Biomedical subjects

R D Treede

Publications and source records attributed to R D Treede.

At least 55 records · Page 3Linked to original sources

PubMed1995

Middle-latency somatosensory evoked potentials after stimulation of the radial and median nerves: component structure and scalp topography.

Somatosensory evoked potentials (SEPs) after radial nerve stimulation are studied less frequently than those after median nerve stimulation. Therefore, little is known about their component structure and scalp topography. We investigated radial nerve SEPs after electrical stimulation at the left wrist. For comparison, the median nerve was also stimulated at the wrist. SEPs were recorded with 15 scalp electrodes (bandpass 0.5-200 Hz) in 27 healthy subjects. The waveform of the radial nerve SEP at a contralateral parietal lead was comparable to that of the median nerve SEP, consisting of P14, N20, P30, and N60. In spite of comparable stimulus intensities, SEP amplitudes were smaller after radial than after median nerve stimulation. Significant latency differences were found only for N20 (earlier for median nerve) and P30 (earlier for radial nerve). The duration of the primary complex N20-P30 thus was significantly shorter for the radial nerve. Whereas N20 and P30 were present with either earlobe or frontal reference, N60 had a prerolandic maximum and was best recorded with a bipolar transverse derivation. In addition, another middle-latency negativity (N110) was found near the secondary somatosensory cortex, which had previously been described only for radial nerve stimulation. In standard SEP derivations, the N110 is riding on the ascending limb of the vertex negativity. It could best be recorded in low temporal leads versus a midline reference. The scalp topographies of P30, N60, and N110 were similar for radial and median nerve stimulation.

Adult↗

PubMed1995

Evoked potentials in a subject with a large-fibre sensory neuropathy below the neck.

The results from experiments in various modalities of evoked potentials are described in a subject with a complete large peripheral neuropathy below the neck. He has no tactile or position sensitivity below that level, but has retained fatigue, pain, and temperature sensation. Percutaneous electrical stimulation of peripheral nerves led to scalp recorded evoked potentials with thresholds and propagation velocities compatible with conduction along A-delta peripheral pathways. CO2 laser evoked potentials were similar to those seen in controls, further support for intact A-delta peripheral fibres. Movement-related cortical potentials (MRCPs) were recorded associated with active and passive movement of the middle finger. The former were normal, evidence that the termination of the MRCP is not dependent on peripheral feedback. By comparing passive MRCPs between controls and the subject it was possible to establish which parts of the potentials are visual and which are proprioceptive and to gain evidence of central reorganisation in the subject. Magnetic brain stimulation was used to show that the subject did not perceive induced movement, had a normal centrally originating silent period, and could focus his attention during real and imagined movement of the finger more successfully than could normal controls.

Attention↗

PubMed1995

Peripheral acute pain mechanisms.

Many studies in several species, including humans, have identified a subset of primary afferent nerve fibres that are activated by potential or actual tissue-damaging stimuli. Discharge patterns of these nociceptive afferents faithfully reproduce some aspects of the applied stimuli (e.g. shape of the stimulus-response function) but not others (e.g. time-course of a sustained stimulus). Since primary nociceptive afferents provide the input to the central nervous system, their encoding properties have to be considered when studying central processing. On the other hand, pain perception correlates with some aspects of nociceptor discharges (e.g. fatigue with repetition of brief heat pulses), but not with others (e.g. absolute thresholds). Therefore, the painfulness of a stimulus cannot be deduced from nociceptor discharges alone; central processing needs to be taken into account, particularly central summation. In addition to the immediate responses of nociceptive afferents to external stimulation, acute pain mechanisms also comprise the short-term plasticity of the nociceptive system as a consequence of prolonged noxious stimulation.

Acute Disease↗

PubMed1993

Equivalent electrical source analysis of pain-related somatosensory evoked potentials elicited by a CO2 laser.

