Nerve SEPs Research Articles

Short and middle-latency Median Nerve (MN) SEPs recorded by depth electrodes in human pre-SMA and SMA-proper

Objective To analyse waveforms, latencies and amplitudes of Median Nerve (MN) SEPs recorded by stereotactically electrodes implanted in the SMA of 14 epileptic patients (9 in pre-SMA,3 in SMA-proper, 2 in both) in order to evaluate which short and middle-latency SEPs are generated in this area and which could be the physiological relevance of these responses. Methods Short and middle-latency MN SEPs were recorded by chronically implanted electrodes in the fronto-temporal cortex and in particular in the mesial frontal region of 14 drug-resistant epileptic patients. MN stimulations of 100 μs were delivered by skin electrodes at the wrist; stimulus intensity was adjusted slightly above the motor threshold. Results The main result of this study is that middle-latency SEPs were originated in pre-SMA but not in SMA-proper as demonstrated by both referential and bipolar recordings. In particular off-line computed bipolar traces between neighbouring contacts implanted in the pre-SMA and in the frontal external regions showed a phase reversal at the deepest contacts located in pre-SMA. Conversely, bipolar recordings between neighbouring contacts implanted in the SMA-proper and in the frontal external regions showed inversion recovery at more superficial contacts, implanted in area 6. Finally, we confirmed that no short-latency MN SEP (and in particular the N30) is originated in the whole SMA. Conclusions Among premotor areas, somatosensory inputs seem to reach pre-SMA and area 6 but not SMA-proper. Significance This study assessed that no scalp SEP in the first 100 ms after MN stimulus could be generated in SMA-proper.

Increase of brain-stem high-frequency SEP subcomponents during light sleep in seizure-free epileptic patients

Objective Three hertz spike-and-wave (SW) occurrence is caused by the abnormal functioning of the same thalamo-cortical loop generating sleep spindles. In fact, SW preferably occurs during light sleep and transitional phases of the vigilance status. Since high-frequency somatosensory evoked potentials (HF-SEPs) are powerfully modulated by sleep and arousal, we verified whether they can reveal abnormalities of arousal-related structures in two patients having showed sporadic SW discharges during light sleep. Methods We recorded right median nerve SEPs in two adult patients who suffered since the infancy from childhood absence epilepsy (CAE). Sleep stage-related changes of HF-SEPs were compared to those observed in five healthy volunteers. Results HF-SEPs decreased during sleep in controls. By contrast, the amplitude of the subcortical component dramatically increased in CAE patients during phase II NREM sleep. Simultaneous EEG showed normally represented sleep spindles, but not SW discharges. Conclusions HF-SEP increase probably reflects the hyperactivation of brain-stem arousal-related structures. During such a hyperactivation no EEG abnormalities were observed. Significance We hypothesize that HF-SEP increase might reflect a protective mechanism against seizure occurrence during light sleep.

Tibial nerve SEPs localized the lesion site in a patient with early tabes dorsalis

There is controversy regarding the initial pathology of tabes dorsalis. In a patient with early tabes dorsalis, tibial nerve somatosensory evoked potentials elicited normal P15, a delayed traveling peak in the lumbar bipolar leads, and absent subsequent components. Based on the comparison with normative data and stimulation at different intensities, the authors conclude that only the slower conducting antidromic motor volleys are preserved, whereas the dorsal root is damaged at its distal end.

Far-field potentials generated by thalamocortical fibers in median nerve SEPs

We previously suggested that P15 in median nerve SEPs is generated by thalamocortical fibers by the mechanism of the junctional potential. In this study, we examined five normal subjects using long-distance bipolar leads over the scalp and aimed to further elucidate the nature of the P15 potential as a junctional potential. As a result, negative potentials were detected in all the sagittal (fronto-occipital) bipolar leads, which coincided with the P15 latency. In contrast, we found no far-field potential in any coronal bipolar lead. Accordingly, a dipolar distribution, frontal negative and occipital positive, is suggested at this latency, indicating the presence of a junctional potential. We suggested that the mechanism of this junctional potential is the bending of the thalamocortical fibers. Computer simulations revealed that the change of the direction of neural propagation can produce a junctional potential. Thalamocortical fibers are angled backwards anatomically. The expected polarity of the dipole generated by this kinking coincides with the observed distribution.

