Median and tibial nerve somatosensory evoked potentials: middle-latency components from the vicinity of the secondary somatosensory cortex in humans

The topography of the middle-latency N110 after radial nerve stimulation suggested a generator in SII. To support this hypothesis, we have tried to identify a homologous component in the tibial nerve SEP (somatosensory evoked potential). Evoked potentials following tibial nerve stimulation (motor+sensory threshold) were recorded with 29 electrodes (bandpass 0.5–500 Hz, sampling rate 1000 Hz). For comparison, the median nerve was stimulated at the wrist. Components were identified as peaks in the global field power (GFP). Map series were generated around GFP peaks and amplitudes were measured from electrodes near map maxima. With median nerve stimulation, we recorded a negativity with a maximum in temporal electrode positions and 106±12 ms peak latency (mean±SD), comparable to the N110 following radial nerve stimulation. After tibial nerve stimulation the latency of a component with the same topography was 131±11 ms (N130). Both N110 and N130 were present ipsi- as well as contralaterally. Amplitudes were significantly higher on the contralateral than the ipsilateral scalp for both median (3.1±2.4 μV vs. 1.7±1.6 μV) and tibial nerve (1.9±1.2 μV vs. 0.6+1 μV). The topography of the N130 can be explained by a generator in the vicinity of SII. The latency difference between median and tibial nerve stimulation is related to the longer conduction distance (cf. N20 and P40). The smaller ipsilateral N130 is consistent with the bilateral body representation in SII.     

Effects of hypothermia on short latency somatosensory evoked potentials in humans

Short latency somatosensory evoked potentials (SSEPs) elicited by median nerve stimulation were monitored in 14 adult patients undergoing cardiac surgery under cardiopulmonary bypass and induced hypothermia. SSEPs were recorded at 1–2°C steps as the body temperature was lowered from 37°C to 20°C to determine temperature-dependent changes. Hypothermia produced increased latencies of the peaks of N₁₀, P₁₄ and N₁₉ components, the prolongation was more severe for the later components so that N₁₀−P₁₄ and P₁₄−N₁₉ interpeak latencies were also prolonged. The temperature-latency relationship had a linear correlation. The magnitude of latency prolongation (msec) with 1°C decline in temperature was 0.61, 1.15, 1.56 for N₁₀,P₄ and N₁₉ components, respectively, and 0.39 and 0.68 for interpeak latencies N₁₀−P₁₄ and P₁₄−N₁₉, respectively. The rise time and duration of the 3 SSEP components increased progressively with cooling. Cortically generated component, N₁₉ was consistently recordable at a temperature above 26°C, usually disappearing between 20°C and 25°C. On the other hand, more peripherally generated components, N₁₀ and P₁₄, were more resistant to the effect of hypothermia; P₁₄ was always elicitable at 21°C or above, whereas N₁₀ persisted even below 20°C. The amplitude of SSEP components had a poor correlation with temperature; there was a slight tendency for N₁₀ and P₁₄ to increase and for N₁₉ to decrease with declining temperature. Because incidental hypothermia is common in comatose and anesthetized patients, temperature-related changes must be taken into consideration during SSEP monitoring under these circumstances.     

Pudendal nerve somatosensory evoked potentials in paediatrics: maturation aspects

Pudendal nerve somatosensory evoked potentials (PN-SSEPs) were recorded in 21 healthy children (age range: 3.3–13.3 years). The dorsal nerve of the penis/clitoris was stimulated and SSEPs were recorded at spinal L1-D12 and at cortical Cz′-Fz. Morphology, latency and amplitude of the cortical SSEPs were evaluated. A cortical response was obtained in all but two subjects. Cortical SSEPs were broader and less defined in shape in the youngest subjects. There was a progressive shortening of the latency of the P and N components during growth. Spinal responses were obtained only in 6 cases. Nine subjects also underwent tibial nerve stimulation. Pudendal and tibial SSEPs differed in their degree of maturation.     

