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     

Nerve,spinal cord and brain somatosensory evoked responses: a comparative study during electrical and magnetic peripheral nerve stimulation

Somatosensory evoked potentials (SEPs) and compound nerve action potentials (cNAPs) have been recorded in 15 subjects during electrical and magnetic nerve stimulation. Peripheral records were gathered at Erb's point and on nerve trunks at the elbow during median and ulnar nerve stimulation at the wrist. Erb responses to electrical stimulation were larger in amplitude and shorter in duration than the magnetic ones when ‘electrical’ and ‘magnetic’ compound muscle action potentials (cMAPs) of comparable amplitudes were elicited. SEPs were recorded respectively at Cv7 and on the somatosensory scalp areas contra- and ipsilateral to the stimulated side. SEPs showed a statistically significant difference in amplitude only for the brachial plexus response and for the ‘cortical’ N20-P25 complex; differences were not found between the magnetic and electrical central conduction times (CCTs) or for the peripheral nerve response latencies. Magnetic stimulation preferentially excited the motor and proprioceptive fibres when the nerve trunks were stimulated at motor threshold intensities.     

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.     

Somatotopy of human hand somatosensory cortex as studied in scalp EEG

We recorded somatosensory evoked potentials (SEPs) in scalp EEGs during stimulation of the median nerve, the ulnar nerve and the individual digits in 3 normal subjects and in 1 epilepsy patients. In this patient we also measured SEPs from chronically indwelling subdural grid electrodes during electrocorticography (ECoG). We applied dipole modelling techniques to study the 3-dimensional intracerebral locations and time activities of the neuronal sources underlying stimulation of different peripheral receptive fields. The sources underlying median nerve SEPs were located an average of 10.8 mm lateral inferior to those underlying ulnar nerve SEPs. Digit SEP sources showed a somatotopic arrangement from lateral inferior to medial superior in the order thumb, index finger, middle finger, ring finger and little finger, with some overlap or reversal for adjacent digits. The average distance between thumb and little finger was 12.5 mm. Thumb, index finger and middle finger were clustered around median nerve cortical representation, whereas ring finger and little finger were arranged around ulnar nerve cortex. In the epilepsy patient, the source localizations obtained in scalp EEGs showed good agreement with those on ECoGs. We conclude that SEPs recorded in scalp EEGs can be used to study functional topography of human somatosensory cortex non-invasively.     

Ipsilateral median somatosensory evoked potentials recorded from human somatosensory cortex

Somatosensory evoked potentials (SEP) to ipsilateral and contralateral median nerve stimulations were recorded from subdural electrode grids over the perirolandic areas in 41 patients with medically refractory focal epilepsies who underwent evaluation for epilepsy surgery. All patients showed clearly defined, high-amplitude contralateral median SEPs. In addition, four patients showed ipsilateral SEPs. Compared with the contralateral SEPs, ipsilateral SEPs were very localized, had a different spatial distribution, were of considerably lower amplitude, had a longer latency (1.2–17.8 ms), did not show an initial negativity, and were markedly attenuated during sleep. Stimulation of the subdural electrodes overlying the sensory hand area was associated with contralateral hand paresthesias, but no ipsilateral hand paresthesias occurred. It was concluded that subdurally recorded cortical SEPs to ipsilateral stimulation of the median nerve (M) reflect unconscious sensory input from the hand possibly serving fast bimanual hand control. The anatomical pathway of these ipsilateral short-latency MSEPs is not yet known. Transcallosal transmission seems unlikely because of the short delay between the ipsilateral and contralateral responses in selected cases. The infrequent occurrence of ipsilateral subdurally recorded SEPs and their low amplitude and limited distribution suggest that they contribute very little to the short-latency ipsilateral median SEPs recorded on the scalp.     

Bit-mapped imaging of somatosensory evoked potentials after stimulation of the posterior tibial nerves and dorsal nerve of the penis / clitoris

Somatosensory evoked potentials (SEPs) to unilateral or bilateral posterior tibial nerve (PTN) stimulation and to stimulation of the dorsal nerve (DN) of the penis / clitoris were recorded on 32 channels in 10 volunteers. SEPs to unilateral PTN stimulation consisted of the classic ‘W’ complex P38-N45-P56-N75 maximal on the ipsilateral central and parietal leads, and two negative waves, N33 and N37, maximal on the contralateral post- and prerolandic areas, respectively. A lemniscal P30 was also recorded. Bilateral PTN stimulation caused, by algebraic summation, the disappearance of both N33 and N37; the W complex was symmetrical and the amplitude of P30 increased. The SEPs to DN stimulation were also symmetrical, and N33 and N37 were absent. These features can be explained by the bilateral character of DN stimulation. They also differed from bilateral PTN SEPs in 3 respects; the absence of P30, the small amplitude and the weaker gradients of field distribution of the ‘W’ complex, and the somewhat different distribution of penile from clitoral or bilateral PTN, N45 and P56. These differences can be explained both by physiological (the different fiber composition of the DN) and anatomical (the deeper localization of the DN cortical receiving area) mechanisms.     

