Cortical generators of somatosensory evoked potentials to median nerve stimulation

In 12 patients with intractable partial seizures, chronically implanted subdural electrodes were used to define the relationship of the epileptogenic focus to cortical functional areas. Cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were recorded from these electrodes. The initial cortical positivity, postrolandic primary cortical potential (PCP), was recorded in all 12 patients with a mean latency of 22.3 +/- 1.6 msec. A potential of opposite polarity, prerolandic PCP, was defined in nine patients with a mean latency of 24.1 +/- 2.7 msec. The latency of the postrolandic PCP was 1.61 +/- 1.59 msec shorter than the prerolandic PCP (p less than 0.01, paired t test). The maximum amplitude postrolandic PCP was 2.1 times larger than the maximum prerolandic PCP (p less than 0.02, paired t test). The phase reversal of the SEPs was compared with the position of the rolandic fissure (RF) defined by electrical stimulation. This study shows that the latency and amplitude characteristics of post- and prerolandic PCPs are significantly different and give support to the concept that they are produced by different generators; and cortical SEPs are helpful in locating the RF.     

Distribution of scalp somatosensory potentials evoked by stimulation of the tibial nerve in man

The scalp distribution of the response to stimulation of the tibial nerve at the medial malleolus was systematically analysed. The somatosensory evoked potential (SEP) was recorded with electrodes placed in a transversal line over the ipsilateral and contralateral postcentral gyri and in a sagittal line over the longitudinal brain fissure. The SEPs recorded over the ipsilateral hemisphere and along the sagittal line were similar to the F response (the response over the foot primary somatosensory region). Over the contralateral hemisphere the waveform of the responses changed obviously from point F to the point C (contralateral hand primary somatosensory region). The C response started with N37, P40 had a longer latency, N50 was not present and the subsequent waves were also considerably different. Mathematical simulation of the responses recorded from the electrodes between points F and C has shown that they represent an electrical algebraic summation of the activity over points F and C. Although the F and C responses may be 2 potentials arising from the opposite sides of a single dipole generator which is located in the medial fissure, it is more probable that the somatosensory evoked potential on tibial nerve stimulation reflects the activity of 2 separate generators.     

Premovement gating of somatosensory evoked potentials after tibial nerve stimulation

Somatosensory evoked potentials (SEPs) are attenuated or gated during movement. The mechanism for this includes both centrifugal gating of afferent input and competition with other afferents caused by the movement (peripheral gating). Using a paradigm in which the signal for triggering movement is the electric stimulus for SEPs, we studied the gating of SEPs after tibial nerve stimulation prior to foot movement, and compared it with that during counting task. Significant gating was found for P40 component, which distributed centrally and ipsilaterally to the side of the stimulation, whereas the contralateral N40 component showed no changes. Dissociated gating of P40 and N40 indicates multiple generators of these components, in contrast to the previous view of a single generator dipole projecting tangentially. Together with the previous findings in median SEPs, these gating phenomena should represent a general mechanism for sensori-motor integration in preparation for limb movement.     

Maturation of somatosensory evoked potentials upon posterior tibial nerve stimulation

Somatosensory evoked potentials produced in response to posterior tibial nerve stimulation were studied in 42 normal infants and children, ages 4 months to 16 years. The maturation of afferent conduction from the lower limb was evaluated for the peripheral nerve, spinal cord, and central nervous system. Although the maturation of conduction in the peripheral nerve (from the ankle to the popliteal fossa and from the popliteal fossa to L₃) was complete by 6 years of age, afferent conduction in the spinal cord (from L₃ to C₇) was not complete until 12 years of age or older. Spinal evoked potentials investigated in the thoracolumbar area revealed a phase-reversed potential located between the lower thoracic spine and upper lumbar spine in over 80% of patients. Reciprocal velocities for the major cortical positive potential P₁ (corresponding to P₃₇ in adults) and its onset, N₁, steadily decreased with age and leveled off at greater than 12 years of age and by 12 years of age, respectively. The propagation velocity from L₃ to the cerebral cortex also increased steadily with age, leveling off at greater than 12 years of age. Accordingly, the maturation of afferent conduction in the central nervous system was not complete until affer 12 years of age.     

