Somatosensory evoked potentials from posterior tibial nerve; normative data

The somatosensory evoked potentials from posterior tibial nerve were studied in a group of normal adults. The latencies of popliteal fossa potential, L3, N33 and P40 waves as well as central conduction time were analyzed as a function of height and age. The correlation of the peripheral conduction velocity with the subject's age was also studied. The corresponding regression formulae were calculated and can be used to predict normal values of these parameters over a wide range of height and age. Standard error estimates are given for all parameters.     

Neurophysiological investigation of cervical spondylosis

The difficulties in diagnosing spinal cord lesions due to the cervical spondylosis is well-known in clinical neurology. In order to investigate the contribution of various neurophysiological examinations in the diagnosis in cervical spondylosis, we examined 70 patients suffering from cervical spondylosis, with peripheral nerve conduction studies, F-wave from the upper limb and electromyography from the corresponding muscles, as well as somatosensory evoked potentials (SEPs) from upper and lower limbs. Patients were separated into four groups: 20 patients had cervical spondylosis symptoms only; 15 patients had symptoms and signs of spinal root involvement; 15 patients had symptoms and signs of myelopathy; and 20 patients had symptoms and signs of both myelopathy and spinal root involvement. A group of 20 normal controls was also studied. In all groups of patients SEPs were the most sensitive electrophysiological study. Low-amplitude N13 and increased conduction time of N9-N13 and central conduction N13-N19 and LP-P27 were the most common finding in SSEP testing. SEPs were affected in many cases without CT-MRI findings of spinal cord pressure. From the above findings, SEPs proved to be the most sensitive diagnostic investigation in cervical spondylosis.     

Median sep and blink reflex in thyroid diseases

Pathological disturbances of thyroid hormones is associated with central and peripheral nervous system disturbances. The aim of this study is to evaluate median nerve stimulated somatosensory evoked potential (SEP) and blink reflex of thyroid patients (hypo and hyperthyroidism). Median SEP was performed in 40 patients (21 with hyperthyroidism and 19 with hypothyroidism). We evaluated the latencies of N9, N11, N13, P9, P11, P14, N20 and P25 waves and the N9-N20, N9-N13, N13-N20 and P14-N20 interpeak latencies. We compared the results of patients with the control group (26 persons). We found that the N20 latency was longer in patients with hyperthyroidism than in the control group and the difference was statistically significant. There was not any statistically significant difference regarding the N9, N11, N13, P9, P11, P14, N20 and P25 latencies and the N9-N20, N9-N13, N13-N20 and P14-N20 interpeak latencies between hypothyroid patients and controls. We performed the blink reflex study in 28 of 40 patients (14 patients with hyperthyroidism and 14 patients with hypothyroidism). Comparing the R1, R2, CR2 (contralateral R2) latencies and durations of the patients and controls, we found that R2 and CR2 duration was shorter in patients with hyperthyroidism. This difference was statistically significant.     

Cortical somatosensory evoked potentials. II. Effects of excision of somatosensory or motor cortex in humans and monkeys

1. To clarify the generators of human short-latency somatosensory evoked potentials (SEPs) thought to arise in sensorimotor cortex, we studied the effects on SEPs of surgical excision of somatosensory or motor cortex in humans and monkeys. 2. Normal median nerve SEPs (P20-N30, N20-P30, and P25-N35) were recorded from the cortical surface of a patient (G13) undergoing a cortical excision for relief of focal seizures. All SEPs were abolished both acutely and chronically after excision of the hand area of somatosensory cortex. Similarly, excision of the hand area of somatosensory cortex abolished corresponding SEPs (P10-N20, N10-P20, and P12-N25) in monkeys. Excision of the crown of monkey somatosensory cortex abolished P12-N25 while leaving P10-N20 and N10-P20 relatively unaffected. 3. After excision of the hand area of motor cortex, all SEPs were present when recorded from the cortical surface of a patient (W1) undergoing a cortical excision for relief of focal seizures. Similarly, all SEPs were present in monkeys after excision of the hand area of motor cortex. 4. Although all SEPs were present after excision of motor cortex in monkeys, variable changes were observed in SEPs after the excisions. However, these changes were not larger than the changes observed after excision of parietal cortex posterior to somatosensory cortex. We concluded that the changes were not specific to motor cortex excision. 5. These results support two major conclusions. 1) Median nerve SEPs recorded from sensorimotor cortex are produced by generators in two adjacent regions of somatosensory cortex: a tangentially oriented generator in area 3b, which produces P20-N30 (human) and P10-N20 (monkey) [recorded anterior to the central sulcus (CS)] and N20-P30 (human) and N10-P20 (monkey) posterior to the CS; and a radially oriented generator in area 1, which produces P25-N35 (human) and P12-N25 (monkey) recorded from the postcentral gyrus near the CS. 2) Motor cortex makes little or no contribution to these potentials.     

