Specific gating of the early somatosensory evoked potentials during active movement

The gating effect of self-paced rapid flexion movements of the fingers on the early somatosensory evoked potentials following electrical stimulation of the median nerve at the wrist was studied in normal volunteers. Triggering of the median nerve stimulation by the EMG signals with a delay of 100 msec showed that the slow positive wave of the movement-associated potential was not directly responsible for the SEP amplitude variations observed. The nerve action potential at Erb's point as well as far-field components P9 and P11 were unchanged by the active movements. Far-field components P13-P14, which are presumably generated in the medial lemniscus, were not significantly modified. An enhancing effect on the widespread N18 component was found, which is in favour of a subcortical gating process. The parietal component N20 was unchanged by active movement interference whereas the frontal P22 component showed a marked suppression. A fronto-parietal dissociation was thus disclosed which could be in favour of separate cortical generators in the debate on the origin of SEP components. An important gating effect was observed on parietal P27 and frontal N30 components, the latter being considerably reduced in amplitude. The parietal P45 component showed no significant alteration. Each component of the early SEPs was thus distinctly influenced by the gating process during active movement interference.     

Task-relevance and temporal synchrony between tactile and visual stimuli modulates cortical activity and motor performance during sensory-guided movement

Sensory-guided movements require the analysis and integration of task-relevant sensory inputs from multiple modalities. This article sought to: (1) assess effects of intermodal temporal synchrony upon modulation of primary somatosensory cortex (S1) during continuous sensorimotor transformations, (2) identify cortical areas sensitive to temporal synchrony, and (3) provide further insight into the reduction of S1 activity during continuous vibrotactile tracking previously observed by our group (Meehan and Staines 2007: Brain Res 1138:148-158). Functional MRI was acquired while participants received simultaneous bimodal (visuospatial/vibrotactile) stimulation and continuously tracked random changes in one modality, by applying graded force to a force-sensing resistor. Effects of intermodal synchrony were investigated, unbeknownst to the participants, by varying temporal synchrony so that sensorimotor transformations dictated by the distracter modality either conflicted (low synchrony) or supplemented (high synchrony) those of the target modality. Temporal synchrony differentially influenced tracking performance dependent upon tracking modality. Physiologically, synchrony did not influence S1 activation; however, the insula and superior temporal gyrus were influenced regardless of tracking modality. The left temporal-parietal junction demonstrated increased activation during high synchrony specific to vibrotactile tracking. The superior parietal lobe and superior temporal gyrus demonstrated increased activation during low synchrony specific to visuospatial tracking. As previously reported, vibrotactile tracking resulted in decreased S1 activation relative to when it was task-irrelevant. We conclude that while temporal synchrony is represented at higher levels than S1, interactions between inter- and intramodal mechanisms determines sensory processing at the level of S1.     

Normal latency values of early cortical somatosensory evoked potentials in children

Somatosensory evoked potentials (SEPs) after median and posterior tibial nerve stimulation were studied in 172 children ranging in age from 1 day to 16 years for the purpose of obtaining normal reference values, for use in analysing pathological cases. The mean onset and peak latencies of the N wave after median nerve stimulation and of the P wave after posterior tibial nerve stimulation were calculated for 12 age groups. N and P latencies decreased from birth to 3 years of age, when they reached their minimal values. The latencies then increased with age, the increase being greater for posterior tibial nerve SEPs than for median nerve SEPs. By contrast, the ascending time (the interval between onset and peak latencies) decreased progressively with age from birth to adolescence.     

Frontal distribution of early cortical somatosensory evoked potentials to median nerve stimulation

The topography of early frontal SEPs (P20 and N26) to left median nerve stimulation was studied in 30 normal subjects and 3 patients with the left frontal bone defect. The amplitudes of P20 and N26 were maximum at the frontal electrode (F4) contralateral to the stimulation and markedly decreased at frontal electrodes ipsilateral to the site of stimulation. There was, however, no latency difference of P20 and N26 between ipsilateral and contralateral frontal electrodes. These results suggest that the origin of the ipsilateral and contralateral P20 and N26 is the same. The wide distribution of P20 and N26 over both frontal areas could be explained by assuming a smearing effect from generators actually located in the rolandic fissure and motor cortex.     

Influence of stimulus repetition rate on cortical somatosensory potentials evoked by median nerve stimulation: implications for generation mechanisms.

