The modulation of somatosensory evoked potentials during the foreperiod of a forewarned reaction time task

During the foreperiod of a forewarned reaction time (RT) task reflexes in the executing limb increase to a lesser extent than those in the contralateral limb. This is possibly due to input modulation. The present study investigates the possibility of cutaneous sensory modulation during motor preparation by studying the amplitudes of somatosensory evoked potentials (SEPs). Eighteen subjects performed a forewarned RT task with the same fingers as the ones which were electrically stimulated. SEPs evoked during the 4 sec preparatory period were compared to those evoked during movement execution and during the resting period after the motor response respectively. During response execution most SEP components showed smaller amplitudes, i.e., they were gated, which agrees with other studies. In the first part of the foreperiod no SEP modulation was observed. Towards the end of the foreperiod, 500 msec before the response stimulus (RS), the amplitude of the contralateral parietal N70-P100 was significantly decreased, while the P45-N70 showed a similar tendency. However, at the same time the P100-N140 was increased in amplitude. The decrease of the intermediate latency components towards the end of the foreperiod is discussed in terms of gating, while the increase in the long latency component is discussed with respect to a decrease in RT on trials where the fingers were stimulated just before the RS, pointing to the role of attentional mechanisms.     

Effect of manipulation and fractionated finger movements on subcortical sensory activity in man

Previous studies have shown that the somatosensory evoked potentials (SEPs) recorded from the scalp are modified or gated during motor activity in man. Animal studies show corticospinal tract terminals in afferent relays, viz. dorsal horn of spinal cord, dorsal column nuclei and thalamus. Is the attenuation of the SEP during movement the result of gating in subcortical nuclei? This study has investigated the effect of manipulation and fractionated finger movements of the hand on the subcortically generated short latency SEPs in 9 healthy subjects. Left median nerve SEPs were recorded with electrodes optimally placed to record subcortical activity with the least degree of contamination. There was no statistically significant change in amplitude or latency of the P9, N11, N13, P14, N18 and N20 potentials during rest or voluntary movement of the fingers of the left hand or manipulation of objects placed in the hand. The shape of the N13 wave form was not modified during these 3 conditions. It is concluded that in man attenuation of cortical waves during manipulation is not due to an effect of gating in the subcortical sensory relay nuclei.     

Dissociation induced by voluntary movement between two different components of the centro-parietal P40 SEP to tibial nerve stimulation

Whether the two earliest cortical somatosensory evoked potentials (SEPs) to tibial nerve stimulation (N37 and P40) are generated by the same dipolar source or, instead, originate from different neuronal populations is still a debated problem. We recorded the early scalp SEPs to tibial nerve stimulation in 10 healthy subjects at rest and during voluntary movement of the stimulated foot. We found that the P40, which reached its highest amplitude on the vertex at rest, changed its topography during movement, since its amplitude was reduced much more in the central than in the parietal traces. These findings suggest that two different components contribute to the centro-parietal positivity at rest: (1) the P37 response, which is parietally distributed and is not modified by movement, and (2) the `real' P40 SEP, which is focused on the vertex and is reduced in amplitude during voluntary movement. Since, also, the N37 response did not vary its amplitude under interference condition, it is possible that the N37 and P37 potentials are generated by the same dipolar source. Other later components, namely P50 and N50, were significantly reduced in amplitude during foot movement. Lastly, the subcortical P30 far-field remained unchanged and this suggests that the phenomenon of amplitude reduction during movement (i.e. gating) occurs above the cervico-medullary junction.     

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.     

Recovery function of somatosensory evoked potentials in juvenile myoclonic epilepsy*

Abstract

Objective: We analysed the recovery function of somatosensory evoked potentials (SEPs) in juvenile myoclonic epilepsy (JME) patients. We hypothesized that there may be disinhibition in the recovery of SEPs at 20–100?ms intervals in JME patients.

Methods: We recorded SEPs and SEP recovery in 19 consecutive patients with JME admitted for a routine follow-up examination, and in a control group composed of 13 healthy subjects who were similar to the patient group regarding age and sex. The recovery function of SEPs was examined using paired stimuli at 30, 40, 60, and 100?ms intervals.

