Scalp-recorded short and middle latency peroneal somatosensory evoked potentials in normals: comparison with peroneal and median nerve SEPs in patients with unilateral hemispheric lesions

Peroneal somatosensory evoked potentials (SEPs) were performed on 23 normal subjects and 9 selected patients with unilateral hemispheric lesions involving somatosensory pathways.Recording obtained from right and left peroneal nerve (PN) stimulations were compared in all subjects, using open and restricted frequency bandpass filters. Restricted filter (100–3000 Hz) and linked ear reference (A1–A2) enhanced the detection of short latency potentials (P1, P2, N1 with mean peak latency of 17.72, 21.07, 24.09) recorded from scalp electrodes over primary sensory cortex regions. Patients with lesions in the parietal cortex and adjacent subcortical areas demonstrated low amplitude and poorly formed short latency peroneal potentials, and absence of components beyond P3 peak with mean latency of 28.06 msec. In these patients, recordings to right and left median nerve (MN) stimulation showed absence or distorted components subsequent to N1 (N18) potential.These observations suggest that components subsequent to P3 potential in response to PN stimulation, and subsequent to N18 potential in response to MN stimulation, are generated in the parietal cortical regions.     

Unmasking of cortical SEP components by changes in stimulus rate: a topographic study

We performed topographic mapping of somatosensory responses to median nerve stimulation delivered at 2, 5 and 10 Hz. Parietal N20 was significantly attenuated in 10 Hz somatosensory evoked potentials (SEPs), while central P22 diminished between 2 and 5 Hz, remaining stable thereafter. The single component most affected by increasing stimulus rate was N30, which abated by more than 50% in 10 Hz SEPs, as compared with basal responses. N30 attenuation disclosed the existence of an earlier negative component, N24, which appeared as a notch on the N30 ascending slope in 2 Hz SEPs, but became a well-defined peak at higher stimulus rates. The N24 negativity was not significantly modified by stimulus rate; it had a parietal counterpart (P24) with the same peak latency and identical behavior during the experimental procedure. Both P24 and N24 could be differentiated from central P22 on the basis of topographical distribution and response to stimulus frequency. P22 topography could be the result of a radially oriented generator, while P24/N24 appeared as the two poles of a neural source tangential to the scalp. P27 was seen in 40% of the subjects only; it is suggested that P27 is itself a composite potential to which the generator of N30 could contribute in part. We conclude that there is no single “optimal” stimulation rate for SEP recording. On the contrary, combination of different frequencies of stimulation should enhance the diagnostic utility of this technique by allowing a more selective assessment of overlapping activities.     

Serial recording of sensory,corticomotor, and brainstem-derived motor evoked potentials in the rat

A method is presented for serial recording of corticomotor evoked potentials (CMEPs), brainstem-derived motor evoked potentials (BMEPs), and somatosensory evoked potentials (SEPs) via permanently implanted cranial screws. One screw was positioned posterior to lambda (posterior screw), and two screws were positioned over the cortical hind limb areas (cortical screws). SEPs were elicited by stimulation of the hind paw and recorded from the contralateral cortex. BMEPs were stimulated via the posterior screw and recorded from both hind limbs, whereas CMEPs were elicited by repeated bipolar stimulation of the cortex and recorded from the contralateral hind limb. BMEPs and CMEPs differed in several points and can be considered as completely separate motor evoked potentials. While BMEPs consisted of a prominent negative peak with short latency (5–7.5 ms), CMEPs were represented by polyphasic signals with long latencies (17–22 ms). The cortical origin of the CMEPs was confirmed by transecting the corticospinal tracts, which abolished the CMEPs but spared the BMEPs. SEPs consisted of three consecutive peaks with mean latencies of the initial peak ranging between 15 and 17 ms. Dorsal column transection also abolished SEPs. In healthy rats, all three signals were recorded for six consecutive weeks. Signal parameters did not change significantly within this observation period. Rats tolerated the screws and the repeated measurements very well and no negative affect on animal behavior was noted. Thus, this method allows serial recording of SEPs, CMEPs, and BMEPs in chronic rat models.     

