Topographical displays of somatosensory evoked potentials

The distribution of somatosensory evoked potentials (SEPs) after stimulation of the median nerve at the wrist was examined in 10 normal subjects using isopotential maps. The latencies of continuous negative and positive peaks were measured in each lead. The differences of the potentials at these latencies were measured in all the leads and the isopotential maps were constructed. The distribution of P0-NI was all similar. The latencies of P0 were almost the same in all the leads at about 13 msec. The distribution of NI-PI-NII was divided into three types--N16-P20-N28 localized in the frontal region, N17-P22-N30 localized in the central region and N19-P25-N33 distributed in the parieto-occipito-temporal regions. The distributions of NII-PII and PII-NIII were all similar, with high amplitudes in the central region. The latencies of PII and NIII were almost the same in all the leads at about 45 msec and 68 msec.     

Somatosensory evoked potentials in Huntington's disease

Scalp recorded somatosensory evoked potentials (SEPs) elicited by left and right median nerve stimulation were obtained in 21 patients with Huntington's disease (HD), 14 individuals at risk (AR) for HD, and 21 non-patient controls matched for age and sex. Although SEP abnormalities were not uniform in the HD group, no HD patient had SEPs that conformed fully to the normal configuration with respect to peak latencies, presence of all components and spatial distribution. The most common abnormality was non-specific in nature, consisting of amplitude reduction or virtual abscence of components after 100 msec. More specific deviations were noted in the early SEP events. In half of the HD patients, peak P30 seemed to occur at approximately 45 msec poststimulus; this peak could have been taken as the normal P45 had it not reversed in phase between the central and frontal leads. In these cases peak P45 prepared to be missing. Peak N20 latency values were longer in the HD group than in the non-patient controls, whereas the P15 latencies did not differ significantly. The conduction time between P15 and N20 was significantly longer in HD patients than the non-patient controls. SEPs of the majority of the ARs were similar to those of the non-patients controls in terms of overall configuration, although mean amplitudes were generally lower for ARs than non-patient controls and 4 ARs exhibited prolonged P15-N20 latency differences.     

Projections of the septum to the lateral hypothalamus

Evoked potentials recorded in the lateral hypothalamus (LH) of the rat to stimulation of the septum were observed to have response components of 3–6, 10–14, and 18–23 msec. These components were elicited from different regions of the septum; the 3–6 and 10–14 msec components from dorsal and midline regions corresponding to the projection field of the precommissural fornix from the hippocampus and the 18–23 msec component from a ventrolateral region corresponding to projections of the stria terminalis. Stimulation of the hippocampus and stria terminalis evoked responses in the LH of similar configuration but with latencies longer than the 10–14 and 18–23 msec components, respectively. Lesions in the dorsal midline and ventrolateral septum attenuated these responses suggesting that the precommissural fornix and stria terminalis are the pathways mediating the septal evoked components. These data provide a neuroanatomical framework for the dual role of the septum on response patterns elicited from the hypothalamus.     

Flash Visual Evoked Potentials of Various Derivations in Dementia of the Alzheimer Type and Vascular Dementia

Background : Recently, evoked potentials have been used for objective monitoring of the cortical function in dementia. The aim of this study was to distinguish dementia of the Alzheimer type (DAT) from vascular dementia (VaD) using flash visual evoked potentials of various derivations.
Methods : A total of 70 patients consulting Tachikawa Medical Center Kashiwazaki Kosei Hospital were divided into four groups, normal adult (29.5 ± 8.5 years, n=16), normal elderly (77.2 ± 4.7 years, n=17), VaD (81.1 ± 8.1 years, n=17) and DAT (77.4 ± 5.6 years, n=20). Red flash stimulation was provided by a pair of goggles. Visual evoked potentials (VEPs) to flash were recorded in accordance with the International 10–20 Electrode System.
Results : The latencies of N130 and P190 of frontal and central derivations were significantly reduced in DAT compared with all other groups (p<0.05). The N130 and P190 latencies were markedly delayed in the normal elderly group compared with the normal adult group (p<0.05). The P3 (P100) latency of occipital derivation was significantly delayed in normal elderly, VaD and DAT groups compared with the normal adult group (p<0.05). In the DAT group, the P190 latency was shortened at central and frontal derivations compared with that at occipital derivation (p<0.05).
Conclusions : The N130 and P190 latencies decreased at frontal and central derivations in DAT. While the reason is still unclear, dysfunction in the central visual system induced by the degeneration of neuronal populations in DAT may cause the apparently reduced latency. Flash VEPs of frontal and central derivations may be useful for the differential diagnosis of DAT from VaD.     

