Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with leukemic reticuloendotheliosis is described who two years following splenectomy developed massive retroperitoneal, abdominal, and mediastinal lymphadenopathy. Therapeutic intervention was necessary because the bulky tumor masses produced disabling pain in the back and chest regions. Low-dose radiation to the involved fields produced prompt regression of the adenopathy along with dramatic pain relief. This case suggests that hairy cells may be quite sensitive to radiation, and this therapeutic modality should be considered, especially when local problems are present.
 ...
PMID:A role for radiation in the treatment of hairy cell leukemia complicated by massive lymphadenopathy: a case report. 615 23

Short radiant heat pulses, emitted by a high power CO2 laser, were used to investigate single nociceptor activity, cerebral potentials and concomitant sensations. Stimuli of 20 and 50 ms duration with different intensities were randomly applied to the hairy skin of the hand. Microelectroneurography was performed from the radial nerve at the wrist; 26 stable recordings were evaluated. Pre- and post-stimulus EEG segments were recorded from vertex versus linked ear lobes. Sensation was assessed on an eight-step category scale, an adjective scale, and by reaction times. In some experiments an A-fibre block was applied in order to isolate C-fibre responses. The main results were: Short heat stimuli activate C-units. In addition one of two identified A delta-units responded. None of the 15 A beta-units investigated was activated by the heat pulses. Short heat stimuli evoked cerebral potentials having a main vertex positive component at about 400 ms. These potentials were ascribed to A delta-fibre input. Laser induced pain consisted of an immediate stinging component, followed by a burning pain which often lasted several seconds. Reaction time to first pain ranged from 400-500 ms. Weak laser stimuli induced non-painful sensations mostly of tactile character. High correlations were found between the number of spikes elicited by a given stimulus and the intensity of the evoked sensation. Intensity discrimination, as evaluated by measures of Signal Detection Theory, was better in the peripheral C-units than in the subjective ratings. If conduction of A-fibres was blocked by pressure, A delta-related cerebral potential components vanished.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Nerve fibre discharges, cerebral potentials and sensations induced by CO2 laser stimulation. 633 9

The peripheral neuronal correlates of heat pain elicited from normal skin and from skin made hyperalgesic following a mild heat injury were studied by simultaneously recording, in humans, evoked responses in C mechanoheat (CMH) nociceptors and the magnitude estimations of pain obtained from the same subjects. Subjects made continuous magnitude ratings of pain elicited by short-duration stimuli of 39-51 degrees C delivered to the hairy skin of the calf or foot before and at varying intervals of time after a heat injury induced by a conditioning stimulus (CS) of 50 degrees C, 100 s or 48 degrees C, 360 s. The stimuli were applied with a thermode pressed against the nociceptor's receptive field. For heat stimulations of normal skin, that is, uninjured skin, pain thresholds in 14 experiments with nine subjects ranged from 41 to 49 degrees C, whereas response thresholds for most of the 14 CMH nociceptors were 41 degrees C (in two cases, 43 degrees C). The latter suggested that spatial summation of input from many nociceptors was necessary at pain threshold. An intensity-response function was obtained for each CMH by relating the total number of nerve impulses evoked per stimulus to stimulus temperature. A corresponding magnitude scaling function for pain was obtained by relating the maximum rating of pain elicited by each stimulus to stimulus temperature. The relation between the subject's scaling function and the intensity-response function of his CMH nociceptor varied somewhat from one experiment to the next, regardless of whether the results were obtained from the same or from different subjects. However, when averages were computed for all 14 tests, there was a near linear relationship between the mean number of impulses elicited in the CMHs and the median ratings of pain, over the range of 45-51 degrees C. It was concluded that the magnitude of heat pain sensation was more closely related to the magnitude of response in a population of CMH nociceptors than in any individual nociceptor. At 0.5 min after the CS, the pain thresholds of most subjects were elevated, and the magnitude ratings of pain elicited by supra-threshold stimuli were lower than pre-CS values (hypoalgesia). Corresponding changes were seen in the increased thresholds and decreased responses (fatigue) of most CMHs. By 5-10 min after the CS, the pain thresholds of most subjects were lower, and their magnitude ratings of suprathreshold stimuli were greater than pre-CS values (hyperalgesia).(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Peripheral neural correlates of magnitude of cutaneous pain and hyperalgesia: simultaneous recordings in humans of sensory judgments of pain and evoked responses in nociceptors with C-fibers. 670 24