Results: The amplitudes of N20-P25 and P25-N33 components were higher in patients with JME. Ten patients had high-amplitude SEPs. By paired stimulation, there was inhibition of SEPs in both groups. The mean recovery percentages of N20-P25 and P25-N33 components at 30, 40, 60, and 100?ms were not different between healthy subjects and patients with JME.

Conclusions: The recovery function of SEP is normal in JME even in the presence of high-amplitude SEPs.     

Somatosensory evoked potentials at rest and during movement in Parkinson's disease: evidence for a specific apomorphine effect on the frontal N30 wave

Studies attempting to relate the abnormalities of the frontal N30 components of the somatosensory evoked potentials (SEPs) to motor symptoms in Parkinson's disease (PD) have shown contradictory results. We recorded the frontal and parietal SEPs to median nerve stimulation in 2 groups of PD patients: a group of 17 patients presenting the wearing-off phenomenon, and a group of 10 untreated PD patients. The results were compared with a group of 13 healthy volunteers of the same age and with a group of 10 non-parkinsonian patients. All parkinsonian and non-parkinsonian patients were studied before (“off” condition) and after a subcutaneous injection of apomorphine (“on” condition). The gating effects of a voluntary movement (clenching of the hand) on the SEPs were also studied for the wearing-off group of PD patients (in states off and on) in comparison with the healthy subjects. At rest and in the off condition the amplitude of the frontal N30 was significantly reduced in the 2 groups of PD patients. We demonstrate that the movement gating ability of the PD patient is preserved in spite of the reduced amplitude of the frontal N30. This result suggests that the specific change in the frontal N30 in PD is not the consequence of a continuous gating of the sensory inflow by a motor corollary discharge. Clinical motor improvement induced by apomorphine was associated with a significant enhancement of the frontal N30 wave. In contrast, the subcortical P14 and N18 waves and the cortical N20, P22, P27 and N45 were not statistically modified by the drug. Apomorphine infusion did not change the absolute reduced voltage of the N30 reached during the movement gating. While the frontal N30 component of the non-parkinsonian patients was significantly lower in comparison to healthy subjects, this wave did not change after the apomorphine administration. In the wearing-off PD patient group the frontal N30 increment was positively correlated with the number of off hours per day. This specific apomorphine sensitivity of the frontal N30 was interpreted as a physiological index of the dopaminergic modulatory control exerted on the neuronal structures implicated in the generation of the frontal N30.     

Abnormalities of parietal and prerolandic somatosensory evoked potentials in Huntington's disease

Cervical, parietal and prerolandic somatosensory evoked potentials (SEPs) to median nerve stimulation at the wrist were recorded with an earlobe reference in 24 patients with Huntington's disease (HD) and in 24 age-matched normal controls. Cortical responses of abnormal wave form and reduced amplitude were constantly observed in HD patients. SEP changes affected more severely the prerolandic (P22/N30) pattern, which could not be recognized in two-thirds of patients, than the parietal (N20/P27) pattern, which could be identified in all cases. The N20 latency and the central conduction time (N13–N20 interval) were significantly increased. The occurrence of abnormalities of central conduction and of a predominant involvement of the prerolandic SEP pattern suggests an impairment of impulse transmission along the somatosensory lemniscal pathway at subcortical, possibly thalamic, level in HD.     

Somatosensory evoked potentials during long-term isometric muscle contraction

The effect of sustained isometric contraction on somatosensory evoked potentials (SEPs) was studied. An attenuation of early SEP components N20--P30, P30--N35) was observed during the last minute of the endurance time. The late components (P45--N55, N55--P100) showed a significant increase of the amplitude during the first minute of the contraction. The amplitude of N35--P45 did not change during voluntary contraction, although it was decreased immediately after the contraction. An increase of the integrated EMG of forearm flexors was observed in the last minute of the endurance time. The maximal voluntary contraction was decreased immediately after the sustained contraction. The observed changes in SEPs could be attributed to possible changes in sensory information and motor command due to motor task.     