Motor and cortical sensory evoked potentials by magnetic stimulation

Motor evoked potentials (MEP) by magnetic stimulation on the scalp and the spinous processes of the 7th cervical (C 7) and 5th lumbar (L 5) vertebrae were studied in 20 normal subjects and 10 patients with the pyramidal tract lesions. The magnetic stimulator composed of two flat helical coils with mean inner diameters of 12.0 and 2.2 cm. The evoked muscle action potentials were recorded from the thenar muscle in the hand and abductor hallucis muscle in the leg. The mean peak latencies of MEP recorded from the thenar muscle were 22.1 +/- 1.7 and 12.8 +/- 0.9 msec at the stimulations on the scalp and C 7, respectively. The central motor conduction time (CMCT) between the cortex and C 7 was 9.1 +/- 1.1 msec. On the other hand, the peak latencies of MEP were 41.0 +/- 3.2 and 21.6 +/- 2.3 msec at the stimulations on the scalp and L 5, respectively. CMCT between the cortex and L 5 was 19.3 +/- 2.3 msec. The patients with pyramidal tract involvements showed delayed peak latencies or absent MEP. The cortical somatosensory evoked potentials (SEP) by the noninvasive magnetic stimulation on the levels of Th 10, Th 12 and L 5 spines, gluteus and ankle were studied in 20 normal subjects and 7 patients with neurological diseases. Cortical components P 2 and N 2 were recorded clearly in all normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Non-invasive evaluation of input-output characteristics of sensorimotor cerebral areas in healthy humans

The topography of scalp SEPs to mixed and sensory median nerve (MN) and to musculocutaneous nerve stimulation was examined in 20 healthy subjects through multichannel (12-36) recording in a 50 msec post-stimulus epoch. MN-SEPs in both frontal leads were characterized by an N18, P20, N24, P28 complex showing maximal amplitude at contralateral parasagittal sites. This was sometimes partly obscured by a wide wave N30 having a fixed latency, but a steep amplitude gradient moving toward the scalp vertex. A P40 component followed, having longer peak latencies, moving the recording sites from contralateral medial parietal toward the vertex and frontal ipsilateral positions. MN-SEPs in contralateral parietal leads contained a widespread N20 with a maximum source posterior to the Cz-ear line. The following P25 enveloped two subcomponents - early and late P25 - having different distributions. The late P25 showed a maximum - coincident with that of wave N20 - which was localized more posteriorly than that of the early P25. An inconstant wave N33 with progressively longer peak latencies from sagittal toward lateral positions was then recorded. MN-SEPs in contralateral central positions showed a well-localized P22 wave in which both the parietal early P25 and the frontal P20 were vanishing. Common or separate generators for frontal, central and parietal SEPs were discriminated by evaluating the influence of stimulus rate and intensity, as well as of general anesthesia and transient CBF deficits, investigated in 7 patients undergoing carotid endarterectomy. Unifocal anodal threshold shocks were separately delivered to each of the scalp electrodes and motor action potentials were recorded from the target muscle in order to delineate the scalp representation of the motor strip for the upper limb and, consequently, to monitor, through SEP tracings, the short-latency sensory input to the motor cortex for hand and shoulder muscles. This was characterized by a boundary zone separating the parietal N20-early P25 complex, from the fronto-central N18-P22 one. This zone had an oblique direction strongly resembling that of the central sulcus.     