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.     

Short-latency somatosensory evoked potentials following median nerve stimulation in Down's syndrome

Short-latency somatosensory evoked potentials (SEPs) following median nerve stimulation were recorded in 42 patients with Down's syndrome and in 42 age- and sex-matched normal subjects. There were no significant differences between the 2 groups in the absolute peak latencies of N9, N11 and N13 components. However, interpeak latencies, N9-N11, N11-N13 and N9-N13, were prolonged significantly in Down's syndrome. These findings suggest impaired impulse conduction in the proximal part of the brachial plexus, posterior roots and/or posterior column-medial lemniscal pathway. Interpeak latency N13-N20, representing conduction time from cervical cord to sensory cortex, was not significantly different between the 2 groups. Cortical potentials N20 and P25 in the parietal area and P20 and N25 in the frontal area were of significantly larger amplitude in Down's syndrome. P25 had double peaks in 16 of 42 normal subjects, but these were not apparent in any of the patients.     

Three-dimensional human somatosensory evoked potentials

Median nerve somatosensory evoked potentials were recorded from 30 normal adults using conventional scalp derivations and an orthogonal bipolar surface electrode montage. This allowed the determination of the spatial orientation of the hypothetical centrally located equivalent dipole derived from the evoked response recorded in 3-dimensional voltage space. The 3-dimensional voltage trajectory describing changes in equivalent dipole orientation and magnitude revealed 4 major apices between 5 and 25 msec, 3 of which corresponded to the traditional P14, N20 and P25 peaks. A fourth apex at 17 msec was not as evident in the conventional recordings and signaled a transition from a vertical P14–N18 generator process to a horizontal N20 generator process. The normal within- and between-subject variability of trajectory apices, segments and planes are described, along with the theoretical and practical implications of this recording technique.     

Effect of sleep stage on somatosensory evoked potentials by median nerve stimulation

The effects of sleep stage on early cortical somatosensory evoked potentials (SEPs) and short-latency components elicited by median nerve stimulation were studied in 12 normal volunteers. The latency of P13 in the awake stage was not significantly different from that in any sleep stage. The latencies of N16, N20 and P20 were significantly prolonged while the amplitude of N20 was decreased during the non-rapid eye movement (NREM) sleep stage. P22, P23 and N24 components showed double peaks (P23a, P23b, N24a, N24b) during the NREM sleep stage in 6 subjects, while N24 showed a single peak and only P22 and P23 showed double peaks in 5 other subjects. The latencies and morphologies of SEPs during rapid eye movement sleep stage were almost the same as those during the awake stage. These findings suggest that NREM sleep affects the latency, amplitude and morphology of N16 and early cortical components.     

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.     

Short-latency somatosensory evoked potentials in brain-dead patients

Ten adult brain-dead patients were evaluated for the presence of clearly defined median nerve short-latency somatosensory evoked potentials (SSEPs). All met clinical criteria recommended by the President's Commission report (1981), had positive apnea tests, and had electrocerebral silent EEGs. P13-P14 and N20 were absent in all scalp-scalp channels, although 3 patients showed P13-P14 in scalp-non-cephalic channels. Of 6 patients showing N13, 3 lacked P13-P14. Our data suggest a characteristic destruction of N20 and rostral P13-P14 generators, with variable rostral-caudal loss of lower generators, SSEPs can provide valuable information about brain-stem activity in the evaluation of suspected brain-dead patients.     

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.     

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.     

Method for single-trial recordings of somatosensory evoked potentials

Evoked potentials (EPs) in response to stimuli are recorded from a human scalp contaminated with noise. To improve the signal-to-noise ratio, averaging methods have been widely used for the recorded data. However, when the waveforms of EP for each stimulus are not identical, the average waveform of the EP deteriorates. Variation of the EP waveform to each stimulus itself is important information for the EP. In this paper, a recording method for single somatosensory evoked potential (SEP) waveform is proposed, in which three kinds of band-pass filters were selectively used during three specific time sectors for each interstimulus interval. For the late section of the interval, an EEG waveform prediction method was applied to eliminate contaminated alpha rhythm components. By using the proposed method, we were successful in detecting the single SEP waveform.     