Single-trial detection for intraoperative somatosensory evoked potentials monitoring

Abnormalities of somatosensory evoked potentials (SEPs) provide effective evidence for impairment of the somatosensory system, so that SEPs have been widely used in both clinical diagnosis and intraoperative neurophysiological monitoring. However, due to their low signal-to-noise ratio (SNR), SEPs are generally measured using ensemble averaging across hundreds of trials, thus unavoidably producing a tardiness of SEPs to the potential damages caused by surgical maneuvers and a loss of dynamical information of cortical processing related to somatosensory inputs. Here, we aimed to enhance the SNR of single-trial SEPs using Kalman filtering and time–frequency multiple linear regression (TF-MLR) and measure their single-trial parameters, both in the time domain and in the time–frequency domain. We first showed that, Kalman filtering and TF-MLR can effectively capture the single-trial SEP responses and provide accurate estimates of single-trial SEP parameters in the time domain and time–frequency domain, respectively. Furthermore, we identified significant correlations between the stimulus intensity and a set of indicative single-trial SEP parameters, including the correlation coefficient (between each single-trial SEPs and their average), P37 amplitude, N45 amplitude, P37-N45 amplitude, and phase value (at the zero-crossing points between P37 and N45). Finally, based on each indicative single-trial SEP parameter, we investigated the minimum number of trials required on a single-trial basis to suggest the existence of SEP responses, thus providing important information for fast SEP extraction in intraoperative monitoring.     

Gating of the early components of the frontal and parietal somatosensory evoked potentials in different sensory-motor interference modalities

Three different interfering conditions were studied during the recording of pre- and postcentral somatosensory evoked potentials (SEPs) following median nerve stimulation at the wrist in 16 normal subjects: active finger movement (MVT), light superficial massage (LSM) and deep muscular massage (DMM) of the hand. Special attention was focused on selective effects on individual SEP components. The frontal N₃₀ component showed the most significant amplitude reduction during the three interfering conditions (76.4% of reduction in MVT, 36.4% in DMM and 32.9% in LSM). In contrast the frontal N₂₃ was not significantly changed and the preceding P₂₂ component was only reduced in the MVT condition.Postcentral N₂₀ was unchanged by the three conditions while P₂₇ was clearly gated by movement but not significantly by LSM and DMM. The three interfering conditions enhanced the parietal N₃₂ and had no significant effect on the parietal P₄₅.An important point was the interindividual variability of these effects and it appeared that group average wave forms would therefore be confusing.The peak latency of some SEP components was changed during the interfering conditions. The most important effect was an increase of postcentral P45 latency which was found to be related to the amplitude enhancement of N₃₂.     

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.     

Sensory Attenuation Assessed by Sensory Evoked Potentials in Functional Movement Disorders

Background

Functional (psychogenic) movement disorders (FMD) have features associated with voluntary movement (e.g. distractibility) but patients report movements to be out of their control. One explanation for this phenomenon is that sense of agency for movement is impaired. The phenomenon of reduction in the intensity of sensory experience when movement is self-generated and a reduction in sensory evoked potentials (SEPs) amplitude at the onset of self-paced movement (sensory attenuation) have been linked to sense of agency for movement.

Methods

We compared amplitude of SEPs from median nerve stimulation at rest and at the onset of a self-paced movement of the thumb in 17 patients with FMD and 17 healthy controls.

Results

Patients showed lack of attenuation of SEPs at the onset of movement compared to reduction in amplitude of SEPs in controls. FMD patients had significantly different ratios of movement onset to rest SEPs than did healthy controls at each electrode: 0.79 in healthy controls and 1.35 in patients at F3 (t = -4.22, p<0.001), 0.78 in healthy controls and 1.12 at patients C3 (t = -3.15, p = 0.004) and 0.77 in healthy controls and 1.05 at patients P3 (t = -2.88, p = 0.007).

Conclusions

Patients with FMD have reduced sensory attenuation as measured by SEPs at onset of self-paced movement. This finding can be plausibly linked to impairment of sense of agency for movement in these patients.     

Reliability and upper normal variability limits of pattern reversal visual evoked potential parameters.

Twenty healthy volunteers aged 21-48 years (10 males, 10 females) were submitted to pattern reversal visual evoked potentials with 15' and 30' checks. The recordings were repeated after 7 days to assess reliability and upper normal variability limits of the following parameters: latencies of N70, P100, N140 and peak-to peak amplitudes of N70-P100, P100-N140. Reliability was tested with intraclass correlation coefficient, which was excellent or good for all parameters. Test-retest variability limits were computed with = 0.01 for absolute latency differences and relative amplitude differences.     