Despite growing clinical and experimental interest in the cortical components of somatosensory evoked potentials (SEPs) little is known about their physiological dynamics, e.g. with changing stimulation parameters. This paper reports the influence of varying stimulus repetition rate from 0.5 to 5 Hz on cortical SEPs up to 60-msec latency after right median nerve stimulation, separately analyzed at frontal (F3), central (C3) and parietal (P3) electrodes. The amplitudes of early frontal P20 and N25, central P14 and N18, and parietal N20 did not change with stimulation rate. Later deflections were significantly modified when their amplitudes were determined with respect to the baseline: at F3 negative N30 and N60 diminished and positive P40 was enhanced with increasing rate of stimulation. At P3 the effects were the reverse, so that positive P27 and P45 were attenuated while negative N34 and N60 were enhanced. At C3 both positive P22 and P40 and negative N60 were reduced. However, the corresponding peak-to-peak amplitudes changed much less. We conclude that SEP waveforms following the earliest cortical deflections are very sensitive to small changes in stimulation frequency. The opposite changes at F3 compared with P3 probably represent the opposite scalp field poles from horizontally oriented generator(s) located within the primary sensorimotor cortex (SMI). We suggest that the rate effects are partly due to selective sensitivity of postexcitatory inhibitory postsynaptic potentials to stimulation frequency.     

Pain-related somatosensory evoked potentials in cortical reflex myoclonus.

To elucidate the sensitivity to pain stimuli in patients with cortical reflex myoclonus, pain-related somatosensory evoked potentials (pain SEPs) following CO2 laser stimulation and conventional electrically-stimulated SEPs (electric SEPs) were compared in four patients with cortical reflex myoclonus. The P25 peak of electric SEPs was considerably enhanced but the P320 potential of pain SEPs was of normal amplitude in all patients. After medication, myoclonus was reduced and the amplitude of P25 was decreased, but P320 showed no change. In our previous study of the scalp distribution in normal subjects, a subcortical site, probably the thalamus, was considered to be the generator source of P320. Because most pain stimuli do not reach the cortex, patients with cortical reflex myoclonus are not sensitive to pain stimuli and P320 in pain SEPs is not enhanced.     

Optimal method to determine the stimulus intensity for median nerve somatosensory evoked potentials.

To find the best method to determine the stimulus intensity for median nerve somatosensory evoked potentials (SEP), we tried to activate muscle or cutaneous branch as preferentially as possible by using ordinary surface stimulation. We minutely moved the stimulating electrode at the wrist in normal subjects and changed the stimulus intensity stepwise at each site. We evaluated the correlation between the amplitudes of the SEP components and peripheral parameters such as the relative intensities to the motor threshold (rMT) or the sensory threshold (rST) and the amplitude of the sensory nerve action potential recorded over the index finger (SNAP2) or that of the compound muscle action potential (CMAP). The sensory parameters (rST and SNAP2) showed better correlation with SEP amplitude than the motor parameters (rMT and CMAP). In an extreme case, stimulation 40% over the motor threshold elicited no N9 response and only a small N20. Adjusting the stimulus intensity at slightly above the motor threshold, as recommended by most guidelines, in such a case would result in an erroneous result. We propose the stimulus intensity resulting in SNAP2 amplitude of 80% of its maximum as the optimal method because it consistently gave almost saturated SEP responses.     

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.     

Prognostic value of early cortical somatosensory evoked potentials after resuscitation from cardiac arrest

Short-latency somatosensory evoked potentials (SEPs) were evaluated in patients after cardiorespiratory arrest to study their pattern of recovery in the acute stage of anoxic-ischaemic coma. Fifty consecutive comatose patients were investigated within 8 h after cardiorespiratory resuscitation. In 30 patients no cortical SEPs were recorded and none of the patients recovered cognition. In 20 patients cortical SEPs were recorded and 5 recovered. The different susceptibility of frontal and parietal cortical structures to anoxia was reflected by the dissociated loss of parietal or frontal potentials in 6 patients. Post-mortem pathology in 15 patients confirmed extensive anoxic-ischaemic damage of cerebral and cerebellar cortex and thalamus in patients without cortical SEPs whereas the histological lesions were restricted to Sommer's sector and Purkinje cells in those with preserved SEPs. SEPs thus reflect the extent of brain damage after cardiorespiratory resuscitation.     