Intraoperative recordings of spinal somatosensory evoked potentials to tibial nerve and sural nerve stimulation

Somatosensory evoked potentials (SSEPs) to stimulation of the tibial nerve at the knee (TN-K) and ankle (TN-A), and the sural nerve at the ankle (SN-A), were recorded from 3 or 4 spinal levels during surgery for scoliosis in 11 neurologically normal subjects. With stimulation of all 3 nerves, the propagation velocity along the spine was nonlinear: it was faster over cauda equina and midthoracic cord than over caudal spinal cord. Over the mid-thoracic cord, TN-K SSEP propagation was faster than that of TN-A and SN-A SSEPs, whereas over the caudal spinal cord these values were similar on stimulation of all 3 nerves. These data suggest that fast conducting second order afferent fiber systems contribute to spinal cord SSEPs evoked by stimulating both mixed and cutaneous peripheral nerves.     

Cortical somatosensory evoked potentials to posterior tibial nerve stimulation in newborn infants

Successful cortical recordings of somatosensory-evoked potentials (SEPs) to posterior tibial nerve (PTN) stimulation were obtained in 21 (87.5%) for P1 and 22 (91.7%) for N1 of 24 infants who were followed up for at least 3 years and had a normal outcome. There were linear decreases with increasing post menstrual age in both P1 and N1 peak latency. Of the four cases with diplegia later, three showed definite abnormalities, no responses and delayed latency in PTN SEPs respectively, however, the other case showed normal responses. Of the three cases with mental retardation, two showed relatively long latency and borderline responses respectively, and the other case showed normal responses. As the pathway of PTN SEPs traverses the periventricular area of the brain likely to be affected by ischemic lesions in premature infants, abnormalities in the responses might indicate a later motor disorder.     

Scalp recorded somatosensory evoked potentials to posterior tibial nerve stimulation in humans

The somatosensory evoked potentials (SEPs) produced by stimulation of the right and left posterior tibial nerves individually and also by their simultaneous stimulation were recorded in 84 adult normal subjects up to 150 msec after the stimulus by electrodes placed on the cranial vertex and by rows of electrodes over the sagittal and coronal lines using references on the ear or in the nasopharynx. The statistical distribution of the latencies of their different peaks was established. The effect of simultaneous stimulation of right and left posterior tibial nerves on the early SEP components was described. Some details of the anatomy of the rolandic sulcus were inferred from the amplitude distribution of these potentials.     

Bipolar recording of short-latency somatosensory evoked potentials after median nerve stimulation

Generators of median short-latency somatosensory evoked potentials were studied with three orthodiagonal pairs of bipolar electrodes. N11 was attributed to the dorsal root and dorsal column volleys. N13 had at least two subcomponents, generator dipoles of which are directed horizontally (N13a) and axially (N13b). N13a was generated in the lower cervical cord. N13b (bipolar) and P14 far-field (noncephalic reference) appeared to originate in the cuneate nucleus or spinocerebellar tracts as well as in the medial lemniscus. Bipolar recordings were useful in localizing cervical cord lesions, which was impossible in conventional monopolar recordings.     

Subcortical somatosensory evoked potentials after posterior tibial nerve stimulation in children

We report our normative data of somatosensory evoked potentials (SEP) after posterior tibial nerve (PTN) stimulation from a group of 89 children and 18 adults, 0.4-29.2 years of age. We recorded near-field potentials from the peripheral nerve, the cauda equina, the lumbar spinal cord and the somatosensory cortex. Far-field potentials were recorded from the scalp electrodes with a reference at the ipsilateral ear. N8 (peripheral nerve) and P40 (cortex) were present in all children but one. N20 (cauda equina) and N22 (lumbar spinal cord) were recorded in 94 and 106 subjects, respectively. P30 and N33 (both waveforms probably generated in the brainstem) were recorded in 103 and 101 subjects, respectively. Latencies increased with age, while central conduction times including the cortical component, decreased with age (up to about age 10 years). The amplitudes of all components were very variable in each age group. We report our normative data of the interpeak latencies N8-N22 (peripheral conduction time), N22-P30 (spinal conduction time), N22-P40 (central conduction time) and P30-P40 (intracranial conduction time). These interpeak latencies should be useful to assess particular parts of the pathway. The subcortical PTN-SEPs might be of particular interest in young or retarded children and during intraoperative monitoring, when the cortical peaks are influenced by sedation and sleep, or by anesthesia.     