Source Reconstruction of Evoked Cortical Activity using Current Density Reconstruction within Realistically Shaped Head Models

It is well known that source reconstruction techniques based on EEG or MEG data are inferior to fMRI in respect to spatial resolution, but superior concerning the temporal resolution. The present contribution aims to demonstrate the power of modern source reconstruction techniques using standardized, realistically shaped volume conductor models in the spatio-temporal analysis of evoked potentials. A standardized approach of current density reconstruction within a volume conductor model derived from the so-called Montreal wharp brain as implemented in the SPM software will be demonstrated. This approach has the possibility to consider a priori source information, i.e., from functional MRI, to focus the source reconstruction results in respect to the source locations. Using this method, the following exemplary work on source localization and the temporal dynamics of evoked potentials will be demonstrated. The attention effects on median nerve SEP localizes at the contralateral S1 cortex, bilateral temporal, the cingulum and the left parietal cortex. Changes in the electrical activity induced by attention were shown to begin earlier than 100 ms post stimulus. Source reconstruction of the auditory mismatch negativity (MMN) revealed a cingulate source and bilateral temporal generators underlying the MMN. Temporal analysis showed that source activity started at around 130 ms post stimulus within the bilateral temporal gyrus followed by source activity within the cingulum peaking at 220 ms. Source reconstruction of the cortical activity during line bisection judgement revealed 5 source regions, corresponding to those evaluated by a previous fMRI study: right middle occipital gyrus, right superior posterior parietal cortex; bilateral inferior occipital gyrus, and right inferior posterior parietal cortex. Temporal deconvolution presented a sequential activation of these areas starting at the primary visual cortex, followed by the right superior posterior parietal, bilateral inferior occipital cortex and right inferior parietal cortex. In the identification of a network processing spontaneous perceptive reversals of the rotating Necker cube we find support for synchronized neuronal oscillatory activity in the correlation between visual area V3 and left SMA. In summary, the presented work demonstrates the applicability of analyzing EEG data in actual clinical neurophysiology for „functional imaging“ and timing within complex networks of cortical activation.

Cognitive impairment and diffuse white matter atrophy in alcoholics

Objective Diffuse brain white matter atrophy is often seen in chronic alcoholics, but its relation with cognitive impairment remains to be solved. In order to address this issue, in alcoholics with cognitive impairment at different levels, we studied relations of the central sensory conduction time (CSCT) or brain magnetic resonance imaging (MRI) findings with the cognitive function. Methods Subjects were 35 alcoholics with mild cognitive impairment (mini-mental state examination score, MMSE, ≥24; mean±SD, 27.7±1.9), 12 with moderate to severe cognitive impairment (MMSE<24; 20.3±2.7), 15 with Alzheimer's disease (AD) (MMSE, 18.9±4.3) (disease control) and 20 healthy volunteers (MMSE, 28.5±1.6) (normal control). Median nerve SEPs were recorded in the all subjects, and the latencies and amplitudes of their N9, N11, P13/14, N20 and P25 components were measured. The ventriculocranial ratio (VCR) and the width of cortical sulci were measured on MRIs. These physiological parameters and MRI findings were compared between the 4 groups of the subject, and correlations between those all features were also analyzed. Results CSCT and VCR were significantly greater in alcoholics with moderate to severe cognitive impairment than those in the other 3 groups. Pearson's product–moment correlation analyses of the alcoholics disclosed that both the CSCT and VCR had significant negative correlations with the MMSE score. Moreover, the CSCT and VCR were positively correlated. Conclusions Both physiological and morphological estimates of the white matter function (CSCT and VCR) had a significant correlation with the cognitive dysfunction. Significance The diffuse white matter atrophy may be one of the factors causing cognitive impairment in chronic alcoholics.

