Changes of short latency somatosensory evoked potential in sleep

We studied how the first negative waves (frontal 'N18' and parietal 'N20') of median somatosensory evoked potentials (SEP) change from waking to sleep in 9 healthy volunteers. Frontal and parietal responses in awake subjects showed multiple fast frequency potentials (FFP) over the ascending and descending phases of the slow negative waves. The main frontal FFP consisted of N16, P17, N18, P18, N19 and P20, with an additional small FFP, n15, over the ascending phase of N16. The parietal FFP included 3 major peaks (N15, P18 and N20) and 3 small FFP (n17, n19 and n20). Frontal FFP, except for n15, were markedly attenuated or totally disappeared in stage II sleep. Only a few FFP were identified in stage IV. The FFP returned in REM sleep, but amplitude was smaller than the waking state. Parietal FFP were also attenuated in NREM and recovered in REM sleep, but these changes were less prominent compared to those of frontal FFP. Latencies of frontal P20 and parietal N20 were prolonged in NREM sleep with greater prolongation of P20 than N20. These returned to waking values in REM sleep. These findings suggest that the frontal and parietal major negative peaks ('N18' and 'N20') consist of multiple physioanatomical substrates mediated through complex thalamocortical projection systems, and that the FFP are closely related to the sleep-wake mechanism possibly reflected by mutual interaction between cortex and the thalamic reticular system.     

Differential auditory processing continues during sleep.

Auditory evoked potentials (AEPs) were used to examine selective stimulus processing in sleep. In waking, repetitive stimuli generate exogenous P1, N1 and P2 components of the auditory evoked potential (AEP). Deviant stimuli generate endogenous cognitive components including the mismatch negativity (MMN), N2 and P3 components. We examined long-latency auditory evoked potentials elicited by repetitive and deviant stimuli during waking and stage II-IV sleep to assess whether stimulus deviance is detected during sleep. The waking P1, N1b and P2 had maximal amplitudes at fronto-central scalp sites, with additional peaks (N1a, N1c) at temporal sites. Deviant tones generated a frontal maximal MMN, and complex novel tones generated an additional P3 component maximal at centro-parietal sites. During stages II-IV sleep N1a, b, c amplitudes were reduced. During stage II sleep all stimuli generated increased P2 amplitudes and a late negative component (N340). Deviant stimuli generated greater P2 and N340 amplitudes than frequent stimuli in stage II sleep, as well as an additional P420 component. In stage III-IV sleep the P420 was absent and the AEP was dominated by a negativity of long duration whose amplitude increased in response to deviant stimuli. These data indicate that auditory evoked activity changes from wakefulness to sleep. The differential response to deviant sounds observed during waking and all sleep stages supports the theory that selective processing of auditory stimuli persists during sleep.     

Short-latency somatosensory evoked potentials in perinatal asphyxia

Ten asphyxiated term newborns were studied in the first 6 months of life with median nerve short-latency somatosensory evoked potentials (SLSEP) and followed subsequently to a mean age of 20 months. Results of SLSEP correlated with subsequent outcome in every patient; normal and abnormal infants at subsequent examination were separable on the basis of prior SLSEP, although the severity of later disability could not be inferred from SLSEP.     

The effects of varying stimulus intensity on P300 during REM sleep.

Event-related potentials (ERPs) are often used to measure the extent of information processing during sleep. Previous studies have indicated that a late positive wave, P300, can be elicited during REM sleep if stimuli are very rare and/or very loud. The present study examined the role of stimulus intensity in eliciting a P300 during REM sleep. Eight subjects were presented with auditory tone pips with an intensity of either 0, 60, 80 or 100 dB SPL. Stimuli were delivered at random with equal probability. Trials were sorted by stage of sleep, stimulus intensity, and presence or absence of rapid eye movements in REM sleep. During the waking state, when subjects read a book, the loud 100 dB stimulus elicited short (P3a) and long latency (P300) positive waves (peaking at 293 and 373 ms respectively). In stage of 2 non-REM sleep, N1 decreased to baseline level while P2 increased in amplitude compared to the waking state. A P300 could not be observed in stage 2 sleep regardless of the level of stimulus intensity. During REM sleep, a late P300 (latency 363 ms) was elicited by the 100 dB stimulus. The earlier positive peak (i.e. P3a) was not apparent. The P300 was reduced in amplitude compared to the waking state. Its amplitude did not differ between phasic and tonic states of REM sleep. A late parietal negative slow wave (SW) was also apparent during REM. Although the SW was larger during phasic compared to tonic REM, the difference was not significant. These data suggest that stimuli which are sufficiently intrusive to elicit a P300 in the waking state continue to do so in REM sleep.     