Cortical somatosensory evoked potentials. I. Recordings in the monkey Macaca fascicularis

1. The anatomic generators of somatosensory evoked potentials (SEPs) to median nerve stimulation in the 10- to 30-ms latency range were investigated in monkeys (Macaca fascicularis) by means of cortical-surface and laminar recordings. 2. Three groups of SEPs evoked by stimulation of the contralateral median nerve were recorded from the hand representation area of sensorimotor cortex: P10-N20, recorded anterior to the central sulcus (CS); N10-P20, recorded posterior to the CS; and P12-N25, recorded near the CS. These potentials were similar in morphology and surface distribution whether the animal was awake or anesthetized. 3. P10-N20 exhibited a polarity inversion to N10-P20 across the CS, both in cortical-surface recordings and in laminar recordings within cortex and white matter of motor and somatosensory cortex. In contrast, P10-N20 and N10-P20 did not exhibit polarity inversion in recordings from the surface and white matter of the crowns of motor and somatosensory cortex, respectively. These results strongly suggest that these potentials are produced by a tangential generator located in the posterior wall of the CS, primarily in area 3b of somatosensory cortex. 4. P12-N25 was largest over the hand area of somatosensory cortex and showed polarity inversion across the crown of somatosensory cortex but not across the crown of motor cortex or across the walls of the CS, suggesting that P12-N25 is due to a radially oriented generator located in areas 1 and 2 of somatosensory cortex. 5. P10-N20 and P12-N25 are thought to be equivalent to the "primary evoked response" recorded from somatosensory cortex of other mammals. 6. These results are very similar to those obtained in human cortical-surface recordings and demonstrate that the monkey P10-N20, N10-P20, and P12-N25 potentials correspond to the human P20-N30, N20-P30, and P25-N35 potentials, respectively. The only appreciable difference in human and monkey SEPs is that the monkey P12-N25 appears to be generated in areas 1 and 2, whereas the human P25-N35 appears to be generated only in area 1. 7. There was no evidence of locally generated activity in areas 3a and 4.     

Somatosensory evoked potentials/fields--exploration of brain function

We have summarized the history of electroencephalography(EEG) since 1875, when a paper by Richard Caton was published describing the first EEG recordings in animals. Somatosensory evoked potentials (SEPs) were recorded by George Dawson in 1951. Thereafter, SEPs were developed for clinical use with other evoked potentials such as auditory evoked potentials(VEPs). To understand evoked potentials, related mechanism of induction of far-fields-potentials(FFP) following stimulation of the median nerve has been discussed. SEPs consisted of P9, N9, N10, P11, N11, N13, P13, P14, N18, N20 and P20/P22. Scalp recorded P9 FFP arises from the distal portion of the branchial plexus as reflected by N9 stationary negative potential recorded over the stimulated arm. Cervical N11 and N13 arise from the root entry zone and dorsal horn, respectively. Scalp recorded P13, P14 and N18 FFP originate from the brainstem. In this communication, magnetoencephalography(MEG) and results of one of our recent studies on somatosensory evoked fields(SEFs) are also discussed. One of the important features of MEG is that magnetic signals detected outside the head arise mainly from cortical currents tangential to the skull. Since the net postsynaptic current follows the orientation of cortical pyramidal cells, the MEG signals mainly reflect activity of the fissural cortex, whereas radial current may remain undetected. In our study, we demonstrated SEFs elicited by compression and decompression of a subject's glabrous skin by a human operator. Their dipoles were tangentially oriented from the frontal lobe to parietal lobe.     

