Stationary potentials after median nerve stimulation: changes with arm position

We previously reported the presence of stationary negative potentials (N3, N6, N9) over the arm ipsilateral to the side of median nerve stimulation. In this study, we examined the effect of different arm positions upon these stationary peaks in 12 normal subjects. When arm position was changed from elbow extended to elbow flexed 90°, we recorded a new negative peak, N4. The peak latency of N4 corresponded to the traveling impulse reaching the distal biceps brachii. With the elbow flexed, N3, N6 and N9 peak latencies significantly shortened compared to those recorded with the arm in the usual elbow extended position. In contrast, with the arm abducted at the shoulder, N6 and N9 latencies were significantly prolonged while N3 remained unchanged. Corresponding latency shifts were also observed in the bipolarly recorded traveling impulse.We consider 2 possible factors for N4 enhancement by elbow flexion. One is the change in conducting volume surrounding the nerve, i.e., increased muscle bulk of biceps brachii. The other is the change in axial orientation of the propagating nerve impulse by 90°. We also propose that the latency shifts of the stationary potential as well as of a travelling wave can be attributed primarily to relaxation or stretching of the nerve trunk with change in arm position.     

Glossopharyngeal evoked potentials in normal subjects following mechanical stimulation of the anterior faucial pillar

The anterior faucial pillar, which is innervated by the glossopharyngeal nerve, is thought to be important in eliciting the pharyngeal swallow in awake humans. Glossopharyngeal evoked potentials (GPEP), elicited by mechanically stimulating this structure, were recorded from 30 normal adults using standard averaging techniques and a recording montage of 16 scalp electrodes. Ten of the subjects experienced a desire to swallow in response to stimulation. Repeatable responses were recorded from all 30 subjects. The GPEPs recorded from the posterior scalp were W-shaped and consisted of P1, N1, P2, N2 and P3 peaks. Mean latencies of P1, N1 and P2 were 11, 16 and 22 msec, respectively, for both left and right pillar stimulation. In contrast, latencies of N2 and P3 varied significantly between left and right pillar stimulation. Mean latencies of N2 and P3 were 27 and 34 msec for left, and 29 and 35 msec for right pillar stimulation. Topographical maps acquired at peak latencies for P1, N1 and P2 revealed consistent asymmetrical voltage distributions between the two hemispheres; the largest responses were recorded from the hemisphere ipsilateral to the side of stimulation. The scalp topography of N2 and P3 varied between male and female subjects as well as between left and right pillar stimulation. These findings support the hypothesis that mechanical stimulation to the anterior faucial pillar alone can elicit repeatable responses from the central nervous system. The integration of this subcortical/cortical activity with that of the medullary swallowing center may play an important role in eliciting the pharyngeal swallow.     

Scalp topography and distribution of cortical somatosensory evoked potentials to median nerve stimulation

Topographies and distributions of cortical SEPs to median nerve stimulation were studied in 8 normal adults and 5 neurological patients. SEPs recorded from C4, P4, Pz, T6-A1A2 derivations to left median nerve stimulation were composed of 2 early negative (N16, N20) and 2 positive components (P12, P23), whereas those recorded from frontal electrodes (Fz, Fp1, Fp2) disclosed 2 early negativities (N16, N24) and 2 early positivities (P12, P20). N20 and P20, and P23 and N24, reversed across the rolandic fissure with no significant difference in their peak latencies. P23 was of slightly shorter latency at C4 than at more posterior electrodes (P4, T6, Pz).In 3 patients with complete hemiplegia but normal sensation, all the early SEP components were normal in scalp distribution and peak latencies except for a decrease of N24 amplitude. In 2 patients with complete hemiplegia and sensory loss no early cortical SEPs were seen. These findings suggest that N20 and P20 are generated as a single horizontal dipole in the central fissure, whereas P23 and N24 are a reflection of multiple generators in pre- and postrolandic regions.     

