Short latency mechanically evoked somatosensory potentials in humans.

Somatosensory potentials evoked by mechanical stimulation were recorded by surface electrodes over (1) the digital nerves in the index finger, (2) the median nerve at the wrist, (3) the median nerve near the axilla, (4) the brachial plexus, (5) the cervical cord at CII, (6) the scalp overlying the somatosensory cortex. Nerve conduction velocities varied inversely with age and ranged from 43 to 68 m/sec. Mechanically evoked potentials recorded from the electrodes overlying the digital nerves were an artifact of the finger movement. All other electrode configurations recorded potentials comparable to those evoked by electrical stimulation of nerves. These mechanically evoked potentials could prove useful in the assessment of clinical disorders of somatosensory function from receptor to cortex in man.     

Effect of stimulus intensity on short latency somatosensory evoked potentials.

The peripheral and central potentials evoked by percutaneous electrical stimulation of the median nerve were investigated in a group of neurologically normal subjects. We found: (1) Motor threshold stimulation gave consistently submaximal responses and probably does not represent an optimal intensity for routine use. (2) The sum of motor plus sensory threshold gave potentials which were consistently at, or close to, maximal in amplitude. This intensity was comfortable for all subjects. (3) When stimulating at intensities above motor threshold, the increase in amplitude of peripheral potentials markedly exceeded that of the central potentials. There was evidence suggesting that amplitudes would decline at very high stimulus intensities. (4) The P13 peak latency and the P13--N9 interpeak latency declined and the N17--P13 interpeak latency increased with increasing intensities of stimulation. The N9 and N18 peak latencies remained stable.     

Hypothermia-induced changes in rat short latency somatosensory evoked potentials

Under general anesthesia, rats were gradually cooled from 37°C to 24°C. Slowly cooling avoided large temperature gradients between central and peripheral nervous systems. Short latency somatosensory potentials were evoked by forepaw stimulation and recorded from skull and depth structures. Cooling progressively increased onset and peak latencies and duration of all potentials. Amplitude of surface and depth recorded potentials decreased with decreasing temperatures except amplitude of surface component I increased. The response of surface and depth components to different rates of stimulation and cooling clearly indicates that cooling slows synaptic transmission much more than fiber conduction. The response of surface and depth recorded potentials to hypothermia suggests that evoked activity in cervical dorsal column and cuneate nucleus contributes to surface component I, that activity in cuneate nucleus, medial lemniscus, and inferior cerebellar peduncle contributes to surface component II, and that activity in thalamocortical fibers and probably cerebellum contributes to surface component III. These conclusions agree with our previous thoughts about the origin of short latency, surface recorded somatosensory evoked potentials.     

Short latency somatosensory potentials in humans.

A sequence of high frequency potentials was averaged from the scalp of 10 normal human subjects during the first 25 msec following median nerve stimulation. There was a large positive component with a peak latency between 18.9 and 22.3 msec localized to the somatosensory area contralateral to stimulation. This was preceded by an early positive potential arising peripherally (peak latency 7.7-9.7) and at least 3 negative to positive deflections which appear to originate in multiple subcortical structures. When corrected for arm length, intersubject variability was less than 5% for all components. With further clarification, this method should allow one to study neural conduction along the entire somatosensory pathway.     

Stage II sleep alters infants' short latency somatosensory evoked potentials

To evaluate the effects of stage II sleep on short latency somatosensory evoked potentials (SLSEP) to median nerve stimulation, we studied 16 normal infants from two to twelve months of age. SLSEP were recorded during waking and stage II sleep. Four channels of parasagittal EEG and behavioral observations were used to classify states. Compared with SEP in the waking state, cerebral potentials in stage II sleep were of much lower amplitude, even vanishing entirely in several infants. In addition, the change from waking to stage II sleep produced significantly longer latencies of the peaks N1, P1, and P2. We suggest performing SLSEP in infants in the waking state in order to assess cerebral somatosensory function.     

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.     

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.     

