Amplitude abnormalities in the scalp far-field N18 of SSEPs to median nerve stimulation in patients with midbrain-pontine lesion

Various amplitude ratios were measured in 20 normal controls and 36 patients with midbrain-pontine, thalamic or putaminal lesions in order to evaluate the amplitude abnormalities in scalp far-field N18 following median nerve stimulation. A study of normal controls showed that the distributions of P9/N18, P14/N18 and N18/P14 + N18 resembled a gaussian distribution and could be used as criteria for determining the decrease in N18 amplitude in each patient. There was a decrease in N18 amplitude, or the absence of N18, in patients with midbrain-pontine lesions, but not in those with thalamic or putaminal lesions.Nine amplitude ratios (P11/P9, P14/P9, N18/P9, P9/P11, P9/P14, P9/N18, N18/P14, P14/N18 and N18/P14 + N18) were compared statistically for normal controls and 3 groups of patients based on non-parametric, Wilcoxon's non-pairs and signed-rank tests. A decrease in N18 amplitude in midbrain-pontine lesion was shown by significant changes in N18/P9, P9/N18, N18/P14, P14/N18 and N18/P14 + N18, no amplitude decreases in P11 and P14 being found from the amplitude ratios of P11/P9, P9/P11, P14/P9 and P9/P14. No significant changes were seen in any of the 9 amplitude ratios when the normal controls and patients with thalamic and putaminal lesions were compared.The amplitude ratios of N18 can be used to detect a decrease in N18 amplitude in patients with midbrain-pontine lesions. The data obtained support the hypothesis that N18 originates in the midbrain-pontine region and that neither the thalamus nor thalamocortical radiation make major contributions to the formation of the N18 peak.     

Origin of scalp far-field N18 of SSEPs in response to median nerve stimulation

To identify the origin of scalp-recorded far-field negativity of short-latency somatosensory evoked potentials to median nerve stimulation (designated N18), direct records were made from the thalamus and ventricular system during 4 stereotaxic and 3 posterior fossa operations.In the thalamus a negative potential with almost the same latency as the scalp N18 was restricted to the Vim nucleus, but there was a large positive potential in the VC nucleus and medial lemniscus. Vim negativity increased in amplitude when high frequency stimulation was given to the median nerve, indicative of a facilitation effect. In contrast, the amplitude of scalp N18 decreased at high frequency stimulus.Direct recordings made through the medulla oblongata to the mid-brain showed a negative potential with gradually increasing latency. Above the upper pons, there was stationary negativity with no latency shift. The similarity between this negative potential and N18 is shown by their having the same latency and same response to the amplitude reduction and latency prolongation produced by high frequency stimulus.Our data suggest that scalp N18 comes from brain-stem activity between the upper pons and the mid-brain rather than from the thalamus.     

Middle-latency somatosensory evoked potentials following median and posterior tibial nerve stimulation in Down's syndrome

Middle-latency somatosensory evoked potentials (SEPs) following median and posterior tibial nerve stimulation were studied in 40 patients with Down's syndrome and in age- and gender-matched healthy controls as well as in middle-aged and aged healthy subjects. In median nerve SEPs, latencies of the initial cortical potentials, N18 and P18, showed no significant difference, but the following potentials N22, P25, N32, P41 and P46 were relatively or significantly shorter in latency in Down's patients than in the controls. Amplitudes of all components in Down's patients were significantly larger than those of age- and gender-matched controls as well as of those of middle-aged healthy subjects, but there was only a small difference in their amplitudes from aged healthy subjects. Results of posterior tibial nerve SEPs were generally consistent with those of median nerve SEPs. Therefore, ‘short latency with large amplitude’ is the main characteristic of middle-latency SEPs in Down's syndrome, possibly related to accelerated physiological aging of the central nervous system.     

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.     

The N18 component of the median nerve SEP is not reduced by vibration

Objective: To study the interference of mechanical vibration of the palm of the hand on the median nerve short-latency SEP components.Methods: Electrically-elicited short-latency median nerve SEP were obtained before and during mechanical vibration (120 Hz) of the palm in two groups of normal individuals (6 in group I and 9 in group II). The amplitude of the different components was compared between the two conditions through non-parametric statistical tests.Results: A significant reduction in the amplitude of the N9, P13/14 and N20 components was detected, however no overall significant changes were detected for the N18 component.Conclusions: Vibration interference reduced all studied components except the N18, these findings are interpreted as supporting evidence for the proposed association between the N18 component and the inhibitory activities elicited in the dorsal column nuclei.     

