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.     

Pudendal nerve somatosensory evoked potentials in paediatrics: maturation aspects

Pudendal nerve somatosensory evoked potentials (PN-SSEPs) were recorded in 21 healthy children (age range: 3.3–13.3 years). The dorsal nerve of the penis/clitoris was stimulated and SSEPs were recorded at spinal L1-D12 and at cortical Cz′-Fz. Morphology, latency and amplitude of the cortical SSEPs were evaluated. A cortical response was obtained in all but two subjects. Cortical SSEPs were broader and less defined in shape in the youngest subjects. There was a progressive shortening of the latency of the P and N components during growth. Spinal responses were obtained only in 6 cases. Nine subjects also underwent tibial nerve stimulation. Pudendal and tibial SSEPs differed in their degree of maturation.     

Somatosensory evoked potentials by electrical stimulation of the third trigeminal branch in humans.

Somatosensory Evoked Potentials by stimulation of the trigeminal nerve (TSEPs) were recorded from 30 healthy subjects (15 males, 15 females; mean age: 45.2 years; range: 21-66 years) in order to assess normative data for clinical purposes. To elicit the TSEPs, electrical square pulses (duration: 0.1 msec; frequency: 3.3 Hz; intensity: 4-6 mA) were delivered by bipolar skin electrodes (cathode over the foramen mentale and anode on the middle of the chin, stimulating the trigeminal third branch). TSEPs were obtained from C3-Fpz and C4-Fpz by twice averaging 1000 responses. Time base was 100 msec; bandpass filter setting was 5-1500 Hz. In our normal subjects the TSEPs were composed of several components (N1, P1, N2, P2 and N3); the components, with the exception of N3, were always bilaterally detectable. Statistical analysis (repeated measures analysis of variance) demonstrated a dependence of TSEP latencies on sex; it did not demonstrate an analogous dependence on either side of stimulation or age. Finally, we propose some guidelines for the evaluation of TSEPs: consider N1, P1, N2 and P2 waves, base the judgement of normality on latencies rather on amplitudes, use differing normative data according to sex.     

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.     

Scalp,basal epidural and intravascular far-field recordings after median nerve stimulation: evidence for a separate N18a potential

Far-field somatosensory evoked potentials (SSEPs) after median nerve stimulation were recorded from scalp- (Fz), epidural(ED) and intravascular electrodes (basilar artery [Bas]) to study the nature of the controversial N18a component of the widespread N18 potential. In healthy volunteers frequently an N18a potential was recorded at Fz. Simultaneous Fz and ED recordings at the pontomesencephalic junction as well as Bas-recordings at the caudal basilar artery showed N18a components identical in latency and shape. With intravascular recordings the shapes differed between the top of the basilar artery and the caudal artery recordings. These findings support the existence of a separate N18a potential. The generator of the N18a is likely to be localized within the upper brainstem.     

Scalp, basal epidural and intravascular far-field recordings after median nerve stimulation: evidence for a separate N18a potential

Far-field somatosensory evoked potentials (SSEPs) after median nerve stimulation were recorded from scalp- (Fz), epidural- (ED) and intravascular electrodes (basilar artery [Bas]) to study the nature of the controversial N18a component of the widespread N18 potential. In healthy volunteers frequently an N18a potential was recorded at Fz. Simultaneous Fz and ED recordings at the pontomesencephalic junction as well as Bas-recordings at the caudal basilar artery showed N18a components identical in latency and shape. With intravascular recordings the shapes differed between the top of the basilar artery and the caudal artery recordings. These findings support the existence of a separate N18a potential. The generator of the N18a is likely to be localized within the upper brainstem.     

The effect of stimulus frequency on post- and pre-central short-latency somatosensory evoked potentials (SEPs)

We assessed the influence of the stimulus frequency on short-latency SEPs recorded over the parietal and frontal scalp of 26 subjects to median nerve stimulation and 16 subjects to digital nerve stimulation. When the stimulus frequency is increased from 1.6 Hz to 5.7 Hz, the amplitude of the N13 potential decreases whereas the P14 remains stable. The amplitude of the N20 is not changed significantly whereas the P22, the P27 and the N30 decrease significantly. In 50% of the subjects 2 components can be seen within the frontal negativity that follows the P22: an early ‘N24’ component, which is not affected by the stimulus rate, and the later N30, which is highly sensitive to the stimulus frequency. The distinct amplitude changes of the N20 and P22 with increasing stimulus frequency is one among other arguments to show that these potentials arise from separate generators.     

