SEPs to median nerve stimulation: normative data for paediatrics

Somatosensory evoked potentials (SEPs) provide neurologists with an assessment of the neuraxis from peripheral nerve to sensory cortex. Their value is particularly relevant in paediatric neurology as sensory clinical examination can be difficult in young infants and children. The clinical utility of SEPs, however, requires knowledge of the alterations in wave form which occur with growth and development. This study presents normative SEP data from 4 months-35 years. Different non-linear maturational months-35 years. Different non-linear maturational patterns were seen in spinal and central segments of the nervous system. The cervical components (N12, N13) changed little in latency until 2-3 years, the N20 decreased in latency until 2-3 years and P22 decreased in latency until 6-8 years, after which latencies increased until adulthood. The greatest latency changes occurred in N12 and N13, the least in N20. Wave form morphology and interpeak latencies also changed with age. Adult morphology was achieved early (from 1 year), but central conduction time (N13-N20) reached adult values only at 6-8 years. This study provides normative values of SEPs during maturation and a functional assessment of pathways known to myelinate and mature at varying rates.     

Comparison of cervical SEPs on median, radial and ulnar nerve stimulation

Cervical responses (SEPs) to stimulation of the median, radial and ulnar nerves were studied in 9 healthy subjects. In recordings from e Cv₇ electrode referenced to a scalp electrode P11 presented a bilobed (P11a+P11b) profile for all three nerves whereas from Cv₂ only P11b appeared as a rule. P11a and P11b were more distinct in the ulnar than in the median and radial nerves. The P11_onset-P13_onset interval was virtually the same for the radial and median nerves and approximately 0.4 msec longer for the ulnar nerve. This difference probably represents the Cv₈ to Cv₆ intramedullary conduction time. An exact evaluation of P11_onset is possible only in low cervical recordings, though the P11_peak may be a useful landmark when recording from Cv₂. P11a would appear to originate at (or near) spinal entry, P11b high in the cervical cord and P13 at supraspinal level.

---

Sommario In nove soggetti, sono state studiate le risposte cervicali da stimolazione dei nervi mediano, radiale ed ulnare. Utilizzando un riferimento cefalico, P11 appare bilobata, registrando da Cv₇, per tutti e tre i nervi, mentre solo la seconda delle due subcomponenti (P11a e P11b, rispettivamente) viene registrata generalmente da Cv₂. P11a e P11b sono meglio distinte fra di loro nel caso del nervo ulnare, che non del radiale o mediano. L'intervallo P11_onset-P13_onset è sovrapponibile fra mediano e radiale e circa 0.45 msec più lungo per il nervo ulnare; questa differenza dovrebbe essere dovuta ad un tempo di conduzione intramidollare fra Cv₈ e Cv₆. Una esatta valutazione di P11_onset è possibile solo a livello cervicale inferiore, mentre il picco P11b può essere utilizzato nel computo delle latenze solo da Cv₂. P11a dovrebbe originare all'ingresso spinale, P11b nel tratto cervicale superiore, P13 a livello sopraspinale.

     

Interference of tactile and pain stimuli on thalamocortical signal processing in humans revealed by median nerve SEPs.

OBJECTIVE: We investigated the interference of tactile and painful stimuli on human early somatosensory evoked potentials (SEPs) including high frequency oscillations (HFOs) to further study thalamocortical processing of somatosensory information. METHODS: Multi-channel median nerve SEPs were recorded during (1) no interference, (2) sensory interference by tactile stimulation to digits 2 and 3, and (3) application of pain to the same digits. Spatio-temporal source analysis separated brain stem (S1), thalamic (S2) and two cortical sources (S3, S4), which were evaluated for the low (20-450 Hz) and high (450-750 Hz) frequency portion of the signal. RESULTS: Low frequency SEPs showed a decrease of activity at cortical source S3 during both conditions, while thalamic source S2 was significantly increased during pain interference. HFOs showed an increase of cortical source S3 and in trend of thalamic source S2 and cortical source S4 during both kinds of interference. CONCLUSIONS: Although the painful stimulus might not be specific for the nociceptive afferents, the present data affirm that at this early stage of sensory information processing within the primary sensory cortex (area 3b, area 1) pain is handled similar to sensory interference. SIGNIFICANCE: HFOs might represent an intrinsic "somatosensory alerting" system which reacts to both interference stimuli in a similar way, therefore indicating an interference without a qualitative evaluation.     

