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 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.     

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.     

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.     

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.     

Validity of median nerve somatosensory evoked potentials in the diagnosis of supraclavicular brachial plexus lesions

Experience with median nerve SEPs in the diagnosis of brachial plexus lesions is analysed in 49 patients selected from a total material of 264 cases with brachial plexus problems tested by SEP techniques. Median nerve SEPs were always compared with the results of SEPs after stimulation of at least one other nerve relevant to the site of the lesion as suspected clinically and electromyographically. All patients presented with unilateral brachial plexus problems and all root lesions were verified by clinical presentation, EMG studies, myelogram or surgery. There were 19 brachial plexus injuries, 13 cases with cervical spondylopathic rediculopaties without myelopathy and 7 patients presented brachial plexopathy with systemic cancer. It was found that median nerve SEPs were always normal in injuries of upper trunk and root avulsions confined to one or two root levels. Median nerve SEPs were abnormal in multiple trunk lesions and multiple root avulsions. In patients with spondylopathic radiculopathies median nerve SEPs were normal apart from one case where involvement of multiple roots was present. Median nerve SEPs were useful in assessing patients presenting brachial plexus problems in the presence of systematic cancer apart from cases where lower trunk involvement was present.In general, median nerve SEPs are useful if they are combined with SEP testing of other nerves anatomically more closely related to the problem as outlined clinically and electromyographically.     

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.     

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.     

Modification of median nerve somatic evoked potentials by prior median nerve,peroneal nerve,and auditory stimulation

In a recovery function design, changes were measured in the somatic evoked potentials (SEP) to right median nerve (RMN) shocks preceded by stimulation of: the same nerve (RMN-RMN); the left median nerve having primary input to the homologous sensory area in the contralateral hemisphere (LMN-RMN); the right peroneal nerve having primary input to a different region of the same hemisphere (RPN-RMN); and the auditory nerve with primary input to a different sensory modality (AUD-RMN). Eight inter-stimulus intervals ranged from zero (simultaneous) to 2.5 sec. It was assumed that the degree of interaction between evoked potentials would be related to the degree to which common neural structures are activated or modulated in response to the stimuli. Results were: (a) the primary somatosensory response N20-P30 was little influenced by other somatic or auditory stimulation, interaction occurring predominantly in the RMN-RMN condition; (b) with increasing latency, components showed increasing interaction across modalities; (c) preceding homolateral stimulation (RPN-RMN) showed no greater interaction than preceding contralateral stimulation (LMN-RMN); (d) N55-P100 differed from the primary somatosensory response N20-P30 by showing greater interaction with other somatic stimuli; and (e) N140-P190 showed similarly shaped recovery functions across stimulus pairs but significant differences in magnitude of interaction. These results show that components with similar wave form and topographical characteristics can have different neurophysiological properties.     

A prospective 1 year follow-up study with somatosensory potentials evoked by stimulation of the posterior tibial nerve in patients with supratentorial cerebral infarction

Somatosensory potentials evoked by stimulation of the posterior tibial nerve (tibial nerve SEPs) were studied in 40 patients with supratentorial non-haemorrhagic cerebral infarction and in 25 control subjects. SEPs were recorded twice in 39 patients and thrice in 35 patients. The first examination was carried out 4–19 days after the onset of the symptoms, the second examination 56–100 days after the stroke, and the third examination 348–393 days after the stroke. Increased side-to-side differences in the P57 and N75 peak latencies and absence of the P40 peak were the most frequent abnormal findings. The latency abnormalities were associated with involvement of the subcortical white matter of the rolandic region. The absence of the P40 peak was, in contrast, closely related to the extension of the infarcted area into the cortical gray matter of during the acute stage, 51% of patients had abnormal SEPs in the second examination and 43% of patients in the third examination. A nearly significant decrease was observed in the number of latency abnormalities, but the number of amplitude abnormalities, including absent responses, did not change during the 1 year follow-up period.     