Sensory and cognitive evoked potentials in a case of congenital hydrocephalus

We studied auditory and visual evoked potentials in D.W., a patient with congenital stenosis of the cerebral aqueduct. Head CT scans revealed marked hydrocephalus with expanded ventricles filling more than 80% of the cranium and compressing brain tissue to less than 1 cm in thickness. Despite the striking neuroanatomical abnormalities, however, the patient functioned well in daily life and was attending a local community college at the time of testing. Evoked potentials provided evidence of preserved sensory processing at cortical levels. Pattern reversal visual evoked potentials had normal latencies and amplitudes. Brain-stem auditory evoked potentials (BAEPs) showed normal wave V latencies. Na and Pa components of middle-latency AEP had normal amplitudes and latencies at the vertex, although amplitudes at lateral electrodes were larger than at the midline. In contrast to the normal sensory responses, long-latency auditory evoked potentials to standard and target tones showed abnormal P3 components. Standard tones (probability 85%), evoked N1 components with normal amplitudes (-3.7 microV) and latencies (103 msec), but also elicited large P3 components (17 microV, latency 305 msec) that were never observed following frequent stimuli in control subjects. Target stimuli (probability 15%) elicited P3s in D.W. and controls, but P3 amplitudes were enhanced in D.W. (to more than 40 microV) and the P3 showed an unusual, frontal distribution. The results are consistent with a subcortical source of the P300. Moreover, they suggest that the substitution of controlled for automatic processes may help high-functioning hydrocephalics compensate for abnormalities in cerebral structure.     

Source location of a 50 msec latency auditory evoked field component

We recorded auditory evoked magnetic fields in response to 128 15 msec duration 1 kHz tone pips from both hemispheres of 6 normal adult males. Auditory evoked potentials were recorded conventionally from a vertex lead. An approximately 50 msec latency component was identified in both the magnetic (called the M50) and EEG (called the P50) recordings. Isofield topographical contour maps were used to estimate M50 source location and depth. With respect to extracranial bony landmarks, M50 source locations were significantly higher and tended to be more posterior, over the left hemisphere. M50 and P50 latencies were not significantly different in 5 of 6 subjects; in one, M50 latencies were significantly longer than P50 latencies over the left hemisphere. Magnetic resonance images in 5 subjects were used to identify the neuroanatomical structure(s) present at the estimated source location. M50 sources appeared to reside in the cortex of the planum temporale in both left and right hemispheres in all 5 subjects.     

Symptomatic and asymptomatic high-grade unilateral internal carotid artery stenosis: scalp topography of event-related potentials (P300) and psychometric testing

Unilateral internal carotid artery (ICA) stenosis may be accompanied by widespread atherosclerosis of extra- and intracranial vessels leading to subtle cognitive disorders. We applied multichannel recording of P300 in 28 patients (68.3 ± 8.1 years; 15 asymptomatic, 13 with a history of transient ischemic attack (TIA)) and compared them with an age- and sex-matched control group. All underwent a visual “odd-ball paradigm” as well as a psychometric test, the Cognitive Performance Test (CPT), testing mainly visual attention and memory. The potentials were derived from 16 electrodes according to the $\text{10}\text{20}$ system against linked mastoids. The latencies and amplitudes of N250 and P300 were measured and their amplitudes additionally mapped. Furthermore, the early sensory exogenous potentials, P1 and N1, within the P300 potentials as well as conventional pattern reversal visual evoked potentials (PVEPs) were evaluated.(1) Both the early exogenous potentials and the conventional PVEPs showed no significant differences among all groups. (2) There were no significant differences between asymptomatic patients and those with a TIA history in all parameters of the P300 complex so that one total patient group was constructed and compared to the controls. (3) Patients' P300 amplitudes showed significant reductions over hemispheres ipsilateral (P ≤ 0.014) and contralateral (P <- 0.044) to the stenosis. (4) The N250 amplitudes were reduced only in the central leads (P <- 0.05). (5) The latencies of N250 potentials were significantly prolonged at many electrodes, not only ipsi- (P <- 0.0007) but also contralateral (P <- 0.022) to the stenosis. (6) The patients' P300 latencies showed significant lengthening only at occipital sites (P ≤ 0.05) compared to controls. (7) In all measured parameters, within the patient group, the differences between hemispheres ipsilateral versus contralateral to the ICA stenoses did not reach statistical significance. (8) The CPT values detected slight cognitive disorders for both patient groups and they correlated significantly with the latencies in many leads. (9) The highest test sensitivity to classify patients versus controls (z score > 2) was reached in P300 maps of TIA patients (77%).An altered P300 indicates electrophysiologically, and CPT behaviorally, subclinical cognitive deficits even in asymptomatic patients with unilateral tight ICA stenoses. Interestingly, no differences between asymptomatic and TIA patients with a high-grade unilateral ICA stenosis could be found.     