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     

Short-latency somatosensory evoked potentials in brain-dead patients

Ten adult brain-dead patients were evaluated for the presence of clearly defined median nerve short-latency somatosensory evoked potentials (SSEPs). All met clinical criteria recommended by the President's Commission report (1981), had positive apnea tests, and had electrocerebral silent EEGs. P13-P14 and N20 were absent in all scalp-scalp channels, although 3 patients showed P13-P14 in scalp-non-cephalic channels. Of 6 patients showing N13, 3 lacked P13-P14. Our data suggest a characteristic destruction of N20 and rostral P13-P14 generators, with variable rostral-caudal loss of lower generators, SSEPs can provide valuable information about brain-stem activity in the evaluation of suspected brain-dead patients.     

Selectivity of attenuation (i.e., gating) of somatosensory potentials during voluntary movement in humans

Attenuation of somatosensory evoked potentials (SEPS) recorded from the scalp during voluntary movement occurs for specific combinations of the finger moved and the peripheral nerve stimulated. The cerebral potential component occurring at a latency of 27 msec (P27) evoked either by stimulation of median nerve at the wrist or by stimulation of 1st and 2nd digit nerves in the fingers were selectively attenuated during movement of 1st digit but were not altered during movement of 5th digit. By contrast, the cerebral P27 component evoked by stimulation of ulnar nerve at the wrist or by stimulation of 5th digital nerve were attenuated during movement of that digit but were not altered during movement of 1st digit. Gating of somatosensory activity is a selective phenomenon occuring when movement involves the areas being stimulated.     

k tibial nerve stimulation: Normative values

Cortical somatosensory evoked potentials to posterior tibial nerve stimulation were obtained in 29 normal controls varying in age and body height. In obtaining these potentials we varied recording derivations and frequency settings. Our recordings demonstrated the following points:

• 1.(1) N20 (dorsal cord potential) and the early cortical components (P2, N2) were the only potentials that were consistently recorded. All other subcortical components (N18, N24, P27, N30) were of relatively low amplitude and not infrequently absent even in normals.
• 2.(2) All absolute latencies other than N2 were correlated with body height. However, interpeak latency differences were independent of body height.
• 3.(3) Below the age of 20, subcortical but not cortical peak latencies correlated with age, but this appeared to be due to changes in body height in this age group.
• 4.(4) Absolute amplitudes and amplitude ratios (left/right and uni/bilateral) showed marked interindividual variability and have very limited value in defining abnormality.
• 5.(5) The use of restricted filter windows facilitated the selective recording of postsynaptic potentials (30–250 Hz) and action potentials (150–1500 Hz).

     

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.     

A method of calculating spinal cord transit time from potentials evoked by tibial nerve stimulation in normal subjects and in patients with spinal cord disease

Somatosensory potentials were evoked by stimulation of the tibial nerve at the ankle and recorded over the spine and scalp in 16 normal subjects and 26 patients with known or suspected spinal cord disease, with the aim of developing a method of measuring spinal sensory conduction velocity using a tolerable number of stimuli, applied unilaterally to alert subjects.In normal subjects N21 was consistently recorded overL1 vertebra and in most subjects a complex, N27/N29/P33, was recorded over the cervical spine referred to the vertex. Constant latencies at different spinal levels and, in one subject, comparison with the latency of the ascending volley indicate that the complex was not derived from the spinal cord but from more rostral structures, and therefore only transit time, rather than velocity, could be measured.In patients with clinically definite multiple sclerrosis, even with minimal clinical signs, the N27/N29/P33 complex was always abnormal. Abnormalities in this and other forms of spinal cord disease were commonly absence or distortion of the complex, prolonged transit time being rare. The clinical value of the method is limited by the very low amplitude of the responses.     

