Mapping of early and late human somatosensory evoked brain potentials to phasic galvanic painful stimulation

In the present study, we modeled the spatiotemporal evolution of human somatosensory evoked cortical potentials (SEPs) to brief median-nerve galvanic painful stimulation. SEPs were recorded (-50 to +250 ms) from 12 healthy subjects following nonpainful (reference), slight painful, and moderate painful stimulations (subjective scale). Laplacian transformation of scalp SEPs reduced head volume conduction effects and annulled electric reference influence. Typical SEP components to the galvanic nonpainful stimulation were contralateral frontal P20-N30-N60-N120-P170, central P22-P40, and parietal N20-P30-P60-P120 (N = negativity, P = positivity, number = latency in ms). These components were observed also with the painful stimulations, the N60, N120, P170 having a longer latency with the painful than nonpainful stimulations. Additional SEP components elicited by the painful stimulations were parietomedian P80 as well as central N125, P170 (cP170), and P200. These additional SEP components included the typical vertex negative-positive complex following transient painful stimulations. Latency of the SEP components exclusively elicited by painful stimulation is highly compatible with the involvement of A delta myelinated fibers/spinothalamic pathway. The topography of these components is in line with the response of both nociceptive medial and lateral systems including bilateral primary sensorimotor and anterior cingulate cortical areas. The role of attentive, affective, and motor aspects in the modulation of the reported SEP components merits investigation in future experiments.     

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.     

Topography and intracranial sources of somatosensory evoked potentials in the monkey. II. Cortical components

Averaged somatosensory evoked potentials (SEPs) and associated multiple unit activity (MUA) were recorded from a series of epidural and intracortical locations following stimulation of the contralateral median nerve in the monkey. Cortical components were differentiated from the earlier subcortical activity and the intracerebral distribution and sources of each cortical potential were determined. Under barbiturate anesthesia the SEP wave form is simplified and can be wholly attributed to two sources. The earliest cortical activity consists of a biphasic P10-N20 wave which is generated in the posterior bank of the central sulcus. A second wave form, P12-N25, originates in the crown of the postcentral gyrus. No other cortical areas are active. In the alert state the morphology of the surface SEP is complex and reflects the interaction of volume conducted activity from several adjacent cortical sources. The wave form overlying the hand area of the postcentral gyrus consists of P12, P20, P40, N45 and P110. Precentral recordings exhibit P10, P13, N13, N20, P24, N45 and P110. Six anatomical sources have been identified. P10 and N20 originate in the posterior bank of the central sulcus including areas 3a and 3b and are volume conducted in an anteroposterior direction. P12 originates in area 1 as well as the anterior portion of area 2. P20 is generated in the medial portion of the postcentral gyrus including area 5. The source of P40 lies within the lateral portion of the parietal lobe including area 7b. Two components were generated in precentral cortex: P13/N13 originates principally in area 4 within the anterior bank of the central sulcus and P24 reflects activity in the anteromedial portion of the precentral gyrus including area 6. The long latency SEP components, N45 and P110, are generated widely within the somesthetic areas of postcentral cortex. The early cortical SEP components recorded in the monkey closely resemble in configuration and topography those recorded from man although the latter are longer in latency, reflecting interspecies differences in the length of conduction pathways as well as in cortical processing time.     

Non-invasive evaluation of input-output characteristics of sensorimotor cerebral areas in healthy humans