Somatosensory evoked potentials in X-linked recessive bulbospinal neuronopathy: a case demonstration.

Clinicopathological findings in X-linked recessive bulbospinal neuronopathy were characterized by loss of myelinated fibers in the fasciculus gracilis and depletion of neurons in the ventral horn throughout the same segments. Clinical profile of this rare motor neuron disease include sign and symptom of lower motor neuron involving bulbar and spinal level with minimal or no sensory deficit. Previous electrodiagnostic findings consist of electrophysiological evidence of anterior horn cell disease and decreased or absent sensory action potentials in the peripheral nerve. The role of somatosensory evoked potential which can uncover the involvement of posterior column has never been probed. We report a 22-year-old man who had a clinical syndrome of X-linked bulbospinal neuronopathy. The peripheral electrodiagnostic studies supported the evidence of prolonged anterior horn cell disease and decreased sensory response. The median SEPs revealed delayed N11-N13 and N13-N20 interpeak latencies representing demyelination in fasciculus gracilis of upper cervical cord. Therefore, the median SEPs, an uninvasive procedure, can be used as a supportive method to identify sensory neuronopathy with posterior column lesion in this syndrome, especially when the patient has no obvious sensory and endocrine symptom.     

Human cortical potentials evoked by stimulation of the median nerve. II. Cytoarchitectonic areas generating long-latency activity

1. The anatomic generators of human median nerve somatosensory evoked potentials (SEPs) in the 40 to 250-ms latency range were investigated in 54 patients by means of cortical-surface and transcortical recordings obtained during neurosurgery. 2. Contralateral stimulation evoked three groups of SEPs recorded from the hand representation area of sensorimotor cortex: P45-N80-P180, recorded anterior to the central sulcus (CS) and maximal on the precentral gyrus; N45-P80-N180, recorded posterior to the CS and maximal on the postcentral gyrus; and P50-N90-P190, recorded near and on either side of the CS. 3. P45-N80-P180 inverted in polarity to N45-P80-N180 across the CS but was similar in polarity from the cortical surface and white matter in transcortical recordings. These spatial distributions were similar to those of the short-latency P20-N30 and N20-P30 potentials described in the preceding paper, suggesting that these long-latency potentials are generated in area 3b of somatosensory cortex. 4. P50-N90-P190 was largest over the anterior one-half of somatosensory cortex and did not show polarity inversion across the CS. This spatial distribution was similar to that of the short-latency P25-N35 potentials described in the preceding paper and, together with our and Goldring et al. 1970; Stohr and Goldring 1969 transcortical recordings, suggest that these long-latency potentials are generated in area 1 of somatosensory cortex. 5. SEPs of apparently local origin were recorded from several regions of sensorimotor cortex to stimulation of the ipsilateral median nerve. Surface and transcortical recordings suggest that the ipsilateral potentials are generated not in area 3b, but rather in other regions of sensorimotor cortex perhaps including areas 4, 1, 2, and 7. This spatial distribution suggests that the ipsilateral potentials are generated by transcallosal input from the contralateral hemisphere. 6. Recordings from the periSylvian region were characterized by P100 and N100, recorded above and below the Sylvian sulcus (SS) respectively. This distribution suggests a tangential generator located in the upper wall of the SS in the second somatosensory area (SII). In addition, N125 and P200, recorded near and on either side of the SS, suggest a radial generator in a portion of SII located in surface cortex above the SS. 7. In comparison with the short-latency SEPs described in the preceding paper, the long-latency potentials were more variable and were more affected by intraoperative conditions.     