Scalp topography of mechanically and electrically evoked somatosensory potentials in man

Scalp topography of somatosensory evoked potentials following mechanical (SEPs(M)) and electrical (SEPs(E)) stimulation of the left middle finger was investigated with linked ear reference in 21 normal young adults. A small plastic ball (touch) or needle (pain) was used for the mechanical stimulation. With mechanical stimulation, at least 3 positive and 3 negative potentials (P19(M), N24(M), P29(M), N36(M), P49(M) and N61(M)) were found in the post-rolandic area contralateral to the stimulation. The wave form in SEPs(M) was similar to those in SEPs(E), but the peak latency of each component in SEPs(M) was 1–4 msec longer than that in SEPs(E). Earlier components such as P19(M), N24(M) and P29(M) were not as clearly recognized as corresponding components in SEPs(E). However, the wave form recorded on the hemisphere ipsilateral to the stimulation or in the frontal area contralateral to the stimulation showed a greater difference from subject to subject. P19(M), N24(M) and P29(M) correlated positively both with arm length and height of the subject. There was no significant difference of the wave form between the linked ear reference and the bipolar (C4-Fz) derivation. Wave form of SEPs(M) by needle stimulation did not significantly differ from that by plastic ball stimulation.     

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 relationship between median nerve somatosensory evoked potential latencies and age and growth parameters in young children

Median nerve somatosensory evoked potentials (SEPs) were recorded in a group of 35 normal children aged 6–36 months and related to body length, body weight and head circumference. Recordings were made while the child was awake using the following derivations: ipsilateral clavicle - Fpz; seventh cervical vertebra (CV7) - Fpz; contralateral C′ - Fpz. the clavicular-Fpz response was bilobed in 77% of the recordings, the initial being designated CL1 and the following negativity, CL2. Early negativities, coincident in latency with CL1 and CL2, were often present inin CV7-Fpz recordings, however, a negativity longer in latency than CL2 was always present, was designated CVN, and preceded a prominent positivity. A scalp-recorded early negativity (N1) and a following positivity (P1) were well defined in all recordings.The latency of CL1, CL2 and CVN increased with an increase in age and stature. In contrast, significant negative correlations were found between the latency of N1, P1, age and statur. The CL1-CVN interpeak latency did not correlate significantly with age, while the central conduction time (CVN-N1) declined with an increase in age and stature. These findings confirmed the complexity of SEP absolute and interpeak latency changes with an increase in age and stature in young children.     

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.     

P30 and N33 of posterior tibial nerve SSEPs are analogous to P14 and N18 of median nerve SSEPs

Generator sources of far-field P30 and N33 components produced bosterior tibial nerve stimulation were compared with those of the P14 and N18 components of median nerve stimulated somatosensory evoked potentials. Intracranial spatio-temporal distributions of P30 and N33 were similar to those of the P14 and N18 obtained by median nerve stimulation. In clinical cases, the changes in P30 and N33 were correlated with those in P14 and N18, indicative that P30 and N33 are derived from activities similar to those that produce P14 and N18.     

Recovery from central apnea: effect of stimulus duration and end-tidal CO2 partial pressure

The present study was designed to investigate the effect of stimulus duration and chemosensory input on the recovery of central respiratory activity from apnea induced by superior laryngeal nerve (SLN) electrical stimulation. Newborn piglets less than 8 days of age were anesthetized, paralyzed, and mechanically ventilated at differing levels of end-tidal CO2 partial pressure (PCO2). The vagi were cut bilaterally in the neck. Integrated phrenic nerve activity was used as the index of respiratory activity. SLN stimulation caused apnea that persisted after stimulus cessation. The length of apnea following stimulus cessation was directly related to stimulus duration and inversely related to end-tidal PCO2. After apnea, respiratory activity returned gradually to the initial control level. The recovery pattern was well described by a linear regression function using the natural logarithm of time as the independent variable. Prolonging stimulus duration progressively inhibited the amount of initial respiratory activity following apnea. On the other hand, the rate of respiratory recovery was independent of stimulus duration and, except at low end-tidal PCO2 following long (30 s) stimuli, was independent of the end-tidal PCO2 level. These results demonstrate that a long-acting central mechanism regulates recovery from apnea induced by SLN stimulation.