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     

Middle-latency somatosensory evoked potentials following median and posterior tibial nerve stimulation in Down's syndrome

Middle-latency somatosensory evoked potentials (SEPs) following median and posterior tibial nerve stimulation were studied in 40 patients with Down's syndrome and in age- and gender-matched healthy controls as well as in middle-aged and aged healthy subjects. In median nerve SEPs, latencies of the initial cortical potentials, N18 and P18, showed no significant difference, but the following potentials N22, P25, N32, P41 and P46 were relatively or significantly shorter in latency in Down's patients than in the controls. Amplitudes of all components in Down's patients were significantly larger than those of age- and gender-matched controls as well as of those of middle-aged healthy subjects, but there was only a small difference in their amplitudes from aged healthy subjects. Results of posterior tibial nerve SEPs were generally consistent with those of median nerve SEPs. Therefore, ‘short latency with large amplitude’ is the main characteristic of middle-latency SEPs in Down's syndrome, possibly related to accelerated physiological aging of the central nervous system.     

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.     

Ipsilateral median somatosensory evoked potentials recorded from human somatosensory cortex

Somatosensory evoked potentials (SEP) to ipsilateral and contralateral median nerve stimulations were recorded from subdural electrode grids over the perirolandic areas in 41 patients with medically refractory focal epilepsies who underwent evaluation for epilepsy surgery. All patients showed clearly defined, high-amplitude contralateral median SEPs. In addition, four patients showed ipsilateral SEPs. Compared with the contralateral SEPs, ipsilateral SEPs were very localized, had a different spatial distribution, were of considerably lower amplitude, had a longer latency (1.2–17.8 ms), did not show an initial negativity, and were markedly attenuated during sleep. Stimulation of the subdural electrodes overlying the sensory hand area was associated with contralateral hand paresthesias, but no ipsilateral hand paresthesias occurred. It was concluded that subdurally recorded cortical SEPs to ipsilateral stimulation of the median nerve (M) reflect unconscious sensory input from the hand possibly serving fast bimanual hand control. The anatomical pathway of these ipsilateral short-latency MSEPs is not yet known. Transcallosal transmission seems unlikely because of the short delay between the ipsilateral and contralateral responses in selected cases. The infrequent occurrence of ipsilateral subdurally recorded SEPs and their low amplitude and limited distribution suggest that they contribute very little to the short-latency ipsilateral median SEPs recorded on the scalp.     

Temperature-dependent hysteresis in somatosensory and auditory evoked potentials

Fourteen adult patients undergoing open heart surgery under induced hypothermia had median nerve, short-latency somatosensory evoked potentials (SSEPs) recorded during cooling (from 36°C to 19°C) and subsequent rewarming. Similar data on another group of patients who had brain-stem auditory evoked potentials (BAEPs) were also analyzed. Hypothermia produced increased latencies of the major SSEP and BAEP components and the latencies returned to normal with subsequent warming. The temperature-latency relationship during the cooling phase was significantly different from that during the warming phase. For SSEP components the temperature-latency relationship was linear during cooling and curvilinear during warming, whereas for BAEP it was curvilinear both during cooling and warming. Furthermore, the regression curves were different during the two phases of temperature manipulation, particularly for temperatures below 30°C both for SSEP and BAEP components. At the onset of warming there was an initial exaggerated warming response on the evoked potential (EP) latencies and amplitude of the EP components. The temperature-latency regression curves were uniformly less steep during the warming phase compared to those during cooling. These findings suggest the existence of hysteresis in the relationship between temperature and EP latencies. The latencies at a given temperature below 30°C depend on whether that temperature is reached during cooling or during warming.