Human cortical potentials evoked by stimulation of the median nerve. II. Cytoarchitectonic areas generating short-latency activity

1. The anatomic generators of human median nerve somatosensory evoked potentials (SEPs) in the 40 to 250-ms latency range were investigated in 54 patients by means of cortical-surface and transcortical recordings obtained during neurosurgery. 2. Contralateral stimulation evoked three groups of SEPs recorded from the hand representation area of sensorimotor cortex: P45-N80-P180, recorded anterior to the central sulcus (CS) and maximal on the precentral gyrus; N45-P80-N180, recorded posterior to the CS and maximal on the postcentral gyrus; and P50-N90-P190, recorded near and on either side of the CS. 3. P45-N80-P180 inverted in polarity to N45-P80-N180 across the CS but was similar in polarity from the cortical surface and white matter in transcortical recordings. These spatial distributions were similar to those of the short-latency P20-N30 and N20-P30 potentials described in the preceding paper, suggesting that these long-latency potentials are generated in area 3b of somatosensory cortex. 4. P50-N90-P190 was largest over the anterior one-half of somatosensory cortex and did not show polarity inversion across the CS. This spatial distribution was similar to that of the short-latency P25-N35 potentials described in the preceding paper and, together with our and Goldring et al. 1970; Stohr and Goldring 1969 transcortical recordings, suggest that these long-latency potentials are generated in area 1 of somatosensory cortex. 5. SEPs of apparently local origin were recorded from several regions of sensorimotor cortex to stimulation of the ipsilateral median nerve. Surface and transcortical recordings suggest that the ipsilateral potentials are generated not in area 3b, but rather in other regions of sensorimotor cortex perhaps including areas 4, 1, 2, and 7. This spatial distribution suggests that the ipsilateral potentials are generated by transcallosal input from the contralateral hemisphere. 6. Recordings from the periSylvian region were characterized by P100 and N100, recorded above and below the Sylvian sulcus (SS) respectively. This distribution suggests a tangential generator located in the upper wall of the SS in the second somatosensory area (SII). In addition, N125 and P200, recorded near and on either side of the SS, suggest a radial generator in a portion of SII located in surface cortex above the SS. 7. In comparison with the short-latency SEPs described in the preceding paper, the long-latency potentials were more variable and were more affected by intraoperative conditions.(ABSTRACT TRUNCATED AT 400 WORDS)     

Developmental changes in point-light walker processing during childhood and adolescence: An event-related potential study

To investigate developmental changes in the neural responses to a biological motion stimulus, we measured event-related potentials (ERPs) in 50 children aged from 7 to 14 years, and 10 adults. Two kinds of visual stimuli were presented: a point-light walker (PLW) stimulus and a scrambled point-light walker (sPLW) stimulus as a control. The sPLW stimulus had the same number of point-lights and the same velocity vector of point-lights as the PLW stimulus, but the initial starting positions were randomized. Consistent with previous ERP studies, one positive peak (P1) and two negative peaks (N1 and N2) were observed at around 130, 200 and 330 ms, respectively, in bilateral occipitotemporal regions, in all age groups. The latency of the P1 component was significantly shorter for the PLW than sPLW stimulus in all age groups, whereas the amplitude was significantly larger for the PLW than sPLW stimulus only for the 7-year-old group. The P1 amplitude and N1 latency were linearly decreased with age. The negative amplitudes of both N1 and N2 components of the PLW stimulus were significantly larger than those of the sPLW stimulus in all age groups. P1-N1 amplitude was changed by development, but not N2 amplitude. These results suggest that the intensity (P1) and timing (N1) of early visual processing for the PLW stimulus changed linearly throughout childhood and P1-N1 amplitude at occipitotemporal electrodes and N1 latency in 10-year-olds, but not 11-year-olds, was significantly larger than that in adults. For the amplitudes of the N2 component in response to PLW and sPLW stimuli in 7–8-year-old subjects were not statistically different from those in adults at occipitotemporal electrodes. These results suggest that the neural response to the PLW stimulus has developed by 10 years of age at the occipitotemporal electrode.     