Serial Median Nerve SEPs and SSEPs in Patients with West Syndrome

Serial Median Nerve SEPs and SSEPs in Patients with West Syndrome

Spinal Cord Temperature

To the Editor:—In their confirmatory study, Kottenberg-Assenmacher et al. concluded that surface hypothermia to a core temperature of 32°C did not depress median nerve somatosensory-evoked potentials (SSEP) amplitude, but did prolong latency. 1This is an important observation, as patients undergoing certain orthopedic and vascular surgical procedures that may result in spinal cord ischemia have SSEPs monitored. Because these patients are often mildly to moderately hypothermic, it is important to know if the spinal cord temperature is at the same core temperature and, if so, what affect spinal cord hypothermia has on SSEPs.In their study, the authors induced hypothermia, and although the mean total duration of the surface hypothermia was not stated, the article inferred that it was acute and transitory. To determine whether there were effects of hypothermia on the spinal cord that affected the SSEPs, we recommend the following:1. Measure the temperature of the spinal cord. This can be approximated clinically by inserting a thermistor-tipped 4-French pulmonary artery catheter via a needle into the subarachnoid space at the lumbar level. Using this technique, the lowest mean cerebrospinal fluid temperature in a case series of patients undergoing spinal cord cooling for thoracoabdominal aneurysm repair was 26.7 ± 3.2°C. 2This technique will provide an indirect, but clinically relevant, measurement of temperature at the spinal cord level. If this were undertaken, the tibial nerve SSEP would need to be measured to determine the effect of spinal cord hypothermia on the SSEP.2. Measure SSEP in patients with acquired poikilothermia in whom steady-state hypothermia can be maintained. MacKenzie et al. published a case series of four patients with acquired poikilothermia who had spontaneous hypothermia maintained at 33.5 ± 0.3°C for a minimum of 4 days. 3The inference is that in poikilothermia, the patient’s central core steady-state temperature is more likely to reflect the local spinal cord temperature. In these patients, hypothermia increased the latency of the central conduction times; however, in this group, only the latencies could be reliably identified.As interest in moderate hypothermia as a neuroprotective technique increases, it is important to definitively answer the question concerning the effect of spinal cord hypothermia on SSEPs.

Pharmacologic and physiologic influences affecting sensory evoked potentials: implications for perioperative monitoring.

Pharmacologic and physiologic influences affecting sensory evoked potentials: implications for perioperative monitoring.

Short-lasting impairment of tactile perception by 0.9Hz-rTMS of the sensorimotor cortex.

To test whether low-frequency repetitive transcranial magnetic stimulation (rTMS) of sensorimotor cortex (SM1) has prolonged effects on somatosensory function, eight subjects were given 900 TMS pulses over the left hand SM1 (0.9Hz, 90% of the resting motor threshold) or at sites 3 cm anterior or posterior to it. Tactile threshold of the right hand was increased for a short duration after rTMS over SM1, but two-point discrimination and median nerve SEPs were unaffected after rTMS at any sites.

Somatosensory evoked potential in neurosyphilis.

Since the development of effective antibiotic therapy, the occurrence of neurosyphilis has become less frequent. The number of syphilitic patients is gradually increasing as a complication in acquired immunodeficiency syndrome, but the diagnosis of neurosyphilis sometimes is difficult. We describe six patients with neurosyphilis and an analysis of their tibial nerve somatosensory evoked potentials. Four of them, including two with no tabes dorsalis symptoms, had delayed P15-N21 or the absence of N21. These abnormalities were ameliorated by treatment for syphilis. Analysis of tibial nerve SEPs provides a useful tool for the diagnosis of neurosyphilis and the evaluation of the extent to which neurosyphilis has progressed.

Determination of median nerve somatosensory evoked potentials in 27 patients with hemiplegia.