Comparison in man of short latency averaged evoked potentials recorded in thalamic and scalp hand zones of representation

Recordings were performed in the thalamus of 13 patients suffering from either abnormal movements or intractable pain, with the aim of delimiting the region to be destroyed or stimulated in order to diminish the syndrome. In 11 of these patients averaged evoked potentials were recorded simultaneously from the scalp and specific thalamus (VP) hand area levels following median nerve stimulation. These recordings were done during the operation or afterwards when an electrode was left in place for a program of stimulation.The latencies of onsets and peaks on the scalp ‘P15’ were compared with those of the VP wave; a clear correspondence was found. Moreover, when increased stimulation was used, both waves began to develop in parallel. Thus in the contralateral ‘P15’ a component exists due to the field produced by the thalamic response. To explain the presence of an ipsilateral scalp ‘P15’ wave, we propose that a second wave having the same latency and a slightly shorter peak exists on the scalp due to a field produced by a brain-stem response. This double origin of ‘P15’ is also shown by the different changes which the ipsilateral and contralateral waves present during changes in alertness.The scalp ‘N18–N20’ is also composed of at least 2 components. The first peak appears on the scalp with a latency shorter than that of the negativity which develops in the thalamus. The N wave, moreover, increases in latency with rapid stimulus repetition. We propose with others that ‘N18’ is a cortical event reflecting the arrival of the thalamo-cortical volley. The second component, ‘N20,’ has a peak latency closely correlated to that of the thalamic negativity. This component was present alone in ‘N’ when rapid stimulation (> 4/sec) was used, which did not change the thalamic response. It must be a field produced by the thalamic negativity.     

Detailed analysis of the latencies of median nerve somatosensory evoked potential components, 2: analysis of subcomponents of the P13/14 and N20 potentials

Detailed analysis of P13/14 and N20 wavelets was performed for 62 normal subjects and patients with various lesions along the somatosensory pathway. A histogram of the latencies of all the identified P13/14 wavelets (measured from P13/14 onset) demonstrated three latency-groups, which were named P13, P14a and P14b subcomponents. The relationship between the three newly identified subcomponents and the conventional naming of P13 and P14 was inconstant, indicating the ambiguity of the latter. P14b was most prominent in the contralateral central region, and therefore a P15 positivity slightly after P14b was often recorded in the CPc-Fz and CPc-CPi leads (CPc and CPi are centroparietal electrodes contralateral and ipsilateral to the stimulation). P14b/P15 was lost even in patients with cortical lesions, and thalamocortical fibers were assumed for its origin. The CPc-Fz and CPi-Fz leads registered a low negativity named broad N13', suggesting frontal predominance of the overall P13/14 complex. Both P13 and P14a were identified in a patient with a pontine lesion, and a caudal brainstem origin for both was suspected due to the onset of two repetitive bursts of the ascending lemniscal volley. We refuted the presynaptic origin of the scalp P13 potential and pointed out that a prolonged and/or polyphasic P11 frequently observed in patients with high cervical lesions can be mistaken as scalp P13. A histogram of the latencies of all the identified negative wavelets of N20 in the CPc-Fz lead (measured from N20 onset) revealed five definite latency-groups, which were named N20a, N20b, N20c, N20d and N20e subcomponents. The highest peak of N20 actually corresponded to either N20b, N20c or N20d, and this uncertainty, which must be related to intracortical processes, resulted in a large instability of the N20 peak latency as well as the age and sex dependence of the N20 onset-peak interval, both of which were demonstrated by our preceding study (Sonoo, M., Kobayashi, M., Genba-Shimizu, K., Mannen, T. and Shimizu, T. Detailed analysis of the latencies of median nerve SEP components, 1: selection of the best standard parameters and the establishment of the normal values. Electroenceph. clin. Neurophysiol., 1996b, 100: 319–331). Negative subcomponents in the CPc-NC lead and positive subcomponents in the Fz-NC lead constituted mirror images of each other, which suggested that these subcomponents were generated within area 3b.     

