Cerebral cortical potentials to pure non-painful temperature stimulation: an objective technique for the assessment of small fibre pathway in man.

In six healthy subjects cortical potentials were evoked by rapidly changing heating or cooling stimuli to the hand. Recordings were made from the contralateral scalp area overlying the sensori-motor cortex, referred to a frontal reference. The potential averaged from 25 stimuli comprised a large positive wave with a mean amplitude of 9.2, SD 1.1 microV for heat and 8.8 SD 1.2 micro V for cold stimulation. The heat evoked potentials had longer peak latencies (range: 280-350 ms) than those elicited by cold stimuli (range: 178-200 ms). A lower amplitude positive wave of a longer latency was also recorded to both modes of stimulation over the corresponding ipsilateral cortex. Cortical thermal evoked potentials were absent in two patients, one with severe selective small fibre neuropathy and the other with syringomyelia, both of whom had high thermal thresholds demonstrated by the technique of Jamal et al. Cerebral potentials evoked by thermal stimuli may represent an alternative approach to the investigation of the central projections of the human small fibre system with both clinical and research potential.     

Corticospinal potentials after transcranial stimulation in humans.

The descending volley evoked in humans by transcranial electrical stimulation of the scalp was recorded with epidural and spinal electrodes. It consisted of an early wave, which increased in amplitude and decreased in latency when the strength of the stimulus was increased. The mean conduction velocity of the early wave was 66, SD 2.5 m/s. At high stimulus intensity this wave was followed by later and smaller waves, which travel at the same speed as the initial potential. The recovery cycle of the descending volley was studied by delivering paired cortical stimuli at time intervals ranging from 0.5 to 10 ms. The early wave evoked by the test stimulus recovered to about 50% at a 1 ms interval and to 100% at a 3.5 ms interval. The later waves could not be tested at short time intervals but with time intervals longer than 3.5 ms they recovered to 100%. It is suggested that the initial and later waves after scalp stimulation are equivalent to the D and I waves seen in animal experiments.     

Knowledge of stimulus timing attenuates human evoked cortical potentials

To determine whether or not knowledge of stimulus timing influences the amplitude and latency of evoked cortical potentials, we have studied the evoked potentials of 24 adults under two contrasting conditions in which people knew or did not know the timing of tone stimuli by means of numerical perceptual cuing. Results demonstrated markedly smaller amplitude and significantly faster latency for the late components of vertex potentials evoked by stimuli whose timing subjects knew in advance. The cognitive act of knowing when auditory stimuli will occur attenuates the amplitude and facilitates the poststimulus timing of cortical evoked potentials.     

Long-latency reflexes in contracted hand and foot muscles and their relations to somatosensory evoked potentials and transcranial magnetic stimulation of the motor cortex.

OBJECTIVE: The cortical relay time (CRT) for V2 of long-latency reflexes (LLRs) in the contracted thenar and short toe flexor muscles was studied. METHODS: LLRs and somatosensory evoked potentials (SEPs) were studied by electrical stimulation of the median or posterior tibial nerve. The CRT for V2 was calculated by subtracting the onset latency of cortical potentials in SEPs and that of motor evoked potentials (MEPs) by transcranial magnetic stimulation (TMS) from the onset latency of V2 in eight healthy subjects. RESULTS: The CRT for the thenar muscles was 11.4+/-0.9 ms (mean +/- SD), as the onset latency was 48.8+/-1.4 ms for V2, 16.0+/-1.2 ms for N20 and 21.3+/-1.1 ms for MEP, respectively. The CRT for the short toe flexor muscles was 3.0+/-1.3 ms, as the onset latency was 80.5+/-4.5 ms for V2, 35.3+/-1.8 ms for P38 and 42.2+/-2.0 ms for MEP, respectively. CONCLUSION: Significantly longer CRT for V2 for the thenar muscles (P<0.001, paired Student's t test) may indicate more synaptic relays as compared to that for the short toe flexor muscles.     