脑白质疏松症短潜伏期躯体感觉诱发电位研究

对24例经CT证实的脑白质疏松症患者进行短潜伏期躯体感觉诱发电位(SLSEP)顶和中央前成分检测。结果,SLSEP总异常率83.3％,时间参数异常率(79.17％)明显比幅度参数异常率(29.11％)高,中央前成分异常率(75％)明显比顶成分异常率(41.7％)高。结论:在脑白质疏松症的临床早期,体感诱发电位可以敏感反映脑电生理的异常,作为临床诊断该病的辅助手段。     

中潜伏期体感诱发电位预测重症脑卒中患者预后的应用价值

目的 探讨中潜伏期体感诱发电位(middle-latency somatosensory evoked potentials,MLSEP)预测急性重症脑卒中患者预后的应用价值.方法 对70例症状出现7 d内的重症脑卒中患者行格拉斯哥昏迷评分(Glasgow Coma Scale,GCS)、短潜伏期体感诱发电位(short-latency somatosensory evoked potentials,SLSEP)和MLSEP检测,6个月后采用改良Rankin评分和生存与死亡两个预后标准进行预后评估.健康对照组20名行SLSEP和MLSEP检测.统计学分析MLSEP、SLSEP和GSC与预后的一致性及预测的准确性.结果 健康对照组均记录到双侧N20、N35和N60,脑卒中组患者MLSEP波形有缺失,而且病灶侧MLSEP各波消失比例明显高于对侧.双侧N60消失与预后不良(Kappa=0.828,P＜0.01)和死亡(Kappa=0.686,P＜0.01)的一致性均最好.预测准确性分析显示:病灶侧N60消失预测不良预后和死亡的敏感性高达100%,较病灶侧N20消失的敏感性(85.7%)提高了14.3%;双侧N60消失预测预后不良的特异性为100%,与双侧N20消失一致;但预测死亡的特异性为82.9%,不如双侧N20消失(97.1%).结论 MLSEP可反映脑损伤程度,预测预后不良的敏感性高于SLSEP,建议将MLSEP和SLSEP联合用于重症脑损伤后的评估与预后的预测.

Abstract：

Objective To explore the effectiveness of using middle-latency somatosensory evoked potentials (MLSEP) to predict the prognosis in patients with acute severe stroke. Methods MLSEP, shortlatency somatosensory evoked potentials (SLSEP), and Glasgow Coma Scale (GCS) were recorded in 70 acute severe supratentorial stroke patients within 1 week after onset. All patients were evaluated with modified Rankin Scale (mRS) and follow-up in 6 months after onset. SLSEP and MLSEP were recorded in 20 normal controls. The consistency between MLSEP, SLSEP, GCS and prognosis, as well as the prognostic authenticity of MLSEP, SLSEP, and GCS were analyzed. Results Bilateral N20, N35, and N60 exited in all normal controls. Some waves of MLSEP were absent in stroke patients, and the proportion of absent waves in ipsilateral MLSEP was higher than in contralateral MLSEP. The consistency between bilateral absence of N60 and unfavorable outcome ( Kappa = 0.828, P ＜ 0.01 ), and between bilateral absence of N60 and death ( Kappa = 0.686, P ＜ 0.01 ) was satisfactory. By using the prognostic authenticity analysis of predictors, the ipsilateral absence of N60 showed the highest sensitivity ( 100% ) for unfavorable outcome and death, which added 14.3% compared with the sensitivity of ipsilateral absence of N20 ( 85.7% ). Bilateral absence of N60 showed a high specificity of 100% for unfavorable outcome, which equaled bilateral absence of N20.However, it showed a lower specificity ( 82.9% ) for death, than bilateral absence of N20 (97.1% ).Conclusions MLSEP was able to reflect the degree of brain injury and showed higher sensitivity than SLSEP for predicting unfavorable outcomes. Therefore combined use of MLSEP and SLSEP in evaluating and predicting the outcomes in brain injuries is suggested.     