Serial recording of sensory, corticomotor, and brainstem-derived motor evoked potentials in the rat

A method is presented for serial recording of corticomotor evoked potentials (CMEPs), brainstem-derived motor evoked potentials (BMEPs), and somatosensory evoked potentials (SEPs) via permanently implanted cranial screws. One screw was positioned posterior to lambda (posterior screw), and two screws were positioned over the cortical hind limb areas (cortical screws). SEPs were elicited by stimulation of the hind paw and recorded from the contralateral cortex. BMEPs were stimulated via the posterior screw and recorded from both hind limbs, whereas CMEPs were elicited by repeated bipolar stimulation of the cortex and recorded from the contralateral hind limb. BMEPs and CMEPs differed in several points and can be considered as completely separate motor evoked potentials. While BMEPs consisted of a prominent negative peak with short latency (5-7.5 ms), CMEPs were represented by polyphasic signals with long latencies (17-22 ms). The cortical origin of the CMEPs was confirmed by transecting the corticospinal tracts, which abolished the CMEPs but spared the BMEPs. SEPs consisted of three consecutive peaks with mean latencies of the initial peak ranging between 15 and 17 ms. Dorsal column transection also abolished SEPs. In healthy rats, all three signals were recorded for six consecutive weeks. Signal parameters did not change significantly within this observation period. Rats tolerated the screws and the repeated measurements very well and no negative affect on animal behavior was noted. Thus, this method allows serial recording of SEPs, CMEPs, and BMEPs in chronic rat models.     

Giant central N20-P22 with normal area 3b N20-P20: an argument in favour of an area 3a generator of early median nerve cortical SEPs?

Generators of early cortical somatosensory evoked potentials (SEPs) still remain to be precisely localised. This gap in knowledge has often resulted in unclear and contrasting SEPs localisation in patients with focal hemispheric lesions. We recorded SEPs to median nerve stimulation in a patient with right frontal astrocytoma, using a 19-channel recording technique. After stimulation of the left median nerve, N20 amplitude was normal when recorded by the parietal electrode contralateral to the stimulation, while it was abnormally enhanced in traces obtained by the contralateral central electrode. The amplitude of the frontal P20 response was within normal limits. This finding suggests that two dipolar sources, tangential and radial to the scalp surface, respectively, contribute concomitantly to N20 generation. The possible location of the N20 radial source in area 3a is discussed. The P22 potential was also recorded with increased amplitude by the central electrode contralateral to the stimulation, while N30 amplitude was normal in frontal and central traces. We propose that the radial dipolar source of P22 response is independent from both N20 and N30 generators and can be located either in 3a or in area 4. This report illustrates the usefulness of multichannel recordings in diagnosing dysfunction of the sensorimotor cortex in focal cortical lesions.     

Effect of stimulus rate on the cortical posterior tibial nerve SEPs: a topographic study

We performed topographical mapping of somatosensory evoked potentials (SEPs) in response to posterior tibial nerve stimulation delivered at 2, 5 and 7.5 Hz in 15 healthy subjects. P37 was significantly attenuated at 5 and 7.5 Hz and the N50 component attenuated only at 5 Hz, its amplitude remaining stable for further increases in stimulus frequency. Frontal N37 and P50 potentials showed no significant decrease when the stimulus repetition frequency was changed from 2 to 7.5 Hz. P60 showed an attenuation of the amplitude only at 7.5 Hz. Latency and scalp topographies of all cortical components examined remained uncharged for the 3 stimulus rates tested The optimal stimulus rate for mapping of tibial nerve SEPs was lower than 5 Hz. The distinct recovery function of the contralateral N37-P50 and ipsilateral P37-N50 responses suggests that these potentials arise from separate generators     

Electric and CO2 laser SEPs in a patient with asymptomatic syringomyelia

We recorded electrically stimulated somatosensory evoked potentials (electric SEPs) and pain-related SEPs following CO₂ laser stimulation (CO₂ laser SEPs) from a 17-year-old patient affected by myotonic dystrophy whose MRI disclosed a large syrinx extending from spinal level C2 to S3. Careful clinical and electromyographic examinations revealed no motor or sensory disturbances, apart from myotonia. The only abnormality noted in median and ulnar nerve short-latency electric SEPs (recorded with a non-cephalic reference electrode) was the absence of cervical component N13, the other SEP responses (N9, N10, N11, P14, N20) being normal. The cutaneous pain threshold and CO₂ laser SEPs (both obtained by a CO₂ laser beam applied to the back of the hand) were normal. Thus cervical component N13 appears to be highly sensitive to the effects of central cord lesions, even when these are asymptomatic.     