Scalp topography and distribution of cortical somatosensory evoked potentials to median nerve stimulation

Topographies and distributions of cortical SEPs to median nerve stimulation were studied in 8 normal adults and 5 neurological patients. SEPs recorded from C4, P4, Pz, T6-A1A2 derivations to left median nerve stimulation were composed of 2 early negative (N16, N20) and 2 positive components (P12, P23), whereas those recorded from frontal electrodes (Fz, Fp1, Fp2) disclosed 2 early negativities (N16, N24) and 2 early positivities (P12, P20). N20 and P20, and P23 and N24, reversed across the rolandic fissure with no significant difference in their peak latencies. P23 was of slightly shorter latency at C4 than at more posterior electrodes (P4, T6, Pz).In 3 patients with complete hemiplegia but normal sensation, all the early SEP components were normal in scalp distribution and peak latencies except for a decrease of N24 amplitude. In 2 patients with complete hemiplegia and sensory loss no early cortical SEPs were seen. These findings suggest that N20 and P20 are generated as a single horizontal dipole in the central fissure, whereas P23 and N24 are a reflection of multiple generators in pre- and postrolandic regions.     

Median nerve somatosensory evoked potentials. Apomorphine-induced transient potentiation of frontal components Clin. Parkinson's disease and in parkinsonism

Somatosensory evoked potentials (SEPs) to median nerve stimulation have been recorded from parietal and frontal districts Clin. 43 parkinsonians, 17 patients with parkinsonism and 35 healthy controls matched for age and sex. Latency/ amplitude characteristics of the parietal P14-N20-P25 and of the frontal P20-N30-P40 wave complexes before and after (10, 20, 30 and 60 min) subcutaneous administration of apomorphine chloride were evaluated Clin. all the 60 patients and Clin. 3 controls. The frontal waves N30 and P40 were either absent or significantly smaller than normal Clin. 31 patients with Parkinson's disease (PD) (72.1%) and Clin. 9 with parkinsonism Clin. baseline records (56.3%). Following apomorphine, the parietal deflections did not significantly vary Clin. amplitude. On the contrary, the frontal complex showed a significant amplitude increase Clin. 27 PD and 8 parkinsonisms (respectively 62.8 and 47.1%): 79.1% of PD and 35.3% of parkinsonisms were improved clinically. Amplitude increase was evident at 10 min after apomorphine, Clin. parallel with clinical improvement, and vanished nearly Clin. coincidence with the end of the clinical effect.     

Clinical and neuroimaging correlates of abnormal short-latency Somatosensory Evoked Potentials in elderly vascular dementia patients: A psychophysiological exploratory study

BACKGROUND: Short Latency Somatosensory Evoked Potentials (SEPs) may serve to the testing of the somatosensory tract function, which is vulnerable and affected in vascular encephalopathy. The aim of the current study was to search for clinical and neuroimaging correlates of abnormal SEPs in vascular dementia (VD) patients. MATERIALS AND METHODS: The study included 14 VD patients, aged 72.93 PlusMinus; 4.73 years, and 10 controls aged 71.20 PlusMinus; 4.44 years. All subjects underwent a detailed clinical examination, blood and biochemical testing, brain MRI and were assessed with the MMSE. SEPs were recorded after stimulation from upper and lower limbs. The statistical Analysis included 1 and 2-way MANCOVAs and Factor analysis RESULTS: The N13 latency was significantly prolonged, the N19 amplitude was lower, the P27 amplitude was lower and the N11-P27 conduction time was prolonged in severely demented patients in comparison to controls. The N19 latency was prolonged in severely demented patients in comparison to both mildly demented and controls. The same was true for the N13-N19 conduction time, and for the P27 latency. Patients with subcortical lesions had all their latencies prolonged and lower P27 amplitude. DISCUSSION: The results of the current study suggest that there are significant differences between patients suffering from VD and healthy controls in SEPs, but these are detectable only when dementia is severe or there are lesions located in the subcortical regions. The results of the current study locate the abnormal SEPs in the white matter, and are in accord with the literature.     

Augmented P22-N31 SEP component in a patient with a unilateral space occupying lesion

A patient presented with a right rolandic space occupying lesion resulting in a decrease of position sense, touch and stereognosis in the left upper limb.SEPs revealed an augmentation of the right hemisphere P22 component co-existing with relative attenuation of all other right hemisphere components. The augmented P22-N31 complex represented a ‘giant’ potential in relation to a control group (> 2.5 S.D.).The data provide further evidence that the P22-N31 complex has separate generators from those responsible for the N20-P27-N33 components parietally and P20-N30 components frontally. The focal nature of the lesion and symptomatology are of interest.     