Electric and CO2 laser SEPs in a patient with asymptomatic syringomyelia

We recorded electrically stimulated somatosensory evoked potentials (electric SEPs) and pain-related SEPs following CO₂ laser stimulation (CO₂ laser SEPs) from a 17-year-old patient affected by myotonic dystrophy whose MRI disclosed a large syrinx extending from spinal level C2 to S3. Careful clinical and electromyographic examinations revealed no motor or sensory disturbances, apart from myotonia. The only abnormality noted in median and ulnar nerve short-latency electric SEPs (recorded with a non-cephalic reference electrode) was the absence of cervical component N13, the other SEP responses (N9, N10, N11, P14, N20) being normal. The cutaneous pain threshold and CO₂ laser SEPs (both obtained by a CO₂ laser beam applied to the back of the hand) were normal. Thus cervical component N13 appears to be highly sensitive to the effects of central cord lesions, even when these are asymptomatic.     

Pain-related somatosensory evoked potentials following CO2 laser stimulation of foot in man

Since our previous study of pain somatosensory evoked potentials (SEPs) following CO₂ laser stimulation of the hand dorsum could not clarify whether the early cortical component NI was generated from the primary somatosensory cortex (SI) or the secondary somatosensory cortex (SII) or both, the scalp topography of SEPs following CO₂ laser stimulation of the foot dorsum was studied in 10 normal subjects and was compared with that of the hand pain SEPs and the conventional SEPs following electrical stimulation of the posterior tibial nerve recorded in 8 and 6 of the 10 subjects, respectively. Three components (N1, N2 and P2) were recorded for both foot and hand pain SEPs. N1 of the foot pain SEPs was maximal at the midline electrodes (Cz or CPz) in all data where that potential was recognized, but the potential field distribution was variable among subjects and even between two sides within the same subject. N1 of the hand pain SEPs was maximal at the contralateral central or midtemporal electrode. The scalp distribution of N2 and P2, however, was not different between the foot and hand pain SEPs. The mean peak latency of N1 following stimulation of foot and hand was found to be 191 msec and 150 msec, respectively, but there was no significant difference in the interpeak latency of Nl-N2 between foot and hand stimulation. It is therefore concluded that NI of the foot pain SEPs is generated mainly from the foot area of SI. The variable scalp distribution of the N7 component of the foot pain SEPs is likely due to an anatomical variability among subjects and even between sides.     

Interactions of somatosensory evoked potentials: simultaneous stimulation of two nerves

To analyse the mechanism by which sensory inputs are integrated, interactions of somatosensory evoked potentials (SEPs) in response to simultaneous stimulation of two nerves were examined in 12 healthy subjects. Right, left and bilateral median nerves were stimulated in random order so that a precise comparison could be made among the SEPs. The arithmetical sum of the independent right and left median nerve SEPs was almost equal within 40 msec of stimulus onset to that evoked by the simultaneous stimulation of bilateral median nerves. However, a difference emerged after 40 msec. The greatest difference was recorded after 100 msec. Sensory information from right and left median nerves may interact in the late phase of sensory processing. Left median, left ulnar, and both nerves together were stimulated. The sum of the SEPs of left median and ulnar nerves was not equal to that evoked by the simultaneous stimulation of the two nerves even at early latencies. Differences between them were first recorded at 14–18 msec and became greater after 30–40 msec. It is suggested that the neural interactions between impulses in the median and ulnar nerves begin below the thalamic level.     

Giant central N20-P22 with normal area 3b N20-P20: an argument in favour of an area 3a generator of early median nerve cortical SEPs?