Hippocampal responses evoked by tooth pulp and acoustic stimulation: Depth profiles and effect of behavior

Averaged evoked potentials and unitary discharges in response to tooth pulp and acoustic click stimuli were recorded from the hippocampus of freely moving rats. The spatial distribution of evoked field responses to tooth pulp stimulation and acoustic clicks were identical. Averaged evoked potentials consisted of a large negative deflection (N1) preceded by a small positive potential (P1). The shortest latency N1 in response to tooth pulp stimulation was recorded from the middle third of the dentate molecular layer and the outer portion of apical dendrites of CA3 (27 ms). The peak latency of N1 was significantly longer (34 ms) in the stratum radiatum of CA1. Laminar profiles of N1 in the dentate gyrus and CA3 were similar to that evoked by electrical stimulation of the medial entorhinal afferents; in CA1 the depth profiles of the potentials were similar to the response profile evoked by the Schaffer collaterals. Largest amplitude P1 was obtained from above the pyramidal layer of CA1 and the hilus. Both sensory modalities were able to modify the discharge rate of neurons in all hippocampal regions. The amplitude of evoked field potentials and cellular responses were dependent upon both the ongoing behavior of the animal and the nature of its response to the stimulus. The largest amplitude evoked potentials were recorded during immobility and slow wave sleep. On the other hand, virtually no potentials were obtained during exploratory behaviors associated with theta EEG activity. The findings indicate that information about sensory stimuli can reach the hippocampus by two distinctive pathways: a short latency inhibitory input via the fimbria-fornix and a longer latency path via the entorhinal cortex. It is suggested that neuronal mechanisms involved in theta EEG block the sequential activation of the unidirectional entorhinal-hippocampal circuitry.     

Event-related potential studies in infants and children.

The current status of event-related potentials (ERPs) in infants and children is discussed based on a review of the relevant literature. Although the N100-P200 component evoked by tone stimuli is clearly detected using an odd-ball paradigm in children over approximately 6 years of age, that component evoked by speech stimuli is not clearly detected until at least 10 years of age. In contrast to the adult N100-P200 component evoked by speech stimuli, infants and young children show a positivity at a latency of about 85-120 ms and a negativity at about 200-240 ms. The definition of P300 in children has not yet been established. P300 latency evoked by both auditory and visual stimuli decreases throughout childhood and reaches the mature value by puberty or young adulthood. However, P300s elicited by auditory and visual stimuli show different developmental time courses from each other, suggesting that they may originate from different neural generators. The Nc component is elicited by a variety of attention-getting events in infants and children. Interestingly, the developmental change in the Nc amplitude parallels the maturational course of synaptogenesis in the frontal cortex, and the Nc latency reaches the mature value at the time when myelinogenesis is complete in the nonspecific thalamic radiation.     

Brain-stem auditory evoked potentials in squirrel monkey (Saimiri sciureus)

To more fully characterize brain-stem auditory evoked potentials (BAEPs) in non-human primates, BAEPs were recorded from chronically implanted epidural electrodes in 10 squirrel monkeys (Saimiri sciureus). The effects of stimulus intensity, repetition rate, and anesthesia (ketamine 20 mg/kg i.m.) on peak latencies and inter-peak intervals were evaluated. Monkey wave forms consisted of approximately 7 peaks (I-VII), each exhibiting similar latencies across sessions, with later peaks exhibiting greater variability. In some subjects, additional peaks (IIa, IIIa) and slow potentials were recorded. The slow potentials provided a substratum for peaks IV through VII. As with human, monkey peaks exhibited systematic changes in latency with changes in stimulus intensity or repetition rate. These shifts included significant decreases in latency with increasing intensity for peaks I-IV and increases in latency with increases in repetition rate for peaks III, V, and VI. Inter-peak intervals were similar to those observed in human. Furthermore, ketamine anesthesia significantly delayed the latencies of most peaks (except I, V, and VII). Some differences between monkey and human BAEPs were evident in the relative amplitude of specific peaks. For example, peak V is typically most prominent in human, while this was true for peak III in monkey. The similarities between unanesthetized monkey and human inter-peak intervals suggest that the times required for impulses to reach particular brain-stem areas are conserved across primate species that vary in brain size. This supports the hypothesis that comparably numbered BAEP peaks in monkey and human index homologous processes. The data also suggest that the differences between animal and human BAEPs commonly reported may result from the use of anesthetics. In summary, unanesthetized monkey BAEPs resemble human BAEPs in morphology, number of peaks, polarity, latency variability, inter-peak intervals, slow potentials superimposed on the high-frequency peaks, and variations in morphology, amplitude, and resolution of peaks as a function of recording site. Thus, unanesthetized monkey BAEPs may be an excellent model for investigating the neural substrates of human BAEP or for determining species differences in acoustic processing among primates.     