The purpose of this study was to localize possible neural sources of pain-related cortical evoked potentials. A brain electrical source analysis was performed on late somatosensory evoked potential data (500-ms window was analyzed) elicited by short heat pulses produced by a CO2 laser. These stimuli activate pain and temperature pathways. The first, fairly small, negative response can be recorded on the scalp about 160 ms from the stimulus (N1 component). The major negativity on the scalp has its peak about 240 ms from the stimulus and is followed by a positivity (N2 and P2 components). A four-dipole model was developed using data following left-hand stimulation. Spatiotemporal source analysis suggested that the N1 component could be generated by contralateral activity in both primary and secondary somatosensory cortices and that N2 could be generated by bilateral activity mainly in secondary somatosensory cortices. A deep dipole in the midline was active during the time range of the negative potentials and seemed to be mostly responsible for the P2 component. This dipole was located too frontally to be thalamic, but it corresponded well to the location of the anterior cingulate gyrus. The model also yielded good fits for right-hand and left-foot stimulation data and, in addition, another set of left-hand data obtained with different electrode spacing in a different group of subjects (residual variances from 2.8% to 3.3%). The model explaining data sets from different body part stimulations varied very little, except with respect to the location of the dipole representing the activity of the primary somatosensory area.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Vasodilator flare due to activation of superficial cutaneous afferents in humans: heat-sensitive versus histamine-sensitive fibers.

Histamine-sensitive nerve endings are assumed to terminate in the superficial epidermis. Heat-sensitive nociceptors that are excited by brief carbondioxide-laser pulses must also terminate within the epidermis, because this infrared radiation has an extinction length of about 10 microns. We now compared laser heat stimuli (10 W, 50 ms, 20 mm2) with intradermal injections of histamine (10(-10) to 10(-8) mol) in their capacity to cause cutaneous vasodilatation (flare) in awake human subjects. Cutaneous blood flow was measured with a two-channel laser-Doppler device. The radiant heat pulses caused a transient cutaneous vasodilatation that spread at least 15 mm from the stimulus site. There was no visible flare and vasodilatation could only be detected by laser Doppler measurements. Although the heat pulses elicited enough nociceptor activity to be perceived as moderately painful, the magnitude of the vasodilatation was smaller and its duration shorter than after the smallest dose of histamine. In contrast, nociceptor activation by heat is usually stronger than by histamine. These data indicate that flare and pain are two different aspects of cutaneous small fiber function.

Histamine↗

PubMed1992

Peripheral and central mechanisms of cutaneous hyperalgesia.

Hyperalgesia after cutaneous injury can be divided into two phenomena: Primary hyperalgesia occurs at the site of injury and is characterized by hyperalgesia to mechanical and heat stimuli. Secondary hyperalgesia occurs outside the injury site and is characterized by mechanical hyperalgesia only. Hyperalgesia in inflammatory processes corresponds to primary hyperalgesia. Hyperalgesia in referred pain and neuropathic pain resembles secondary hyperalgesia (Table 3). Evidence for the latter would be strengthened if hyperalgesia to cooling stimuli, which is observed in neuropathic pain, was also demonstrated in referred pain and in secondary hyperalgesia. Some of the more likely neural mechanisms to explain primary and secondary hyperalgesia are illustrated in Fig. 8. Primary hyperalgesia to heat stimuli has a counterpart in the sensitization of peripheral nociceptors to heat stimuli (Fig. 8A), leading to similar changes in central neurons. In addition, the enlargement of the mechanical receptive field of primary afferent nociceptors to include the site of injury may account for the primary hyperalgesia to mechanical stimuli (Fig. 8B). In the literature, there are some contradictions with respect to the stimulus modalities to which hyperalgesia and sensitization occur. In spite of the well-documented sensitization of primary afferent nociceptors to heat stimuli, there are few studies on its molecular mechanisms. On the other hand, there is pharmacological evidence for a peripheral mechanism of primary mechanical hyperalgesia, but little direct evidence that nociceptors can be sensitized to mechanical stimuli by injury. This contradiction should spawn further investigations into the mechanical response properties of nociceptors and into the molecular mechanisms of heat sensitization. Secondary hyperalgesia to mechanical stimuli is likely due to the sensitization of central pain signalling neurons (CPSNs). This sensitization could involve only input from nociceptors (Fig. 8C), since mechanical pain thresholds after a cutaneous injury are of the same order as those of nociceptors. Central sensitization could also be the result of enhanced connectivity between low-threshold mechanoreceptors and CPSNs (Fig. 8D). This form of sensitization may account for the pain to light touch associated with neuropathic pain. Receptive field plasticity is a prevalent property of dorsal horn neurons and probably plays a vital role with regard to hyperalgesia. The molecular mechanisms of synaptic plasticity are currently subject to intense experimental investigation and may provide new insights on the mechanisms of pain and hyperalgesia.

