT within the average (30 trials) were studied by fractionating off-line the original averages in three subaverages. After stimulation of the right median nerve oscillations on P300 amplitude and latency were observed. After stimulation of the left median nerve there was a trend toward a decrease of the P300 amplitude that reached significance at the electrode P3 for patients (p = 0.014) and at the electrode P4 for controls (p = 0.025). The P300 latency showed variations for patients and controls. The mean-RT was prolonged across the subaverages only for schizophrenics, reaching significance after stimulation of the right median nerve. Paranoid and nonparanoid schizophrenic patients showed similar results on P300 and RT parameters across the subaverages. These results are discussed in terms of the influence of motivation and task involvement on the P300 amplitude. These could be unspecific factors that account for the habituation of the P300 along the examination.     

Interference of vibrations with input transmission in dorsal horn and cuneate nucleus in man: a study of somatosensory evoked potentials (SEPs) to electrical stimulation of median nerve and fingers

Summary The effects of 50 Hz palm vibrations on somatosensory potentials (SEPs) evoked by electrical stimulation of the median nerve at the wrist and of the 2nd and 3rd fingers were studied in 10 normal subjects. Vibrations were found to produce attenuation of the N13 spinal and P14 brainstem potentials and of the N20 contralateral parietal response. Brachial plexus (N9, P9) and dorsal column (P11) responses were not modified by vibrations. These SEP findings show: 1) that vibrations do not interfere at the periphery with the processing of brief ascending volleys triggered by an electrical stimulus and 2) that such an interference does occur in spinal dorsal horn and cuneate nucleus. Reduced input transmission in the cuneate nucleus is likely to be responsible for perceptual alterations induced by vibrations.     

Planar vector projection of short-latency median nerve somatosensory evoked potentials

A planar vector projection of short-latency somatosensory evoked potentials (SEP) following stimulation of the median nerve was obtained by recording SEP over Fpz-Oz and T3-T4 and plotting the amplitudes on both channels at corresponding time points against each other. The resulting curve showed three successive loops pointing ipsilateral occipital (N1), contralateral occipital (N2) and ipsilateral frontal (N3) to the stimulated side. Normal values for latency, amplitude and direction of these loops were obtained from 10 normal adults. N1 can be attributed to the cuneate nucleus and medial lemniscus, N2 to the primary somatosensory cortex and N3 to the frontal cortex.     

Sensory nerve somatosensory evoked potentials (SEP) in the evaluation of patients with sciatica: false P1 latency prolongation may be due to admixture of dermatomal SEP.

Patient-reported stimulus-related radiating sensory symptoms within the territory of the stimulated nerve have been used to verify stimulation in sensory nerve scalp recorded somatosensory evoked potentials (SEP). The main aim of the present study of false positive P1 latency prolongation in lumbosacral sensory nerve SEP was to investigate whether elicitation of such symptoms secures adequate sensory nerve stimulation. Nerve roots were studied on the asymptomatic side in 64 patients with unilateral sciatica. Saphenous (L4), superficial peroneal (L5), and sural (S1) nerve SEP were registered in all patients. Pretibial dermatomal SEP were registered in ten of them. Stimulation was equidistant from the registration electrode in all SEP registrations. The false positive rate was lower in saphenous nerve SEP with than without verified supramaximal stimulation (1/30 vs. 6/22, P = 0.03) in spite of radiating stimulus-related sensory symptoms in both groups. This difference was not caused by subclinical myelographic nerve root compression or general peripheral nerve dysfunction. The P1 latency was longer in the pretibial dermatomal SEP than in the saphenous and superficial peroneal nerve SEP with the same conduction distance (mean difference 4.7 (95% CI = 3.8 to 5.6) and 4.4 ms (95% CI = 3.4 to 5.4), respectively). It is concluded that dermatomal SEP have longer P1 latency than sensory nerve SEP. Verified supramaximal nerve simulation is recommended to avoid false results due to admixture of dermatomal to sensory nerve SEP.     

帕金森病患者正中神经和胫神经体感诱发电位研究

目的:同时观察帕金森病患者正中神经和胫神经体感诱发电位的异常并推测其发生机制。方法:选择30名帕金森病患者和20名健康对照者,刺激正中神经,记录顶叶体感诱发电位的N20、P25、N30波,额叶的P20、N30波的潜伏期和波幅。刺激胫神经,记录顶叶体感诱发电位的P40、N50、P60波的潜伏期和波幅。结果:帕金森病患者上肢额叶N30和下肢N50波幅明显降低(P<0·05)。结论:帕金森病患者上下肢SEP同时出现异常是黑质纹状体系统多巴胺缺乏的结果,下肢N50波幅比上肢N30与临床症状的严重性更有相关性。     

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.     

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。     

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.     

Observations of the posterior tibial nerve SEP of patients requiring extradural spinal surgery

The cortical potentials evoked by posterior tibial nerve stimulation were examined in a series of 141 hospital patients requiring extradural spinal surgery. One hundred and five patients were neurologically intact, while in 36 some deficit was present. In the intact subjects, the absolute latencies of the main medium-latency peaks (N30, P40, N50, P60) were found to vary with height and age. There were no additional gender-related differences. The latencies of the deficit group were longer than those of the intact group but only marginally useful as a clinical discriminator; their amplitudes were not significantly lower than those of the intact group. A model for variations in SEP latency is suggested.     

Cerebral Dynamics of SEPs to Non-Painful and Painful Cutaneous Electrical Stimulation of the Thenar and Hypothenar

Early, middle and late latency somatosensory evoked potentials (SEPs) elicited by cutaneous electrical stimulation (painful vs. non-painful) of right and left hands were recorded. The aims were to study (1) if lifelong use of dominant right hand would result in different SEP topographies compared to non-dominant left hand stimulation, (2) if painful and non-painful stimuli resulted in different SEP activation patterns for the different latency components and (3) if these results were consistent between two areas of the hand. Electrical stimuli were applied cutaneously above the thenar and hypothenar muscles of the left and right hand. A two-way repeated measures ANOVA was used to test the effects of laterality and intensity for a given peak amplitude and latency. Statistical results yielded no significant difference in peak amplitude for either thenar and hypothenar between the two hands. In contrast, a significant difference in amplitude was observed for 6 components for each stimulus location when the two intensities were compared. These components were found at early, middle and late latencies. No significant latency shift was observed between the two hands. Only the P30 component showed a significant latency shift for both locations with the painful condition having the shorter latency. Thus, life-long use of the dominant hand does not generate detectable changes in cortical evoked activity to sensory input from the skin above thenar and hypothenar muscles. Several SEP components across the time course (0-400 ms) showed increased amplitude when the stimulus was increased from non-painful to painful intensity.     

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.