Postural sway and brain potentials evoked by visual depth stimuli

This study measured the postural sway and brain potentials evoked by a visual depth stimulus. Thirteen subjects maintained standing posture on a force platform, and were administered two types of depth stimuli, strong and weak. The latency and amplitude of evoked potentials as well as changes in center of foot pressure (CFP) and the electromyogram (EMG) were examined. CFP displacement was found to change according to stimulus intensity. In the occipital lobe, evoked potentials exhibited a triphasic peak, with the first positive peak at approximately 120 ms (P120), the first negative peak at approximately 160 ms (N200), and the second positive peak at approximately 260 ms (P250). Brain evoked potentials correlated with CFP displacement as well as the latency of onset of EMG response. Onset of EMG response was probably related to the P120 component, whereas CFP displacement was related to the P250 component.     

脑干听觉诱发电位在面肌痉挛显微血管减压术中的应用价值

目的探讨脑干听觉诱发电位（BAEPs）V波潜伏期和（或）波幅的变化与面肌痉挛（HFS）显微血管减压术（MVD）后听力损失的应用价值。 方法选取中日友好医院神经外科自2015年9月至2019年8月行MVD治疗的HFS患者的临床资料，分析MVD始末BAEPs的V波潜伏期和波幅的变化以及手术前后听力状况的改变，听力学评估采用平均纯音听力阈值及言语识别率改变。根据美国耳鼻咽喉头颈外科学会分级方法，将术后患者听力分为听力未明显下降组和听力明显下降组。收集术中全程的BAEPs改变，并将BAEPs的V波术中改变分为：无显著异常，单纯V波潜伏期（LwV）延长>1.5 ms，单纯V波波幅（AwV）下降>50%，LwV延长>1.5 ms且AwV下降>50%，LwV延长>1.5 ms或AwV下降>50%，对5组分类模式下术后听力损伤程度与分组的相关性进行统计分析，并分析4组BAEPs改变对术后听力损伤的预测价值。 结果本研究纳入的1009例行MVD治疗的HFS患者中，943例患者听力未明显下降，66例患者术后听力异常，术中BAEPs监测波形无显著改变，术后出现听力下降5例（0.6%）；术中仅LwV延长>1.5 ms，术后出现听力下降4例（18.2%）；术中仅AwV降低>50%，术后出现听力下降19例（25.0%）；术中"LwV延长>1.5 ms且AwV降低>50%"，术后出现听力下降38例（64.4%）；术中"LwV延长>1.5 ms或AwV降低>50%"，术后出现听力下降61例（38.8%）。各组的阳性预测值比较，结果显示"LwV延长>1.5 ms且AwV降低>50%"最高；"LwV延长>1.5 ms或AwV下降>50%"组的敏感度最高；"LwV延长>1.5 ms且AwV下降>50%"组的特异度最强。 结论术中BAEPs监测可为MVD术者提供听力参考。术末V波潜伏期延长1.5 ms且波幅降低50%以上阳性预测值最高。术中根据BAEPs监测结果及时调整手术策略，可有效改善术后听力障碍的发生率。     

Action potentials of cat masseter muscle motor neurons evoked by stimulation of low-frequency infraorbital nerve afferents

The responses of masseter motoneurons evoked by stimulation of the low-threshold infraorbital afferents by different number of stimuli were investigated in cats under chloralose-nembutal anesthesia. It is shown that 3-4 succesive stimuli (1.2 of threshold) evoked action potentials in masseter motoneurons if their frequency was above 300/s. Stimulation of the infraorbital nerve by paired stimuli produced action potentials in these motoneurons when the interval between the stimuli was 1.3-4.0 ms. With longer intervals only facilitation of the second EPSP was observed, the degree of facilitation varying from 0.2 to 1.0. A conclusion is made that the masseter motoneurons discharges can be produced by activation of the infraorbital nerve. A -fibres probably connected to rapidly adapting receptors of the vibrissae.     

Brainstem auditory-evoked potentials studied with paired stimuli in multiple sclerosis patients

In 19 patients with definite multiple sclerosis (MS) brainstem auditory-evoked potentials (BAEP) with paired stimuli were recorded. Only hearing pathways without abnormalities in usual BAEP were examined. The latencies of wave III and wave V were significantly increased with the paired-stimulus technique (using paired-click intervals of 1.5 and 4.0 ms duration) compared to single clicks. In 4 patients (21%) paired-click BAEP latencies exceeded the critical values of normal subjects. This technique might give new possibilities in detecting minor lesions in MS patients.     

The refractory period of fast conducting corticospinal tract axons in man and its implications for intraoperative monitoring of motor evoked potentials.