Animals↗

PubMed1992

The plasticity of cutaneous hyperalgesia during sympathetic ganglion blockade in patients with neuropathic pain.

In order to investigate the plasticity of cutaneous sensory abnormalities in neuropathic pain, we monitored sensory and vasomotor effects of diagnostic sympathetic ganglion blocks in 24 patients, who suffered from chronic pain and cutaneous hyperalgesia following peripheral nerve or tissue injury. Ongoing pain was rated on a visual analogue scale, and pain evoked by innocuous tactile and cooling stimuli (hyperalgesia) on a verbal rating scale. Skin temperatures were determined at symmetric sites. In two patients, cutaneous blood flow was measured with a laser Doppler device. The sympathetic blocks led to a significant reduction of the group mean ongoing pain (40%) and cutaneous hyperalgesia (50%). Between patients, however, there was a large variability that could not be related merely to adequacy of sympathetic blockade. Neither the magnitude of change in skin temperature nor the final skin temperature after the block correlated with the amount of pain relief. The relief of hyperalgesia, however, correlated with the relief of ongoing pain. Nine patients experienced pain relief of greater than 50%. In these patients, the time course of hyperalgesia relief was similar to the time course of relief of ongoing pain. Pain relief occurred simultaneously with or a few minutes before cutaneous vasodilatation. During the block, even vigorous mechanical or cold stimuli did not rekindle hyperalgesia. In all patients, pain and hyperalgesia returned within a day after the block. In three patients tested, passive warming of the limb to the temperature achieved by the sympathetic block had negligible effects on pain and hyperalgesia. The hyperalgesia of sympathetically maintained pain is thought to be due to sensitization of central pain-signalling neurons to mechanoreceptor input. The present data indicate that this sensitization is highly plastic even when the disease has persisted for months or years. It could be reversed within minutes by a sympathetic blockade, but returned when sympathetic block subsided. Mechanoreceptor input by itself was not sufficient to maintain or rekindle the central sensitization. This supports the hypothesis that low-grade activity of nociceptors, possibly due to development of alpha-adrenergic sensitivity after injury, is involved in the maintenance of central sensitization.

Adult↗

PubMed1992

Sensory and movement-related cortical potentials in nociceptive and auditory reaction time tasks.

The processing of a sensory stimulus leading to a simple motor command was studied with scalp-recorded long latency cortical potentials in humans. Two sensory modalities were tested in their ability to activate descending motor pathways: auditory stimuli and painful cutaneous stimuli produced by a CO2 laser. Subjects were asked to react to stimuli with voluntary index finger movements. The stimulus-related and movement-related cortical potentials were recorded simultaneously with five midline electrodes on the scalp. The auditory reaction time, measured from the stimulus to the onset of electromyogram (EMG), was faster (150 ms) than the laser reaction time (350 ms). The onset of EMG of finger movements occurred only after the first negative components following auditory or laser stimuli but before the positive components. The latency from the auditory negativity to the onset of EMG was about 50 ms and the latency from the laser negativity to the onset of EMG was about 110 ms. This finding indicates that not only the peripheral afferent conduction but also central processing takes longer in a pain-related somatosensory task than in an auditory task. The frontal peak of Motor Potential (fpMP), a cortical potential related to the sensory feedback from movement, occurred with a constant latency after the onset of EMG (100 ms) and was unaffected by the task.

Adult↗

PubMed1991

Mechanically insensitive afferents (MIAs) in cutaneous nerves of monkey.