Mechanically and electrically evoked somatosensory potentials in humans: Scalp and neck distributions of short latency components

Short latency somatosensory potentials evoked by electrical stimulation of the median nerve as well as by mechanical stimulation on the nail of the index finger were recorded from 10 normal adults using a noncephalic reference (the forearm contralateral to the stimulus). Potentials were recorded from 15 electrode locations extending from the level of the 4th thoracic through the 7th, 4th and 2nd cervical vertebrae to the scalp at O_z, P₄, P₃, A₂, A₁, C₄, C_z, C₃, F₄, F₃ and F_pz. In general, all the components of potentials evoked by mechanical stimulation had electrically evoked counterparts with comparable surface distributions and variations between subjects. Some of the electrically evoked components, which were low in amplitude and variable in occurrence between subjects, did not have mechanically evoked counterparts. Possible generators of the components detected are discussed based on their surface distribution and polarity reversals. A comparable study on patients with well localized lesions must be performed in order to support or disprove the generators proposed.     

The effects of a supratentorial mass lesion on brain-stem auditory evoked potentials and short latency somatosensory evoked potentials

Nineteen patients with unilateral supratentorial mass lesion and without any evident clinical signs of transtentorial herniation were studied with Computed Tomography (CT), brain-stem evoked potentials (BAEPs) and central conduction time (CCT) of short latency somatosensory evoked potentials (SEPs). Sixteen had tumours, two had intracranial haematoma and one had chronic subdural haematoma. CT detected the initial signs of transtentorial herniation in every case. Preoperative I-V interpeak latency (IPL) was significantly (M+2SD) prolonged in 26% of cases on the lesion side and in 21% of cases on the opposite side. The mean I-V IPL was significantly prolonged both on the lesion side and the opposite side (P < 0.01, P < 0.02, respectively). Suppression of Wave V (M-2SD) was seen only in two cases, however, the mean amplitude of Wave V was significantly decreased both on the lesion side and on the opposite side (P < 0.001, P < 0.01, respectively). CCT of SEPs was significantly (M+2SD) prolonged in 33% of cases on the lesion side and in only 13% on the opposite side. The mean CCT was, however, significantly prolonged both on the lesion and on the opposite side (P < 0.001, P < 0.02, respectively). Postoperative I-V IPL was significantly prolonged in only 11% of cases while the mean I-V IPL was still significantly prolonged (P < 0.07) and the mean amplitude of Wave V was still suppressed (P < 0.001) on the lesion side. On the other hand, there was neither abnormality of I-V IPL nor suppression of Wave V on the opposite side. Postoperative CCT was significantly prolonged in 43% of cases and the mean CCT was also significantly (P < 0.01) prolonged on the lesion side. However, there was no prolongation of CCT on the opposite side. Preoperative findings of both BAEPs and SEPs show the abnormality due to the supratentorial lesion and postoperative findings of these potentials indicate both the effects of surgical decompression and the residual abnormalities due to the supratentorial mass lesion.     

Short latency somatosensory evoked potentials in infants

Short latency somatosensory evoked potentials (SEPs) to unilateral median nerve electrical stimulation were recorded from normal infants at birth and at 2, 4, 6, 8, 10 and 12 months of age. Three channels were recorded: Erb's point-Fz; C II (over 2nd cervical vertebra)-Fz; contralateral C' (2 cm posterior to C3 or C4)-Fz. Sweep time = 50 msec. At birth, the C II potential was seen in all infants; the Erb's point and C' potentials were seen in two-thirds. All older infants had well developed potentials at all sites. The mean latency of the Erb's point potential was stable over time. The latency of the C II potential decreased with maturation. At C', 4 components were seen, the latencies of which decreased with maturation: N1, P1, N2 and P2. The duration of N1 and P1 decreased with maturation. Standard deviations were relatively small for latencies and large for amplitudes. SEPs were adversely affected by using the 60 c/sec filter. Increasing the low frequency filter from 1 to 30 c/sec changed SEP, particularly in younger infants. Abnormal SEPs were seen in prematures surviving periventricular hemorrhage.     