Evoked potentials during REM sleep reflect dreaming.

Polygraphic recordings were collected for 11 normal subjects during sleep and wakefulness in order to investigate characteristics of the rapid eye movement (REM) associated potentials. EEGs were averaged using 5 different triggering points: (1) saccade onset under the normal ambient illumination, (2) saccade onset in the total darkness, (3) onset of REMs during REM sleep, (4) flash during REM sleep, and (5) flash during stage 2 sleep. In the central area, positive potentials appeared with waking saccades under the normal ambient illumination (P240L) and REMs (P185R). The latency of P185R associated with REMs was significantly shorter than that of P240L associated with waking saccades. These findings suggest that P185R is evoked by PGO waves occurring just before the REM. A small positive potential appeared in the occipital area with waking saccade under the normal ambient illumination (P260L) and REMs in the total darkness (P250R). Conspicuous absence of these waves for waking saccades in the total darkness suggests that P250R accompanied with REMs reflects activities involved with the cognitive processes occurring when a subject scans a dream image during REM sleep.     

The effect of state on sensory gating: comparison of waking, REM and non-REM sleep.

OBJECTIVES: Auditory sensory gating is an electrophysiological assay that has been employed in clinical and basic research to clarify the neurobiological basis of perceptual and attentional impairments associated with schizophrenia and other diseases. In addition to genetically-linked characteristics, this measure also exhibits potentially confounding sensitivity to behavioral state, most notably acute stress. The goal of the present study is to determine if auditory sensory gating of evoked potential component P50 ('P1') could be measured during rapid eye movement (REM) sleep, as an alternative to the waking state. METHODS: The suppression of vertex-recorded auditory evoked potential components, P30, P50 and N100, was measured as a function of stimulus redundancy using the paired-click paradigm during all-night sleep in 10 control subjects. Average evoked responses were computed separately for 30 min periods of waking, REM sleep, and non-REM (stage 2) sleep. RESULTS: Evoked response component P50 exhibited suppression to the paired-click stimulus during REM sleep, not significantly different than waking. Suppression of wave N100 was significantly poorer during both sleep stages than waking. Component P30 was not suppressed in response to repetitive stimuli under any state of vigilance. CONCLUSIONS: In addition to waking, response suppression of evoked potential component P50 can be measured during REM sleep, thus allowing the separation of trait- and state-dependent effects in future investigations of auditory sensory gating.     

Machine classification of infant sleep state using cardiorespiratory measures

We examined the potential to classify sleep and waking state over the first 6 months of life in normal infants using only cardiac and respiratory measures. Twelve hour all-night polygraph recordings which included EEG, eye movement, whole body movement, facial muscle electromyographic, cardiac, and respiratory activity from 25 normal infants were collected at 1 week, and at 1, 2, 3, 4, and 6 months of age. Each minute of these recordings was classified into quiet sleep, waking, or rapid eye movement sleep by trained observers using EEG and somatic criteria. Respiratory rate and variability, heart rate and variability, and cardiac interbeat interval variation at respiratory and lower frequencies from 12 of the 25 infants were used as measures in discriminant analyses of sleep state for test on the 13 remaining infants. Using all 7 cardiac and respiratory measures, sleep states were classified with an accuracy approximating that attained by trained observers who had available all polygraph tracings (84.8% overall correct classification). Using only cardiac measures, the accuracy of classification decreased slightly, with an overall correct classification of 82.0%. Using only respiratory measures, the accuracy of classification diminished further, with an overall correct classification of 80.0%. Cardiac and respiratory measures provide quantifiable indications of sleep and waking states over the first 6 months of life in normal infants.     

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.     