The topography of scalp SEPs to mixed and sensory median nerve (MN) and to musculocutaneous nerve stimulation was examined in 20 healthy subjects through multichannel (12-36) recording in a 50 msec post-stimulus epoch. MN-SEPs in both frontal leads were characterized by an N18, P20, N24, P28 complex showing maximal amplitude at contralateral parasagittal sites. This was sometimes partly obscured by a wide wave N30 having a fixed latency, but a steep amplitude gradient moving toward the scalp vertex. A P40 component followed, having longer peak latencies, moving the recording sites from contralateral medial parietal toward the vertex and frontal ipsilateral positions. MN-SEPs in contralateral parietal leads contained a widespread N20 with a maximum source posterior to the Cz-ear line. The following P25 enveloped two subcomponents - early and late P25 - having different distributions. The late P25 showed a maximum - coincident with that of wave N20 - which was localized more posteriorly than that of the early P25. An inconstant wave N33 with progressively longer peak latencies from sagittal toward lateral positions was then recorded. MN-SEPs in contralateral central positions showed a well-localized P22 wave in which both the parietal early P25 and the frontal P20 were vanishing. Common or separate generators for frontal, central and parietal SEPs were discriminated by evaluating the influence of stimulus rate and intensity, as well as of general anesthesia and transient CBF deficits, investigated in 7 patients undergoing carotid endarterectomy. Unifocal anodal threshold shocks were separately delivered to each of the scalp electrodes and motor action potentials were recorded from the target muscle in order to delineate the scalp representation of the motor strip for the upper limb and, consequently, to monitor, through SEP tracings, the short-latency sensory input to the motor cortex for hand and shoulder muscles. This was characterized by a boundary zone separating the parietal N20-early P25 complex, from the fronto-central N18-P22 one. This zone had an oblique direction strongly resembling that of the central sulcus.     

Maturation of near-field and far-field somatosensory evoked potentials after median nerve stimulation in children under 4 years of age.

OBJECTIVES: The maturation of subcortical SEPs in young children. METHODS: Median nerve SEPs were recorded during sleep in 42 subjects aged 0-48 months. Active electrodes were at the ipsilateral Erb's point, the lower and upper dorsal neck, and the frontal and contralateral centroparietal scalp; reference electrodes were at the contralateral Erb's point, the ipsilateral earlobe and the frontal scalp; bandpass was 10-3000 Hz. The peaks were labelled by their latencies in adults. RESULTS: The peak latencies of N9 (brachial plexus potential) decreased exponentially with age during the first year, but increased with height thereafter. The interpeak latencies (IPLs) N9-N11, which measure conduction between brachial plexus and dorsal column, decreased with age (linear regression). The IPLs N11-P13 and N11-N13b, which measure conduction between the dorsal column and approximately the cervico-medullary junction, did not change across this age range. The IPLs N13a-N20, N13b-N20 and P13-N20, which measure central conduction, showed negative exponential regressions with rapidly decreasing latencies during the first year of life and slowly decreasing latencies thereafter. CONCLUSIONS: Maturation of the peripheral segments of the somatosensory pathway progresses more rapidly than that of the central segments. The maturation of central conduction is not completed within the first 4 years of age. Our maturational data may serve as a reference source for subsequent developmental and clinical studies.     

Cortical and subcortical somatosensory evoked potentials to median nerve stimulation in man

In order to define the precise locations of precentral and postcentral gyri during neurosurgical operations, somatosensory evoked potentials to contralateral median nerve stimulation were recorded from the cerebral cortex in 19 cases with organic cerebral lesions which located near the central sulcus. In addition to that, distribution patterns of early components of SEPs were displayed by Nihonkoden Atac 450 in 3 cases who had bone defects after wide decompressive craniectomy but were without any sensory disturbances In 4 cases, in whom deep electrodes were inserted for the stereotaxic operations or other reasons, frontal subcortical SEPs were recorded in order to know the origins of frontal components of SEPs. From the parietal cortex, N19, P22 and P23 were observed. And from the frontal cortex, P20 and N25 were obtained. Their average peak latencies were as follows; (table; see text) Because all subjects had organic lesion in the brain, the peak latencies were a little bit longer, and their standard deviations were larger than those in normal cases. Usually, clear-cut phase reversal could be observed between N19 and P20 across the central sulcus. So, the precentral and postcentral gyri were easily identified during the operations. N19 and P23 appeared over the wide areas of the parietal cortex. Also, P20 and N25 were recorded almost whole areas of the frontal cortex. On the other hand, P22 appeared from relatively restricted part of the postcentral gyrus where sensory hand area might have been located. Depth recording from the frontal subcortical area revealed that P20 could be recorded from the bilateral frontal subcortical areas and there observed no phase reversal between the cortical and subcortical SEPs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Somatosensory evoked potentials during the ideation and execution of individual finger movements