Effects of hypothermia on brainstem auditory evoked potentials in humans

Ten adult patients who underwent open heart surgery under induced hypothermia had brainstem auditory evoked potentials (BAEPs) recorded at 1 degree- to 2 degrees C-steps as body temperature was lowered from 36 degrees C to 20 degrees C to determine temperature-dependent changes. Hypothermia produced increased latencies of BAEP waves I, III, and V; the prolongation was more severe for the later components with the result that interpeak latencies I-III, III-V, and I-V were also prolonged. The temperature-latency relationship was nonlinear and best expressed by exponential curve. The latencies of waves I, III, V and the interpeak latency I-V increased roughly 7% for each 1 degree C drop; they doubled at a temperature around 26 degrees C. The amplitude of the BAEP components had a quasiparabolic relationship to temperature; the amplitude rose with hypothermia to 28 degrees or 27 degrees C, but decreased linearly with further cooling. All BAEP components were present at temperatures above 23 degrees C and absent below 20 degrees C. With rewarming, the changes reversed and BAEPs returned to initial prehypothermia status.     

Short latency somatosensory evoked potentials in Charcot-Marie-Tooth Disease

9 patients with Charcot-Marie-Tooth Disease (CMTD) of intermediate type (PMA type II, 10), all from the same family, presented with a significant increase of the interpeak N9-N13 latency. This increase is already present in the pre-symptomatic phase of the disease and there is no significant difference between the various patients of different ages and clinical severity, indicating that the lesions appears very early and tends to establish itself equally early. Similar behaviour is also seen in the distal conduction velocity along the sensitive fibres, while the more proximal areas seem to be relatively spared. The authors interpret these data as an expression of a distal central peripheral sensory neuropathy. In contrast, the lesion of the peripheral motor fibres, particularly in the legs, has a different and more severe pattern of evolution. Alterations in central conduction time (N13-N20) were not seen in any of the 9 patients studied.     

Effects of stimulus intensity on latency and conduction time of short-latency somatosensory evoked potentials.

We studied the effect of stimulus intensity on latencies of short-latency somatosensory evoked potentials (SSEP) by measuring both onset and peak latencies individually. The latencies of N9, N13, N20 and N9-N13 peripheral conduction time (PCT) of median nerve (MN) SSEP, and N8, N23, P37 and N8-N23 PCT of tibial nerve (TN) and sural nerve (SN) SSEP significantly shortened with increasing stimulus intensity by onset latency measurement. However, those latencies by peak latency measurement were less significantly shortened or had only a trend of latency shortening without statistical significance. In contrast to PCT, N13-N20 central conduction time (CCT) of MN-SSEP and N23-P37 CCT of TN- or SN-SSEP showed no latency changes with the increased stimulus intensity by both onset and peak latencies measurement. As peak latencies had greater interindividual variability than onset latencies shown by larger standard deviation, shortening of onset latencies were more consistent than that of peak latencies. We think shortening of onset latencies indicates the recruitment of faster conduction fiber along with increased stimulus intensity. As the degree of latency shortening was less if stimulus intensity was above 2.5 times sensory threshold, the stimulus intensity greater than 2.5 times the sensory threshold should be used for clinical application.     

Somatosensory evoked potentials from the thalamic sensory relay nucleus (VPL) in humans: correlations with short latency somatosensory evoked potentials recorded at the scalp

Somatosensory evoked potentials (SEPs) were recorded in humans from an electrode array which was implanted so that at least two electrodes were placed within the nucleus ventralis posterolateralis (VPL) of the thalamus and/or the medial lemniscus (ML) of the midbrain for therapeutic purposes. Several brief positive deflections (e.g., P11, P13, P14, P15, P16) followed by a slow negative component were recorded from the VPL. The sources of these components were differentiated on the basis of their latency, spatial gradient, and correlation with the sensory experience induced by the stimulation of each recording site. The results indicated that SEPs recorded from the VPL included activity volume-conducted from below the ML (P11), activity in ML fibers running through and terminating within the VPL (P13 and P14), activity in thalamocortical radiations originating in and running through the VPL (P15, P16 and following positive components) and postsynaptic local activity (the negative component). The sources of the scalp-recorded SEPs were also analyzed on the basis of the timing and spatial gradients of these components. The results suggested that the scalp P11 was a potential volume-conducted from below the ML, the scalp P13 and P14 were potentials reflecting the activity of ML fibers, the small notches on the ascending slope on N16 may potentially reflect the activity of thalamocortical radiations, and N16 may reflect the sum of local postsynaptic activity occurring in broad areas of the brain-stem and thalamus.     