Obstructive-sleep apnea syndrome: brain oxygenation measured with near-infrared spectroscopy. Preliminary results]

This study assessed cerebral oxygenation in four obstructive sleep apnea syndrome (SAOS) patients (age = 51.8 +/- 15 years, apnea-hypopnea index = 68-125 per hour), during sleep and waking time, using near infrared spectoscopy (NIRS), during a standard polysomnography. Oxyhemoglobin (HbO2, reflecting cerebral oxygenation), total hemoglobin (Hbt, reflecting cerebral blood volumes) and cerebral oxygen saturation (SaO2c = HbO2/Hbt), were compared to the data obtained in four snorers not presenting apneas (age = 51.8 +/- 6.6, apnea-hypopnea index = 2.6-6.2 per hour) examined in the same way. The main result was that HbO2 values were reduced in SAOS patients, both during sleep (at stage 2: 52.54 +/- 9.60 mumol/L versus 73.80 +/- 11.70 mumol/L) and during waking state (53.67 +/- 7.20 mumol/L versus 63.05 +/- 5.55 mumol/L). Hbt was also reduced in apneic patients as compared to snorers during waking state (72.73 +/- 13.90 mumol/L versus 96.05 +/- 6.30 mumol/L). During sleep, Hbt increased in a similar way for snorers and apneics (12.4% versus 13%), whereas HbO2 values were constant for apneics. SaO2c paralleled SaO2p in snorers and apneics, values for SaO2c being 20-30% lower than values for SaO2p. The difference in the values was probably due to the use of different monitoring techniques. Cerebral oxygenation and cerebral blood volumes were continuously low in apneic patients, and peripheral hypoxia was associated with same-range cerebral hypoxia. Cerebral hemodynamic mechanisms related to sleep, although in part efficient in apneic patients, were not able to increase cerebral oxygenation up to normal values.     

Sleep but not hyperventilation increases the sensitivity of the EEG in patients with temporal lobe epilepsy

PURPOSE: To evaluate the relative impact of 3 and 5 min of hyperventilation (HV) and different sleep stages on the sensitivity of the interictal EEG in focal epilepsy. METHODS: We examined 20 patients with temporal lobe epilepsy (TLE, 85%) or extratemporal epilepsy during EEG-monitoring. We compared 6 min EEG (12 epochs of 30s) during/after each: (a) waking; (b) 5 or 3 min of HV; (c) sleep stages 1, 2, 3/4 and REM regarding the frequency of epileptiform discharges (ED). The Wilcoxon matched pairs signed rank test was used. The main endpoint was the comparison of 5 min of HV with sleep stage 2. RESULTS: During sleep stage 2, ED were more frequent than during/after 5 min of HV (P=0.002). Compared to the waking EEG, all NREM-sleep stages activated ED. Sleep stage 2 was associated with the strongest activation. There was no difference between the waking state and REM-sleep. Compared to the waking EEG, neither 3 nor 5 min of HV showed an activation of ED. CONCLUSION: In patients with TLE, sleep stage 2 shows a significantly higher sensitivity for ED than 5 min of HV. Compared to the waking EEG, HV showed no activating effect on ED. These results suggest that in patients with the clinical diagnosis of TLE (and possibly other focal epilepsies) measures to record sleep stage 2 (such as sleep deprivation) should be increased whereas HV appears to be dispensable in this setting.     

N20-P25、N18消失在深昏迷预后判断中的价值

目的评价短潜伏期体感诱发电位(shortlatencysomatosensoryevokedpotentials,SLSEP)N20P25、N18消失在深昏迷患者预后判断中的作用。方法运用便携式诱发电位仪,对95例深昏迷患者进行SLSEP检测,记录脑皮质电位N20P25和周围电位N13,44例患者同时记录脑皮质下电位N18。结果95例患者N20P25均消失(100%),8例患者因有周围神经损伤未记录到周围电位N13;44例患者中脑皮质下电位N18消失者38例(86.4%)。结论95例患者SLSEP检查结果与临床判断完全吻合。在脑功能判断中,N20P25敏感性较高,N18特异性较高,二者均消失高度提示脑功能预后不良。     

