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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Spreading vasodilatation of the axon reflex type was evoked by contact heat stimulation of the hairy skin in the human forearm (13.3 cm2 stimulus area) and was detected by laser Doppler flowmetry at 8, 19 and 30 mm distance. 2. From a base temperature of 35 degrees C, rapidly rising short heat stimuli (4 degrees C s-1, 2 s plateau) elicited vasodilatation at an average threshold of 39.4 degrees C. For slowly rising sustained heat stimuli (64 s duration) the average threshold was 39.6 degrees C (n.s.) Laser Doppler flowmetry revealed a rapid onset within about 4 s, a long duration of several minutes beyond the end of the stimulus, and a rapid spread of vasodilatation to remote skin areas. These characteristics are typical for vasodilatation by an axon reflex of nociceptive afferents. 3. Axon reflex thresholds matched the lower range of C fibre nociceptor heat thresholds. Thermal stimuli that were adjusted to elicit about half-maximal phasic responses in warm fibres (steps from 30 to 35 degrees C), but were below the range of C fibre nociceptor thresholds, did not cause any vasodilatation. 4. Pain thresholds were higher than axon reflex thresholds for both rapidly and slowly rising heat stimuli and strongly depended on the stimulus pattern (40.1 degrees C for rapidly rising stimuli and > 43 degrees C for slowly rising stimuli). This observation is consistent with recent reports that the phasic response of nociceptive afferents is essential to overcome the summation requirements at central synapses. 5. In conclusion, axon reflex vasodilatation in response to heat stimuli in the hairy skin of humans is elicited by activation of heat-sensitive nociceptors, even in the absence of a conscious perception of heat pain. The dissociation of pain and vasodilatation thresholds supports the concept of two operating ranges of primary nociceptive afferents. Warm fibres do not contribute to axon reflex vasodilatation in the hairy skin of the human forearm. Release of vasoactive peptides by nociceptive primary afferents may also contribute to local heat-evoked vasodilatation at temperatures above 40 degrees C.
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PMID:Heat-evoked vasodilatation in human hairy skin: axon reflexes due to low-level activity of nociceptive afferents. 900 68

The cutaneous sensory units labeled C-fiber polymodal nociceptors have a broadly coherent set of responsive characteristics. These include; (a) elevated thresholds to mechanical stimulation and to heat; (b) excitation by irritant and algesic chemicals; and (c) sensitization by injury or algesic substances. These characteristics and the match between the signals produced by C-polymodal nociceptors to pain-causing stimuli and human reports of pain indicate a probable causal connection. Nevertheless, there are indications that this population of sensory units may contain functionally-distinct subtypes. Some human C-polymodal nociceptors have been reported to be excited by histamine at low concentrations, whereas much of the population lacks such responsiveness. Further, in vitro studies of the effects of non-steroidal anti-inflammatory agents and low pH on sensitization suggest distinctions in the responsiveness of different elements whose general characteristics place them into the C-polymodal category. The enhanced responsiveness of C-polymodal nociceptors after heat stimulation or exposure to acidity has a probable relationship to the primary hyperalgesia produced after injury to hairy skin or in the presence of inflammation. Furthermore, the alterations of C-polymodal nociceptor characteristics after partial nerve injury and sympathectomy imply a change in phenotype of neurons spared by denervation and are suggestive of a possible relationship to sympathetically related pain and post-sympathetic neuralgias. These evidences of plasticity in responsiveness of a set of sense organs putatively associated with cutaneous pain represent lessons in the adaptability of biological mechanisms, and clues to the pathophysiology of pain.
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PMID:Cutaneous polymodal receptors: characteristics and plasticity. 900 26