"Initial-" and "change-orienting reactions": an analysis based on visual single-trial event-related potentials

The present study was concerned with brain potentials elicited by, respectively, the first of a series of stimuli ("initial-orienting reaction", I-OR), and infrequent deviants ("change-orienting reaction", C-OR). Single-trial event-related potentials (ERPs) to visual stimuli were estimated from recordings at Oz, Pz, Cz and Fz. The design included both a habituation series as well as a series of occasional deviant trials against a background of standards. This was done with both task-relevant and neutral stimuli, and in two interstimulus interval (ISI) conditions: 2.45 s and 8.45 s. In the latter ISI condition, skin conductance responses (SCRs) were recorded as well. Decrease (Habituation) in the habituation series was found for a non-specific N1, a posteriorly distributed P3, and the SCR, but not for P2-N2. Deviant stimuli produced an enhancement of the central P2-N2, the P3, the N1 (on the first few deviant trials only, in both ISI conditions), and the SCR (with task-relevant stimuli only). Elongation of ISI delayed both short-term and long-term decrease of P3, but had no effect on enhancement of P2-N2 due to stimulus deviance. It was concluded that, with respect to ERP parameters, the I-OR is marked by the N1, whereas the C-OR coincides with the P2-N2.     

糖尿病患者的体感诱发电位

应用电子计算机迭加平均技术,记录了23名正常人和25例糖尿病患者的电刺激正中神经和胫后神经的体感诱发电位(somatosensory evoked potentials,SEPs)。结果发现,大部分患者均有SEPs成份峰值潜伏期的延长,以及正中神经和胫后神经传入纤维传导速度的减慢;部分患者有中枢传导时间(N13-N20传导时间和P40-N80传导时间)的延长。此外,外周神经三相电位的波形也出现异常变化。这些结果提示,糖尿病患者不仅可出现外周神经传导功能障碍,而且也可出现中枢神经传导功能异常。     

Reconsiderations about the abnormalities of somatosensory evoked potentials in motor neuron disease

The frequency of involvement of sensory pathways in motor neuron disease (MND) remains the matter of controversy. For this reason the purpose of the present work was to test how often sensory system involvement might be detected by somatosensory evoked potentials (SEP) studies and then to verify the presence of alteration of the sensory conduction and to detect the frequency of abnormalities of somatosensory peripheral, spinal, subcortical and cortical potentials in MND. SEP were tested after median nerve stimulation at the wrist, recorded from Erb's point, Ce2, Ce7 and scalp. Pearson's correlation coefficients test and Wilcoxon rank-sum test were used for statistical analysis. 74 patients (22 women and 52 men) were examined. Mean age of patients was 54.07 +/- 11.24 years; mean duration of the disease -19.25 +/- 15.87 months. SEP were abnormal in 39 of 74 patients (about 53%) whereas the sensory NCV in median nerve was abnormal in 14 of 74 patients (19%). The most frequent pattern of abnormalities consisted of the absence or delay of cortical responses. The mean values of SEP latencies (N9, N11, N13, N20 and P25) were significantly increased in MND patients (p < 0.05) as compared with controls. The N9 and N11 latencies correlated with the duration of the disease. The results of our study (concerning a large group of MND patients) suggest that the involvement of sensory pathways is not rare in MND.     

Interference of vibrations with input transmission in dorsal horn and cuneate nucleus in man: a study of somatosensory evoked potentials (SEPs) to electrical stimulation of median nerve and fingers

Summary The effects of 50 Hz palm vibrations on somatosensory potentials (SEPs) evoked by electrical stimulation of the median nerve at the wrist and of the 2nd and 3rd fingers were studied in 10 normal subjects. Vibrations were found to produce attenuation of the N13 spinal and P14 brainstem potentials and of the N20 contralateral parietal response. Brachial plexus (N9, P9) and dorsal column (P11) responses were not modified by vibrations. These SEP findings show: 1) that vibrations do not interfere at the periphery with the processing of brief ascending volleys triggered by an electrical stimulus and 2) that such an interference does occur in spinal dorsal horn and cuneate nucleus. Reduced input transmission in the cuneate nucleus is likely to be responsible for perceptual alterations induced by vibrations.     