Different neuronal contribution to N20 somatosensory evoked potential and to CO2 laser evoked potentials: an intracerebral recording study.

OBJECTIVE: To investigate the possible contribution of the primary somatosensory area (SI) to pain sensation. METHODS: Depth recordings of CO2 laser evoked potentials (LEPs) and somatosensory evoked potentials (SEPs) were performed in an epileptic patient with a stereotactically implanted electrode (Talairach coordinates y=-23, z=40) that passed about 10 mm below the hand representation in her left SI area, as assessed by the source of the N20 SEP component. RESULTS: The intracerebral electrode was able to record the N20 SEP component after non-painful electrical stimulation of her right median nerve. The N20 potential showed a phase reversal in the bipolar montage (at about 31 mm from the midline), which confirms that the electrode was located near its generator in area 3b. In contrast, no reliable response was recorded from the SI electrode after painful CO2 laser stimulation of the right hand. An N2-P2 response was evoked at the vertex electrode (Cz), thus demonstrating the effectiveness of the delivered CO2 laser stimuli. CONCLUSIONS: Since the N20 SEP component originates from the anterior bank of the post-central gyrus (area 3b), our result suggests that this part of SI does not participate in LEP generation. In fact, the previously published LEP sources in the SI area estimated from scalp recordings are about 10-17 mm posterior of the electrode in our patient, suggesting that they are more likely located in area 1, 2 or posterior parietal cortex.     

Multichannel recording of median nerve somatosensory evoked potentials.

OBJECTIVES: Clinical applications of multichannel (>or=64 electrodes) electroencephalography (EEG) have been limited so far. Amplitude variability of evoked potentials in healthy subjects is large, which limits their diagnostic applicability. This amplitude variability may be partially due to spatial undersampling of anatomical variations in cortical generators. In the present study, we therefore investigated whether 128-channel recordings of somatosensory evoked potentials (SEPs) can reduce this amplitude variability in healthy subjects. Additionally, we explored the relation between amplitude and age. METHODS: We recorded median nerve SEPs using a 128-channel EEG system in 50 healthy subjects (20-70 years) and compared N20, P27, and P45 amplitude as obtained with a 128-channel analysis method - based on butterfly plots and spatial topographies - and as obtained using a conventional one-cortical-channel configuration and analysis. Scalp and earlobe references were compared. RESULTS: Although amplitude variability itself was not reduced, a reduced coefficient of variation was obtained with the 128-channel method due to higher SEP amplitudes, compared to the conventional one-channel method, independent of reference. CONCLUSION: These results suggest that at the cost of some additional preparation time, the 128-channel method can measure SEP amplitude more accurately and might therefore be more sensitive to physiological and pathological changes. For optimal amplitude estimation, we recommend to increase the number of centroparietal electrodes or, preferably, to perform at least a 64-channel recording.     

Lumbar-spinal somatosensory evoked potentials in the rat after stimulation of the tibial nerve

Spinal somatosensory evoked potentials after stimulation of the tibial nerve were recorded from the lumbospinal cord of rats. Their components and the respective latencies recorded over L5/6 and L1/2 in 40 normal animals are described. Using this method exact statements concerning lesions particularly of the proximal segment of the peripheral nerves and their roots can be made.     

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.     