Effect of sleep stage on somatosensory evoked potentials by median nerve stimulation

The effects of sleep stage on early cortical somatosensory evoked potentials (SEPs) and short-latency components elicited by median nerve stimulation were studied in 12 normal volunteers. The latency of P13 in the awake stage was not significantly different from that in any sleep stage. The latencies of N16, N20 and P20 were significantly prolonged while the amplitude of N20 was decreased during the non-rapid eye movement (NREM) sleep stage. P22, P23 and N24 components showed double peaks (P23a, P23b, N24a, N24b) during the NREM sleep stage in 6 subjects, while N24 showed a single peak and only P22 and P23 showed double peaks in 5 other subjects. The latencies and morphologies of SEPs during rapid eye movement sleep stage were almost the same as those during the awake stage. These findings suggest that NREM sleep affects the latency, amplitude and morphology of N16 and early cortical components.     

Short-latency somatosensory evoked potentials following median nerve stimulation in Down's syndrome

Short-latency somatosensory evoked potentials (SEPs) following median nerve stimulation were recorded in 42 patients with Down's syndrome and in 42 age- and sex-matched normal subjects. There were no significant differences between the 2 groups in the absolute peak latencies of N9, N11 and N13 components. However, interpeak latencies, N9-N11, N11-N13 and N9-N13, were prolonged significantly in Down's syndrome. These findings suggest impaired impulse conduction in the proximal part of the brachial plexus, posterior roots and/or posterior column-medial lemniscal pathway. Interpeak latency N13-N20, representing conduction time from cervical cord to sensory cortex, was not significantly different between the 2 groups. Cortical potentials N20 and P25 in the parietal area and P20 and N25 in the frontal area were of significantly larger amplitude in Down's syndrome. P25 had double peaks in 16 of 42 normal subjects, but these were not apparent in any of the patients.     

Topographic analyses of somatosensory evoked potentials following stimulation of tibial,sural and lateral femoral cutaneous nerves

Using topographic maps, we studied the scalp field distribution of somatosensory evoked potentials (SEPs) in response to the stimulation of the tibial (TN), sural (SN) and lateral femoral cutaneous (LFCN) nerves in 24 normal volunteers. Cortical peaks, i.e., N35, P40, N50 and P60 were generally dominant in the contralateral hemisphere for the LFCN-SEP, whereas all peaks except N35 had dominance in the ipsilateral hemisphere for TN- and SN-SEPs. The findings imply that ipsilateral or contralateral peak dominance for the lower extremity SEP is determined by where the cortical leg representation occurs. As a result, mesial hemisphere representation results in peak dominance projected to the hemisphere ipsilateral to stimulation. Representations at the superior lip of the interhemispheric fissure or lateral convexity lead to midline or contralateral peak dominance. These findings also suggest that the paradoxically lateralized P40 is not the result of a positive field dipole shadow generated by the primary negative wave in the mesial hemisphere, but is the primary positive wave, analogous to P26 of the median nerve SEP. Accordingly, contralaterally dominant N35 is likely equivalent to the first cortical potential of N20 in the median nerve SEP. The difference in vector directions of potential fields between N35 and P40 may account for the opposite hemispheric dominance for these peaks in TN- and SN-SEPs.     

Median nerve somatosensory evoked potentials in profound hypothermia for ascending aorta repair

Median nerve somatosensory evoked potentials (SEPs) were recorded in 9 patients undergoing profound hypothermia for surgical repair of the aortic arch. In addition to the known increase in peak latencies, hypothermia gave rise to the appearance of peaks (‘P13,’ ‘N14’) inconsistently recognized at normothermia; moreover, profound hypothermia is associated with the disappearance of cortical activities around 20°, of subcortical waves at lower temperatures. The practical implications of the results are 3-fold: firstly, they suggest that the ‘P13’ and P14 should both be intracranially generated, at a pre- and postsynaptic level with respect to the cuneate nucleus, respectively; secondly, they show that some discrepancies between previous papers dealing with SEPs and hypothermia can be explained by differences in the choice of the reference; thirdly, they bring some suggestions on a better use of SEPs to monitor patients undergoing aortic arch surgery.     