Contributions of evoked discharge in nociceptors with C-fibers to the temporal profiles of magnitude judgments of pain by humans were determined for heat stimulations of the skin before and after the development of hyperalgesia (increased sensitivity to pain) produced by a mild heat injury. Human subjects continuously rated the magnitude of pain evoked by short-duration heat stimuli of 39-51 degrees C delivered to the hairy skin of the arm or leg (calf or foot) before and after the development of hyperalgesia produced by a conditioning stimulus (CS) of either 50 degrees C for 100 s or 48 degrees C for 360 s. During heat stimulations of the leg in humans, magnitude judgments of pain were obtained simultaneously with recordings of evoked discharges in single C-fiber mechanoheat (CMH) nociceptive afferent fibers. Seven fibers were studied before and after the CS. In other experiments, magnitude ratings of pain evoked by heat stimulations of the arm were compared with heat-evoked discharges in 21 CMH nociceptive afferent fibers innervating the hairy skin of the wrist or hand in anesthetized monkeys. From CMH responses obtained in each species, median response latencies were calculated as well as poststimulus time (PST) histograms--the latter plotting mean frequency of discharge versus time during each stimulus. In these analyses, the times of action potentials in CMHs were calculated as they would occur at entry to the lumbar or cervical spinal cord in humans, taking into account the temporal dispersion that should occur because of differing conduction velocities. These results were then compared with response latencies for pain and the temporal profiles of pain ratings made by individual subjects. Comparisons were made for data obtained before the CS (normal skin) and those obtained 10 min after the CS in heat-sensitized (hyperalgesic) skin. For normal skin, PST histograms of mean frequencies of discharge were similar for CMHs with similar heat thresholds (41-43 degrees) in the anesthetized monkey and the awake human. Despite minor discrepancies, there were similarities in the changes in these histograms for monkey and human CMHs following heat sensitization after the CS. It was concluded that CMHs in monkeys and humans have similar response magnitudes and temporal profiles of response to heat. The major differences in the temporal profiles of CMH responses and human pain ratings were the latencies at which CMH responses and pain ratings began, reached maximum, and ended.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Time-intensity profiles of cutaneous pain in normal and hyperalgesic skin: a comparison with C-fiber nociceptor activities in monkey and human. 673 35

Pain thresholds in humans were determined for heat stimulations of the skin before and after a mild injury induced by a single conditioning stimulus (CS) of 50 degrees C and 100 sec duration. The same stimuli were delivered to the receptive fields of C fiber and A fiber mechanoheat-sensitive nociceptors (CMH and AMH nociceptors, respectively) and of low threshold warm and cold receptors in the anesthetized monkey and to the receptive fields of CMH nociceptors recorded percutaneously from the peroneal nerve of awake humans. Pain thresholds in normal skin were matched only by the response thresholds of CMH and not AMH nociceptors. Immediately following heat injury, some pain thresholds and CMH response thresholds were elevated, but by 5 to 10 min after the CS, pain and CMH thresholds were lowered to 2 to 6 degrees C below normal (hyperalgesia and nociceptor sensitization). No other type of cutaneous receptor studied exhibited changes in threshold similar to those observed for pain and for CMH nociceptors. The magnitude of hyperalgesia in humans and the magnitude of sensitization of CMH nociceptors in monkeys following heat injury were greater for hairy than for glabrous skin. The time course of the development of hyperalgesia was not altered by ischemia or conduction block in A fibers. The results support the conclusion that altered activity in CMH nociceptors is a major peripheral determinant of cutaneous hyperalgesia following a mild heat injury to the skin.
 ...
PMID:Peripheral neural mechanisms of cutaneous hyperalgesia following mild injury by heat. 708 82