Subcortical and cortical somatosensory potentials evoked by posterior tibial nerve stimulation: normative values

Cortical somatosensory evoked potentials to posterior tibial nerve stimulation were obtained in 29 normal controls varying in age and body height. In obtaining these potentials we varied recording derivations and frequency settings. Our recordings demonstrated the following points: N20 (dorsal cord potential) and the early cortical components (P2, N2) were the only potentials that were consistently recorded. All other subcortical components (N18, N24, P27, N30) were of relatively low amplitude and not infrequently absent even in normals. All absolute latencies other than N2 were correlated with body height. However, interpeak latency differences were independent of body height. Below the age of 20, subcortical but not cortical peak latencies correlated with age, but this appeared to be due to changes in body height in this age group. Absolute amplitudes and amplitude ratios (left/right and uni/bilateral) showed marked interindividual variability and have very limited value in defining abnormality. The use of restricted filter windows facilitated the selective recording of postsynaptic potentials (30-250 Hz) and action potentials (150-1500 Hz).     

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.     

Topography and cortical generators of somatosensory potentials evoked by median nerve stimulation in the cat

Epidural and cortical mapping of somatosensory evoked activity after median nerve stimulation was performed under barbiturate anaesthesia in 6 cats. Depth profiles were made to confirm the site of the cortical generators. The area studied revealed two cortical generators in SI and one in SII. In all cases polarity changes in intracortical tracks were demonstrated. The peak latency of all these generators was 12 msec. In SI a P8 was also a consistent finding in epidural, epicortical and intracortical measurements. No evidence, however, could be obtained for a cortical origin of the P8. The most rostral generator of the P12 was localized in the posterior sigmoid gyrus (area 3a). The N12 originates from the dorso-medial bank of the coronal sulcus in SI (area 2). Histological evidence for these projections was obtained with use of electrode markation. Within the second somatosensory area one source was active; the P12 originated just lateral to the anterior aspect of the suprasylvian sulcus in the anterior ectosylvian gyrus.     

Maturational study of short-latency somatosensory evoked potentials after posterior tibial nerve stimulation in infants and children

SSEPs produced in response to PTN stimulation were studied in 41 normal infants and children from 4 months to 16 years in age. SSEPs were recorded on the scalp with reference electrodes attached to the contralateral knee, shoulder and earlobe. Four positive SSEPs, PI, PII, PIII and PIV, named in order of appearance, and one negative SSEP, N0, were recorded as FFPs on the scalp with the cKn reference. Following these FFPs, the cortical component P1 which corresponded to P37 in adults was recorded. Preceding P1, another negative wave, N1, could be recognized solely at Cz' mainly at the onset of P1. P1 and N1 could be identified in all children with derivations with noncephalic references, although they could not be identified in 5 of 41 children with a Cz' - Fpz derivation. PI, bilobed in configuration, was considered to originate at the sacral plexus or entry to the spinal canal. PII was the least reproducible potential and was considered to originate at the dorsal root, dorsal horn or conus medullaris. PIII, PIV and N0 were considered to originate at the cervical cord, brain stem and thalamus, respectively. With the peak latencies of PI, PII, PIII, PIV, N0, N1 and P1, the RV was calculated in order to eliminate the influence of body height. The RV of the later appearing components leveled off in the older age categories. The RV of P1 reached a steady level at 3 years of age. RVs of PII and PIII appeared to level off by the age of 6 years. The RV of PIV leveled off by the age of 9 years. RVs of N0 and N1 leveled off by the age of 12 years, and that of P1 decreased until over 12 years of age. Furthermore, to eliminate the influence of naturation in the peripheral nerves, the RV was obtained from PI-PIV, PI-P1, PIV-P1 and N1-P1 interpeak latencies. The RVs of these 4 interpeak latencies all decreased until over 12 years of age. Accordingly, the maturation of afferent conduction in the central nervous system after PTN stimulation appeared to be complete after 12 years of age.     