Scalp somatosensory evoked potentials (SEPs) were recorded in 10 volunteers after median nerve stimulation, in four experimental conditions of hand movements performance/ideation, and compared with the baseline condition of full relaxation. The experimental conditions were (a) self-improvised hand-finger sequential movements; (b) the same movements according to a read sequence of numbers; (c) mental ideation of finger movements; and (d) passive displacement of fingers in complete relaxation. Latencies and amplitudes of the parietal (N20, P25, N33, and P45) and frontal peaks (P20–22, N30, and P40) were analyzed. Latencies did not vary in any of the paradigms. Among the parietal complexes, only the P25-N33 amplitude was significantly reduced in (a), (b), (c), and (d) and the N20-P25 was reduced in (a) and (d); among frontal waves, N30 and P40 were significantly reduced (20–75%) in (a) and (b). Coronal electrodes showed amplitude decrements maximal at the frontal-rolandic positions contralateral to the stimulated side. © 1996 John Wiley & Sons, Inc.     

Scalp topography of human somatosensory evoked potentials: the effect of interfering tactile stimulation applied to the hand

A detailed topographical analysis of human SEPs in response to median nerve stimulation was performed, with and without concurrent tactile stimulation of the hand. Twenty-eight recording sites on the scalp and neck were referred to earlobe and non-cephalic reference electrodes. The following components were identified in the control wave form: N10, N11, N13, P14, N19, P20, P22, N22, N29, P30 and P44. The interference wave form showed significant attenuation of P14, N19, P20, P22 and N29, while P30 was abolished. N10, N11, N13 and N22 remained unchanged and P44 was enhanced. In the interference wave form there also appeared an N33 component, supplanting P30 over the posterior contralateral quadrant, and a P36 frontally. The pattern of changes was best demonstrated by subtracting the interference from the control response to derive a 'difference' wave form. This consisted of 'P'14, 'N'19, 'P'21, 'P'32 and 'N'36 components. The last 2 were of large amplitude over the posterior contralateral quadrant and frontal cortex, respectively, and overlapped for at least 10 msec of their duration. The results indicate that the interfering effect occurred at the level of the brain-stem or above. The topography of the difference wave form suggests that the 'P'32 and 'N'36 components may be attributable to a generator situated in the posterior bank of the central sulcus (Brodmann's area 3b), concerned with the processing of input from cutaneous mechanoreceptors. It is proposed that the P22 and N22 components of the control and interference wave forms may be due to a generator located at the bottom and in the anterior bank of the central sulcus (area 3a).     

Somatosensory evoked potentials in minor cerebral ischaemia: diagnostic significance and changes in serial records

Frontal, central and parietal short and middle latency somatosensory evoked potentials (SEPs) arising after stimulation of the contralateral median nerve were studied in 10 normal adults. Stable SEPs were recorded: a frontal P21-N30 complex and an N20-P23-P28-N35-P42 complex in the centro-parietal region. The use of a chin reference electrode allowed identification of (the thalamic) P15 and N18. SEP studies of 20 patients with unilateral cerebral ischaemia were also performed, about 4 and 18 days after the stroke. In 13 out of 18 patients with a minor stroke (TIA, RIND and PNS) abnormalities of the frontal and/or parietal SEPs were demonstrated. Improvement in these SEPs occurred in 5 cases. In two patients who suffered from a major ischaemic deficit, the SEPs were highly abnormal and did not show any change in the course of time. SEP studies may be useful for the diagnosis of minor cerebral ischaemia as well as quantification of recovery; an even more important indication for this neurophysiological method might be detection of subclinical lesions in patients who have suffered from transient cerebral ischaemia even weeks before the SEP studies are carried out.     