改良的下肢SLSEP检测方法对糖尿病近端神经病的诊断意义

目的：探讨改良的短潜伏期体感诱发电位（SLSEP）（改变记录点）的检测方法对糖尿病性近端神经病的诊断意义。方法：排除脑卒中、腰颈椎病及其它疾病引起的神经肌肉疾病,肌电图检查排除有神经病变体征同时常规神经传导检测异常的糖尿病（DM）患者,将符合标准的61例2型DM患者分为3组：有神经病体征而常规神经传导检测正常（Ⅰ组）20例,无神经病体征且常规神经传导检测正常（Ⅱ组）21例和无神经病体征而常规神经传导检测异常（Ⅲ组）20例,与30例正常人均行改良的SLSEP测定。结果：改良的胫神经SLSEP反映下肢感觉神经近端功能的参数总异常率以DM有神经病变症状肢体亚组（Ⅰ组）（n=27）所占的比例最高（85％,23／27）,SLSEP反映神经近端功能的N13、N24峰的感觉神经传导速度（SCV）和N13N24、N9-N24峰间SCV,与对照组比较差异均有显著意义（P〈0．01）;DMⅡ组虽然无神经病变体征并且神经传导测定无异常,但与对照组比较,N13-N24峰间SCV异常肢体率却有显著差异（P〈0．01）。DMⅢ组SLSEP各参数异常率普遍较高（20％～72．5％）,但以反映神经远端功能的N9峰SCV异常率最高。结论：改良的SLSEP检测是对常规SCV检测的一种补充,可以提供感觉纤维近端信息,对有周围神经损害症状而常规SCV测定正常的DM患者其诊断意义尤为显著。SLSEP还有利于发现DM患者亚临床症状。     

皮层运动诱发电位监测在脑中央区术中的应用

目的:探讨在全凭静脉麻醉下,使用皮层运动诱发电位(MEP)对脑中央区手术进行术中监测的方法。方法:使用皮层电极对12例中央区肿瘤患者进行诱发电位术中监测,在中央后回感觉皮层区相应部位记录皮层体感诱发电位(SEP)的N20-P25波,沿中央后回功能区皮层向前移动电极,直至记录到一个波型相反(位相倒置)、波幅相近的波型P20-N25,将其定为运动中枢刺激点。使用高频串刺激(TS)直接刺激该点,在上肢肌肉记录MEP。结果:12例患者均能成功地记录到MEP。术中注意保护此区,术后患者症状无明显加重,被监测的上肢肌力无明显减退。结论:对于脑中央区手术,在全凭静脉麻醉下找出运动中枢刺激点并作MEP监测(术中注意保护此区)是一种优良的术中监测手段。     

Synaptic organization of eighth nerve afferents to cat dorsal cochlear nucleus

The synaptic organization of eighth nerve afferents to the dorsal cochlear nucleus (DCN) of cats was studied using extracellular field potential analyses. The eighth nerve was electrically stimulated and potentials produced in the DCN characterized using single shocks, paired shocks, repetitive stimulation, and one-dimensional current source-density (CSD) analysis. Field potentials and CSD profiles were correlated with the laminated cytoarchitecture of the DCN. At least four major temporally discrete components can be identified in field potentials evoked by a single shock to the eighth nerve. The amplitude and polarity of these events depends on the layers in which they are recorded. A brief positive-negative deflection (the P1-N1) is present in all layers but is maximal in the deeper layers 3 and 4. The N1 has a peak latency of approximately 0.8 ms in these layers. The N1 in the deep layers is followed by a large negative potential, termed the N2, with a peak latency of about 1.6 ms. In the superficial layers (1 and 2), the N1 is followed by a small positive potential (the P2) occurring nearly simultaneously with the N2, Immediately following the N2 is another negative potential that is most clearly observed in layer 2. The layer 2 negative wave is termed N3 and is also identifiable on the repolarizing phase of the N2 in layers 3 and 4. The N3 in layer 2 can be followed by a positive potential, the P4. Simultaneous with the P4 is a small negative wave ion layer 1, termed the N4. The P4-N4 complex is observed in about half the recordings. Frequency-following tests indicate that both the N1 and N2 waves can follow shock trains up to 333 Hz. The N1 remains nearly constant in amplitude up to about 300 Hz and decreases as the stimulus frequency is raised to 500 Hz. The N2 decrements more rapidly than the N1 at frequencies above about 250 Hz and is considerably reduced at 500 Hz. The N2 sometimes shows an increased amplitude (by about 20-40%) between 100 and 250 Hz. A paired-shock paradigm was used to characterize further potentials. The N1 was little affected by prior stimulation for intervals greater than 5 ms. The N2 and N3 generally showed a small facilitation for shock intervals from about 7 to 30 ms, with a return to base line at longer intervals. The N4 and P4 (when present) were profoundly depressed for intervals from 7 to about 30 ms, with recovery to control values by 50 ms.(ABSTRACT TRUNCATED AT 400 WORDS)     