Effect of stimulus intensity on subcortical and cortical somatosensory evoked potentials by posterior tibial nerve stimulation

The effects of stimulus intensity on subcortical and cortical somatosensory evoked potentials (SEPs) to posterior tibial nerve (PTN) stimulation were studied in 16 normal controls. Stimulus intensity was evaluated as a function of sensory threshold (S). Motor threshold (M) varied between 1 S and 2 S. The amplitude of N18 (afferent volley immediately before it enters the spinal canal) increased approximately linearly up to at least 4.5 S. N20 (dorsal cord potential) also demonstrated a linear increase up to at least 4 S but the rate of increase was significantly smaller. All central components (subcortical brain-stem components P27 and N30, and cortical components N1 and P2) showed an even smaller rate of increase which was non-linear and reached a plateau at 3 S. The relatively higher rate of increase of N18 as compared with N20 was most probably due to the recording of sensory impulses plus antidromic impulses in motor fibers. The smaller rate of increase and early saturation of all the central components compared with N20 suggests that of all the afferent fibers generating N20 only the low threshold fibers participate in the generation of more central components. Stimulus intensities of 3 S are recommended for clinical studies of the central SEPs to PTN stimulation.     

Visual and somatosensory evoked cortical potentials in multiple sclerosis.

The diagnostic value of the pattern reversal evoked cortical potential (VEP) and the somatosensory evoked cortical potential (SEP) has been compared in 50 patients with established or suspected multiple sclerosis. A prolonged latency of VEP was found in 96% of definite cases of multiple sclerosis, 58% of probable cases, and 20% of possible cases. A prolonged latency of SEP by stimulation of median or peroneal nerves or both was found in 86% of definite cases of multiple sclerosis, 83% of probable cases, and 50% of possibe cases. When combining the results of all three tests the diagnostic yield increased to 100%, 92%, and 50%, respectively.     

On the significance of giant somatosensory evoked potentials in cortical myoclonus.

Four patients with cortical myoclonus were studied. All had reflex muscle jerking and grossly enlarged somatosensory evoked responses (SEPs) following electrical stimulation of the digital nerves. In addition, three of the patients had spontaneous or action-induced myoclonus. Back-averaging the EEG from these spontaneous muscle jerks showed a large positive wave over the contralateral somatomotor cortex which preceded the jerk by about 20 ms. Administration of lisuride (0.1 mg iv) reduced the severity of the reflex and spontaneous myoclonus, but had no effect on, or increased the size of the SEP. Two of the patients also received 1 mg clonazepam iv. As with lisuride, the severity of myoclonic jerking was reduced although the size of the SEP was increased. It is concluded that the usual association between giant SEPs and reflex muscle jerking can be abolished by acute administration of lisuride and clonazepam in patients with cortical myoclonus.     

Effects of stimulus intensity on posterior tibial nerve somatosensory evoked potentials.

Relationships between stimulus intensity and peak latencies and amplitudes in posterior tibial nerve somatosensory evoked potential patterns were evaluated in ten healthy subjects. Eight intermediate latency peaks between 30 and 125 milliseconds (ms) after stimulus onset and seven amplitudes were analyzed. In general, there was a decrease in latency with each increase in stimulus intensity over a five step intensity range between 5 and 19 milliamps (mA) for most peaks. Similarly, increases in amplitudes generally occurred with increases in stimulus intensity for most peaks. Later peaks N105 and P115 as well as amplitudes P90-N105 and N105-P115 were least sensitive to stimulus intensity changes. The greatest changes in peak latency and amplitude occurred as stimulus intensity was increased from 7 to 11 mA. Beyond 11 mA relatively little change was observed in either peak latencies or amplitudes. Under anesthesia, by contrast, there was no stimulus intensity-peak latency interaction and beyond 11 mA there were decreases in amplitudes. Possible reasons for these findings are discussed.     

How response inhibition modulates nociceptive and non-nociceptive somatosensory brain-evoked potentials.

OBJECTIVE: To examine and compare the modulation of nociceptive somatosensory laser-evoked potentials (LEPs) and non-nociceptive somatosensory electrically-evoked potentials (SEPs) by brain processes related to response inhibition. METHODS: A warning auditory tone was followed by either an electrical or a laser stimulus. Subjects performed a Go/Nogo task in which they were instructed to respond to the laser stimulus and refrain from responding to the electrical stimulus in half of the runs. In the other half, they performed the opposite. The paradigm allowed a direct, within-subject comparison of the electrophysiological correlates of brain processes related to the Go/Nogo task in both somatosensory submodalities. RESULTS: In the Nogo-condition, SEPs displayed an enhanced N120 (early Nogo-response), a reduced vertex P240 and enhanced frontal P3 (late Nogo-responses). In contrast, LEPs only displayed late Nogo-related responses (reduced vertex P350 and enhanced frontal P3). CONCLUSIONS: The early Nogo-related enhancement of SEPs may reflect brain processes specific to the processing of non-nociceptive somatosensory stimuli. Later components of the Nogo-response may reflect cortical activity common to the processing of both nociceptive and non-nociceptive somatosensory stimuli. SIGNIFICANCE: Response inhibition significantly modulates both LEPs and SEPs. Part of these activities may be specific of the eliciting stimulus modality.     

