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.     

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.     

Serial recording of median nerve stimulated subcortical somatosensory evoked potentials (SEPs) in developing brain death

Subcortical somatosensory evoked potentials (SEPs) to median nerve stimulation were recorded serially in 35 patients during the evolution towards brain death and in brain death. Neuropathological alterations of the central nervous system down to the C1/C2 spinal cord segment in brain death are well known. SEP components supposed to be generated above this level should be lost in brain death, while components generated below should not be altered. Erb's point, scalp and neck potentials were recorded at C3/4, or over the spinous process C7, using an Fz reference. In 10 patients additional montages, including spinous process C2-Fz, a non-cephalic reference (Fz-contralateral shoulder) and a posterior to anterior neck montage (spinous process C7-jugulum) were used. The cephalic referenced N9 and N11 peaks remained unchanged until brain death. N9 and N11 decreased in parallel in amplitude and increased in latency after systemic effects like hypoxia or hypothermia occurred. The cephalic referenced 'N14' decreased in amplitude and increased in latency after the clinical brain death syndrome was observed, while N13 in the posterior to anterior neck montage remained unchanged. The alteration of 'N14' went parallel to the decrease of the P14 amplitude. The subcortical SEPs in the cephalic referenced lead are supposed to be a peak composed by a horizontally orientated dorsal horn generated N13 and a rostrally orientated P14 arising at the level of the foramen magnum. The deterioration of the non-cephalic referenced P14 and of its cephalic referenced reflection 'N14' seems to provide an additional objective criterion for the diagnosis of brain death.     

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.     

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.

     

Serial median nerve SEPs and SSEPs in patients with West syndrome

We studied serial median nerve somatosensory evoked potentials (SEPs) and short latency somatosensory evoked potentials (SSEPs) in 17 patients with West syndrome. Four of the 7 patients with absent SEPs in the initial examination showed recognizable SEPs in the follow-up studies, associated with improvement of electroencephalogram (EEG). This indicated that SEPs were variable with condition of epilepsy and lack of initial SEPs was not always a poor prognostic factor for seizure control and developmental outcome. Persistent lack of SEPs, however, indicated poor outcome of seizures, EEG and development. Central conduction time in SSEPs did not correlate with seizure or developmental outcome.     

Short latency somatosensory evoked potentials following median nerve stimulation in children

We investigated short latency somatosensory evoked potentials (SSEP) to median nerve stimulation in normal children and children with neurological disorders. The waveform of SSEP in normal children was almost the same as that in adults. The peak latency and interpeak latency in normal children changed during their development. Moreover, after 3 years of age, each peak latency was positively correlated with the body length and arm length. Each peak latency per 1 m of body length decreased with age. We examined SSEP in children with various neurological disorders and found that SSEP was useful for evaluating sensory functions and somatosensory damages in children who were unable to cooperate in clinical examinations. Using SSEP, we could estimate the distal margin of the lesion in the somatosensory pathway, but it was difficult to determine the accurate range of the lesion.     

Intermediate and long latency SEPs in relation to clinical disability in traumatic brain injury patients

Intermediate (0-60 ms) and long latency (0-500 ms) somatosensory evoked potential (SEP) patterns were compared in terms of their relationship to degree of clinical disability in severe traumatic brain injury patients. Long latency (LL) SEP patterns correlated significantly with clinical disability as measured by the Disability Rating scale while intermediate latency (IL) SEP patterns did not. Evoked potential abnormality (EPA) scores based upon LL SEP patterns appear better able to reflect extent and severity of brain dysfunction and overall clinical condition than do IL SEP patterns for severe traumatic brain injury patients.     

The effects of sleep on median nerve short latency somatosensory evoked potentials

The effects of sleep on median nerve short latency somatosensory evoked potentials were studied in 7 subjects made up of 6 patients being evaluated for seizure disorders by all-night electroencephalograms and 1 normal healthy volunteer. The median nerve was stimulated at the wrist, and the peripheral (N9), subcortical (P13) and early cortical (N1, P2) evoked potentials were recorded during full wakefulness and natural night-time sleep. Sleep-wake state was monitored by the simultaneously obtained polysomnogram. The latencies of the cortical responses were prolonged during non-rapid eye movement (NREM) sleep. In 3 of the subjects P2 was consistently bifid during NREM sleep only. The second component of the bifid potential, 3-4 msec longer in latency than the first, appeared to be selectively enhanced during NREM sleep whereas the first component tended to become less prominent or even disappear. This suggests that the 2 peaks have different generators that are affected differently by NREM sleep. These are clinically relevant findings for interpretation of routine clinical studies.     