Evoked potentials as a tool for the investigation of human sleep

This review summarizes studies of evoked potentials (EPs) applied to the investigation of human sleep and of sleep disorders. The first part is devoted to studies dealing with the nature, mechanisms and extent of information processing during sleep. EP studies suggest that the brain's ability to detect salient stimuli persists during even the deepest sleep stages, while discrimination of the stimulus' intrinsic significance and/or semantic content may persist only in stage II and paradoxical sleep (PS). Deviance detection in non-rapid eye movement (NREM) sleep is reflected by amplitude recovery of K-complexes elicited by stimulations that differ from the background. The evoked K-complex appears to be formed by two functionally different modules. The first may be related to the discrimination of relevant information. The second appears more sensitive to stimulus salience than to its intrinsic significance. In PS, the EP signs of stimulus discrimination are similar to those observed during waking. Thus, if the possibilities of information processing are fairly similar during stage II and PS, their respective neural mechanisms are not the same, as judged by their electrophysiological counterparts. The second part of the paper reviews clinical application of EPs to the study of sleep/wake disorders. While early potentials are of little use for diagnosis of sleep disorders, the cognitive P300 may help to quantify cognitive slowing and pathological sleepiness. However, intersubject variability restrains the use of these techniques in individual patients. A promising approach is the utilization of late responses to the study of sleep inertia with the use of "forced awakening" recording paradigms.     

The effects of sleep on median nerve short latency somatosensory evoked potentials

The effects of sleep on median nerve short latency somatosensory evoked potentials were studied in 7 subjects made up of 6 patients being evaluated for seizure disorders by all-night electroencephalograms and 1 normal healthy volunteer. The median nerve was stimulated at the wrist, and the peripheral (N9), subcortical (P13) and early cortical (N1, P2) evoked potentials were recorded during full wakefulness and natural night-time sleep. Sleep-wake state was monitored by the simultaneously obtained polysomnogram. The latencies of the cortical responses were prolonged during non-rapid eye movement (NREM) sleep. In 3 of the subjects P2 was consistently bifid during NREM sleep only. The second component of the bifid potential, 3-4 msec longer in latency than the first, appeared to be selectively enhanced during NREM sleep whereas the first component tended to become less prominent or even disappear. This suggests that the 2 peaks have different generators that are affected differently by NREM sleep. These are clinically relevant findings for interpretation of routine clinical studies.     

Somatosensory evoked potentials and magnetic fields elicited by tactile stimulation of the hand during active and quiet sleep in newborns.

OBJECTIVE: Our objective was to characterize the effects of sleep stages on tactile somatosensory evoked responses in full-term newborns. METHODS: Somatosensory evoked potentials (SEPs) and magnetic fields (SEFs) to tactile stimulation of the tip of the index finger and/or thenar eminence were measured from 14 healthy newborns. The stimulus was a gentle tap produced by a moving membrane driven by an air-pressure pulse. RESULTS: SEPs and SEFs to tactile stimulation of the skin were similar in waveform and latency to SEPs known to be produced by electrical stimulation of the fingertip of neonates. The two most distinguishable positive deflections of SEPs, P1 and P2, within 300 ms of the stimulation, and their magnetic counterparts were clearly smaller in active compared to quiet sleep. CONCLUSIONS: Our study demonstrates for the first time that it is possible to record SEFs in neonates, and that clear late cortical somatosensory responses are produced by tactile stimulation. In addition, the effect of sleep stage on these responses indicates differences in the processing of the incoming information, at least in the somatosensory modality, in active and quiet sleep. SIGNIFICANCE: Tactile stimulation may be useful as a completely non-invasive technique for studying the physiology of the somatosensory system in neonates. Methodologically, since the effect of sleep stage is profound, one must carefully monitor the sleep stages in studies of event-related responses in newborns, or else this effect may confound the phenomena being studied.     