Neuronal generators of the visual evoked potentials: intracerebral recording in awake humans

Flash and pattern reversal visual evoked potentials were recorded in awake patients undergoing stereotactic procedures for severe dyskinetic disorders resistant to medical treatment. The nucleus ventralis lateralis thalami was reached via an occipital approach. VEPs were recorded on the scalp at the entrance of the intracerebral electrode, and serially from sites at different depths. A polarity reversal of the surface recorded wave form took place as the intracerebral electrode was advanced beneath the surface cortical layers. As concerns F-VEPs, most of the scalp activity mirrored the potentials recorded down to the depth of 70-65 mm from the thalamus. The largest amplitude of intracerebral F-VEPs was obtained from recording sites at 50-70 mm from the thalamus, i.e., in the depth of the calcarine fissure. A negative wave, peaking around 47-50 msec, became evident in recording sites at 30-40 mm from the thalamus but vanished as the electrode was advanced farther. In only one patient could we record a small negative wave, peaking at 33 msec, in the vicinity of the corpus geniculatum externum. Furthermore, the oscillatory activity recorded from the scalp appeared to be generated in the cortical layers. PR-VEPs also underwent polarity reversal as the electrode traversed the cortex. PR-VEPs disappeared more superficially than F-VEPs. No PR-evoked activity could be recorded in the vicinity of the corpus geniculatum externum. We conclude that slow and fast components of VEPs recorded from the scalp are entirely generated in cortical layers.     

Spinal and far-field components of human somatosensory evoked potentials to posterior tibial nerve stimulation analysed with oesophageal derivations and non-cephalic reference recording

Somatosensory evoked potentials (SEPs) were elicited by stimulation of the right posterior tibial nerve at the ankle in 20 experiments on 18 normal adults. A non-cephalic reference on the left knee was used throughout (with triggering of averaging cycles from the ECG), except for recording the peripheral nerve potentials. The responses were recorded along the spine, from oesophageal probes and from the scalp. The peripheral nerve volley propagated at a mean maximum conduction velocity (CV) of 59.2 m/sec served to identify the spinal entry time (mean 19.7 msec) at spinal segments S1-S3, under the D12 spine. This entry time coincided with the onset of the N21 component which was interpreted as the dorsal column volley and considered equivalent to the neck N11 of the median nerve SEP. The large voltage of the spinal response at the D12 spine probably results from summation of N21 with a fixed latency N24 potential that phase reverses at oesophageal recording sites into a P24. The N24-P24 reflects a horizontal dipole in the dorsal horn and is equivalent to the N13-P13 of the neck SEP to median nerve stimulation. Spinal conduction between D12-C7 spines was spuriously overestimated because the true length of the dorsal spinal cord is shorter by about 13% than the distance measured on the skin over the dorsal convexity. This correction should be applied routinely and it leads to a mean maximum spinal CV of 57 m/sec. Several positive far fields with widespread scalp distribution and stationary latencies have been identified. The P17 (over spine and head) reflects the peripheral nerve volley at the upper buttock. The P21 is synchronous with the N21 at the D12 spine and reflects the initial volley in the dorsal column. No far-field equivalent has been found for the N24-P24, due to the horizontal axis of the corresponding dipole. The P26 far field reflects the ascending volley at spinal levels D10-D4. The P31 reflects the initial volley in the medial lemniscus. The P40 at Cz represents the cortical response of the foot projection. Average central CVs were calculated and discussed.     

Effects of age, gender, and stimulus side on the scalp topography of somatosensory evoked potentials following posterior tibial nerve stimulation.

This is the first thorough study to evaluate the effects of age, gender, and stimulus side on the scalp topographies of somatosensory evoked potentials (SEPs) following stimulation of the posterior tibial nerve by using computerized bit-mapped color images and the significance probability mapping method. Seventy-four normal subjects whose ages ranged from 7 to 88 years were studied. Topographic mappings of most components in aged subjects were significantly different from those in young subjects, mainly because of higher amplitudes of the components in the aged group. However, scalp distribution of each component did not show a large difference among different age groups. There was a tendency that amplitudes in women were larger than those in men, and the gender differences of some components were significantly larger for some age groups. Stimulus side and handedness caused no significant difference in amplitudes and topographies of the components. These results were very similar to our previous results of the scalp topographies of SEPs following median nerve stimulation.