Temporal correspondence of intracranial,cochlear and scalp-recorded human auditory nerve action potentials

Conventional, vertex-ipsilateral ear records (‘A’), as well as 3-channel Lissajous' trajectories (3-CLTs) of auditory brain-stem evoked potentials (ABEPs) were recorded from the scalp simultaneously with tympanic membrane electrocochleograms (‘TME’) and auditory nerve compound action potentials (‘8-AP’) recorded intracranially using a wick electrode on the auditory nerve between the internal auditory meatus and the brain-stem. The recordings were made during surgical procedures exposing the auditory nerve.The peak latency recorded from ‘TME’ corresponded to trajectory amplitude peak ‘a’ of 3-LLT and to peak ‘I’ of the ‘A’ channel ABEP. Peak latency of ‘8-AP’ was slightly longer than the latency of peak ‘II’ of ‘A’ when ‘8-AP’ was recorded from the root entry zone and the same or shorter when recorded from the nerve trunk. ‘8-AP’ peak latency was shorter than trajectory amplitude peak ‘b’ of 3-CLT regardless of where the wick electrode was along the nerve. Peak latencies from all recordings sites clustered into two distinct groups—those that included N1 from ‘TME’, peak ‘I’ of the ‘A’ record and trajectory amplitude peak ‘a’ of 3-CLT, and those that included the negative peak of ‘8-AP’ and trajectory amplitude peak ‘b’ of 3-CLT, as well as peak ‘II’ of the ‘A’ record, when present. In one case, the latency of peak ‘II’ and trajectory amplitude peak ‘b’ was manipulated by changing the conductive properties of the medium surrounding the auditory nerve.These results are consistent with other evidence proposing: (1) the most distal (cochlear) portion of the auditory nerve is the generator of the first ABEP component (‘I’, ‘a’); (2) the proximal auditory nerve is the major contributor to the ‘A’ channel ABEP component ‘II’; (3) in addition to the auditory nerve, more central structures participate in the generation of the 3-CLT ‘b’ component.     

Determination of conduction times of the peripheral and central parts of the sensory pathway using evoked somatosensory potentials

Determination of conduction times of the peripheral and central parts of the sensory pathway using evoked somatosensory potentials. Acta physiol. pol., 1985, 36 (3): 216-223. Simultaneous recording of the somatosensory evoked potentials (SEP) from Erb's point, neck and scalp allows investigation of the peripheral and central conduction times. The early components of the SEP produced by stimulation of the median nerve at the wrist were recorded using standardized electrode locations in 15 normal subjects. The difference of the latencies between the first peak of the cortical response (N20) and the peak of the neck response (N14) reflects, probably, the conduction time between the dorsal column nuclei and the cortex. Its value was 6 +/- 0.7 msec. The conduction time difference (between peak Erb's point response (N9) and N14) was 5.5 +/- 0.5 msec and it reflected the peripheral conduction time. For diagnostic application the lower limit of the response amplitudes was determined also for every component.     

The development of the somatosensory evoked potential in the unanaesthetized fetal sheep

Somatosensory evoked potentials were recorded in utero from 13 chronically instrumented fetal lambs (97 to 148 days of gestation) following electrical stimulation of the upper lip or upper limb. Several clear and reproducible peaks were observed. Following upper lip stimulation, peaks were seen with mean peak latencies of 9, 13.2, 17.8, 21.3, 33.8 and 206 ms at a gestational age of 125 days. Similar peaks, but of slightly later mean latencies, were seen following limb stimulation. These peaks demonstrated significant gestational age related falls in peak latencies (P less than 0.05). Several of the mid to late latency peaks, notably those occurring at 21.3, 33.8 and 206 ms, demonstrated changes (P less than 0.05) in both latency (longer in low voltage) and amplitude (reduced in low voltage) dependent on electrocorticographic state. Rate of stimulus presentation also had a significant effect on both amplitude and latency of several peaks (P less than 0.05) with this effect lessening with advancing gestational age. Evoked potentials can thus be successfully obtained from chronically instrumented fetal lambs and provide a useful indice for studies of neural maturation.     