Sudomotor functions were studied in 27 patients suffering from reflex sympathetic dystrophy (RSD) according to the criteria established by Bonica (18 women, 9 men; mean age 50 +/- 12.3 years; median duration of disease 8 weeks, range 2-468 weeks). To measure local sweating rates, two small chambers (5 cm2) were affixed to corresponding areas of hairy skin on the affected and unaffected limbs. Dry nitrogen gas was passed through the chambers (270 ml/min) and evaporation was recorded at both devices with hygrometers. Thermoregulatory sweating (TST) was induced by raising body temperature (intake of 0.5 1 hot tea and infra-red irradiation). Local sweating was also induced through an axon reflex (QSART) by transcutaneous iontophoretic application of carbachol (5 min, 1 mA). In addition, skin temperature was measured on the affected and unaffected side by infra-red thermography. Mean skin temperature was significantly higher on the affected side (P < 0.003). In spite of the temperature differences, there was no difference in basal sweating on the affected and unaffected side. However, both methods of sudomotor stimulation lead to significantly greater sweating responses on the affected compared to the unaffected side (TST: P < 0.05, QSART: P < 0.004). Latency to onset of sweating was significantly shorter on the affected side under both test conditions (P < 0.04 and P < 0.003, respectively). Sweat responses were not correlated to absolute skin temperature but were probably related to the increased blood flow on the affected side. Our findings imply a differential disturbance of vasomotor and sudomotor mechanisms in affected skin. Whereas vasoconstrictor activity is apparently lowered, sudomotor output is either unaltered or may even be enhanced.
Pain 1997 Jan
PMID:Sudomotor function in sympathetic reflex dystrophy. 906 12

A psychophysical investigation was carried out to examine whether heat hyperalgesia exists within the secondary mechanical hyperalgesia zone surrounding a capsaicin injection site on hairy skin. A non-contact laser stimulator was used to deliver temperature controlled stimuli to sites within and outside the zone of mechanical hyperalgesia. Heat testing was carried out before and after the intradermal injection of 50 micrograms of capsaicin into the volar forearm. The zones of mechanical hyperalgesia to punctate and stroking stimuli and the region of flare were also mapped after the capsaicin injection. Heat pain thresholds inside the secondary mechanical hyperalgesic zone were not significantly different from thresholds outside the secondary mechanical hyperalgesia zone. In addition, pain ratings to an ascending series of heat stimuli delivered inside the zone of secondary hyperalgesia were not significantly different from pain ratings outside the zone of secondary hyperalgesia. Thus, there was no evidence for heat hyperalgesia within the zone of secondary hyperalgesia to punctate mechanical stimuli. Though the areas of punctate and stroking hyperalgesia were correlated, no correlation existed between the magnitude of capsaicin evoked pain and the areas mechanical hyperalgesia to punctuate and stroking stimuli or the area of flare. This suggests that independent mechanisms may mediate evoked pain, central sensitization that leads to mechanical hyperalgesia, and axon reflexive flare.
Pain 1996 Dec
PMID:Secondary hyperalgesia to mechanical but not heat stimuli following a capsaicin injection in hairy skin. 912 30

The behaviour of 101 calves was evaluated during (n = 73) and after (n = 28) thermical dehorning without anaesthesia. Cortisol in saliva (n = 68) was measured in 68 calves. A simulation of dehorning was carried out as a control in most of the animals. The area around the horn bud was examined histologically in 20 calves of different ages (newborn until 3-4 months old). Additionally, the influence of dehorning cows with a wire-saw under anaesthesia on behaviour (n = 16), cortisol in saliva (n = 23), and the milk yield was examined. Independent of the calves' age, the horn bud and the surrounding hairy area were well innervated. For all calves dehorning without anaesthesia was a painful experience. During dehorning calves showed distinct pain and defense reactions. Most reactions were observed more often when the calves were dehorned as when dehorning was simulated. The cortisol in saliva was significantly increased after dehorning. In summary, we have to conclude that calves have a well developed nociceptive system from birth on. Therefore calves should only be dehorned using anaesthesia. Despite the anaesthesia, dehorning was stressful for the cows, as measured by a significant increase of cortisol in saliva. Moreover, cows showed pain reactions when the effects of the anaesthesia diminished. Dehorning had only a short effect on the milk yield of the cows.
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PMID:[Ethological, physiological and histological aspects of pain and stress in cattle when being dehorned]. 915 26