Twenty-seven in-patients with hemiplegia following brain injury were studied by using upper extremity median nerve somatosensory evoked patentials (SVEP), Brunnstrom assessment in hemiplegic hand and assessment of the patients' activities of daily lioing (ADL) (Barthel index). The upper extremity median nerve SEP on the affected and normal sides was determined. By using Kovindha standard, upper extremity median nerve SEP was graded in accordance with N20. The correlation between the differences of SEP N20 amplitude and the latencies on the both sides and the Barthel index scores was analyzed. A Spearman correlation analysis was made between the median nerve SEP N20 grades and Brunnstrom stages in hand or ADL on the affected side. The results showed that upper extremity median nerve SEP grades were positively correlated with those of the Brunnstrom stages in hand (r1 = 0.6925, P1 < 0.01). The correlation coefficient between SEP N20 grades and patients' ADL grades was r2 = 0.5015, P2 < 0.01. It was concluded that upper extremity median nerve SEP could be used as a sensitive electrophysiological predictor to clinically assess hemiplegic hand function. SEP N20 might play a role in predicting the ADL of the patients with hemiplegia to some extent, but could not be used as a sensitive predictor to directly observe and predict the ADL of the patients.

Cutaneous and mixed nerve silent periods in syringomyelia

Objectives and methods: We studied cutaneous and mixed nerve silent periods (CSP, MNSP) in 4 patients with cervical syringomyelia documented by magnetic resonance imaging who on clinical examination presented with unilateral hypalgesia and hypothermesthesia. In addition, we recorded upper and lower extremity somatosensory and motor evoked potentials (SEP, MEP), and cortical silent periods. Results: In all patients, CSP and the later portion of MNSP were absent or shortened on their affected side, while both were normal on their unaffected side. In all patients, SEP latencies were normal following both median and tibial nerve stimulation. In two patients, the amplitude N13 (median nerve SEP), and in one patient each the amplitudes N20 (median nerve SEP) and P37 (tibial nerve SEP) were reduced. Central motor conduction time was prolonged to abductor digiti minimi muscle in one patient on the affected side, but was normal to tibialis anterior muscle in all patients. Cortical silent periods where present bilaterally in spite of unilateral complete absence of CSP and MNSP in two subjects tested. Loss of CSP and MNSP were a sensitive parameter of spinal cord dysfunction in syringomyelia. The cervical median nerve SEP response N13 reflected gray matter involvement, while corticospinal tract dysfunction was less frequently observed. Conclusion: Our data suggest that CSP and later portion of MNSP are generated at the spinal level by the same small myelinated A-δ fibers, and that their central network is distinct from large diameter fiber afferents and efferents.

Abnormal somatosensory evoked potentials indicate compressive cervical myelopathy in mucopolysaccharidoses.

Compressive myelopathy at the cranio-cervical junction is a complication of mucopolysaccharidoses (MPS). To detect cervical myelopathy we recorded median and posterior tibial nerve SEPs in 15 patients aged 2.4-33.4 years (median 8.8 years) with MPS I-S (n = 3), MPS IVA (n = 8) and MPS VI (n = 4). In addition to the cortical waveforms we recorded the subcortical median nerve SEPs N13b and P13 generated near the cranio-cervical junction and the lemniscal P30 after posterior tibial nerve stimulation. MRI studies in 13 subjects revealed spinal cord compression at the cranio-cervical junction in 10 patients; 5 patients had an increased signal intensity on the T2-weighted initial MRI indicating high cervical myelomalacia and 4 patients had clinical signs of cervical myelopathy. We did not find a relationship between the SEPs and spinal cord compression. Abnormal SEPs were found in the patients with MRI evidence of myelomalacia (sensitivity 1.0, specificity 1.0) and correspondingly in the patients with clinical signs (sensitivity 1.0, specificity 0.91). The SEPs consequently deteriorated in 2 subjects of 7.3 and 10.3 years of age. Abnormal SEPs indicated subclinical cervical myelopathy in 3 subjects. Cervical cord compression may be present before occurrence of clinical or electrophysiological evidence of myelopathy. However, we feel that the SEP analysis is useful to detect functional impairment of the cervical cord in patients with MPS.