Generators of early cortical somatosensory evoked potentials (SEPs) still remain to be precisely localised. This gap in knowledge has often resulted in unclear and contrasting SEPs localisation in patients with focal hemispheric lesions. We recorded SEPs to median nerve stimulation in a patient with right frontal astrocytoma, using a 19-channel recording technique. After stimulation of the left median nerve, N20 amplitude was normal when recorded by the parietal electrode contralateral to the stimulation, while it was abnormally enhanced in traces obtained by the contralateral central electrode. The amplitude of the frontal P20 response was within normal limits. This finding suggests that two dipolar sources, tangential and radial to the scalp surface, respectively, contribute concomitantly to N20 generation. The possible location of the N20 radial source in area 3a is discussed. The P22 potential was also recorded with increased amplitude by the central electrode contralateral to the stimulation, while N30 amplitude was normal in frontal and central traces. We propose that the radial dipolar source of P22 response is independent from both N20 and N30 generators and can be located either in 3a or in area 4. This report illustrates the usefulness of multichannel recordings in diagnosing dysfunction of the sensorimotor cortex in focal cortical lesions.     

Evaluation of reference sites for scalp potentials evoked by painful and non-painful sural nerve stimulation

The objective of this study was to evaluate reference sites for recording the middle- and long-latency scalp potentials elicited by painful and non-painful sural nerve stimulation. Somatosensory evoked potentials (SEPs) were recorded from the scalp, the mastoid, the earlobe, the neck, and the wrist. Each site was referenced to the sterno-vertebral (SV) electrode, which is a balanced non-cephalic reference with essentially no ECG contamination.There was little or no activity recorded between the wrist and SV, and the SV was located within a region extending from the rostral neck to the wrist where the potentials were stable over space. Hence, the SV reference is indifferent for the middle- and long-latency potentials evoked by painful and non-painful sural nerve stimulation. There was, however, significant activity recorded from the earlobe and mastoid, sites which are frequently used as references for the SEP. It is important that investigators using these cephalic references to study the middle- and long-latency peaks of the SEP be aware of this activity as it will distort SEPs recorded from single sites and the SEP scalp topography, distortions which could unnecessarily complicate their interpretation.     

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.     

Right or left ear reference changes the voltage of frontal and parietal somatosensory evoked potentials

Short-latency cortical somatosensory evoked potentials (SEPs) to left median nerve stimulation were recorded with either the left or right earlobe as reference. With a right earlobe reference the voltage of the parietal N20 and P27 was reduced while the voltage of the frontal P20 and N30 was enhanced. The effects were consistent, but their size varied with the SEP component considered and also among the subjects. Analysis of SEPs at different scalp sites and at either earlobe suggested that the ear contralateral to the side stimulated picked up transient potential differences, depending a.o. on side asymmetry and geometry of the neural generators as disclosed in topographic mapping. For example, the right ear potential can be shifted negatively by the right N20 field evoked by left median nerve stimulation. The changes involve the absolute potential values, but not the time features of the gradients of potential fields. Scalp current density (SCD) maps are not affected. The results are pertinent for current discussions about which reference to use and document the practical recommendation of recording short-latency cortical SEPs with a reference at the ear ipsilateral (not contralateral) to the side of stimulation.     

Cortical potentials evoked by epidural stimulation of the cervical and thoracic spinal cord in man

Scalp somatosensory evoked potentials (SEPs) were recorded after electrical stimulation of the spinal cord in humans. Stimulating electrodes were placed at different vertebral levels of the epidural space over the midline of the posterior aspect of the spinal cord. The wave form of the response differed according to the level of the stimulating epidural electrodes. Cervical stimulation elicited an SEP very similar to that produced by stimulation of upper extremity nerves, e.g., bilateral median nerve SEP, but with a shorter latency. Epidural stimulation of the lower thoracic cord elicited an SEP similar to that produced by stimulation of lower extremity nerves. The results of upper thoracic stimulation appeared as a mixed upper and lower extremity type of SEP. The overall amplitudes of SEPs elicited by the epidural stimulation were higher than SEPs elicited by peripheral nerve stimulation. In 4 patients the CV along the spinal cord was calculated from the difference in latencies of the cortical responses to stimulation at two different vertebral levels. The CVs were in the range of 45–65 m/sec. The method was shown to be promising for future study of spinal cord dysfunctions.     

