The somatosensory central conduction time: physiological considerations and normative data

The somatosensory central conduction time (CCT) can be measured from the peak of N13 to the peak of N20 (peak CCT) or from the onset of N11 to the onset of N20 (onset CCT). The onset and peak CCT were measured concomitantly in 40 normal subjects and the mean peak CCT was significantly shorter than the mean onset CCT. Records with different reference electrodes (linked earlobes, F3, over the ipsilateral parietal scalp, non-cephalic reference in some subjects) showed no significant latency change of the N11 onset, the N20 onset, the peak and onset CCT in contrast with the significant latency changes of the N13 and N20 peak with different montages. The onset CCT was divided by the onset of the P14 far-field in 2 parameters, the N11-P14 interval predominantly concerned with spinal conduction and the P14-N20 interval which reflected only supraspinal conduction. The onset and peak CCT, the N11-P14 and P14-N20 intervals were not correlated with height or age. Three independent recording sessions over 1 year in 16 subjects showed that the parameters were reproducible. From the physiological point of view the onset and peak CCT are different parameters and the anatomical correlates of both parameters are discussed.     

Somatosensory evoked potential recovery (SEP-R) in various neurological disorders

Recovery functions of somatosensory evoked potentials were studied by the paired stimulation technique in 61 patients with various neurological disorders. A less suppressive or hyperexcitable phase at short intervals, which had been shown in myoclonic patients, was seen in 22 patients. This abnormality was observed even in patients without myoclonus or involuntary movements, which suggests that this phenomenon is not mainly due to some dysfunction causing myoclonus or movement disorders. Less suppression at short intervals was observed for both N20-P25 and P25-N33 components in most of them. Less suppressive recovery of the N20-P25 component with normal recovery of the P25-N33 component was shown only in 3 patients with subcortical lesions with relative sparing of the cortical elements (Binswanger's subcortical encephalopathy). We conclude that less suppressive recovery of only the N20-P25 component suggests the presence of subcortical lesions.     

Brain-stem somatosensory dysfunction in a case of long-standing left hemispherectomy with removal of the left thalamus: a nasopharyngeal and scalp SEP study

We have studied median nerve somatosensory evoked potentials (SEPs) in a patient who had undergone early surgical removal of the left cerebral hemisphere and left thalamus. Stimulation of the right side evoked normal latency P9, P11 and P13 potentials at scalp as well as at nasopharyngeal (NP) leads, while P14 and N18 potentials were absent. These SEP abnormalities, that have been described previously in cervico-medullary lesions and in comatose patients with upper brain-stem involvement, suggest that in our patient the removal of the left thalamus has caused retrograde degeneration of the cuneate-thalamic projections. Moreover, this study confirms that P13 and P14 potentials have different generators.     

Sphingosine and FTY720 modulate pacemaking activity in interstitial cells of Cajal from mouse small intestine

Interstitial cells of Cajal (ICCs) are the pacemakers of the gastrointestinal tract, and transient receptor potential melastatin type 7 (TRPM7) and Ca²⁺ activated Cl⁻ channels (ANO1) are candidate the generators of pacemaker potentials in ICCs. The effects of D-erythro-sphingosine (SPH) and structural analogues of SPH, that is, N,N-dimethyl-Derythro-sphingosine (N,N-DMS), FTY720, and FTY720-P on the pacemaking activities of ICCs were examined using the whole cell patch clamp technique. SPH, N,N-DMS, and FTY720 decreased the amplitudes of pacemaker potentials in ICC clusters, but resting membrane potentials displayed little change. Also, perfusing SPH, N,N-DMS, or FTY720 in the bath reduced both inward and outward TRPM7-like currents in single ICCs, and inhibited ANO1 currents. The another structural analogue of SPH, FTY720-P was ineffective at the pacemaker potentials in ICC clusters and the TRPM7-like currents in single ICCs. Furthermore, FTY720- P had no effect on ANO1. These results suggest that SPH, N,N-DMS, and FTY720 modulate the pacemaker activities of ICCs, and that TRPM7 and ANO1 channels affect intestinal motility.     

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.     

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?).     

Absence of spinal N13-P13 and normal scalp far-field P14 in a patient with syringomyelia

Short latency somatosensory evoked potentials to median or ulnar nerve stimulation were recorded in a patient with syringomyelia. Scalp-recorded far-field P14 was clearly preserved, but spinal N13-P13 components disappeared. Our findings support the hypothesis that spinal N13-P13 is generated by structures intrinsic to the cervical cord, most likely in the ventral central gray matter.     