Influence of concurrent tactile stimulation on somatosensory evoked potentials following posterior tibial nerve stimulation in man

A topographical study was made of SEPs following stimulation of the right posterior tibial nerve at the ankle, with and without concurrent tactile stimulation of the soles of either foot or the palm of the right hand. Effects of the interfering stimulus were best demonstrated by subtracting the wave forms to derive ‘difference’ potentials.The majority of SEP components were significantly attenuated by tactile stimulation of the ipsilateral foot, and the difference wave form was of similar morphology to the control response. Components of opposite polarity peaking at 39 msec were consistent with the field of a cortical generator with dipolar properties, situated in the contralateral hemisphere just posterior to the vertex with the positive poles oriented towards the ipsilateral side. By analogy with median SEP findings, these potentials were believed to originate in the foot region of area 3b where neurones are mainly concerned with cutaneous sensory processing.When the tactile stimulus was applied to the contralateral foot, difference potentials maximally recorded just posterior to the vertex were of smaller amplitude but similar morphology to ipsilateral foot difference components. This suggested the possibility that input from the two lower extremities may converge at cortical or subcortical level, the effect being manifested in the response of certain neurones in area 3b. With both contralateral foot and ipsilateral hand stimulation, other difference potentials were present which suggested that there may be cortical regions responding to combinations of sensory stimuli applied to various parts of the body surface.     

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.     

Effects of halothane on intraoperative scalp-recorded somatosensory evoked potentials to posterior tibial nerve stimulation in man

Somatosensory evoked potentials (SEPs) were monitored in 116 patients receiving halothane anesthesia during spinal fusion surgery. Whereas it has been generally assumed that the use of halogenated inhalational anesthetics should be avoided with SEP monitoring because of their purported deleterious effects on scalp-recorded sensory responses, we found that reproducible SEPs were obtained throughout the surgical procedure in 91% of the cases we monitored while using halothane at concentrations of 0.25–2.0%. In those cases in which halothane was delivered continuously at 0.5%, reproducible evoked responses were recorded in 96% (75 of 78) of the patients. Our data demonstrated 3 major effects of halothane on the SEP: (a) a small but significant decrease in the average amplitude of the first two components (N₂₅ and P₃₀), (b) a significant increase in the average latency of the late positive component (P₅₃) of the wave form, and (c) occasional obliteration of components N₂₅, N₄₀, P₅₃, and N₇₁,but never of P₃₀. These effects did not, in most cases, interfere with our ability to obtain clinically useful recordings. Our results suggest that in many instances the use of halothane anesthesia can be combined successfully with the recording of intraoperative SEPs.     

Long sensory tracts (cuneate fascicle) in cervical somatosensory evoked potential after median nerve stimulation

Low amplitude high frequency waves (LHW) were investigated in normal and patient cervical somatosensory evoked potentials after median nerve stimulation (CSEP) in parallel to normal and patient conducted somatosensory evoked potentials (SEP) after tibial nerve stimulation. Normal recordings were obtained in five subjects undergoing dorsal root entry zone (DREZ) coagulation for pain relief. Patient recordings were obtained in 11 subjects suffering from either syringomyelia, spinal cord tumour, or both. All recordings were made intraoperatively from the dorsal spinal cord surface using the subpial recording technique. Normal CSEP showed typical triphasic potential starting with an initial P9, followed by N13 and a final positivity, P1. Numerous LHW were superimposed on slow triphasic potential. To improve the visibility of LHW, slow triphasic potential was removed from the original CSEP. Potentials thus obtained contained only high frequency components of CSEP, i.e. LHW. They were compared with conducted SEP after tibial nerve stimulation. Comparison revealed similarities in high frequency, low amplitude and general wave form, LHW thus showing characteristics of conducted potential. Duration was found to be significantly shorter than normal duration in both patient LHW (Student's t-test, P<0.0005) and patient conducted SEP (Student's t-test, P=0.064). A shorter duration was associated with worsening of configuration in patient LHW and patient conducted SEP. These changes of LHW could not be connected with distortion of N13 seen in patient CSEP. A shorter duration and worsening of configuration in patient LHW were most prominent in cases with a loss of vibration and posture senses, but were also observed in cases where only pain and temperature senses were affected. We therefore concluded that cuneate fascicle is the most likely generator of LHW, although the participation of other cervical long sensory tracts, e.g. spinothalamic tract, cannot be ruled out.     