A problem in the study of nociceptors is that intense stimuli are used to locate the receptive field (RF), and thus the receptor may be damaged before the first responses are recorded. In addition, some nociceptors do not respond to the mechanical stimuli often used to search for the RF. To overcome these problems, an electrical search technique was developed to locate the RF of cutaneous nociceptors. In the hairy skin of anesthetized monkey, we used this technique to locate the RF of 63 A delta-fibers and 22 C-fibers that had extremely high thresholds or were unresponsive to mechanical stimuli. We refer to these afferents as mechanically insensitive afferents (MIAs). Ten A delta-fiber MIAs had a short latency response to stepped heat stimuli and could be responsible for first pain sensation. Five A delta-fiber MIAs and one C-fiber MIA did not respond to mechanical or heat stimuli but did respond to injection into the electrical RF of an artificial inflammatory soup containing histamine, bradykinin, prostaglandin E1, and serotonin. These chemoreceptors might be responsible for the pain and itch sensations that result from chemical stimuli. Some MIAs became more responsive to mechanical stimuli after injection into the RF of the inflammatory soup and, thus, may contribute to the hyperalgesia to mechanical stimuli associated with cutaneous injury. A large proportion of the A delta-fiber (48%) and C-fiber (30%) afferents in this study were insensitive to mechanical stimuli. The role of these MIAs in sensation needs to be studied further. The electrical search technique enables a systematic study of these afferents to be performed. This technique may also be of use to identify and characterize dorsal horn neurons that have inputs from MIAs.

Action Potentials↗

PubMed1991

Topical application of clonidine relieves hyperalgesia in patients with sympathetically maintained pain.

Patients with reflex sympathetic dystrophy or causalgia characteristically have ongoing pain and pain to light touch (hyperalgesia). Some of these patients obtain relief of their pain following interruption of sympathetic function to the affected area and, therefore, have sympathetically maintained pain (SMP). Evidence suggests that the pain and hyperalgesia in SMP are related to activation of peripheral adrenergic receptors. We wished to determine the contribution of alpha 1- and alpha 2-adrenergic receptors in SMP and thus examined the effects of local application of adrenergic agents in patients with SMP. The alpha 2-adrenergic agonist clonidine, available as a transdermal patch, was delivered topically to the patients' hyperalgesic skin. In four patients with SMP, clonidine eliminated or substantially reduced hyperalgesia to mechanical and cold stimuli. In three of these patients the effects were confined to the skin region beneath the patch, suggesting a peripheral and not central effect. The relief of hyperalgesia was not due to a local anesthetic effect since touch thresholds were unaffected. Topical clonidine did not relieve hyperalgesia of similar severity for two other patients whose hyperalgesia and pain were unaffected by sympathetic ganglion blocks (i.e., diagnosed as having sympathetically independent pain). In two SMP patients, intradermal injection of norepinephrine or phenylephrine (a specific alpha 1-adrenergic agonist) at a site treated with clonidine evoked intense pain and rekindled the pre-clonidine hyperalgesia at that site. It is likely that clonidine locally blocks the release of norepinephrine via activation of alpha 2 receptors on the sympathetic terminals. This study suggests, therefore, that SMP is mediated via alpha 1-adrenergic receptors located in the affected tissue.

Administration, Cutaneous↗

PubMed1991

Cerebral potentials evoked by painful, laser stimuli in patients with syringomyelia.

Brief cutaneous heat stimuli generated by a CO2 laser were used to elicit late somatosensory evoked cerebral potentials (SEPc) in 10 patients with syringomyelia. For comparison, early and late cerebral potentials in response to electrical nerve stimuli (SEPn) were recorded in the same session. In 8 patients with localized impairment of pain and temperature sensitivity we found complete absence of SEPc after stimulation of the affected area; in another patient with similar sensory deficits, the SEPc was grossly attenuated and delayed. In 1 patient with intact pain sensitivity but absent temperature sensitivity, a well defined SEPc could be recorded. Both early cortical SEPn and late SEPn in response to conventional nerve stimuli were normal in all patients and thus did not differentiate control and affected areas. These data indicate that alteration of SEPc correlates with altered pain sensitivity in patients with a circumscribed spinal lesion. SEPc may thus be used as a neurophysiological test in the assessment of hypalgesic dermatomes.

Brain↗

PubMed1991

Systemic alpha-adrenergic blockade with phentolamine: a diagnostic test for sympathetically maintained pain.