Two distinct cervical N13 potentials are evoked by ulnar nerve stimulation

To investigate the dual nature of the posterior neck N13 potential, we attempted to establish the presence of a latency dissociation between caudal (cN13) and rostral (rN13) potentials on stimulating the ulnar nerve, in view of its lower radicular entry compared to the median nerve. SEPs were evaluated in 24 normal subjects after both median and ulnar nerve stimulation. cN13 was prominent in the lower cervical segments, and rN13 was localized mainly in the upper ones using anteroposterior and longitudinal bipolar montage, respectively. The N9-cN13 interpeak latency did not differ significantly from N9-rN13 when stimulating the median nerve. On the other hand, the N9-rN13 interpeak was significantly longer than the N9-cN13 interpeak when the ulnar nerve was stimulated. The rN13 presented the same latency as P13-P14 far-field potentials in 17 out of 24 ulnar nerves tested. Therefore, the ulnar nerve stimulation evokes two distinct posterior neck N13 potentials. It is widely accepted that the caudal N13 is a postsynaptic potential reflecting the activity of the dorsal horn interneurons in the lower cervical cord. We suggest that the rostral N13 is probably generated close to the cuneate nucleus, which partly contributes to the genesis of P13-P14 far-field potentials.     

Discrepancy between SEPs directly recorded from the dorsal column nuclei following upper and lower limb stimulation in patients with syringomyelia

Somatosensory evoked potentials (SEPs) in response to electrical stimulation of the median nerve (MN) and posterior tibial nerve (PTN) were studied in 2 patients with syringomyelia. Intraoperative recordings were made from the surface of the dorsal column nuclei as well as from the scalp. Following MN stimulation, there was a preservation of scalp-recorded P9, P11, P13 and N20, however, there was an absence of spinal N13-P13. The dorsal column SEPs to MN stimulation were normal, characterized by a major negativity (N1), preceded by a small positivity (P1) and followed by a large positivity (P2). On the other hand, there was little or no cortical response (P37) to PTN stimulation. The dorsal column SEPs to PTN stimulation showed a disappearance of the normal P1′-N1′-P2′ configuration, being replaced by a series of small spiky waves. The syringomyelic cavity may have thus compressed the gracile dorsal column which courses more medially than the cuneate pathway, causing desynchronization of the dorsal column SEPs. These findings suggest that dorsal column pathway arising from the lower limb is more vulnerable than that from the upper limb when a cervical syrinx is present.     

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.     

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     

Median nerve somatosensory evoked potentials. Apomorphine-induced transient potentiation of frontal components Clin. Parkinson's disease and in parkinsonism

Somatosensory evoked potentials (SEPs) to median nerve stimulation have been recorded from parietal and frontal districts Clin. 43 parkinsonians, 17 patients with parkinsonism and 35 healthy controls matched for age and sex. Latency/ amplitude characteristics of the parietal P14-N20-P25 and of the frontal P20-N30-P40 wave complexes before and after (10, 20, 30 and 60 min) subcutaneous administration of apomorphine chloride were evaluated Clin. all the 60 patients and Clin. 3 controls. The frontal waves N30 and P40 were either absent or significantly smaller than normal Clin. 31 patients with Parkinson's disease (PD) (72.1%) and Clin. 9 with parkinsonism Clin. baseline records (56.3%). Following apomorphine, the parietal deflections did not significantly vary Clin. amplitude. On the contrary, the frontal complex showed a significant amplitude increase Clin. 27 PD and 8 parkinsonisms (respectively 62.8 and 47.1%): 79.1% of PD and 35.3% of parkinsonisms were improved clinically. Amplitude increase was evident at 10 min after apomorphine, Clin. parallel with clinical improvement, and vanished nearly Clin. coincidence with the end of the clinical effect.     

Recovery function of somatosensory evoked potentials in juvenile myoclonic epilepsy*

Abstract

Objective: We analysed the recovery function of somatosensory evoked potentials (SEPs) in juvenile myoclonic epilepsy (JME) patients. We hypothesized that there may be disinhibition in the recovery of SEPs at 20–100?ms intervals in JME patients.