Maps of somatosensory evoked potentials (SEPs) to mechanical (tapping) stimuli: comparison with P14, N20, P22, N30 of electrically elicited SEPs

Bit mapped color imaging of SEPs was recorded from 19 derivations in 11 healthy volunteers after electrical stimulation of the median nerve at the wrist, index finger digital nerve stimulation, and mechanical stimulation of the index fingertips by an electromechanically driven vibrating thin metallic plate. The latencies of SEP components increased for the various stimulation modalities, being shortestafter median nerve stimulation at the wrist and longest after mechanical stimulation of the index fingertips.The scalp distribution of SEPs to mechanical stimuli was, however, the same as other SEPs, independently of the stimulation employed, and components corresponding to N20 and P22 were recorded only contralaterally to the stimulated side.     

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.     

Comparison of scalp distribution of short latency somatosensory evoked potentials (SSEPs) to stimulation of different nerves in the lower extremity

SSEPs to stimulation of the CPN at the knee and PTN, PN and SN at the ankle were recorded from 15 cephalic sites and compared in 8 normal subjects. The configuration, amplitude, peak latency and distribution of P27, N35 (CPN) and P37, N45 (PTN, PN and SN) were analyzed. The configuration and distribution of SSEPs to stimulation of the 3 nerves at the ankle were similar across subjects. Both P37 and N45 were greatest in amplitude at the vertex and at recording sites ipsilateral to the side of stimulation. At contralateral sites either negative (N37) or negative, positive, negative potentials were recorded. The peak latency of N37 was the same or slightly less than that of P37. CPN-SSEPs were lower in amplitude and their configuration and scalp distribution showed much greater intersubject variability. This suggests that complex mechanisms which variably interact with one another are reflected in scalp SSEPs to CPN stimulation at the knee. The larger amplitude plus the minimal intersubject variability in morphology and topography of PTN-SSEPs indicate that this nerve is the most suitable for routine clinical use.     

Somatosensory evoked potentials recorded from the posterior pharynx to stimulation of the median nerve and cauda equina

Somatosensory evoked potentials (ppSEPs) in response to stimulation of the median nerve at the wrist and the cauda equina at the epidural space (the L4 level) were recorded from the posterior wall of the pharynx in 15 patients who underwent spinal surgery under general anesthesia, using disc electrodes attached to the endotracheal tube, and compared with segmental spinal cord potentials (seg-SCPs) that were recorded simultaneously from the posterior epidural space (PES). ppSEPs consisted of the initially positive spike (P9) followed by slow positive (P13) and negative (N22) waves. The P13 and N22 of ppSEPs had phase reversal relationship with the P2 and N2 recorded from the PES, respectively. The peak latencies of P9 (9.40 ± 0.7 ms) (mean ± SD), P13 (13.1 ± 0.9 ms), and N22 (22.0 ± 2.1 ms) of ppSEPs coincided with those of P1, N1 and P2 of seg-SCPs, respectively. ppSEPs were recorded more clearly with a reference electrode on the dorsal surface of the neck than with the reference electrode at the earlobe or back of the hand. The threshold and maximal stimulus intensities were also similar between the ppSEPs and seg-SCPs. Thus, the P9, P13, and N22 components of ppSEPs were thought to have the same origin as the P1, N1 and P2 of seg-SCPs, respectively. Therefore, the P9, P13 and N22 of ppSEPs may reflect incoming volleys through the root, synchronized activities of the interneurons and primary afferent depolarizations (PAD), respectively. ppSEPs in response to cauda equina stimulation showed that the latencies of the two initial components (4.6 ± 0.4 and 6.4 ± 0.6 ms) corresponded to those of the SCPs recorded from the PES (4.6 ± 0.3 and 6.3 ± 0.5 ms), suggesting that these potentials reflect impulses conducting through the spinal cord, similar to epidurally recorded SCPs.     