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.     

Serial changes in somatosensory evoked potentials following cerebral infarction

The relationship between somatosensory evoked potentials (SEPs) and recovery from stroke was investigated in 12 patients. All had suffered recent cerebral infarction. SEPs were performed within the first week, 6 weeks, 3 months and 6 months after stroke onset. Improvement of initially abnormal SEPs was maximal in the first 6 weeks and this correlated closely with the period of maximum clinical improvement. The results of this study suggest that the major effect of stroke on on SEPs occurs acutely and is little affected by secondary degenerative processes.     

Somatosensory evoked potentials recorded from the posterior pharynx to stimulation of the median nerve and cauda equina

Somatosensory evoked potentials (ppSEPs) in response to stimulation of the median nerve at the wrist and the cauda equina at the epidural space (the L4 level) were recorded from the posterior wall of the pharynx in 15 patients who underwent spinal surgery under general anesthesia, using disc electrodes attached to the endotracheal tube, and compared with segmental spinal cord potentials (seg-SCPs) that were recorded simultaneously from the posterior epidural space (PES). ppSEPs consisted of the initially positive spike (P9) followed by slow positive (P13) and negative (N22) waves. The P13 and N22 of ppSEPs had phase reversal relationship with the P2 and N2 recorded from the PES, respectively. The peak latencies of P9 (9.40 ± 0.7 ms) (mean ± SD), P13 (13.1 ± 0.9 ms), and N22 (22.0 ± 2.1 ms) of ppSEPs coincided with those of P1, N1 and P2 of seg-SCPs, respectively. ppSEPs were recorded more clearly with a reference electrode on the dorsal surface of the neck than with the reference electrode at the earlobe or back of the hand. The threshold and maximal stimulus intensities were also similar between the ppSEPs and seg-SCPs. Thus, the P9, P13, and N22 components of ppSEPs were thought to have the same origin as the P1, N1 and P2 of seg-SCPs, respectively. Therefore, the P9, P13 and N22 of ppSEPs may reflect incoming volleys through the root, synchronized activities of the interneurons and primary afferent depolarizations (PAD), respectively. ppSEPs in response to cauda equina stimulation showed that the latencies of the two initial components (4.6 ± 0.4 and 6.4 ± 0.6 ms) corresponded to those of the SCPs recorded from the PES (4.6 ± 0.3 and 6.3 ± 0.5 ms), suggesting that these potentials reflect impulses conducting through the spinal cord, similar to epidurally recorded SCPs.     

Hypothalamic evoked potentials to vagus and sciatic nerve stimulation

Hypothalamic evoked potentials to stimulation of the cervical portion of the vagus nerve and the sciatic nerve were recorded in experiments on cats anesthetized with chloralose and immobilized with succinylcholine. When both monopolar and bipolar recording techniques were used the focus of maximal activity of both "visceral" and "somatic" evoked potentials was located in the supramammillary and posterolateral region of the hypothalamus. Responses in the tuberal and anterior hypothalamus occurred in most experiments after a longer latent period, their amplitude was lower, and they were less stable. Evoked potentials in the focus of maximal activity of the posterior hypothalamus are similar in all parameters to responses of the mesencephalic reticular formation. Evoked potentials to stimulation of the visceral nerve have a higher threshold of generation and a lower amplitude than the "somatic" responses and they are inhibited more strongly when the frequency of stimulation is increased. Evoked potentials arising in the hypothalamus in response to stimulation of the vagus and sciatic nerves are regarded as nonspecific responses of reticular type.L. A. Orbeli Institute of Physiology, Academy of Sciences of the Armenian SSR, Erevan. Translated from Neirofiziologiya, Vol. 5, No. 3, pp. 253–260, May–June, 1973.