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.     

Effects on median nerve SEPs of tactile stimulation applied to adjacent and remote areas of the body surface

Study of the influence of continuous tactile stimulation on somatosensory evoked potentials (SEPs) following electrical stimulation of the median nerve revealed an effect due to interfering input from both adjacent and remote regions of the body surface. The distribution of the effect was demonstrated by subtracting the 'interference' from the 'control' response to derive a 'difference' wave form. Tactile stimulation of the thumb ipsilateral to the stimulated median nerve produced a difference wave form in which a marked phase reversal was apparent between pre- and post-central areas for 2 complexes, at latencies of approximately 20 and 30 msec. It is proposed that this may have been due to partial 'saturation' of a generator in the hand region of area 3b in the primary somatosensory cortex (SI), which was then unable to respond fully to the median nerve impulse. A similar effect was observed when the interfering stimulus was applied to the ipsilateral little finger, possibly reflecting a process of 'surround inhibition.' Tactile stimulation of more remote regions (principally the face and contralateral hand) resulted in consistent difference wave forms in which the early components (less than 30 msec latency) had scalp distributions differing from one another but consistent with influence on generators in the face or hand region of the second somatosensory cortex (SII). Later potentials consistently identifiable in the difference wave forms were similar for all locations of the interfering stimulus apart from the ipsilateral thumb and were distributed in accordance with a proposed generator in the parietal 'association' cortex.     

Short latency somatosensory evoked responses to median nerve stimulation in healthy humans: electric and magnetic recordings

Somatosensory Evoked Potentials (SEPs) and Somatosensory Evoked magnetic Fields (SEFs) to median nerve stimulation at wrist were recorded in 5 healthy subjects and the components between 15 and 30 ms after the stimulus were evaluated on the hemiscalp contralateral to the stimulated wrist. SEPs were measured by means of a 32-channel recorder and compared with SEFs obtained via multiple measurements with a 4-channel sensor. Equivalent dipole localization was carried out for the magnetic components peaking at about 15, 20 and 24 ms. The scalp distribution of SEPs, illustrated by bit mapped color images, were qualitatively explained by three separate sources. The first is described as a tangentially oriented dipole placed behind the Central Sulcus and responsible for the parietal N20-"late P25" waves and for the frontal P20-N30 ones. The second is represented by a radieal dipole placed just in front of the Central Sulcus and pointing towards the motor strip, responsible for the rolandic P22 component. The third is just behind the Central Sulcus and is radieally oriented towards the surface of the postcentral sensory area for the "early P25" parietal wave. The SEFs distributions, illustrated by color isofield contour maps, were quantitatively explained by a unique tangential dipole localized, with good resolution, well behind the Sulcus for the 15 ms waves and slightly frontal to this site for the waves peaking at around 20 and 24 ms. The equivalent dipole has been localized at a depth of about 5 cm (15 ms component), 2 cm (20 ms components) and 4 cm (24 ms component), across the studied subjects. It is stressed that the dipole responsible for the magnetic pattern is likely to be the same tangential dipole responsible for a part of the electric pattern. Due to their radieal orientation, the other two dipoles, proposed for the SEPs maps, would be mostly undetectable by a magnetic investigation.     