Scalp-recorded oscillatory potentials evoked by transient pattern-reversal visual stimulation in man

Replicable oscillatory potentials, time-locked to pattern stimuli (9.0° central; counterphase reversal at 2.13 Hz) were dissociated from conventional, broad-band VEPs recorded in healthy volunteers at occipital scalp locations by high-pass digital filtering at 17.0–20.0 Hz. Nine consecutive wavelets were identified with a 56.4 ± 8.4 msec mean latency of the first replicable wavelet and mean peak-to-peak amplitude varying between 0.9 and 2.0 μV. The first 2 wavelets had significantly shorter latencies than wave N70 of unfiltered VEP, whereas the last 2 wavelets had longer latencies than N145. Latency and amplitude values varied as a function of contrast and spatial frequency of the stimulus, with shorter latencies and larger amplitudes at 60–90% contrast level and tuning of amplitude at 5.0 c/deg. All wavelets were correlated with wave P100 of unfiltered VEP, while a correlation with N70 of VEP was observed only for those wavelets with latencies in the range of wave P100. Two patients with documented brain lesions involving the visual system are described as examples of oscillatory responses occurring irrespective of filter bandpass and instead of the expected conventional VEP when the generation of these is interfered with by brain pathology. A substantial cortical contribution to the origin of the oscillatory response is conceivable. It is suggested that the oscillatory response to pattern-reversal stimulation reflects events in the visual system that are parallel to, and partly independent of, the conventional VEP, with potential application in research or for clinical purposes.     

Topography of somatosensory evoked potentials to median nerve stimulation in patients with cerebral lesions

Scalp distributions and topographies of early cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were studied in 22 patients with 5 different types of cerebral lesion due to cerebrovascular disease or tumor (thalamic, postcentral subcortical, precentral subcortical, diffuse subcortical and parieto-occipital lesions) in order to investigate the origins of frontal (P20, N24) and central-parietal SEPs (N20, P22, P23).In 2 patients with thalamic syndrome, N16 was delayed in latency and N20/P20 were not recorded. No early SEP except for N16 was recorded in 2 patients with pure hemisensory loss due to postcentral subcortical lesion. In all 11 patients with pure hemiparesis or hemiplegia due to precentral subcortical lesion N20/P20 and P22, P23/N24 components were of normal peak latencies. The amplitude of N24 was significantly decreased in all 3 patients with complete hemiplegia. These findings support the hypothesis that N20/P20 are generated as a horizontal dipole in the central sulcus (3b), whereas P23/N24 are a reflection of multiple generators in pre- and post-rolandic fissures. P22 was very localized in the central area contralateral to the stimulation.Topographical studies of early cortical SEPs are useful for detecting each component in abnormal SEPs     

Direct recording of somatosensory evoked potentials in the vicinity of the dorsal column nuclei in man: their generator mechanisms and contribution to the scalp far-field potentials

Somatosensory evoked potentials (SEPs) in the vicinity of the dorsal column nuclei in response to electrical stimulation of the median nerve (MN) and posterior tibial nerve (PTN) were studied by analyzing the wave forms, topographical distribution, effects of higher rates of stimulation and correlation with components of the scalp-recorded SEPs. Recordings were done on 4 patients with spasmodic torticollis during neurosurgical operations for microvascular decompression of the eleventh nerve. The dorsal column SEPs to MN stimulation (MN-SEPs) were characterized by a major negative wave (N1; 13 msec in mean latency), preceded by a small positivity (P1) and followed by a large positive wave (P2). Similar wave forms (P1′-N1′-P2′) were obtained with stimulation of PTN (PTN-SEPs), with a mean latency of N1′ being 28 msec. Maximal potentials of MN-SEPs and PTN-SEPs were located in the vicinity of the ipsilateral cuneate and gracile nuclei, respectively, at a level slightly caudal to the nuclei. The latencies of P1 and N1 increased progressively at more rostral cervical cord segments and medulla, but that of P2 did not. A higher rate of stimulation (16 Hz) caused no effects on P1 and N1, while it markedly attenuated the P2 component. These findings suggest that P1 and N1 of MN-SEPs, as well as P1′ and N1′ of PTN-SEPs, are generated by the dorsal column fibers, and P2 and P2′ are possibly of postsynaptic origin in the respective dorsal column nuclei.The peak latency of N1 recorded on the cuneate nucleus was identical with the scalp-recorded far-field potential of P13–14 in all patients, while no scalp components were found which corresponded to P2. These findings support the previous assumption that the scalp-recorded P13–14 is generated by the presynaptic activities of the dorsal column fibers at their terminals in the cuneate nucleus.