The diagnosis of sympathetically maintained pain (SMP) is typically established by assessment of pain relief during local anesthetic blockade of the sympathetic ganglia that innervate the painful body part. To determine if systemic alpha-adrenergic blockade with phentolamine can be used to diagnose SMP, we compared the effects on pain of local anesthetic sympathetic ganglion blocks (LASB) and phentolamine blocks (PhB) in 20 patients with chronic pain and hyperalgesia that were suspected to be sympathetically maintained. The blocks were done in random order on separate days. Patients rated the intensity of ongoing and stimulus-evoked pain every 5 min before, during, and after the LASB and PhB. Patients and the investigator assessing pain levels were blinded to the time of intravenous administration of phentolamine (total dose 25-35 mg). The pain relief achieved by LASB and PhB correlated closely (r = 0.84), and there was no significant difference in the maximum pain relief achieved with the two blocks (t = 0.19, P greater than 0.8). Nine patients experienced a greater than 50% relief of pain and hyperalgesia from both LASB and PhB and were considered to have a clinically significant component of SMP. We conclude that alpha-adrenergic blockade with intravenous phentolamine is a sensitive alternative test to identify patients with SMP.

Adult↗

PubMed1991

Laser-evoked cerebral potentials in the assessment of cutaneous pain sensitivity in normal subjects and patients.

Heat stimuli, applied to the skin by non-contact radiation pulses emitted by a CO2-laser, activate simultaneously both A-delta (mean conduction velocity 14 m/s) and C-fibres (0.8 m/s), which terminate in the most superficial skin layers. Correspondingly, brief heat stimuli elicit two pain sensations with mean reaction times of about 500 ms and 1400 ms. Similarly, two evoked potential waveforms were observed in the electroencephalogram: the late components N240/P370 and the ultralate components N1050/P1250. The shape of the two components was reproducible in independent samples of healthy volunteers. In patients with dissociated sensory loss, the laser evoked cerebral potentials are affected, depending on the kind of disturbed nerve and tracts. This is shown in patients with syringomyelia, encephalomyelitis disseminata, myelitis, Brown-Sequard syndrome, Wallenberg syndrome. In cases with hereditary motor and sensory neuropathy type I or with neurosyphilis, ultralate potentials are observed as correlates of delayed pain perception in the affected body areas. The laser evoked cerebral potentials reflected the clinical disorder of pain sensitivity in most cases, whereas somatosensory evoked potentials in response to conventional nerve stimuli failed in objectifying the diagnosis. As such, evoked cerebral potentials in response to laser heat stimuli applied to the hairy skin can be used for an overall examination of the functional integrity of peripheral small fibres, anterolateral tracts and thalamocortical projections.

Brain↗

PubMed1990

Intradermal injections of bradykinin or histamine cause a flare-like vasodilatation in monkey. Evidence from laser Doppler studies.

The spreading cutaneous vasodilatation (flare) that follows a cutaneous injury is readily visible in humans but cannot be visualized in monkey. To determine if monkeys exhibit this neurally mediated reaction, cutaneous blood flow changes after intradermal injections of bradykinin and of histamine were monitored in the hairy skin of pentobarbital anesthetized monkeys. Using a laser Doppler device, recordings of cutaneous blood flow were made at distances of 15 and 25 mm from the injection of 50 microliters of saline, bradykinin (10(-3) M) and histamine (10(-3) M). These sites were beyond the radius of the wheal caused by bradykinin (6.3 mm) or histamine (6.8 mm). At both recording sites, both drugs caused an increase in blood flow that was significantly larger than that caused by the injection of the same volume of saline. These results provide evidence that although a flare is not visible in monkey skin, a flare-like vasodilatation does occur over an area of at least 50 mm diameter.

Animals↗

PubMed1990

Comparison of heat and mechanical receptive fields of cutaneous C-fiber nociceptors in monkey.