Psychophysical experiments were done to test the possibility that a single receptor population signals both itch and pain by generating different patterns of activity for each type of stimulus. Electrical stimulation of hairy skin evoked pruritus in 92% of the subjects tested, and for the majority the pruritus elicited by electrical stimulation felt the same as that provoked by cowhage. The intensity of pruritus increased with the frequency of stimulation with no change in the quality of the sensation from itch to pain. Electrical stimulation of human skin with response patterns obtained from individual cat polymodal nociceptive neurons to pain- and itch-producing stimuli caused no differences in the quality of the evoked pruritic sensations. These results do not support the idea that the same population of primary sensory neurons can produce both itch and pain by changing their pattern of discharge.
 ...
PMID:Itch evoked by electrical stimulation of the skin. 714 37

High-threshold mechanoreceptors (mechanical nociceptors) with myelinated axons were electrophysiologically identified in hairy skin of the cat as described by Burgess and Perl ('67). Such elements possess receptive fields consisting of a number of punctate areas from which maximal firing can be elicited by intense (skin-damaging) mechanical stimuli. The spots of the receptive field are separated from each other by unresponsive regions, i.e., by skin areas from which responses cannot be evoked by stimuli effective at the spots. Fine steel pins were inserted to bracket closely a number of the spotlike responsive areas for each of several units. After aldehyde perfusion of the animal, osmification of the tissue and embedding in plastic, the marked skin zones were examined in semithin and ultrathin sections at the light and electron microscopic level. Near each delineated area, a thinly myelinated axon was found that could be traced to the papillary layer where it loses its myelin sheath. Unmyelinated axons accompanied by thin Schwann cell processes were then traced and found to penetrate the epidermal basal lamina in one of the papillae. At the epidermal penetration site, the axons contained both clear round, and large, dense core vesicles; at this level, the surrounding Schwann cell cytoplasm exhibited numerous pinocytotic vesicles. The zone of penetration may constitute the receptive apparatus. Some of these axons have been traced within the basal epidermal layer where they become surrounded by keratinocytes, lose their Schwann sheath, and apparently terminate. This overall morphological pattern was consistently present in the demarked areas of focal responsiveness, and was rare in the surrounding skin; this and its difference from other cutaneous neural endings suggest that the intraepidermal axon-Schwann cel complex constitutes the receptive structure for myelinated mechanical nociceptors. It is suggested that such complexes are the sense organs responsible for initiating the sensation of pricking pain produced by localized mechanical injury of the skin.
 ...
PMID:Fine structure of myelinated mechanical nociceptor endings in cat hairy skin. 722 37

1. Ramped heat stimuli were used to compare the effects of rate of temperature change on the responses of monkey nociceptors and on heat pain threshold in human subjects. Recordings were made from twenty-five cutaneous C fibre mechano-heat nociceptors (CMHs) innervating the hairy skin in the anaesthetized monkey. Heat pain thresholds were determined on the volar forearm of eight human subjects using a converging staircase technique. 2. The heat pain threshold decreased as stimulus ramp rate increased. In contrast, the CMH heat threshold, defined as the surface temperature at which the first action potential occurred, increased as stimulus ramp rate increased. Thus, the properties of the heat stimulus that dictate heat pain threshold are different from the properties of the heat stimulus that govern the initiation of a response in nociceptors. 3. Peak discharge frequency of CMHs during the heat ramp increased with stimulus ramp rate. Heat pain threshold was correlated with achievement of a minimum discharge rate in nociceptors (0.5 Hz), rather than with the threshold for action potential initiation.
 ...
PMID:Response of C fibre nociceptors in the anaesthetized monkey to heat stimuli: correlation with pain threshold in humans. 756 15