Changes in short latency SEPs (S-SEPs) to median nerve stimulation in brain dead patients

Short latency SEPs (S-SEPs) to median nerve stimulation consist of positive waves of P1, P2, P3 and P4, followed by negative waves of N 16 and N 19. These potential reflect activities of peripheral nerve, dorsal column of the cervical cord and medial lemniscus. The origins of these waves are considered as follows, P1--peripheral part of the brachial plexus, P2--the entry into the spinal cord or the dorsal column, P3--dorsal column nucleus or upper cervical cord, P4--the medial lemniscus, N 16--rostral brain stem or the thalamus, and N 19--thalamocortical projection or the cortex. The purpose of the present study is to elucidate changes of S-SEPs in brain dead patients. Fifteen brain dead patients were examined with S-SEPs. In addition to that, thirteen cases with lesions of subcortical or the brain stem but not in the state of brain death were studied for the controls. S-SEPs with non-cephalic references, conventional SEPs with earlobe reference and the evoked potentials at the Erb's point were recorded in all these cases. Serial recordings were performed in six brain dead cases during the process of rostro-caudal deterioration of the brain stem functions due to cerebral herniation. In the state of brain death, only P1 and P2 were recorded in eleven cases, and in three cases, only P1 was recorded. The other case with anoxic brain damage showed flat S-SEPs and the evoked potentials at the Erb's point could merely be obtained by the supramaximal stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Contribution of cutaneous and muscle afferent fibres to cortical SEPs following median and radial nerve stimulation in man

Somatosensory evoked potentials were recorded after stimulation of motor and cutaneous nerves in the upper limb. Stimulation of the thenar motor branch of the median nerve and the deep motor branch of the radial nerve produced only broad, ill-defined and small-amplitude scalp-recorded responses. In contrast, stimulation of purely cutaneous nerves (digital and the superficial radial) gave responses of large amplitude. The cortical responses following combined deep and superficial radial nerve stimulation were of smaller amplitude than the two individual responses combined. These findings suggest that, contrary to an earlier report (Gandevia et al. 1984), muscle afferents do not make a major positive contribution to the scalp-recorded cortical responses produced by electrical stimulation of mixed nerves in the upper limb.     

Frontal SEPs and parietal SEPs following median nerve stimulation--clinical correlation and consideration of their generation sites

In order to know the characteristics of frontal and parietal SEP components following median nerve stimulation, 25 patients with unilateral cerebral lesions above the thalamus were examined, and their SSEPs were carefully compared with the clinical and radiological findings. In 10 normal subjects, there were three cortical components of the frontal SEPs (P 20-N 28-P 44) and four those components of the parietal SEPs (N 18-P 22-N 26-P 42). In patient's group, central conduction times (CCTs) between components P 13 and each cortical component were measured and the latency differences between normal side and affected side were calculated. When the latency differences increased over 3 S.D. from the mean of the control values or the some cortical components disappeared, they were regarded as abnormal. According to the combination of the abnormalities in frontal and parietal SEPs, three groups were classified as follows: group 1; frontal and parietal SEPs were normal (n = 10), group 2; frontal and parietal SEPs were both affected (n = 10), group 3; parietal SEPs were affected but frontal components were preserved in normal range (n = 5). CT scan showed that the region from internal capsule to cortex around the central sulcus remained intact in the patients of group 1, while this region was involved in various degrees in all cases of the group 2. In patients of group 3, frontal or parietal regions were variously affected. Both the motor and sensory functions were mainly intact in group 1, and disturbed in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of passive tactile co-activation on median ulnar nerve representation in human SI

In animals simple passive co-activation causes a fusion and expansion of the involved cortical representations. We used passive tactile finger co-activation for 40 min to investigate cortical representational changes in the human somatosensory cortex. Magnetic source imaging revealed that the euclidean distance between median and ulnar nerve somatosensory evoked fields (SEF) was significantly reduced after application of 600 synchronous airpuff stimuli to the fingertips of four fingers. In the control experiment without co-activation no significant change in distance was observed. Perception threshold and spatial two-point discrimination were not affected by the synchronous stimulation. This is in contrast to blind three-finger Braille readers who frequently mislocalize stimuli applied to the reading fingers. This points to a lack of behavioural relevance or the short duration of co-activation.     

Ipsilateral and contralateral SEP components following median nerve stimulation: effects of interfering stimuli applied to the contralateral hand

Somatosensory evoked potentials (SEPs) recorded over the hemisphere ipsilateral and contralateral to the electrically stimulated median nerve were analysed in the presence or absence of interfering movement, tactile and vibratory activity in the contralateral hand. In the control wave forms the early potentials recorded over the ipsilateral frontal region, P19 and N25, showed apparent phase reversal with N19 and P25 respectively in the contralateral parietal region and were therefore considered to be produced by the same generator in the primary sensory cortex. All other potentials recorded over the ipsilateral hemisphere were of the same polarity and similar latency to potentials present contralaterally, and their amplitude diminished progressively with distance from the contralateral hemisphere. They were therefore believed to be volume-conducted from the contralateral hemisphere, rather than originating in the ipsilateral hemisphere through uncrossed ascending pathways or interhemispheric connections. The distribution of effects produced by interfering activity in the contralateral hand was demonstrated by subtracting the 'interference' from the 'control' response to derive a 'difference' wave form. Difference potentials present over the contralateral scalp were consistent with influence on generators in the contralateral hemisphere. In particular, voluntary movement of the contralateral hand resulted in difference potentials distributed in accordance with a proposed generator in area 3a or 4. No consistent difference potentials were found in the ipsilateral parietal region. In the ipsilateral frontal region, however, an upward potential whose latency was around 55 msec was proposed to be due to a generator in the supplementary motor area of the contralateral hemisphere.     