Steady-state analysis of somatosensory evoked potentials

We report the development of a new method for frequency domain analysis of steady-state somatosensory evoked potentials (SEPs) to amplitude-modulated electrical stimulation, which can be recorded in significantly less time than traditional SEPs. Resampling techniques were used to compare the steady-state SEP to traditional SEP recordings, which are based on signal averaging in the time domain of cortical responses to repetitive transient stimulation and take 1–2 min or more to obtain a satisfactory signal/noise ratio. Median nerves of 3 subjects were stimulated continuously with electrical alternating current at several modulation frequencies from 7 to 41 Hz. Amplitude modulation was used to concentrate the power in higher frequencies, away from the modulation frequency, to reduce the amount of stimulus artifact recorded. Data were tested for signal detectability in the frequency domain using the T_circ² statistic. A reliable steady-state response can be recorded from scalp electrodes overlying somatosensory cortex in only a few seconds. In contrast, no signal was statistically discriminable from noise in the transient SEP from as much as 20 s of data. This dramatic time savings accompanying steady-state somatosensory stimulation may prove useful for monitoring in the operating room or intensive care unit.     

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.     

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.     

Estimation of conduction velocity of the spino-thalamic tract in man

This is the first report of estimating conduction velocity (CV) of the slowly conducting somatosensory spinal tracts or the spino-thalamic tract (STT) in man. The CV of the STT was measured by recording somatosensory evoked potentials (SEPs) following CO₂ laser stimulation of the hand and foot, which was previously shown to cause pain or heat sensation by activating cutaneous nociceptors and by its ascending signals through Aδ fibers and probably STT. When the CV of Aδ fibers was assumed to be 10–15 m/sec, the CV of STT was found to be approximately 8–10 m/sec in normal young subjects. It was slightly slower in subjects over 60 years of age. In contrast, the CV of the posterior column, which was calculated based on SEPs following electrical stimulation of the median and posterior tibial nerves, was approximately 50–60 m/sec.     

Right or left ear reference changes the voltage of frontal and parietal somatosensory evoked potentials

Short-latency cortical somatosensory evoked potentials (SEPs) to left median nerve stimulation were recorded with either the left or right earlobe as reference. With a right earlobe reference the voltage of the parietal N20 and P27 was reduced while the voltage of the frontal P20 and N30 was enhanced. The effects were consistent, but their size varied with the SEP component considered and also among the subjects. Analysis of SEPs at different scalp sites and at either earlobe suggested that the ear contralateral to the side stimulated picked up transient potential differences, depending a.o. on side asymmetry and geometry of the neural generators as disclosed in topographic mapping. For example, the right ear potential can be shifted negatively by the right N20 field evoked by left median nerve stimulation. The changes involve the absolute potential values, but not the time features of the gradients of potential fields. Scalp current density (SCD) maps are not affected. The results are pertinent for current discussions about which reference to use and document the practical recommendation of recording short-latency cortical SEPs with a reference at the ear ipsilateral (not contralateral) to the side of stimulation.     

The assessment of severe head injury by short-latency somatosensory and brain-stem auditory evoked potentials

The relative prognostic value of short-latency somatosensory evoked potentials (SEPs) and brain-stem auditory evoked potentials (BAEPs) was assessed in 35 patients with post-traumatic coma. Analysis of the evoked potentials was restricted to those recorded within the first 4 days following head injury. Abnormal SEPs were defined as an increase in central somatosensory conduction time or an absence of the initial cortical potential following stimulation of either median nerve. Abnormal BAEPs were classified as an increase in the wave I–V interval or the loss of any or all of its 3 most stable components (waves I, III and V) following stimulation of either ear. SEPs reliably both good and bad outcomes. All 17 patients in whom SEPs were graded as normal had a favourable outcome and 15 of 18 patients in whom SEPs were abnormal had an unfavourable outcome. Although abnormal BAEPs were associated with an unfavourable outcome in almost all patients (6 of 7), only 19 of 28 patients with normal BAEPs had a favourable outcome. The finding of normal BAEPs was therefore of little prognostic significance. These results confirm the superiority and greater sensitivity of the SEP in detecting abnormalities of brain function shortly after severe head trauma.     