Neural generators of N18 and P14 far-field somatosensory evoked potentials studied in patients with lesion of thalamus or thalamo-cortical radiations

Somatosensory evoked potentials (SEPs) to electrical stimulation of the right or left median nerve were studied in 4 patients with hemianesthesia and a severe thalamic or suprathalamic vascular lesion on one side. The SEPs were recorded with a non-cephalic reference. The normal side of each patient served as his or her own control. The lesion consistently abolished the parietal N20-P27-P45 and the prerolandic P22-N30 SEP components. It did not significantly affect the P9-P11-P14 positive far fields, nor the widespread bilateral N18 SEP component. This allowed N18 features to be studied without interference from cortical components. It is proposed that N18 reflects several deeply located generators in brain stem and/or thalamus whereas N20 represents the earliest cortical response of the contralateral post-central receiving areas.     

Topographical displays of somatosensory evoked potentials

The distribution of somatosensory evoked potentials (SEPs) after stimulation of the median nerve at the wrist was examined in 10 normal subjects using isopotential maps. The latencies of continuous negative and positive peaks were measured in each lead. The differences of the potentials at these latencies were measured in all the leads and the isopotential maps were constructed. The distribution of P0-NI was all similar. The latencies of P0 were almost the same in all the leads at about 13 msec. The distribution of NI-PI-NII was divided into three types--N16-P20-N28 localized in the frontal region, N17-P22-N30 localized in the central region and N19-P25-N33 distributed in the parieto-occipito-temporal regions. The distributions of NII-PII and PII-NIII were all similar, with high amplitudes in the central region. The latencies of PII and NIII were almost the same in all the leads at about 45 msec and 68 msec.     

The relationship between human long-latency somatosensory evoked potentials recorded from the cortical surface and from the scalp.

In scalp recordings, stimulation of the median nerve evokes a number of long-latency (40-300 msec) somatosensory evoked potentials (SEPs) whose neural origins are unknown. We attempted to infer the generators of these potentials by comparing them with SEPs recorded from the cortical surface or from within the brain. SEPs recorded from contralateral sensorimotor cortex can be characterized as "precentral," "postcentral," or "pericentral." The scalp-recorded P45, N60 and P100 potentials appear to correspond to the pericentral P50, N90 and P190 potentials and are probably generated mainly in contralateral area 1 of somatosensory cortex. The scalp-recorded N70-P70 appear to correspond to the precentral and postcentral N80-P80 and are generated mainly in contralateral area 3b of somatosensory cortex. The scalp-recorded N120-P120 appear to correspond to the intracranial N100-P100 and are probably generated bilaterally in the second somatosensory areas. N140 and P190 (the "vertex potentials") are probably generated bilaterally in the frontal lobes, including orbito-frontal, lateral and mesial (supplementary motor area) cortex. The supplementary sensory area probably generates long-latency SEPs, but preliminary recordings have yet to confirm this assumption. Most of the proposed correspondences are speculative because the different conditions under which scalp and intracranial recordings are obtained make comparison difficult. Human recordings using chronically implanted cortical surface electrodes, and monkey studies of SEPs which appear to be analogs of the human potentials, should provide better answers regarding the precise generators of human long-latency SEPs.     

Postcentral origin of P22: evidence from source reconstruction in a realistically shaped head model and from a patient with a postcentral lesion

The source of the radial field of P22 was previously attributed either to the precentral (area 4) or postcentral (area 1) gyrus, on the basis of interpretation of potential maps recorded on the skin or cortex, respectively. The present study used dipole localization within realistically shaped head models and constrained the inverse solution by using the individual cortex and the normals on it, as derived from MR-tomography. In all normal subjects in which a sufficient solution was obtained (6 of 10, goodness of fit above 90%, and relative power of above 94.4% in principal-component analysis) the P22 source resided at the crown of the postcentral gyrus. Further evidence came from a patient with a postcentral lesion (area 1) and loss of P22, while N20-P20 was preserved.     