Changes of short latency somatosensory evoked potential in sleep

We studied how the first negative waves (frontal 'N18' and parietal 'N20') of median somatosensory evoked potentials (SEP) change from waking to sleep in 9 healthy volunteers. Frontal and parietal responses in awake subjects showed multiple fast frequency potentials (FFP) over the ascending and descending phases of the slow negative waves. The main frontal FFP consisted of N16, P17, N18, P18, N19 and P20, with an additional small FFP, n15, over the ascending phase of N16. The parietal FFP included 3 major peaks (N15, P18 and N20) and 3 small FFP (n17, n19 and n20). Frontal FFP, except for n15, were markedly attenuated or totally disappeared in stage II sleep. Only a few FFP were identified in stage IV. The FFP returned in REM sleep, but amplitude was smaller than the waking state. Parietal FFP were also attenuated in NREM and recovered in REM sleep, but these changes were less prominent compared to those of frontal FFP. Latencies of frontal P20 and parietal N20 were prolonged in NREM sleep with greater prolongation of P20 than N20. These returned to waking values in REM sleep. These findings suggest that the frontal and parietal major negative peaks ('N18' and 'N20') consist of multiple physioanatomical substrates mediated through complex thalamocortical projection systems, and that the FFP are closely related to the sleep-wake mechanism possibly reflected by mutual interaction between cortex and the thalamic reticular system.     

Short latency somatosensory evoked potentials in children with autism

SSEP were recorded in normal volunteer, autism, MBD and MR groups in order to find electrophysiological evidence of a brain lesion. Peak latencies per 1 m body length, P1/H, P2/H and P3/H in MR, and P3/H in autism, were greater than those in normal controls. The values of interpeak latencies per 1 m body length, P1-P3/H and P2-P3/H in autism and MR, were greater than those in normal controls. These in MBD were not different from in normal controls. The cause of the increase in P1/H in MR is unknown. The increases in P1-P3/H and P2-P3/H suggest that in autism and MR there is brainstem dysfunction. It is not clear whether there is a relationship among autism, MBD and MR.     

Short latency somatosensory evoked potentials in patients with syringomyelia

Short latency somatosensory evoked potentials (SSEPs) following median nerve and posterior tibial nerve stimulation were studied in six patients with syringomyelia. Three patients had Chiari malformations, two patients experienced fracture of the spine and one patient had a cauda equina ependymoma. SSEPs following median nerve stimulation were abnormal in all patients, of which five patients showed abnormal SSEPs only in the unilateral stimulation on the side of sensory deficits. SSEPs obtained from three out of eight upper extremities which showed no disturbance of deep sensation, were abnormal, so SSEPs were able to detect subclinical abnormality indicating dorsal column dysfunction. Abnormal patterns of SSEPs were classified in three types as follows; Type 1: disappearance of P13, N16 and N18 (3 cases), Type 2: the prolonged interpeak latency P11-P13 (2 cases), and Type 3: abnormal N16 and N18 with preserving P13 (1 case with Chiari malformation). P9 and P11 were present without prolonged latencies in all cases. SSEPs following posterior tibial nerve stimulation were abnormal in two of the three tested patients. Those two patients had disturbance of deep sensations in the lower extremities. All patients underwent surgical treatment, syringo-peritoneal shunt in four patients, foramen magnum decompression with syringo-subarachnoid shunt in one patient, and total removal of an ependymoma of the cauda equina with syringotomy in one patient. Postoperative neurological improvement were found in three patients, of which two cases also showed improvement in SSEPs. On the contrary SSEPs were unchanged in two patients with posttraumatic syringomyelia, whose postoperative neurological condition was also unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)