Modification of median nerve somatic evoked potentials by prior median nerve,peroneal nerve,and auditory stimulation

In a recovery function design, changes were measured in the somatic evoked potentials (SEP) to right median nerve (RMN) shocks preceded by stimulation of: the same nerve (RMN-RMN); the left median nerve having primary input to the homologous sensory area in the contralateral hemisphere (LMN-RMN); the right peroneal nerve having primary input to a different region of the same hemisphere (RPN-RMN); and the auditory nerve with primary input to a different sensory modality (AUD-RMN). Eight inter-stimulus intervals ranged from zero (simultaneous) to 2.5 sec. It was assumed that the degree of interaction between evoked potentials would be related to the degree to which common neural structures are activated or modulated in response to the stimuli. Results were: (a) the primary somatosensory response N20-P30 was little influenced by other somatic or auditory stimulation, interaction occurring predominantly in the RMN-RMN condition; (b) with increasing latency, components showed increasing interaction across modalities; (c) preceding homolateral stimulation (RPN-RMN) showed no greater interaction than preceding contralateral stimulation (LMN-RMN); (d) N55-P100 differed from the primary somatosensory response N20-P30 by showing greater interaction with other somatic stimuli; and (e) N140-P190 showed similarly shaped recovery functions across stimulus pairs but significant differences in magnitude of interaction. These results show that components with similar wave form and topographical characteristics can have different neurophysiological properties.     

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.     

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.     

Nasopharyngeal recordings of somatosensory evoked potentials document the medullary origin of the N18 far-field

Because the nasopharyngeal electrode provides non-invasive access to the ventral brain-stem at the medullo-pontine level we used it for recording somatosensory evoked potentials (SEPs) to median nerve stimulation (non-cephalic reference). After the P9 and P11 far-fields, the nasopharyngeal SEPs disclosed a negative-going component which was interpreted as the near-field equivalent of the P14 scalp far-field generated in the caudal part of the medial lemniscus. Nasopharyngeal SEPs also revealed a large N18 with voltage and features strikingly similar to those of the scalp-recorded N18 far-field. These results suggest that N18 is generated in the medulla and not more rostrally in the brain-stem. The use of a nasopharyngeal electrode as reference for topographic brain mapping is discussed. The paper documents the feasibility and relevance of nasopharyngeal recordings for non-invasive analysis of short-latency SEPs.     

Scalp-recorded short and middle latency peroneal somatosensory evoked potentials in normals: comparison with peroneal and median nerve SEPs in patients with unilateral hemispheric lesions

Peroneal somatosensory evoked potentials (SEPs) were performed on 23 normal subjects and 9 selected patients with unilateral hemispheric lesions involving somatosensory pathways.Recording obtained from right and left peroneal nerve (PN) stimulations were compared in all subjects, using open and restricted frequency bandpass filters. Restricted filter (100–3000 Hz) and linked ear reference (A1–A2) enhanced the detection of short latency potentials (P1, P2, N1 with mean peak latency of 17.72, 21.07, 24.09) recorded from scalp electrodes over primary sensory cortex regions. Patients with lesions in the parietal cortex and adjacent subcortical areas demonstrated low amplitude and poorly formed short latency peroneal potentials, and absence of components beyond P3 peak with mean latency of 28.06 msec. In these patients, recordings to right and left median nerve (MN) stimulation showed absence or distorted components subsequent to N1 (N18) potential.These observations suggest that components subsequent to P3 potential in response to PN stimulation, and subsequent to N18 potential in response to MN stimulation, are generated in the parietal cortical regions.     