Abnormal cortical responses to somatosensory stimulation in medication-overuse headache

Background

Medication-overuse headache (MOH) is a frequent, disabling disorder. Despite a controversial pathophysiology convincing evidence attributes a pivotal role to central sensitization. Most patients with MOH initially have episodic migraine without aura (MOA) characterized interictally by an absent amplitude decrease in cortical evoked potentials to repetitive stimuli (habituation deficit), despite a normal initial amplitude (lack of sensitization). Whether central sensitization alters this electrophysiological profile is unknown. We therefore sought differences in somatosensory evoked potential (SEP) sensitization and habituation in patients with MOH and episodic MOA.

Methods

We recorded median-nerve SEPs (3 blocks of 100 sweeps) in 29 patients with MOH, 64 with MOA and 42 controls. Episodic migraineurs were studied during and between attacks. We measured N20-P25 amplitudes from 3 blocks of 100 sweeps, and assessed sensitization from block 1 amplitude, and habituation from amplitude changes between the 3 sequential blocks.

Results

In episodic migraineurs, interictal SEP amplitudes were normal in block 1, but thereafter failed to habituate. Ictal SEP amplitudes increased in block 1, then habituated normally. Patients with MOH had larger-amplitude block 1 SEPs than controls, and also lacked SEP habituation. SEP amplitudes were smaller in triptan overusers than in patients overusing nonsteroidal anti-inflammatory drugs (NSAIDs) or both medications combined, lowest in patients with the longest migraine history, and highest in those with the longest-lasting headache chronification.

Conclusions

In patients with MOH, especially those overusing NSAIDs, the somatosensory cortex becomes increasingly sensitized. Sensory sensitization might add to the behavioral sensitization that favors compulsive drug intake, and may reflect drug-induced changes in central serotoninergic transmission.

     

Somatosensory evoked potentials: Correlations with height

Somatosensory evoked potentials (SEPs) to median and posterior tibial nerve stimulation were studied in 160 subjects aged 20–90 years. Height was highly correlated with latencies of spinal and cortical SEPs (N13, N20, N22, and P40). Although tibial central conduction (N22-P40) was also highly correlated with height, median conduction (N13–N22) was not correlated with the latter.Multiple correlation and regression analysis showed that except for the median N13–N20 latency, height provided the best prediction of the remaining SEP latencies. Age alone was not correlated with SEP latencies, but its significance was observed when age and height were considered together as the predictors. Effects of age and height on SEP latencies were independent of gender.The present data indicate that except for the N13–N20 conduction, height is the most important parameter for SEP latencies and can be used for construction of normograms.     

Evoked potential findings in Behçet's disease. Brain-stem auditory,visual, and somatosensory evoked potentials in 44 patients

We studied 54 patients with Behçet's disease, 41 males and 13 females, mean age 28 years. Forty-four patients had auditory brain-stem evoked potential (BAEP) recordings, 39 had pattern reversal visual evoked potentials (VEP), 27 had median nerve somatosensory evoked potential (SEP) recordings, and 25 tibial nerve SEPs. BAEPs were abnormal in 16 patients (52%) with neurological manifestations and in 4 (31%) without, because of decreased amplitude of wave V, prolonged I–III or III–V interpeak latencies, or uncertain/absent waves III and/or V. Eleven patients (40%) with neurological symptoms and 3 patients (25%) without, had abnormal VEPs. Absent potentials, decreased amplitude, with or without prolonged P100 latency, were found in 75% of the cases, the rest had prolonged P100 latency only. Median SEPs were abnormal in 8 patients (38%) with neurological manifestations. Four patients (21%) had abnormal tibial SEPs. Decreased amplitude with or without mild slowing in central conduction was the predominant SEP abnormality. SEPs were normal in all patients without neurological symptoms. In total, 84% of patients with, and 38% of patients without, neurological symptoms had abnormalities of one or more EP modality.When used cautiously, EP studies in Behçet's disease might be helpful to separate neuro-Behçet from other disorders with similar symptomatology, to disclose subclinical CNS involvement, to evaluate and monitor CNS disease activity, and to provide objective measures of treatment response.