OBJECTIVE: To determine the absolute and relative refractory period (RRP) of fast conducting axons of the corticospinal tract in response to paired high intensity (HI or supramaximal) and moderate intensity (MI or submaximal) electrical stimuli. The importance of the refractory period of fast conducting corticospinal tract axons has to be considered if repetitive transcranial electrical stimulation (TES) is to be effective for eliciting motor evoked potentials (MEPs) intraoperatively. METHODS: Direct (D) waves were recorded from the epidural space of the spinal cord in 14 patients, undergoing surgical correction of spinal deformities. To assess the absolute and RRPs of the corticospinal tract, paired transcranial electrical stimuli at interstimulus intervals (ISI) from 0.7 to 4.1 ms were applied. Recovery of conditioned D wave at short (2 ms) and long (4 ms) ISI was correlated with muscle MEP threshold. The refractory period for peripheral nerve was tested in comparison to that for the corticospinal tract. In four healthy subjects sensory nerve action potentials of the median nerve were studied after stimulation with paired stimuli. RESULTS: HI TES revealed a mean duration of 0.82 ms for the absolute refractory period of the corticospinal tract, while MI stimulation resulted in a mean refractory period duration of 1.47 ms. Stimuli of HI produced faster recovery of D wave amplitude during the RRP. Furthermore, short trains of transcranial electrical stimuli did not elicit MEPs when D wave showed incomplete recovery. A similar influence of stimulus intensity on recovery time was found for the refractory period of peripheral nerve. CONCLUSIONS: The recovery of D wave amplitude is dependent upon stimulus intensity. High intensity produces fast recovery. This is an important factor for the generation of MEPs. When HI TES is used to elicit MEPs, short and long ISIs are equally effective. When MI TES is used to elicit MEPs, only a long ISI of 4 ms is effective.     

Auditory brain-stem, middle- and long-latency evoked potentials in mild cognitive impairment.

OBJECTIVE: Mild cognitive impairment (MCI) is a selective episodic memory deficit in the elderly with a high risk of Alzheimer's disease. The amplitudes of a long-latency auditory evoked potential (P50) are larger in MCI compared to age-matched controls. We tested whether increased P50 amplitudes in MCI were accompanied by changes of middle-latency potentials occurring around 50 ms and/or auditory brain-stem potentials. METHODS: Auditory evoked potentials were recorded from age-matched controls (n = 16) and MCI (n = 17) in a passive listening paradigm at two stimulus presentation rates (2/s, 1/1.5 s). A subset of subjects also received stimuli at a rate of 1/3 s. RESULTS: Relative to controls, MCI subjects had larger long-latency P50 amplitudes at all stimulus rates. Significant group differences in N100 amplitude were dependent on stimulus rate. Amplitudes of the middle-latency components (Pa, Nb, P1 peaking at approximately 30, 40, and 50 ms, respectively) did not differ between groups, but a slow wave between 30 and 49 ms on which the middle-latency components arose was significantly increased in MCI. ABR Wave V latency and amplitude did not differ significantly between groups. CONCLUSIONS: The increase of long-latency P50 amplitudes in MCI reflects changes of a middle-latency slow wave, but not of transient middle-latency components. There was no evidence of group difference at the brain-stem level. SIGNIFICANCE: Increased slow wave occurring as early as 50 ms may reflect neurophysiological consequences of neuropathology in MCI.     

Abnormalities of cortical excitability and cortical inhibition in cervical dystonia