The effects of stimulus rates upon median,ulnar and radial nerve somatosensory evoked potentials

We examined the effect of stimulus rates on the somatosensory evoked potential (SEP) amplitude following stimulation of the median nerve (MN) and the ulnar nerve (UN) at the elbow or wrist, and the radial nerve (RN) at the wrist in 12 normal subjects. We measured the amplitude of frontal (P14-N18-P22-N30) and parietal peaks (P14-N20-P26-N34) at a stimulus rate of 1.1, 3.5 and 5.7 Hz. The amplitude attenuation was found at frontal P22 and N30 and to a lesser degree at parietal N20 and P26 peaks with an increasing stimulus rate from 1.1 to 5.7 Hz. The amplitude attenuation was greatest at the elbow when compared to the wrist stimulation for both MN and UN. The attenuation was least for wrist stimulation for the RN. The UN block by local anesthesia just distal to the stimulus electrode at the elbow abolished the amplitude attenuation caused by the fast stimulus rate. The observed amplitude attenuation with the faster stimulus rate is probably due, in part, to interference from the “secondary” afferent inputs. The secondary afferent inputs arise from peripheral receptor stimulation (muscle, joint and/or cutaneous) as a subsequent effect of efferent volleys initiated from the point of stimulation. The greater number of peripheral receptors being activated as more proximal sites of stimulation in a mixed nerve would result in greater attenuation of the SEP recorded from scalp electrodes. We postulate that the attenuation of frontal peaks by the fast stimulus rate is due to the frontal projection of interfering “secondary” afferent inputs.     

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.     

Origin of frontal N15 component of somatosensory evoked potential in man

Origin of the frontal somatosensory evoked potential (SEP) by median nerve stimulation was investigated in normal volunteers and in patients with localized cerebrovascular diseases, and the following results were obtained.

• 1.(1) In normal subjects, SEPs recorded at F3 (or F4) contralateral to the stimulating median nerve were composed of P12, N15, P18.5 and N26. Similar components were recognized in SEP recorded at Fz.
• 2.(2) In patients in whom putaminal or thalamic hemorrhages had destroyed the posterior limbs of the internal capsules, frontal N15 and parietal N18 (N20) disappeared. These components were also absent in patients with cortical (parietal) infarctions. Among these patients, the thalamus was not affected in cases with putaminal hemorrhages and cortical infarctions.

These facts indicate that the generator of the frontal N15 does not exist in the thalamus but that it originates from the neural structure central to the internal capsule, which suggests a similarity to the generator of the parietal N18.Because N15 was recorded in the midline of the frontal region with shorter latency than parietal N18, the frontal N15 might represent a response to the sensory input of the frontal lobe via the non-specific sensory system.     

Latency and amplitude abnormalities of the scalp far-field P14 to median nerve stimulation in multiple sclerosis. A SEP study of 122 patients recorded with a non-cephalic reference montage

The frequency and characteristics of P14 abnormalities were investigated in 122 patients with probable (68), or definite (54) multiple sclerosis by recording SEPs to median nerve stimulation with a non-cephalic reference montage. The most frequent SEP abnormality found in our series (62% of abnormal results) combined latency increase and amplitude reduction of P14. Interindividual variability, inherent in absolute amplitude measurements, was by-passed by calculating the ration between the amplitudes of far-field P9 and P14 components, which proved to be normally distributed in controls. In spite of the strong association (P ⪡ 0.001) between the P9–P14 interpeak interval (IPL) and the P9/P14 amplitude ratio in MS patients, the latter parameter was found to be the only abnormality in 12 patients whose P9–P14 and P14–N20 IPLs were normal. Also IPLs were increased in 12 patients with normal P14 amplitudes. These results suggest that adding the P9/P14 amplitude criterion to standard IPL data might be useful to detect conduction troubles in MS patients.     

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.     

Peri-rolandic and fronto-parietal components of scalp-recorded giant SEPs in cortical myoclonus

Scalp topography of giant SEPs to median nerve stimulation was studied in 4 patients with cortical myoclonus of various etiology. The positive peak (P30) at the contralateral parietal area was simultaneously accompanied by a negative peak at the frontal area (N30), and at least one of these two peaks was enhanced in 2 patients. Another positive peak (P25) and a negative peak (N35) were also identified at the peri-rolandic area with different latency from P30 and N30, respectively, in all patients. N35 was enhanced in 3 patients, and P25 in 2 patients. It is concluded that, as seen in normal subjects, tangential (P30-N30) and radial (P25 and N35) components of SEPs are most likely distinguishable in giant SEPs, and that either one or both of those components is enhanced in different ways depending on the patients.     

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.     

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

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