Functional anatomy of human hand sensorimotor cortex from spatiotemporal analysis of electrocorticography.

We measured chronic electrocorticography (ECoG) of sensorimotor cortex during contralateral median nerve stimulation in 6 patients with partial seizures evaluated for surgery. We analyzed the spatiotemporal structure of the somatosensory evoked response (SER) using multiple source modeling to investigate functional anatomy of its neuronal sources. Two dipole sources in postcentral gyrus explained the large majority of the first 60 msec of the SER, indicating a subregion of hand somatosensory cortex generating this activity. The source locations agreed with normal functional anatomy from cortical stimulations, intraoperative photographs, and postoperative neurological examinations after focal excisions. The time patterns of both sources were biphasic like the previously described N20-P30 and P25-N35 peaks. The spatiotemporal patterns of both sources overlapped. Spatiotemporal analysis with multiple dipole sources appears useful to determine the number, locations, and spatiotemporal field patterns of cortical regions active during peripheral somatosensory stimulation and reveals simplicity in the macroscopic functional anatomy of dynamic human sensorimotor cortex.     

Frontal distribution of early cortical somatosensory evoked potentials to median nerve stimulation

The topography of early frontal SEPs (P20 and N26) to left median nerve stimulation was studied in 30 normal subjects and 3 patients with the left frontal bone defect. The amplitudes of P20 and N26 were maximum at the frontal electrode (F4) contralateral to the stimulation and markedly decreased at frontal electrodes ipsilateral to the site of stimulation. There was, however, no latency difference of P20 and N26 between ipsilateral and contralateral frontal electrodes. These results suggest that the origin of the ipsilateral and contralateral P20 and N26 is the same. The wide distribution of P20 and N26 over both frontal areas could be explained by assuming a smearing effect from generators actually located in the rolandic fissure and motor cortex.     

"Gating" of human short-latency somatosensory evoked cortical responses during execution of movement. A high resolution electroencephalography study.

The present study aimed at investigating gating of median nerve somatosensory evoked cortical responses (SECRs), estimated during executed continuous complex ipsilateral and contralateral sequential finger movements. SECRs were modeled with an advanced high resolution electroencephalography technology that dramatically improved spatial details of the scalp recorded somatosensory evoked potentials. Integration with magnetic resonance brain images allowed us to localize different SECRs within cortical areas. The working hypothesis was that the gating effects were time varying and could differently influence SECRs. Maximum statistically significant (p<0. 01) time-varying gating (magnitude reduction) of the short-latency SECRs modeled in the contralateral primary motor and somatosensory and supplementary motor areas was computed during the executed ipsilateral movement. The gating effects were stronger on the modeled SECRs peaking 30-45 ms (N30-P30, N32, P45-N45) than 20-26 ms (P20-N20, P22, N26) post-stimulus. Furthermore, the modeled SECRs peaking 30 ms post-stimulus (N30-P30) were significantly increased in magnitude during the executed contralateral movement. These results may delineate a distributed cortical sensorimotor system responsible for the gating effects on SECRs. This system would be able to modulate activity of SECR generators, based on the integration of afferent somatosensory inputs from the stimulated nerve with outputs related to the movement execution.     

Subcortical somatosensory evoked potentials after posterior tibial nerve stimulation in children