Maturation of near-field and far-field somatosensory evoked potentials after median nerve stimulation in children under 4 years of age

Objectives: The maturation of subcortical SEPs in young children.Methods: Median nerve SEPs were recorded during sleep in 42 subjects aged 0–48 months. Active electrodes were at the ipsilateral Erb's point, the lower and upper dorsal neck, and the frontal and contralateral centroparietal scalp; reference electrodes were at the contralateral Erb's point, the ipsilateral earlobe and the frontal scalp; bandpass was 10–3000 Hz. The peaks were labelled by their latencies in adults.Results: The peak latencies of N9 (brachial plexus potential) decreased exponentially with age during the first year, but increased with height thereafter. The interpeak latencies (IPLs) N9–N11, which measure conduction between brachial plexus and dorsal column, decreased with age (linear regression). The IPLs N11–P13 and N11–N13b, which measure conduction between the dorsal column and approximately the cervico-medullary junction, did not change across this age range. The IPLs N13a–N20, N13b–N20 and P13–N20, which measure central conduction, showed negative exponential regressions with rapidly decreasing latencies during the first year of life and slowly decreasing latencies thereafter.Conclusions: Maturation of the peripheral segments of the somatosensory pathway progresses more rapidly than that of the central segments. The maturation of central conduction is not completed within the first 4 years of age. Our maturational data may serve as a reference source for subsequent developmental and clinical studies.

Intra- and postoperative factors determining neurological complications after surgery under deep hypothermic circulatory arrest: a retrospective somatosensory evoked potential study

Objectives: Intraoperative median nerve SEP monitoring uses the disappearance of cortical and brain stem activities as the criterion to determine that brain cooling is sufficient in deep hypothermic circulatory arrest (CA) surgery. This study presents the results of a retrospective SEP analysis of intraoperative events that engendered neurological complications.Methods: Median nerve SEP monitoring was performed on 58 consecutive patients who underwent surgery under deep hypothermic CA. The monitoring was retrospectively analyzed and compared with intraoperative events, and postoperative symptoms.Results: Intraoperative SEP abnormalities were observed in 9 out of the 16 patients who presented neurological complications. Among the 7 others, the abnormalities either were present preoperatively (n=2), occurred postoperatively (n=3) or only involved the lower limbs (n=2). Although the mere inspection of the intraoperative SEPs was insufficient to determine the origin of the alterations, their comparison with intraoperative events facilitated the identification of hemodynamic factors in 7 cases and embolism in two cases. There were no patients in whom CA per se caused neurological complications.Conclusions: Intraoperative SEP monitoring helps identify intraoperative events responsible for neurological complications and prevent these in subsequent procedures. However, the neurological complications of deep hypothermic CA can also be due to pre- or postoperative factors that escape the domain of intraoperative monitoring.

Somatosensory evoked potentials in very preterm infants

Objective: Cross-sectional and longitudinal reference values of cortical N1 peak latency of the median nerve SEP in very preterm infants.Methods: In infants in a placebo control group within an l-thyroxine supplementation trial, born at less than 30 weeks’ gestation, cortical N1 peak latency was measured at 2 weeks, at term and at 6 months corrected age. Cross-sectional N1 latency values obtained in 50 infants and complete series of longitudinal values obtained in 15 infants were analyzed in relation to postmenstrual age (PMA).Results: Mean N1 latency decreased from 66 ms at 2 weeks to 38 ms at term and 20 ms at 6 months corrected age. Possible confounding factors did not have any significant effect on N1 latency at 2 weeks or at term age except cranial ultrasound abnormalities at 2 weeks of age.Conclusions: Longitudinal N1 latency values were consistent with cross-sectional N1 latency values. The observed N1 latency at term and at 6 months corrected age suggest that extrauterine maturation of the somatosensory pathway in infants born at less than 30 weeks’ gestation is delayed by extrauterine life.

Tibial nerve somatosensory evoked potentials during EEG suppression in sevoflurane anaesthesia

Objectives and Methods: Cortical tibial nerve somatosensory evoked potentials (TSEPs) were recorded from 10 subjects in sevoflurane anaesthesia in order to study TSEP during EEG suppression.Results: With a stimulation frequency less than one per second the major component was a positive wave which had maximal amplitude parietally ipsilaterally to stimulus and mean latency of 46.1 ms. It probably corresponds to the P40 wave. It was preceded by a widespread smaller positive wave, which corresponds to the subcortical P30 wave. In two patients a high amplitude negative wave, a couple of milliseconds before the positive wave, and maximal parietally contralateral to stimulus, was seen. All later waves were absent.Conclusion: The results are in agreement with our previous results from median nerve SEPs showing that the first cortical response from primary somatosensory cortex is enhanced, and later waves are suppressed. Hence, recording TSEPs during EEG suppression provides a way to record the activity of the primary somatosensory cortex accurately and rapidly due to the very good signal to noise ratio, so that even single responses to stimuli can be seen without averaging. Our results suggest that new cortical generators, which are not recordable awake, may be discovered in some patients.