Velocity-dependent suppression of somatosensory evoked potentials during movement

Sensory transmission is known to be impaired during movement of the stimulated body part. This phenomenon is manifested by a decrease of perceptual acuity and a correlated decrease in the size of somatosensory evoked potentials (SEPs). The goal of the present study was to define the relationship between SEP amplitude and speed of movement. SEPs were elicited by brief (25 msec) loading of the wrist flexor muscles. Stimuli were applied while the wrist joint was stationary or moving voluntarily at one of several velocities. In all subjects, SEP amplitude was approximately inversely related to speed of movement at the time of stimulation. The findings refine and extend studies suggesting the velocity dependence of sensory suppression during movement.     

Effect of movement on dipolar source activities of somatosensory evoked potentials.

The early scalp somatosensory evoked potentials (SEPs) to median and tibial nerve stimulation were recorded at rest and during voluntary movement of the stimulated hand and foot, respectively. Both tibial and median nerve SEP distributions at rest could be explained by four-dipole models, in which one dipole was activated at the same latency as the subcortical far field and the three remaining dipolar sources were located in the perirolandic region contralateral to the stimulated side. Voluntary movement reduced all cortical dipoles in strength, while the subcortical one remained unchanged, suggesting that the effect of movement occurs above the cervicomedullary junction. In animals, cutaneous inputs are suppressed during movement and we therefore interpreted the depression of activity in the primary somatosensory cortex induced by movement as due to selective "gating" of cutaneous afferents. Because the reduction in strength of the cortical dipoles was generally lower during passive than active movement, both centrifugal and centripetal mechanisms probably contribute to the phenomenon of "gating." Copyright 1999 John Wiley & Sons, Inc.     

Effects of intrathecal baclofen on lumbosacral and cortical somatosensory evoked potentials.

We analyzed lumbosacral and cortical somatosensory evoked potentials in three spinal cord injury patients undergoing evaluation of intrathecal baclofen infusion for management of spasticity. The cauda equina propagating root wave (R wave) and conus medullaris postsynaptic responses (S and P waves) were analyzed before and during baclofen infusion. Baclofen abolished the concomitantly recorded H-reflex and markedly suppressed the P wave amplitude and area. The S wave amplitude and area were suppressed to a lesser degree. In contrast, there were no significant changes in cortical somatosensory evoked potentials.     

Predictive value of neurological examination for early cortical responses to somatosensory evoked potentials in patients with postanoxic coma

Bilateral absence of cortical N20 responses of median nerve somatosensory evoked potentials (SEP) predicts poor neurological outcome in postanoxic coma after cardiopulmonary resuscitation (CPR). Although SEP is easy to perform and available in most hospitals, it is worthwhile to know how neurological signs are associated with SEP results. The aim of this study was to investigate whether specific clinical neurological signs are associated with either an absent or a present median nerve SEP in patients after CPR. Data from the previously published multicenter prospective cohort study PROPAC (prognosis in postanoxic coma, 2000–2003) were used. Neurological examination, consisting of Glasgow Coma Score (GCS) and brain stem reflexes, and SEP were performed 24, 48, and 72 h after CPR. Positive predictive values for predicting absent and present SEP, as well as diagnostic accuracy were calculated. Data of 407 patients were included. Of the 781 SEPs performed, N20 s were present in 401, bilaterally absent in 299, and 81 SEPs were technically undeterminable. The highest positive predictive values (0.63–0.91) for an absent SEP were found for absent pupillary light responses. The highest positive predictive values (0.71–0.83) for a present SEP were found for motor scores of withdrawal to painful stimuli or better. Multivariate analyses showed a fair diagnostic accuracy (0.78) for neurological examination in predicting an absent or present SEP at 48 or 72 h after CPR. This study shows that neurological examination cannot reliably predict absent or present cortical N20 responses in median nerve SEPs in patients after CPR.     

Spatial attention modulates the cortical somatosensory representation of the digits in humans

The topographic organization of the primary somatosensory cortex adapts to alterations of afferent input. Here, electric source imaging was used to show that spatial attention modifies cortical somatosensory representations in humans. The cortical representation of the electrically stimulated digit 2 (resp. digits 2 and 3) of the right hand was more medial along the somatosensory area 3b in subjects who focused attention on digit 4 of the right hand, while it was more lateral when subjects attended digit 4 of the contralateral hand. This effect was very fast since the direction of attention was changed every 6 min. The results indicate that cortical somatosensory representations not only depend on afferent input but vary when spatial attention is directed towards different parts of the body.