Methods: We recorded SEPs and SEP recovery in 19 consecutive patients with JME admitted for a routine follow-up examination, and in a control group composed of 13 healthy subjects who were similar to the patient group regarding age and sex. The recovery function of SEPs was examined using paired stimuli at 30, 40, 60, and 100?ms intervals.

Results: The amplitudes of N20-P25 and P25-N33 components were higher in patients with JME. Ten patients had high-amplitude SEPs. By paired stimulation, there was inhibition of SEPs in both groups. The mean recovery percentages of N20-P25 and P25-N33 components at 30, 40, 60, and 100?ms were not different between healthy subjects and patients with JME.

Conclusions: The recovery function of SEP is normal in JME even in the presence of high-amplitude SEPs.     

Augmented P22-N31 SEP component in a patient with a unilateral space occupying lesion

A patient presented with a right rolandic space occupying lesion resulting in a decrease of position sense, touch and stereognosis in the left upper limb.SEPs revealed an augmentation of the right hemisphere P22 component co-existing with relative attenuation of all other right hemisphere components. The augmented P22-N31 complex represented a ‘giant’ potential in relation to a control group (> 2.5 S.D.).The data provide further evidence that the P22-N31 complex has separate generators from those responsible for the N20-P27-N33 components parietally and P20-N30 components frontally. The focal nature of the lesion and symptomatology are of interest.     

Somatosensory evoked potentials and magnetic resonance imaging in syringomyelia

Somatosensory evoked potentials (SEPs) to median and posterior tibial stimulation were obtained in 22 patients with syringomyelia. All patients had magnetic resonance imaging (MR) which defined the maximum transverse diameter of the syrinx as well as its longitudinal extension. SEP was abnormal in 16 (72%) patients. Median and posterior tibial SEPs were abnormal in 11 and 15 patients respectively. Both tests were abnormal in 10 patients. Ten patients showed absence of one or more central potentials (P/N13, N20, N22) and 7 patients demonstrated increased conduction times (N9–N20, P/N13–N20, N22–P40). The mean maximum transverse diameter of the syrinx was 7.5 mm in patients with normal SEPs and 16.2 mm in patients with abnormal SEPs. Abnormal SEP was observed in all 5 patients with loss of position sense, in 9 of 13 (69%) with loss of superficial pain and temperature, and 1 of 2 patients with motor deficit only. Central SEP abnormalities were observed in 3 of 5 patients with sensory deficits indistinguishable from a peripheral neuropathy and in 2 patients in the asymptomatic extremity. Three of 4 patients with syringomyelia and Chiari malformation had a normal SEP.     

Somatosensory evoked potentials: Correlations with height

Somatosensory evoked potentials (SEPs) to median and posterior tibial nerve stimulation were studied in 160 subjects aged 20–90 years. Height was highly correlated with latencies of spinal and cortical SEPs (N13, N20, N22, and P40). Although tibial central conduction (N22-P40) was also highly correlated with height, median conduction (N13–N22) was not correlated with the latter.Multiple correlation and regression analysis showed that except for the median N13–N20 latency, height provided the best prediction of the remaining SEP latencies. Age alone was not correlated with SEP latencies, but its significance was observed when age and height were considered together as the predictors. Effects of age and height on SEP latencies were independent of gender.The present data indicate that except for the N13–N20 conduction, height is the most important parameter for SEP latencies and can be used for construction of normograms.     

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.     

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.     

Auditory event-related potentials in obstructive sleep apnea: effects of treatment with nasal continuous positive airway pressure

Event-related potentials (ERPs) were recorded in 47 patients with obstructive sleep apnea (OSA) syndrome prior to and after 6 weeks of treatment with continuous positive airway pressure (CPAP). Compared with a control group, the OSA patients showed ERP abnormalities: lengthened P3 latencies and decreased N2-P3 amplitudes. After 6 weeks of CPAP treatment, there was a highly significant improvement in the abnormal ERPs: the P3 and N2 latencies were shortened, but remained longer than in controls, and the N2-P3 and N1-P2 amplitudes were increased. No correlations could be established with various sleep variables. ERPs may be used as an electrophysiological marker of brain dysfunction; treatment of OSA with CPAP is probably responsible for functional brain modifications. On the other hand, possible relationships between the ERP abnormalities and the neuropsychological disorders observed in OSA remain to be established.     

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.