Age-related changes of auditory event-related potential (P300) in children

Auditory event-related potentials (ERPs) were recorded from 53 neurologically normal children of 5 to 15 years of age, and 8 healthy adults. To clarify the developmental changes and to obtain a normative value in childhood, the latency and amplitude of ERPs (N100, P200, N200, and P300) were examined. ERPs were elicited with the auditory oddball paradigm. P300 components were detected in all subjects. A strong positive correlation was demonstrated between latencies of two trials, and a small latency difference between trials was interpreted as being clinically unimportant. A significant negative correlation was observed between P300 latency and age during childhood (latency (msec) = -9.81 X (Age) + 459: r = 0.75, p less than 0.01). A mild negative correlation was also observed between N100, P200 and N200 latency and age. P300-topography of amplitude showed various patterns in young childhood, but in adolescence a maximum point was Pz in almost all subjects. These findings suggest that auditory ERPs can be easily measured in childhood and are useful for objective evaluation of the cognitive function.     

Auditory evoked potential development in early childhood: a longitudinal study.

Serial recordings of auditory evoked potentials (AEPs) to clicks were obtained using a vertex-mastoid derivation from 16 normal children during sleep over an age span from near birth to age 3. The AEP components studied were: N0 (38 +/- 10 msec), P1 (79 +/- 24 msec), N1 (109 +/- 39 msec), P2 (186 +/- 35 msec), N2 (409 +/- 97 msec), P3A (554 +/- 116 msec), P3B (757 +/- 121 msec) and P3 (728 +/- 128 msec). Amplitudes and latencies of the components were calculated and regressions of the measures on age were computed for the group as a whole, for each subject and for subsets of the data based on sleep stage, sex, order of stimulus presentation and a rearing/race factor. For the group as a whole the latencies of P1, P2, P3, and P3B decreased with age. The amplitudes of P1N1 and the N2P3 waves increased with age. Most change occurred during the first year of life. In general, the changes with age were also found to hold across all of the factors examined, although individuals varied widely in the degree to which they conformed to the trends found for the data as a whole. The amount contributed by each of the factors mentioned above to the total variance was estimated. The proportions varied for different EP components but, in general, age, sleep state, and subject factors other than rearing/race and sex accounted for most variance. One half to 5/6 of the unexplained variance in AEP latencies and amplitudes (i.e., that not due to age, sleep state, etc.) occurred across rather than within subjects. For both the group as a whole and for individual children, P2 and N2 latencies were found to exhibit the greatest stability across time. The results of the longitudinal study reported here were in good agreement with those of a previous study from this laboratory which utilized a cross-sectional design.     