Cortical excitability and cortico-cortical inhibition were examined in twenty-one patients suffering from idiopathic rotational cervical dystonia. Polymyography of cervical muscles, somatosensory evoked potential recordings, and paired transcranial magnetic stimulation were used to assess the dystonic disorder. The results were compared with those obtained in a group of sixteen healthy age-matched volunteers. Statistically significant differences between the patient group and the control group were found when the amplitude values of the mean P22/N30 component measured at F [3, 4] and C[3, 4]' electrode positions were compared. The mean amplitude of P22/N30 in both of these electrode positions contralaterally to the direction of head deviation was significantly higher in the patient group (p ≤ 0.05). The mean side-to-side P22/N30 amplitude ratio was calculated in both groups in the F[3, 4] and C[3, 4]' electrode positions: there was a significant difference between the two groups. The mean ratio (calculated contralaterally/ipsilaterally in the patient group and left/right side in the control group) was significantly higher in the patient group (p ≤ 0.05). There were statistically significant differences between the two groups when the mean values of MEP amplitudes following paired stimuli at short and medium interstimulus intervals (ISI)) were compared. The percentage of amplitude reduction registered at short ISI was significantly lower in the patient group when both 3 ms ISI and 5 ms ISI were considered, and when the hemisphere contralateral to the direction of head deviation was stimulated. There was also a difference (with the short ISI) when the hemisphere ipsilateral to the direction of head deviation was stimulated, but this difference was not significant (p < 0.5). Almost all of the amplitude changes following the paired stimulus at the longer ISI, i. e. 10, 15, and 20 ms were significantly different when the patient group was compared with control group: when the ipsilateral hemisphere was stimulated, the amplitude of conditioned responses was significantly higher following all three paired stimuli (with 10, 15, and 20 ms ISI) at the p ≤ 0.05 significance level; when the contralateral hemisphere was stimulated, they were significantly higher following the 10 and 20 ms ISI paired stimuli (significance level p ≤ 0.05). The interhemispheric difference in the patient group was significant only for the paired stimuli using 3 and 5 ms (short) ISI and 15 and 20 ms (medium) ISI. There was a significantly decreased inhibition at 3 and 5 ms ISI when the hemisphere contralateral to the direction of head deviation was stimulated, as compared with the hemisphere ipsilateral (p ≤ 0.05). Similarly, there was a significantly increased facilitation at 15 and 20 ms when the hemisphere contralateral to the direction of head deviation was stimulated, as compared with the hemisphere ipsilateral (p ≤ 0.05). The results indicate that a disorder of both cortical excitability and intracortical inhibition exists in patients with cervical dystonia, and that this disorder is lateralized, i. e. it is located within the hemisphere contralateral to the direction of head deviation. Received: 5 March 2002, Received in revised form: 1 August 2002, Accepted: 2 August 2002 Correspondence to Doc. MUDr Petr Kaňovsky, CSc.     

Basal ganglia involvement in sensory and cognitive processing. A depth electrode CNV study in human subjects.

OBJECTIVE: Intracranial recordings were taken from the basal ganglia (BG) in order to explore the possible role of the BG in the cognitive processing of sensory information. METHODS: Ten patients with intractable temporal lobe epilepsy, who were candidates for epilepsy surgery, underwent intracranial recordings with depth electrodes. A frontal approach was used for the insertion of diagonal depth electrodes into the amygdalo-hippocampal complex (AH complex). These electrodes passed through the BG. The putamen was explored in 8 patients; the nucleus caudatus and pallidum were explored in two patients. The contingent negative variation (CNV) paradigm was tested using auditory warning stimuli and visual imperative stimuli followed by a hand flexion. The auditory and visual middle and late latency potentials evoked by the warning and imperative stimuli were analyzed. RESULTS: (1) Auditory evoked potentials (EPs): the amplitude potential gradient was observed with latencies of (a) 150-195ms (9 patients); (b) 215-290ms (9 patients); and (c) 350-600ms (10 patients). Negative potentials, with latencies of 100 and 110ms were observed in two patients. (2) Visual EPs: (a) 160-195ms (9 patients); (b) 210-295ms (9 patients); and (c) 330-550ms (7 patients). Negative potentials with latencies between 100 and 120ms were observed in 4 patients. CNV was obtained from the BG in 8 patients; a phase reversal was observed twice. CONCLUSIONS: (1) The BG generate middle and late latency EPs in a cognitive paradigm linked to the motor task. (2) The BG generate CNV. (3) The BG could play an integrative role in the processing of sensory, cognitive, and motor information.     

Direct demonstration of the effect of lorazepam on the excitability of the human motor cortex.

OBJECTIVES: The present study explored the effects of lorazepam, a benzodiazepine with agonist action at the GABA(A) receptor, on human motor cortex excitability as tested using transcranial magnetic stimulation. METHODS: We recorded directly the descending volley evoked by single and paired transcranial magnetic stimulation from the spinal cord of a conscious subject with a cervical epidural electrode before and after a single oral dose of lorazepam. We evaluated the effects of lorazepam on the descending volleys evoked by a single magnetic stimulation and paired cortical stimulation using the intracortical inhibition paradigm (subthreshold conditioning stimulus) and the short latency intracortical facilitation paradigm (suprathreshold conditioning stimulus). RESULTS: Using a single magnetic stimulus lorazepam decreased the amplitude of the later I waves in the descending volley; this was accompanied by a decrease in the amplitude of the evoked EMG response. Using the intracortical inhibition paradigm lorazepam increased the amount of corticocortical inhibition, particularly at 4 and 5 ms interstimulus intervals. There was no effect on the amount of facilitation observed in the short latency intracortical facilitation paradigm. CONCLUSIONS: The present findings provide direct evidence that lorazepam increases the excitability of inhibitory circuits in the human motor cortex.     