Latency and amplitude variability in serial median nerve SEP recordings

Objectives: Intra-individual variability of SEP parameters was investigated by serial SEP recordings.Methods: Median nerve SEP of 53 normal subjects (mean age 25.5±2.7 years) were evaluated. Recordings were repeated 1 week, 2 weeks, and 6 months after the initial recording.Results: Mean values of latencies from right median nerve stimulation were slightly longer (+0.1 ms) as compared to the left. The intra-individual (within stimulation side) variance did not depend on the time interval between recordings. The total within-stimulation-side variance of latencies was 0.056 ms2 for N20 (C3/4′ vs. Fz), 0.070 ms2 for N13 (C7 vs. Fz), 0.048 ms2 for N10 (Erb's point vs. Fz), 0.111 ms2 for P9 (C3/4′ vs. contralateral forearm), and 0.148 ms2 for P14 (C3/4′ vs. contralateral forearm), and was about 3 times smaller than between-side variability with regard to cortical or spinal potentials. Upper limits for latency differences and lower limits for amplitude ratios in repeated recordings, as well as upper and lower limits for between-side latency differences and amplitude ratios were calculated, using F distributions with worst-case assumptions for degrees of freedom and error probability P=0.05. Upper limits of within-stimulation-side latency differences were 0.55 ms for N20, 0.62 ms for N13, 0.51 ms for N10, 0.78 ms for P9, and 0.90 ms for P14, and corresponding lower limits of amplitude ratios were 0.69, 0.62, 0.66, 0.45, and 0.50, respectively.Conclusions: Our results demonstrate a small systematic, and a larger random difference between right and left side stimulation, one arising from the peripheral, and the other one from the central pathway proximal to the source of N10.

Bulbocavernosus-reflex latencies and pudendal nerve SSEP compared to penile vascular testing in 669 patients with erectile failure and other sexual dysfunction.

The purpose of this current study was to find out the coincidence of pathological penile vascular supply with pathological data in Bulbocavernosusreflex latency (BCR-L) measurements and Pudendal Nerve SSEP (PudSSEP) recordings. Six hundred and sixty-nine males (642 with erectile dysfunction, 27 with different sexual disturbances) (mean age 49.3 y, range 17-76 y) underwent consecutively a battery of neurophysiological investigations together with pharmacotesting of cavernous bodies combined with duplex sonography of penile arteries. Pathological vascular findings were indicated in 286 men (43%), pathological neurophysiological findings in 264 men (39%). Normal findings in both investigations (vascular and neurophysiological) were encountered in 252 men (38%); 131 men (19%) revealed pathological data exclusively in the neurophysiological parameters, 153 (23%) exclusively in the vascular parameters and 133 (20%) in both. The highest percentages of pathological findings were observed in patients with diabetes mellitus (110 out of 131, 88%) and patients who had sustained pelvic trauma or surgery (36 out of 44, 82%), in contrast to the lowest percentage in patients with a proven psychogenic etiology (10 out of 38, 26%). Somewhat surprising was the rather high proportion of vascular impairment in patients with defined neurological diseases such as alcohol abuse (20 out of 51, 43%), polyneuropathy (PNP) of various etiology (9 out of 19, 47%), lumbosacral radiculopathies (26 out of 65, 40%), and CNS diseases (24 out of 52, 46%), about half of them coinciding with pathological neurophysiological findings. Even if the validity of BCR-L measurement and PudSSEP recordings in the assessment of neurogenic impotence was controversely discussed, we conclude that in a large number of impotent males both neurogenic and vascular factors are responsible for the onset of erectile dysfunction.