We report our normative data of somatosensory evoked potentials (SEP) after posterior tibial nerve (PTN) stimulation from a group of 89 children and 18 adults, 0.4-29.2 years of age. We recorded near-field potentials from the peripheral nerve, the cauda equina, the lumbar spinal cord and the somatosensory cortex. Far-field potentials were recorded from the scalp electrodes with a reference at the ipsilateral ear. N8 (peripheral nerve) and P40 (cortex) were present in all children but one. N20 (cauda equina) and N22 (lumbar spinal cord) were recorded in 94 and 106 subjects, respectively. P30 and N33 (both waveforms probably generated in the brainstem) were recorded in 103 and 101 subjects, respectively. Latencies increased with age, while central conduction times including the cortical component, decreased with age (up to about age 10 years). The amplitudes of all components were very variable in each age group. We report our normative data of the interpeak latencies N8-N22 (peripheral conduction time), N22-P30 (spinal conduction time), N22-P40 (central conduction time) and P30-P40 (intracranial conduction time). These interpeak latencies should be useful to assess particular parts of the pathway. The subcortical PTN-SEPs might be of particular interest in young or retarded children and during intraoperative monitoring, when the cortical peaks are influenced by sedation and sleep, or by anesthesia.     

Gating of the early components of the frontal and parietal somatosensory evoked potentials in different sensory-motor interference modalities.

Three different interfering conditions were studied during the recording of pre- and postcentral somatosensory evoked potentials (SEPs) following median nerve stimulation at the wrist in 16 normal subjects: active finger movement (MVT), light superficial massage (LSM) and deep muscular massage (DMM) of the hand. Special attention was focused on selective effects on individual SEP components. The frontal N30 component showed the most significant amplitude reduction during the three interfering conditions (76.4% of reduction in MVT, 36.4% in DMM and 32.9% in LSM). In contrast the frontal N23 was not significantly changed and the preceding P22 component was only reduced in the MVT condition. Postcentral N20 was unchanged by the three conditions while P27 was clearly gated by movement but not significantly by LSM and DMM. The three interfering conditions enhanced the parietal N32 and had no significant effect on the parietal P45. An important point was the interindividual variability of these effects and it appeared that group average wave forms would therefore be confusing. The peak latency of some SEP components was changed during the interfering conditions. The most important effect was an increase of postcentral P45 latency which was found to be related to the amplitude enhancement of N32.     

Color imaging of parietal and frontal somatosensory potential fields evoked by stimulation of median or posterior tibial nerve in man

Somatosensory evoked potentials (SEPs) to median or fingers or posterior tibial nerve stimulation were recorded with earlobe reference in normal young adults. A system of 16 electrodes on the scalp served to create bit-mapped images of the potential fields at 1 msec intervals. The P14 (median SEP) or P30 (tibial SEP) far fields thought to reflect the afferent volley in the medial lemniscus produced widespread positivity over the scalp. Subsequent components had a characteristic focal distribution suggesting that they reflected one or more generators in cortical areas. For the median SEP, the parietal N20 and the prerolandic P22 showed differences in onset and offset times as well as distribution that precluded their being related to the same generator. While N20 was contralateral, P22 extended ipsilaterally. P22 may be generated in the motor area 4 and the supplementary motor area. P22 was also distinct from the P27 field restricted to the contralateral parietal region. The frontal N30 had a bilateral distribution and the P45 presented variable features. For the tibial SEP, no phase reversal was confirmed between the parietal P38 (midline-ipsilateral focus) and N33 (contralateral focus). N37 over the contralateral prerolandic region might reflect a generator in the motor region. P58 was more symmetrically distributed than P38, possibly because it reflected generators more posteriorly on the parietal convexity. N75 had a widespread field with focus on the ipsilateral side of midline.     

Methyl bromide myoclonus: an electrophysiological study

We report a case of myoclonus from overnight exposure to methyl bromide. Myoclonus was either spontaneous or induced by somatosensory stimulation or voluntary movements, multifocal and sometimes generalized. Median SEP showed normal size P14-N20, but giant parietal P25, N33 and frontal P22-N30 waves. Back-averaging showed a biphasic EEG spike of maximal amplitude at the central region contralateral to the corresponding myoclonic jerk recorded from abductor pollicis brevis and preceding it by a short interval consistent with conduction in corticospinal pathways. Long latency reflexes from cutaneous and mixed nerve stimulation were enhanced. The above electrophysiological findings suggest that myoclonus following methyl bromide poisoning belongs to the cortical reflex myoclonus category.