金尔伦(盐酸纳洛酮)治疗急性中、重型脑外伤的神经电生理研究

目的：通过诱发电位（EP）监测,探讨金尔伦（盐酸纳洛酮）治疗急性中,重型脑外伤的疗效,方法：对40例急性中,重型脑外伤患者者随机,双盲治疗,前3天剂量为每日0．3mg/kg,后7天剂量为4.8mg/日,于用药前,用药后30分钟,24小时,72小时,120小时监测正中神经短潜伏期体感诱发电位（SLSEP）和脑干听觉诱发电位（BAEP）,揭盲后分为金尔伦治疗组和对照组,对金氽伦治疗组与对照组诱发电位进行统计学分析,结果：金尔伦治疗级SLSEP的N13－N20峰间潜伏期（N13－N20IPL）及BAEP的I－V波峰间潜伏期（I－VIPL）在用药手均较对组缩短且有显著性差异,P＜0．05,结论,诱发电位监测结果表明,金尔伦能有效改善急性脑外伤患者异常的神经网络生理指标,对于急性中,重型脑外伤有明显的治疗作用。     

Spontaneous awakening from sleep in infants

Spontaneous awakenings from sleep were studied in a group of 20 infants whose sleep-waking patterns were recorded polygraphically for 24 h. While 10 infants were orally fed the other 10 underwent continuous feeding for various gastrointestinal diseases. Spontaneous awakening from sleep was analysed with regard to the prior sleep state, age and feeding condition. Infants awoke preferentially out of REM sleep and less often out of non-REM sleep. The feeding condition had no significant influence on the distribution of awakenings. The propensity for REM awakenings was significantly greater than would have been expected according to the REM sleep amount. This tendency was more pronounced for younger (less than or equal to 3 months) than for older (greater than or equal to 4 months) infants. REM sleep episodes which were interrupted by awakenings were significantly shorter than uninterrupted ones, since awakenings occurred predominantly shortly after REM sleep onset. It is proposed that the specific pattern of brain activity during REM sleep facilitates the transition from sleep into the waking state, particularly in the youngest infants.     

Changes in forebrain function from waking to REM sleep in depression: preliminary analyses of [18F]FDG PET studies.

Based on recent functional brain imaging studies of healthy human REM sleep, we hypothesized that alterations in REM sleep in mood disorder patients reflect a functional dysregulation within limbic and paralimbic forebrain structures during that sleep state. Six unipolar depressed subjects and eight healthy subjects underwent separate [18F]2-fluoro-2-deoxy-D-glucose ([18F]FDG) PET scans during waking and during their first REM period of sleep. Statistical parametric mapping contrasts were performed to detect changes in relative regional cerebral glucose metabolism (rCMRglu) from waking to REM sleep in each group as well as interactions in patterns of change between groups. Clinical and EEG sleep comparisons from an undisturbed night of sleep were also performed. In contrast to healthy control subjects, depressed patients did not show increases in rCMRglu in anterior paralimbic structures in REM sleep compared to waking. Depressed subjects showed greater increases from waking to REM sleep in rCMRglu in the tectal area and a series of left hemispheric areas including sensorimotor cortex, inferior temporal cortex, uncal gyrus-amygdala, and subicular complex than did the control subjects. These observations indicate that changes in limbic and paralimbic function from waking to REM sleep differ significantly from normal in depressed patients.     

Hind limb somatosensory evoked potentials in the monkey: the effects of distal axonopathy

Computer-averaged short-latency somatosensory evoked potentials (SLSEP) to unilateral stimulation of the peroneal nerve were recorded from surface electrodes overlying the peripheral nerve, cauda equina, spinal cord, brainstem, and contralateral sensorimotor region. Seven monkeys were studied under normal conditions and at various stages of distal axonopathy induced by systematic acrylamide intoxication. With the use of a noncephalic reference, a series of five small-amplitude positive components were identified that precede the initial cortical activity. On the basis of timing and topography of the components, the source of the first one, SLSPEP1, was localized to the lumbar dorsal root fibers and that of the second, SLSEP2, to the ascending spinal tracts, principally gracile fasciculus. Bipolar recordings of the SLSEP2 overlying the rostral extreme of the cervical spinal cord provided a sensitive measure of the onset of distal axonopathy. Changes in the timing of this component antedated both abnormalities of spinal or peripheral nerve conduction and behavioral signs of intoxication. The initial alteration was specific to stimulation of the hind limb and was associated with early morphological change limited to the terminal and preterminal portions of the long axons in the gracile fasciculus.