1. Receptive-field properties were investigated in cutaneous C-fiber nociceptive afferents (CMH) responsive to mechanical and heat stimuli. Teased-fiber techniques were used to record from 28 CMHs that innervated the hairy skin of upper or lower limb in anesthetized monkeys. 2. The response to mechanical stimuli was studied with the use of calibrated von Frey probes. The response to heat stimuli was studied with the use of a laser thermal stimulator that provided stepped increases in skin temperature with rise times to the desired temperature near 100 ms. The size of the receptive field (RF) for mechanical stimuli was determined by use of a suprathreshold stimulus that consisted of a 0.5-mm-diam probe that exerted a 200-mN force (10 bar). The size of the heat RF was determined by use of a 49 degrees C stimulus applied to a 7.5-mm-diam area for 1 s. 3. Heat thresholds were determined with an ascending series of stimulus intensities and were found to be stable over many hours: they ranged from 37 to 46 degrees C (mean, 41.1 degrees C). Mechanical thresholds ranged from 1.3 to 7.3 bar (mean, 3.3 bar). There was no correlation between mechanical and heat thresholds. Both thresholds extended well below the corresponding psychophysical pain thresholds in the literature. This suggests that spatial and/or temporal summation of C-fiber input are important for pain induced by either stimulus modality. 4. Mechanical RF diameters ranged from 3.3 to 9.6 mm (mean, 4.7 mm); heat RF diameters ranged from punctate (less than 1 mm) to 9.5 mm (mean, 4.3 mm). There was a significant linear correlation between mechanical and heat RF sizes with a slope of one. The distance between the center of the mechanical RF and the center of the heat RF along one axis ranged from 0 to 1.1 mm (mean, 0.4 mm). These data indicate that the heat RFs coincided with the mechanical RFs. 5. Within the mechanical RF determined with the suprathreshold stimuli, all CMHs had one or more punctate areas of maximal mechanical sensitivity where mechanical threshold was lowest. Heat excitability extended greater than 2 mm beyond these mechanically sensitive spots. Because lateral transmission of the heat stimulus is small, this indicates that heat transduction occurs outside the regions of maximal mechanical sensitivity. 6. Both the threshold to heat and the response magnitude at suprathreshold intensities depended on the percentage of the RF area overlapped by the heat stimulus. This indicates that multiple transducer sites probably contribute to the total evoked response.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1990

Modulation of pain-related somatosensory evoked potentials by general anesthesia.

The aim of the present study was to assess if late somatosensory evoked cerebral potentials (SEPs) in response to painful electrical stimuli are a sensitive indicator for analgesic treatment during general anesthesia. For this purpose, a pain model developed for the quantification of drug-induced analgesia in awake volunteers was used in 10 patients scheduled for elective abdominal hysterectomy. Before induction of anesthesia, stimuli were adjusted to two and three times the pain threshold for each individual. Late auditory evoked potentials (AEPs, 30 dB hearing level) and spontaneous electroencephalogram were also evaluated. After control recordings, anesthetic treatments were varied in the following sequences: (a) 0.8% (end-tidal) halothane with 70% nitrous oxide (HN); (b) 0.8% halothane in oxygen (H1); (c) same anesthetic condition as in H1, but the SEP and AEP stimulus intensities were increased to 15 times pain threshold and to 70 dB hearing level, respectively (H2); and (d) fentanyl (0.25 mg) was given with 0.8% halothane in oxygen with no further change in stimulus intensities (HF). In treatments HN and H1, blood pressure and heart rate increases to pain stimuli were abolished, and SEPs and AEPs were both suppressed. Increasing the somatosensory stimulus intensity (treatment H2) stimulated heart rate and arterial pressure responses and again elicited the SEPs. However, AEP components remained suppressed with increased auditory stimulus intensity. Addition of fentanyl (HF) suppressed SEP amplitudes and stimulus-induced hemodynamic responses. Our results suggest that late SEPs in response to painful stimuli change with different analgesic levels.

Adult↗

PubMed1988

Late somatosensory evoked cerebral potentials in response to cutaneous heat stimuli.

Late components of cerebral potentials evoked by brief heat pulses applied to various skin sites were used to monitor the afferent pathways of pain and temperature sensitivity. Radiation at 10.6 micron wave length generated by a CO2 laser stimulator predominantly activates superficial cutaneous A delta and C nociceptors and elicits late and ultralate cerebral potentials. This paper deals with the investigation of the component structure and topography of the A delta fibre mediated late potentials, which were compared with the corresponding late potentials in response to standard electrical nerve stimuli. In the upper limb both stimulus types evoked a large positive potential (nerve: 260 msec, skin: 390 msec latency), preceded by a negativity (nerve: 140 msec, skin: 250 msec). Whereas these components were always maximal at the vertex, an earlier negativity appeared over the somatosensory projection area (nerve: 70 msec, skin: 170 msec). After stimulation of the lower limb all latencies were delayed by 20-30 msec. As a rule, the heat-evoked potentials appeared about 100 msec later than the corresponding potentials after electrical nerve stimulation. Similarities in interpeak latencies and scalp topography indicated similar cerebral processing.

Adult↗

PubMed1988

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.

Afferent Pathways↗