Habituation and sensitization in rat auditory evoked potentials: a single-trial analysis with wavelet denoising.

In this work, systematic changes of single-trial auditory evoked potentials elicited in rats were studied. Single-trial evoked potentials were obtained with the help of wavelet denoising, a very recently proposed method that has already been shown to be useful in the analysis of scalp human evoked potentials. For the evoked components in the 13-24-ms range (i.e. P13, N18, P20 and N24), it was possible to identify slow exponential decreases in the peak amplitudes, most likely related to a slow habituation process, while for N18, an initial increase in amplitude was also found. On the contrary, the slower components (N38 and N52) habituated within a few trials, and we therefore propose that they are related to a different functional process. The outcomes of the present study show that wavelet denoising is a useful technique for analyzing evoked potentials in rats at the single-trial level. In fact, in the present study it was possible to obtain more information than the one described in previous related works. This allows the study of other forms of learning processes in rats with the aid of evoked potentials. Finally, the outcomes of this study may have some relevance for the comparison of human and rat evoked potentials.     

High frequency vibration induced gating of subcortical and cortical median nerve somatosensory evoked potentials: different effects on the cervical N13 and on the P13 and P14 far-field SEP components.

Subcortical and cortical somatosensory evoked potentials (SEP) to median nerve stimulation were recorded before, during and after high frequency (270 Hz) vibration of the fingers 1-3 in 8 healthy subjects. A marked decrease of the amplitude of all potentials was observed. The attenuation of the sensory nerve action potential (SNAP) of the median nerve and the attenuation of SEP components N9, N11 and N13 showed no differences, while the attenuation of the subcortical P14 component was significantly higher. This is in accordance with a generator of the cervical N13 in the interneurons beside the lemniscal pathway. The cortical N20 (post-rolandic) was significantly more decreased in amplitude than P14 while P22 (pre-rolandic) remained reduced in amplitude like P14. An increased latency of the far-field subcortical P14 was observed, while P13 recorded in the same montage remained unchanged in latency. These findings suggest different generators of these peaks. A generator of P14 above the nucleus cuneatus is confirmed. A presynaptic generator of P13 is suspected.     

Nerve conduction study, electromyography and somatosensory evoked potentials in non-Friedreich early onset cerebellar ataxia. A comparative study with Friedreich's ataxia and late onset cerebellar ataxia.

Electrophysiological findings in 14 patients with non-Friedreich early onset cerebellar ataxia are reported. Nerve conduction studies showed reduction of sensory action potential amplitudes in 7 cases associated in 3 with a decrease of sensory conduction velocities. Six subjects also exhibited a chronic neurogenic pattern to standard needle electromyography. Motor conduction velocities were normal in all cases; only two cases showed an increase in distal motor latencies. Short-latency somatosensory evoked potentials following median nerve stimulation revealed a prolonged central conduction time (N13-N20 interpeak latency) in 7 cases, compatible with supraspinal damage of the somatosensory pathways. These electrophysiological data are compared with those obtained in two reference groups of patients, respectively affected by Friedreich's ataxia and olivo-ponto-cerebellar atrophy.