Modality-specific organization for cutaneous and proprioceptive sense in human primary sensory cortex studied by chronic epicortical recording

Modality specificity of human primary somatosensory cortex was studied by recording somatosensory evoked potentials (SEPs) from subdural electrodes in a patient with intractable focal motor seizure. A newly developed device was used for selectively activating proprioception. The spatial and temporal distributions of proprioception-related SEPs elicited by brisk passive flexion movement at the proximal interphalangeal (PIP) joint of the middle finger (4 degrees in 25 ms) were quite different from those to cutaneous sense evoked by electric stimulation of the digital nerve at the same site. It was for the first time demonstrated that proprioception-related SEPs following passive finger movement do not originate in area 3b, which was clearly activated by cutaneous stimulation, and that other sites at the sensorimotor cortex such as areas 2, 3a and 4 possibly contribute to the cortical processing of proprioception.     

Pain-related somatosensory evoked potentials following CO2 laser stimulation of foot in man

Since our previous study of pain somatosensory evoked potentials (SEPs) following CO₂ laser stimulation of the hand dorsum could not clarify whether the early cortical component NI was generated from the primary somatosensory cortex (SI) or the secondary somatosensory cortex (SII) or both, the scalp topography of SEPs following CO₂ laser stimulation of the foot dorsum was studied in 10 normal subjects and was compared with that of the hand pain SEPs and the conventional SEPs following electrical stimulation of the posterior tibial nerve recorded in 8 and 6 of the 10 subjects, respectively. Three components (N1, N2 and P2) were recorded for both foot and hand pain SEPs. N1 of the foot pain SEPs was maximal at the midline electrodes (Cz or CPz) in all data where that potential was recognized, but the potential field distribution was variable among subjects and even between two sides within the same subject. N1 of the hand pain SEPs was maximal at the contralateral central or midtemporal electrode. The scalp distribution of N2 and P2, however, was not different between the foot and hand pain SEPs. The mean peak latency of N1 following stimulation of foot and hand was found to be 191 msec and 150 msec, respectively, but there was no significant difference in the interpeak latency of Nl-N2 between foot and hand stimulation. It is therefore concluded that NI of the foot pain SEPs is generated mainly from the foot area of SI. The variable scalp distribution of the N7 component of the foot pain SEPs is likely due to an anatomical variability among subjects and even between sides.     

Direct recording of somatosensory evoked potentials in the vicinity of the dorsal column nuclei in man: their generator mechanisms and contribution to the scalp far-field potentials

Somatosensory evoked potentials (SEPs) in the vicinity of the dorsal column nuclei in response to electrical stimulation of the median nerve (MN) and posterior tibial nerve (PTN) were studied by analyzing the wave forms, topographical distribution, effects of higher rates of stimulation and correlation with components of the scalp-recorded SEPs. Recordings were done on 4 patients with spasmodic torticollis during neurosurgical operations for microvascular decompression of the eleventh nerve. The dorsal column SEPs to MN stimulation (MN-SEPs) were characterized by a major negative wave (N1; 13 msec in mean latency), preceded by a small positivity (P1) and followed by a large positive wave (P2). Similar wave forms (P1′-N1′-P2′) were obtained with stimulation of PTN (PTN-SEPs), with a mean latency of N1′ being 28 msec. Maximal potentials of MN-SEPs and PTN-SEPs were located in the vicinity of the ipsilateral cuneate and gracile nuclei, respectively, at a level slightly caudal to the nuclei. The latencies of P1 and N1 increased progressively at more rostral cervical cord segments and medulla, but that of P2 did not. A higher rate of stimulation (16 Hz) caused no effects on P1 and N1, while it markedly attenuated the P2 component. These findings suggest that P1 and N1 of MN-SEPs, as well as P1′ and N1′ of PTN-SEPs, are generated by the dorsal column fibers, and P2 and P2′ are possibly of postsynaptic origin in the respective dorsal column nuclei.The peak latency of N1 recorded on the cuneate nucleus was identical with the scalp-recorded far-field potential of P13–14 in all patients, while no scalp components were found which corresponded to P2. These findings support the previous assumption that the scalp-recorded P13–14 is generated by the presynaptic activities of the dorsal column fibers at their terminals in the cuneate nucleus.     