1. Mechano- and heat-sensitive A fibre nociceptors (AMHs) and C fibre nociceptors (CMHs) in hairy skin (forty-six AMHs and twenty-one CMHs) and in glabrous skin (fifty-nine AMHs and ten CMHs) of anaesthetized monkeys were tested with a 30 s, 53 degrees C heat stimulus, delivered by a laser thermal stimulator (0.1 s rise time, 7.5 mm diameter). 2. Two types of heat response were observed in hairy skin AMHs. Type I AMHs had a peak discharge towards the end of the stimulus, response latencies to heat of up to several seconds, a median heat threshold greater than 53 degrees C, and a mean conduction velocity of 25 m s-1 (n = 33). Type II AMHs had a peak discharge within 1-3 s, a mean response latency of 120 ms, a median heat threshold of 46 degrees C, and a mean conduction velocity of 15 m s-1 (n = 13). Type I AMH fibres were sensitized to heat, whereas heat responses of type II AMHs were suppressed following the intense heat stimulus. 3. In glabrous skin, only type I AMHs were found. The absence of type II AMHs is consistent with the absence of first pain to heat in glabrous skin. 4. C fibre nociceptors in hairy skin had a peak discharge near stimulus onset, a mean response latency of 100 ms and a median heat threshold of 41 degrees C. Heat responses of CMHs in glabrous skin were not significantly different from those in hairy skin. 5. Only type II AMHs had response latencies that were short enough to explain first pain to heat. Heat thresholds of type II AMHs were significantly higher than those of CMHs. 6. These results suggest two different heat transduction mechanisms in nociceptive afferents. For one, heat energy is quickly transduced into action potentials, and the peak discharge is reached soon after stimulus onset. For the other, the transduction of heat is distinctly slower, and the peak discharge occurs near the end of the stimulus. Chemically mediated sensitization may be involved in the second transduction mechanism.
 ...
PMID:Evidence for two different heat transduction mechanisms in nociceptive primary afferents innervating monkey skin. 777 55

Extravascular activation of thrombocytes may contribute to nociceptor excitation and pain, since platelets store and, upon stimulation, release potential algogenic substances such as serotonin, histamine and precursor molecules of bradykinin. To test this hypothesis, a skin-nerve preparation of rat hairy skin, in vitro, was used that allows to record and characterize single afferent nerve fibers. In a first protocol, receptive fields of nociceptive C-fibers, at the corium side of the skin patch, were exposed to adenosine diphosphate (ADP), to heparinized human platelet-rich plasma (PRP) and to PRP activated by ADP. Such activated platelets excited 9/11 units characterized as mechano-heat responsive C-nociceptors (CMH); peak discharges of more than 10 spikes/s were observed. After application of activated PRP, 4/5 high threshold mechanosensitive C-units and 4/5 mechano-cold sensitive C-units became responsive to heat stimulation but only few of these fibers were excited (1/5 in each group). In a second series of experiments the exposure to native PRP was prolonged to test for the effect of spontaneous platelet activation resulting from cutaneous collagen. Prolonged exposure did, but not significantly, enhance fiber discharge. During subsequent exposure to activated PRP, the discharge commenced, on average, after a significant delay of about three minutes. With this protocol 5/7 CMH units were driven by activated platelets. Following both protocols, mechanical (v.Frey) and thermal thresholds of the CMH units were not significantly altered. The findings demonstrate that nociceptors can indeed be driven and sensitized by activated platelets. This pain inducing mechanism may be relevant to certain clinical conditions, and it appears promising to scrutinize the chemical factors involved.
 ...
PMID:Activated human platelets in plasma excite nociceptors in rat skin, in vitro. 804 82


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>