Recovery of peripheral and central responses to median nerve stimulation

We recorded the responses to paired stimuli delivered to the median nerve at the wrist in 8 healthy adult volunteers, in order to characterize the recovery of function after a single conditioning stimulus. Responses were recorded over the nerve at the ipsilateral elbow and in the Erb's point region, over the second cervical spinous process, and over the contralateral 'hand area' of the scalp. The data from 1 subject were discarded because of possible artifactual contamination. In the others, the peripheral responses recovered both in latency and amplitude over a time period that accorded with previously published studies. We found, however, that the recovery periods for latency and amplitude of the responses recorded over the spine and scalp were prolonged compared with the corresponding values for the peripheral responses. Except for the responses recorded over the scalp, the recovery of amplitude either preceded or occurred at the same time as latency. By contrast, for the responses recorded over the scalp, there was a delay in the recovery of amplitude compared with latency. The differences in recovery period that we found at different levels of the nervous system are presumably related to structural and electrophysiological differences in afferent pathways, the presence of interposed synapses, and the intrinsic refractory properties of central neuronal populations.     

Dynamic activation of distinct cytoarchitectonic areas of the human SI cortex after median nerve stimulation.

MEG recordings visualized non-invasively a serial mediolateral activation of the human somatosensory 3b area followed by a stationary activation of area 1 after median nerve stimulation. Somatosensory evoked fields (SEFs) were recorded over the hand area contralateral to the right median nerve stimulation at the wrist in six normal subjects. A newly developed MEG vector beamformer technique applied to the SEFs revealed two distinct sources (areas 3b and 1) in the primary somatosensory cortex (SI) during the primary N20m-P22m response in all subjects. The first source was located in area 3b, which started to move sequentially toward mediolateral direction 0.7 ms prior to the peak of N20m and ended its movement 1.4 ms after the peak with a total distance of 11.2 mm. We speculate that the movement reflects a sequential mediolateral activation of the pyramidal cells in area 3b, which is mediated by horizontal connections running parallel to the cortical surface. The second source in area 1, located 5.6 mm medial and 4.2 mm posterior to the first source, was active 1.0 ms after the N20m peak. Then, the first source became inactive and the second source was dominant. In sharp contrast with the first source, the second source was stationary. The different behavior of these two components (moving vs stationary) indicates independent parallel inputs to area 3b and area 1 from the thalamus.     

Cortical generators of somatosensory evoked potentials to median nerve stimulation

In 12 patients with intractable partial seizures, chronically implanted subdural electrodes were used to define the relationship of the epileptogenic focus to cortical functional areas. Cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were recorded from these electrodes. The initial cortical positivity, postrolandic primary cortical potential (PCP), was recorded in all 12 patients with a mean latency of 22.3 +/- 1.6 msec. A potential of opposite polarity, prerolandic PCP, was defined in nine patients with a mean latency of 24.1 +/- 2.7 msec. The latency of the postrolandic PCP was 1.61 +/- 1.59 msec shorter than the prerolandic PCP (p less than 0.01, paired t test). The maximum amplitude postrolandic PCP was 2.1 times larger than the maximum prerolandic PCP (p less than 0.02, paired t test). The phase reversal of the SEPs was compared with the position of the rolandic fissure (RF) defined by electrical stimulation. This study shows that the latency and amplitude characteristics of post- and prerolandic PCPs are significantly different and give support to the concept that they are produced by different generators; and cortical SEPs are helpful in locating the RF.     

Early deflections of cerebral magnetic responses to median nerve stimulation

We have recorded early components of somatosensory evoked magnetic fields with a sensitive 7-channel first-order gradiometer using a wide recording passband (0.05-2000 Hz) and high sampling frequency (8000 Hz). The left median nerve was stimulated at the wrist and responses were recorded over the right hemisphere. The responses typically consisted of a N20m peaking at 18-20 msec, a small P22m peaking at 21-23 msec and a P27m peaking at 29-31 msec. The topography of N20m could be explained by a tangential current dipole in the posterior wall of the central sulcus (probably in area 3b). The equivalent dipoles of P27m were located on average 10 mm antero-medially to the sources of N20m. This suggests that P27m may get a contribution from the anterior wall of the central sulcus. An increase of stimulus repetition rate from 2 to 5 Hz decreased the amplitude of P27m more than that of N20m, which implies that these two deflections are generated by different neural networks.     