Short latency somatosensory evoked potentials in infants

Short latency somatosensory evoked potentials (SEPs) to unilateral median nerve electrical stimulation were recorded from normal infants at birth and at 2, 4, 6, 8, 10 and 12 months of age. Three channels were recorded: Erb's point-Fz; C II (over 2nd cervical vertebra)-Fz; contralateral C' (2 cm posterior to C3 or C4)-Fz. Sweep time = 50 msec. At birth, the C II potential was seen in all infants; the Erb's point and C' potentials were seen in two-thirds. All older infants had well developed potentials at all sites. The mean latency of the Erb's point potential was stable over time. The latency of the C II potential decreased with maturation. At C', 4 components were seen, the latencies of which decreased with maturation: N1, P1, N2 and P2. The duration of N1 and P1 decreased with maturation. Standard deviations were relatively small for latencies and large for amplitudes. SEPs were adversely affected by using the 60 c/sec filter. Increasing the low frequency filter from 1 to 30 c/sec changed SEP, particularly in younger infants. Abnormal SEPs were seen in prematures surviving periventricular hemorrhage.     

The influence of interfering input from the peroneal nerve on tibial-nerve somatosensory evoked potential.

Using a conditioning-test paradigm, we studied the recovery function of tibial nerve somatosensory evoked potentials (SEPs) conditioned by preceding peroneal nerve stimulation. The inter-stimulus intervals (ISIs) ranged from 0 to 400 msec, where 0 msec indicated simultaneous arrival of tibial and peroneal nerve volleys at the L1 spine. The recovery curve was W-shaped, showing two peaks of SEP suppression, maximum at 6 msec ISI (1st phase) and 50-75 ISI msec (2nd phase). In the 1st phase suppression, we found distinct differences in wave forms between 0-2 msec ISI and 4-6 msec ISI. At 0-2 msec ISI, P40-N50-P60 amplitude decreased and latencies shortened, while P31 and N35 were unchanged. At 4-6 msec ISI, all peaks, possibly excluding P31, were markedly depressed. We attribute the former change to an "occlusive effect" and the latter to an "inhibitory effect," each mediated via a central synaptic network between the two nerves. The attenuation of the 2nd but not the 1st phase suppression by peroneal nerve block distal to the stimulating electrodes provided evidence that the 2nd phase suppression resulted primarily from interfering afferent signals generated by peroneal nerve peripheral receptors, activated by foot movement.     

Latency differences of N20, P40/N60, P100/N140 SEP components after stimulation of proximal and distal sites of the median nerve.

The latencies of SEP N20, P40, N60, P100, and N140 components were measured after stimulation of two different sites, and the differences in relation to conduction velocity and their central functions are discussed. Subjects were 8 healthy right-handed males (age 22-31 years, height 164-184 cm). An electrical pulse of 200micro sec duration with an intensity of 2 times the motor threshold was delivered to the wrist and to the elbow alternately at a random rate of 0.1 to 0.3 Hz. Recording electrodes were Cz', C3', and C4' referenced to linked ears. Analysis time was 50 msec before and 450 msec after the stimulus. The band pass was 0.5 Hz to 2 kHz. Subjects were asked to mentally count the number of stimuli. The averaging was interrupted after every 16 to 24 stimuli and checked to determine whether the subject was attentive to the stimuli by verifying the number of stimuli counted. A total of 100 responses each from elbow and wrist stimuli were averaged. Differences in peak latency between elbow and wrist stimuli for N20, P40, N60, P100, and N140 were 3.7 +/- 0.7 msec, 5.0 +/- 1.8, 4.3 +/- 1.2, 8.1 +/- 6.3, and 7.4 +/- 2.6 msec, respectively. According to the latency differences, SEP components can be divided into 3 groups: the shortest difference for N20, medium difference for P40 and N60 and longest difference for P100 and N140. Similar latency differences and similar potential distribution for P40 and N60, and for P100 and N140, and their differences from N20 confirmed that each of N20, P40/N60, and P100/N140 has a different function centrally. In addition, central processing time was longer with the more distal site stimulation.     

Visual evoked potential in man: early oscillatory potentials.

Short latency visual evoked oscillatory potentials to bright light stimulation were recorded from the scalp of 15 normal human adult subjects. The onset latencies of these potentials recorded over anterior frontal and posterior scalp regions were 9--17 msec and 13--24 msec, respectively. The frequency of the oscillations was about 100 c/sec. These potentials were widespread in their distribution over the scalp but were most prominent at midline and parasagittal recording locations. Like similar potentials recorded in animals, it seems that these potentials arise in both subcortical and cortical visual structures. The mechanism underlying the generation of these potentials and their possible functional significance are discussed.     