Intracortical evoked potentials of cats elicited by punctate visual stimuli in receptive field peripheries

Intracortical visual evoked potentials, related to stimulus eccentricity from receptive field center, were investigated as a possible measure of interaction among adjacent populations of cortical neurons. Displacement of the stimuli from field center resulted in (1) a progressive decline in amplitude of the primary potential and (2) an enhancement or development of longer latency (60–100 ms) ‘secondary’ potentials often not apparent with field center stimulation.     

Altered automatic face processing in individuals with high-functioning autism spectrum disorders: Evidence from visual evoked potentials

Individuals with autism spectrum disorders (ASDs) have different automatic responses to faces than typically developing (TD) individuals. We recorded visual evoked potentials (VEPs) in 10 individuals with high-functioning ASD (HFASD) and 10 TD individuals. Visual stimuli consisted of upright and inverted faces (fearful and neutral) and objects presented subliminally in a backward-masking paradigm. In all participants, the occipital N1 (about 100 ms) and P1 (about 120 ms) peaks were major components of the evoked response. We calculated “subliminal face effect (SFE)” scores by subtracting the N1/P1 amplitudes and latencies of the object stimuli from those of the face stimuli. In the TD group, the SFE score for the N1 amplitude was significantly higher for upright fearful faces but not neutral faces, and this score was insignificant when the stimuli were inverted. In contrast, the N1 amplitude of the HFASD subjects did not show this SFE in the upright orientation. There were no significant group differences in SFE scores for P1 amplitude, latency, or N1 latency. Our findings suggest that individuals with HFASD have altered automatic visual processing for emotional faces within the lower level of the visual cortex. This impairment could be a neural component of the disrupted social cognition observed in individuals with HFASD.     

Modulation of upper extremity motor evoked potentials by cutaneous afferents in humans.

The excitability of motoneurons controlling upper limb muscles in humans may vary with cutaneous nerve stimulation. We investigated the effect of noxious and non-noxious conditioning stimuli applied to right and left digit II and right digit V on motor evoked potentials (MEPs) recorded from right thenar eminence, abductor digiti minimi, biceps and triceps brachii muscles in twelve healthy subjects. Transcranial magnetic stimulation (TMS) was applied at interstimulus intervals (ISI) ranging from 40 to 160 ms following conditioning distal digital stimulation. TMS and transcranial electrical stimulation (TES) were compared at ISI 80 ms. Painful digital stimulation caused differential MEP amplitude modulation with an early maximum inhibition in hand muscles and triceps brachii followed by a maximum facilitation in arm muscles. Stimulation of different digits elicited a similar pattern of MEP modulation, which largely paralleled the behavior of cutaneous silent periods in the same muscles. Contralateral digital stimulation was less effective. MEPs following TMS and TES did not differ in their response to noxious digital stimulation. MEP latencies were shortened by cutaneous stimuli. The observed effects were stimulus intensity dependent. We conclude that activation of A-alpha and A-delta fibers gives rise to complex modulatory effects on upper limb motoneuron pools. A-delta fibers initiate a spinal reflex resulting in MEP amplitude reduction in muscles involved in reaching and grasping, and MEP amplitude facilitation in muscles involved in withdrawal. These findings suggest a protective reflex mediated by A-delta fibers that protects the hand from harm. A-alpha fibers induce MEP latency shortening possibly via a transcortical excitatory loop.     

Ultralate cerebral potentials as correlates of delayed pain perception: observation in a case of neurosyphilis.

Evoked cerebral potentials were investigated in a patient with neurosyphilis, who showed the symptoms of delayed pain perception in the lower limbs: a pinprick to the legs was perceived with a latency of more than one second. After stimulation with CO2 laser radiant heat pulses, evoked cerebral potentials of upper limbs were observed in a latency range comparable to those of healthy subjects, with a negative peak at 250 ms and a positive peak at 370 ms. In contrast, after application of laser stimuli to body sites with delayed pain perception, latency of the evoked potentials drastically increased with a vertex negativity at 1300 ms and a positivity at 1420 ms. Evoked potential measurements with conventional electrical stimuli did not show any difference between affected and unaffected body sites, that is, stimulation of the affected body sites did not produce pathological potentials.