Effects of hypoglycemia on functional magnetic resonance imaging response to median nerve stimulation in the rat brain.

The authors studied the effects of a standardized mild-moderate hypoglycemic stimulus (glucose clamp) on brain functional magnetic resonance imaging (fMRI) responses to median nerve stimulation in anesthetized rats. In the baseline period (plasma glucose 6.6 +/- 0.3 mmol/L), the MR signal changes induced by median nerve activation were determined within a fixed region of the somatosensory cortex from preinfusion activation maps. Subsequently, insulin and a variable glucose infusion were administered to decrease plasma glucose. The goal was to produce a stable hypoglycemic plateau (2.8 +/- 0.2 mmol/L) for 30 minutes. Thereafter, plasma glucose was restored to euglycemic levels (6.0 +/- 0.3 mmol/L). In the early phase of insulin infusion (15 to 30 minutes), before hypoglycemia was reached (4.7 +/- 0.3 mmol/L), the activation signal was unchanged. However, once the hypoglycemic plateau was achieved, the activation signal was significantly decreased to 57 +/- 6% of the preinfusion value. Control regions in the brain that were not activated showed no significant changes in MR signal intensity. Upon return to euglycemia, the activation signal change increased to within 10% of the original level. No significant activation changes were noted during euglycemic hyperinsulinemic clamp experiments. The authors concluded that fMRI can detect alterations in cerebral function because of insulin-induced hypoglycemia. The signal changes observed in fMRI activation experiments were sensitive to blood glucose levels and might reflect increases in brain metabolism that are limited by substrate deprivation during hypoglycemia.     

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 potential (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.     

Short-latency components of evoked potentials to median nerve stimulation recorded by intracerebral electrodes in the human pre- and postcentral areas.

OBJECTIVE: To study whether sensory afferents of the hand projected directly to the primary motor cortex (M1) as they have been well electrophysiologically described in monkeys but not in humans. METHODS: We recorded intracerebrally in the central areas (pre- and/or postcentral gyrus) somatosensory evoked potentials (SEPs) to median nerve stimulation in 5 (4 women, 1 man; age 14-37 years) epileptic patients during presurgical evaluation. RESULTS: The primary somatosensory cortex (S1) showed negative-positive components peaking at about 20 and 30 ms, respectively. By contrast, M1 disclosed SEPs of two types of waveforms depending on the portion of the precentral gyrus explored by the different contacts of the electrode. Here, we demonstrated, for the first time, in the medial portion of M1, shaped like an omega in the axial plane, corresponding to the motor hand area, the occurrence of a primary negative component as in S1, but of higher amplitude and peaking at about 4 ms later. In other respects, the lateral portion of M1 disclosed positive-negative components peaking at about 21 and 31 ms, respectively. CONCLUSIONS: These electrophysiological findings, based on accurate spatial and temporal resolution of intracerebral recordings, suggested that somatosensory inputs from the hand projected directly to M1 in its medial portion.     

Dipole modelling of median nerve SEPs in normal subjects and patients with small subcortical infarcts.

Somatosensory evoked potentials (SEPs) to median nerve stimulation were analyzed by means of spatio-temporal dipole modelling in 6 normal subjects and 8 patients with small infarcts in the thalamo-cortical radiation or thalamus. The SEPs could be modelled by a tangentially and a radially oriented equivalent dipole in the region of the contralateral cortical hand area and an equivalent dipole located in the region of the brain-stem. In 3 patients with absence or reduction of amplitudes of cortically generated SEP components, the activity of both cortical dipoles was lost or reduced. In 2 patients the frontally recorded SEP component P20 was lost; in one of them the activity of mainly the tangential dipole was reduced.     

Origins of short latency somatosensory evoked potentials to median nerve stimulation

Short latency SEPs recorded in hand-scalp, ear-scalp and upper neck-scalp leads with stimulation of the median nerve were examined in 27 normal subjects and in 11 selected patients with unilateral complete loss of position sense in order to provide information concerning the generator sources of these potentials. Evidences obtained from both normal subjects and patients suggest the following origins for these short latency SEPs. In hand reference recording, P1 may arise in the brachial plexus just beneath the clavicle, P2 in the cervical dorsal column, P3 mainly in the caudal brain stem, and P4 primarily in the brain stem lemniscal pathways and partly in the thalamus. The initial negative potential recorded in upper neck-scalp leads may originate largely in the cervical dorsal columns. The early positive potential recorded in ear-scalp leads may reflect activity mainly in the brain stem lemniscal pathways and partly in the thalamus. The initial negative component of the cortical SEPs (N1) may arise in the thalamus, and the subsequent positive component (P1) may reflect activity in the primary somatosensory cortex.