Interactions of somatosensory evoked potentials: simultaneous stimulation of two nerves

To analyse the mechanism by which sensory inputs are integrated, interactions of somatosensory evoked potentials (SEPs) in response to simultaneous stimulation of two nerves were examined in 12 healthy subjects. Right, left and bilateral median nerves were stimulated in random order so that a precise comparison could be made among the SEPs. The arithmetical sum of the independent right and left median nerve SEPs was almost equal within 40 msec of stimulus onset to that evoked by the simultaneous stimulation of bilateral median nerves. However, a difference emerged after 40 msec. The greatest difference was recorded after 100 msec. Sensory information from right and left median nerves may interact in the late phase of sensory processing. Left median, left ulnar, and both nerves together were stimulated. The sum of the SEPs of left median and ulnar nerves was not equal to that evoked by the simultaneous stimulation of the two nerves even at early latencies. Differences between them were first recorded at 14–18 msec and became greater after 30–40 msec. It is suggested that the neural interactions between impulses in the median and ulnar nerves begin below the thalamic level.     

Pyramidal tract function during onset of brain death

In 51 patients with primary brain lesions, who fulfilled the criteria of brain death, sequential recording of transcranial magnetic evoked potentials (TMEPs) and somatosensory evoked potentials (SEPs) were performed.In all comatose patients with apnoeic cranial nerve areflexia the TMEP could not be elicited, while the response after cervical magnetic stimulation was always preserved. Similarly, no cortical SEPs were preserved in apnoeic cranial nerve areflexia; however, the cervical somatosensory response was preserved in 44%.In deteriorating patients with coma grade III TMEPs were preserved in 3 instances, while cortical SEPs were already absent. Current brain death criteria, however, were not challenged, as TMEPs were absent in all 51 patients, at the latest when apnoea was noted.     

Topography of somatosensory evoked potentials to median nerve stimulation in patients with cerebral lesions

Scalp distributions and topographies of early cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were studied in 22 patients with 5 different types of cerebral lesion due to cerebrovascular disease or tumor (thalamic, postcentral subcortical, precentral subcortical, diffuse subcortical and parieto-occipital lesions) in order to investigate the origins of frontal (P20, N24) and central-parietal SEPs (N20, P22, P23).In 2 patients with thalamic syndrome, N16 was delayed in latency and N20/P20 were not recorded. No early SEP except for N16 was recorded in 2 patients with pure hemisensory loss due to postcentral subcortical lesion. In all 11 patients with pure hemiparesis or hemiplegia due to precentral subcortical lesion N20/P20 and P22, P23/N24 components were of normal peak latencies. The amplitude of N24 was significantly decreased in all 3 patients with complete hemiplegia. These findings support the hypothesis that N20/P20 are generated as a horizontal dipole in the central sulcus (3b), whereas P23/N24 are a reflection of multiple generators in pre- and post-rolandic fissures. P22 was very localized in the central area contralateral to the stimulation.Topographical studies of early cortical SEPs are useful for detecting each component in abnormal SEPs     

The effect of stimulus frequency on post- and pre-central short-latency somatosensory evoked potentials (SEPs)

We assessed the influence of the stimulus frequency on short-latency SEPs recorded over the parietal and frontal scalp of 26 subjects to median nerve stimulation and 16 subjects to digital nerve stimulation. When the stimulus frequency is increased from 1.6 Hz to 5.7 Hz, the amplitude of the N13 potential decreases whereas the P14 remains stable. The amplitude of the N20 is not changed significantly whereas the P22, the P27 and the N30 decrease significantly. In 50% of the subjects 2 components can be seen within the frontal negativity that follows the P22: an early ‘N24’ component, which is not affected by the stimulus rate, and the later N30, which is highly sensitive to the stimulus frequency. The distinct amplitude changes of the N20 and P22 with increasing stimulus frequency is one among other arguments to show that these potentials arise from separate generators.