Peripheral and central conduction abnormalities in diabetes mellitus

OBJECTIVES: To investigate peripheral and central somatosensory conduction in patients with diabetes. METHODS: The authors recorded sensory nerve action potentials and 5-channel somatosensory evoked potentials (SEPs) with noncephalic reference after median nerve stimulation in 55 patients with diabetes and 41 age- and height-matched normal subjects. The authors determined onset or peak latencies of the Erb's potential (N9) and the spinal N13-P13 and the cortical N20-P20 components, and obtained the central conduction time (CCT) by onset-to-onset and peak-to-peak measurements. RESULTS: Both onset and peak latencies of all SEP components were prolonged in patients with diabetes. The mean onset CCT in the diabetic group was 6.3 +/- 0.5 msec (mean +/- SD)-significantly longer than that in the control group (6.1 +/- 0.2 msec)-whereas no significant difference was found in the peak CCT. The amplitudes of N9 and N13-P13 components (but not N20-P20) were significantly smaller in the diabetic group. The peripheral sensory conduction velocity was also decreased in the diabetic group, but there was no significant correlation between peripheral conduction slowing and the onset of CCT prolongation. CONCLUSIONS: Diabetes affects conductive function in the central as well as peripheral somatosensory pathways. The CCT abnormality does not coincide with lowering of the peripheral sensory conduction. The current results do not favor a hypothesis that a central-peripheral distal axonopathy plays an important role in development of diabetic polyneuropathy.     

Abnormalities of short-latency somatosensory evoked potentials in parkinsonian patients

Twenty-two patients (16 affected by parkinsonian syndromes, 6 by other neurological diseases) and 12 age-matched controls were examined. Short-latency somatosensory evoked potentials were recorded from 30 scalp electrodes in the 45-52 msec following separate left and right median nerve stimulation at the wrist. Bit-colour maps were generated on a 4096 pixel matrix via quadratic interpolation. Peak latencies and amplitudes of the parietal, central and frontal components were evaluated. Moreover, the amplitude ratios between parietal and frontal components on the same hemiscalp and between peaks on homologous right and left scalp districts were taken into account. The unique significant difference between parkinsonians and controls was represented by a depressed frontal N30 wave. This peak was absent in 3 and reduced in 7 out of 16 parkinsonians, with an overall abnormality rate of 47% of the examined arms. Average maps pooling data of parkinsonians and controls confirmed the presence of reduced evoked activity for the whole duration of wave N30 on those mid- and parasagittal frontal districts where this peak is maximally represented in normals. A similar abnormality was found in 1 of the 6 non-parkinsonian neurological patients suffering from a meningioma of the falx compressing the left supplementary motor area. Possible pathophysiology of such wave N30 abnormalities in parkinsonians is discussed.     

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.     

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.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pattern reversal visual evoked potentials in awake rats

A method for recording pattern reversal evoked potentials (PREPs) from awake restrained rats has been developed. The procedure of Onofrj et al. [26] was modified to eliminate the need for anesthetic, thereby avoiding possible interactions of the anesthetic with other manipulations of interest. Rats were restrained in a harness and placed in front of a pattern generating TV screen displaying a black and white alternating square wave grating. Using various stimulation and recording parameters, normative data are presented from 141 adult male Long-Evans hooded and 11 adult male Sprague-Dawley albino rats. Reliable waveforms were recorded with five identifiable peaks. The labels and mean latencies of these peaks in hooded rats were: N1, 47.3 msec; P1, 65.7 msec; N2, 83.3 msec; P2, 94.4 msec: and N3, 129.8 msec. Spatial acuity functions generated with PREPs gave acuity estimates which corresponded closely to values determined behaviorally for hooded and albino rats [4,11].