SEPs in two patients with localized lesions of the postcentral gyrus

Scalp distributions of median nerve SEPs were studied in normal controls and 2 patients with localized lesions of the postcentral gyrus. In controls, parieto-occipital electrodes registered N20-P27 while frontal electrodes registered P20-N27. Other small components, parieto-occipital P22 and frontal N22, were recognized in about half of the control records. The wave forms at a frontal and a parieto-occipital electrode, both distant from the central region, formed exact mirror images of each other concerning N20-(P22)-P27 and P20-(N22)-N27. Electrodes near the central region contralateral to the stimulation registered cP22-cN30 (central P22 and central N30). When the postcentral gyrus was damaged, N20/P20-P27/N27 and cP22-cN30 were eliminated and the only remaining components were a frontal negative wave (frN) and a contralateral parieto-occipital positive wave (poP). Digital nerve stimulation also evoked poP and frN in both cases. In case 2, poP coincided with P22 of the non-affected side. The following generators were proposed; N20/P20-P27/N27: area 3b, cP22-cN30: areas 1 and 2, poP/early frN (= P22/N22): area 4 at the anterior wall of the central sulcus (due to direct thalamic inputs to motor cortex), late frN: uncertain (SMA?, SII?).     

The origin of the scalp recorded P14 following electrical stimulation of the median nerve: intraoperative observations

Direct and far-field recorded somatosensory evoked potentials (SEPs) obtained from 2 patients during neurosurgical procedures are presented. A previous report (Møller et al. 1986) has suggested that the P14 component of the SEP following median nerve stimulation is generated at the cuneate nucleus. The present data suggest that the scalp recorded P14 component (scalp-noncephalic electrode derivation) is generated rostral to the junction of the cervical cord and the medulla.     

Dermatomal and mixed nerve somatosensory evoked potentials in the diagnosis of neurogenic thoracic outlet syndrome

To evaluate the diagnostic utility of dermatomal and mixed nerve somatosensory evoked potentials (SEPs) in patients with thoracic outlet syndrome (TOS) and to compare their value with routine electrodiagnostic methods, we studied a group of 44 patients with neurogenic TOS and 30 healthy controls. In addition to bilateral median and ulnar SEPs, evoked potentials were recorded after stimulation of C6 and C8 dermatomes from the first and fifth digits, respectively. The patients were classified into 3 groups according to the nature of their clinical condition. The abnormality rate for both ulnar and C8 dermatomal SEPs was 100% in a small group of patients with severe neurological signs like atrophy. In groups of patients with lesser degrees of neurogenic damage, abnormality rates for ulnar and C8 dermatomal SEPs on affected limb(s) were 67 and 50%, respectively. Same abnormality rates were 25 and 18% in patients with only subjective symptoms. In patients with objective neurological signs, the major increase in sensitivity was with electromyography (EMG). Abnormalities of routine nerve conduction studies and F-wave latency were observed in patients with severe neurogenic damage. We concluded that the most useful tests in the diagnosis of neurogenic TOS are needle EMG and ulnar SEPs.     

The assessment of severe head injury by short-latency somatosensory and brain-stem auditory evoked potentials

The relative prognostic value of short-latency somatosensory evoked potentials (SEPs) and brain-stem auditory evoked potentials (BAEPs) was assessed in 35 patients with post-traumatic coma. Analysis of the evoked potentials was restricted to those recorded within the first 4 days following head injury. Abnormal SEPs were defined as an increase in central somatosensory conduction time or an absence of the initial cortical potential following stimulation of either median nerve. Abnormal BAEPs were classified as an increase in the wave I–V interval or the loss of any or all of its 3 most stable components (waves I, III and V) following stimulation of either ear. SEPs reliably both good and bad outcomes. All 17 patients in whom SEPs were graded as normal had a favourable outcome and 15 of 18 patients in whom SEPs were abnormal had an unfavourable outcome. Although abnormal BAEPs were associated with an unfavourable outcome in almost all patients (6 of 7), only 19 of 28 patients with normal BAEPs had a favourable outcome. The finding of normal BAEPs was therefore of little prognostic significance. These results confirm the superiority and greater sensitivity of the SEP in detecting abnormalities of brain function shortly after severe head trauma.     

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.     

Questions regarding the sequential neural generator theory of the somatosensory evoked potential raised by digital filtering

Digital bandpass filtering (300–2500 Hz) designed for zero phase shift was applied to somatosensory evoked potentials recorded with cephalic bipolar montages. Four consistent negative and corresponding positive peaks with latencies of about 16, 18, 19, and 20 msec were elicited with median nerve stimulation. Peroneal nerve stimulation also elicited 4 reproducible negative-positive peaks having latencies of about 24, 26, 28, and 30 msec. Interpeak latencies measured 1.3 ± 0.2 msec and 1.8 ± 0.25 msec for median and peroneal elicited SEPs respectively. Becaise cephalic bipolar recordings cancel most far-field potentials, multiple generators cannot account for all the additional components seen. It is hypothesized that some of the high frequency components recorded are due to activity in recurrent intrathalamic neuronal networks.