Origin of component N16 in short latency somatosensory evoked potentials (SSEP) to median nerve stimulation--correlation between component N16 and thalamus

Short latency somatosensory evoked potentials (SSEP) to median nerve stimulation consists of four main subcortical components, namely P 9, P 11, P 13 and N 16 which appears before cortial N 18. However, the origin of component N 16 is a subject of controversy. In an attempt to learn about the generator source(s) of component N 16, SSEP was recorded from 25 patients with various focal lesions of the brain stem and/or thalamus, and abnormalities of the each potential was correlated to the clinically and radiologically defined site of the lesions. Furthermore, the effects of the different frequency in stimulation were also investigated in 6 normal subjects, because latency changes of each component might contribute to the understanding of the generation. Recordings were obtained from 13 patients with brain stem lesion which included 3 cases with pontine hemorrhage, 3 cases with pontine tumor, 3 cases with cerebello-pontine angle tumor, one case of pontine angioma, one case of chordoma, one case of tentorial tumor and one case of MLF syndrome. SSEP changes in these cases were classified into four types as follows: type 1: no response over the base line was recorded, type 2; some responses over the base line were recorded but N 16 was uncertain, type 3; component N 16 was clearly identified but its latency was significantly prolonged, type 4; component N 16 was divided into two peaks. Bilateral abnormality on SSEP with splitted combination of these four types in various degree was observed. Furthermore, these SSEP abnormalities were seen even in the some cases without sensory disturbance. On the other hand, component N 16 was clearly identified in all 12 patients with thalamic lesion which included 11 cases with thalamic hemorrhage and one case with thalamic tumor on the effected side. Comparison of latency and amplitude between normal side and affected side statistically showed no laterality of components P 9, P 11 and P 13, but a tendency of delay in latency of component N 16 on the affected side. Different stimulus repetition rate revealed some other characteristics of each component. Electrical stimuli to median nerve at the wrist were delivered at rates of 3, 6, 9, 12, 15, 18, 21, 24 and 27 Hz. Latencies of components P 9, P 11, P 13, N 16 in Fro.-Cv 7 lead and component N 18 in Par.-Erb lead were measured and all latency changes were calculated relative to the 3 Hz stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)     

Short latency somatosensory evoked potentials from radial, median and ulnar nerve stimulation in man

Short latency somatosensory evoked potentials (SEPs) were elicited by stimulation at the wrist of median, radial, and ulnar nerves, singly or in combination, using normal subjects. Amplitude of P10 was strikingly lower with radial stimulation than with median stimulation, while ulnar-derived P10 was intermediate in amplitude. This difference probably reflects the antidromic firing of motor fibers contained in median nerves as compared with the superficial branch of radial nerve, which is entirely sensory. Beyond P10, there appear to be no significant differences between median, radial and ulnar-derived SEPs. With simultaneous stimulation of several nerves within one arm, larger potentials were sometimes achieved but with poorer definition of P12 and P14. The clinical utility of radial, ulnar, and median stimulation for localizing peripheral lesions derives from the distinct anatomical pathways of the stimulated fibers through the brachial plexus and from the separable motor and sensory components of P10. SEP is less invasive than EMG; this fact, plus its freedom from sampling error, make it potentially more suitable than conventional EMG for sequentially following a patient's clinical course.     

Changes of middle latency somatosensory evoked potentials (SEPs) and alpha rythmicity associated with oculomotor processes

OBJECTIVES: To evaluate median nerve somatosensory evoked potentials (SEPs) and alpha waves during different eye conditions. METHODS: Median SEPs and occipital electroencephalographs (EEG) were recorded in 6 eye conditions: eye-closed (EC), goggle (G), goggle+saccade (GS), saccade (S), eye-opened (EO) and pursuit (P), in 8 normal adults. Subjects saccaded their eyes reacting to auditory cues to watch a diode on the right or left side alternatively during the S condition, or imitated the same saccadic eye-movement as that in the S condition during the GS condition. In the P condition, subjects traced a small circle moving on a computer screen. RESULTS: Compared with the EC and G conditions, N30 (P25-N30 or P14-N30) amplitudes in C4' were significantly larger and the mean amplitude and power of the alpha band was significantly attenuated in the other 4 conditions. The amplitude and power of the alpha band differed significantly between the GS and S conditions, whereas N30 amplitudes were similar between the two conditions. N30-P45 or P45-N60 amplitudes in C4' were significantly larger in the P condition than in other conditions. CONCLUSIONS: Present findings suggest that different neural mechanisms cause alpha blocking and the modification of middle latency SEPs associated with oculomotor control.