In order to investigate the usefulness of immunohistochemical detection of regenerating axons as a correlate of functional recovery, reinnervation of mouse foot pads, hairy skin, and muscle were studied at several intervals along 3 months after sciatic nerve crush using immunohistochemical markers PGP 9.5 and CGRP. These histological results were compared with functional recovery of sweat glands (SGs), plantar muscles, and pain sensibility. One week after nerve injury all neural functions were abolished in the operated hindpaw of all mice, no CGRP-immunoreactive (-ir) fibers were seen in the samples studied, while PGP 9.5 immunofluorescence remained at dim levels within nerve trunks, but disappeared from terminal innervation. The first PGP 9.5- and CGRP-ir regenerating fibers were seen at 15-16 days postoperation (dpo) in dermal nerve trunks of dorsal hairy skin and some days later in dermal trunks of foot pads. Regenerating nerve fibers progressed along the periphery of the dermis reinnervating the different dermal appendages. At 25 dpo all target organs were reinnervated. The first SGs activated by pilocarpine reappeared by 16 dpo and increased in number to 88% of control counts. Nociceptive responses reappeared at 17 dpo and reached 100% of control values. The first PGP immunofluorescence in neuromuscular junctions was seen at 16 dpo, while the first muscle action potentials were recorded at 19 dpo, and the potentials amplitude increased to 66% of controls. Good correlations were found between morphological and functional results of reinnervation. However, the density and distribution of nerve profiles in the tissues studied did not reach normal levels, while neural functions conveyed by small fibers reached levels similar to controls.
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PMID:Comparison of immunohistochemical and functional reinnervation of skin and muscle after peripheral nerve injury. 922 52

Electrical stimulation of the mental nerve evokes two suppression periods SP1 and SP2 in masseter muscle activity bilaterally. In order to investigate a possible nociceptive origin of the suppression periods, we compared the reflex responses evoked by electrical stimulation and by selective activation of nociceptors in hairy skin using painful infrared laser stimuli. The SP was elicited during more than 90% maximal voluntary contraction. Thresholds for detection, pain, and SP in the mental nerve area were determined by the method of limits. A suppression period was evoked by laser stimuli in nine of ten subjects bilaterally. The mean onset latency was 46.9 ms, the mean duration 58.9 ms. The electrical threshold of SP1 (9 mA) was 7.7 x I(0), about 20% smaller than I(P), and significantly higher than I(SP2) (4.7 mA). The onset latencies and durations were 11.7 ms and 21 ms for SP1, and 45 ms and 42.7 ms for SP2 (stimulus intensity 2 x I(P)). The mean difference in onset latencies between laser SP and electrically evoked SP1 was 35.1 +/- 6.2 ms, which closely matches the nociceptor response latency to a laser heat pulse. Based on the threshold and the onset latency we conclude that at least SP1 and laser SP are nociceptive in origin and mediated by group III fibers.
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PMID:Nociceptive masseter inhibitory reflexes evoked by laser radiant heat and electrical stimuli. 929 12

A retrospective study of 37 patients with haematological malignancy (21 acute myeloid leukaemia, 11 acute lymphoid leukaemia, two lymphoma, two hairy cell leukaemia, one Hodgkin's disease) and histologically documented mucormycosis was conducted to evaluate the clinical characteristics and ascertain the factors which influenced the outcome from mycotic infection. Patients were admitted to 18 haematology divisions in tertiary care or university hospitals in Italy between 1987 and 1995. Fever, thoracic pain, dyspnoea and cough were the most frequent presenting symptoms. At the onset, 89% patients were neutropenic (neutrophil counts < 0.5 x 10(9)/l) with a median duration of previous neutropenia of 14 d (range 6-60). The most frequent sites of infection were lungs (81%), CNS (27%), sinus (16%), liver (16%) and orbital space (10%). Only three patients were asymptomatic. A correct in vivo diagnosis was made in only 13 (35%) patients. When performed, thoracic and cranial CT scan were the most useful diagnostic investigations. Despite the fact that 26 febrile patients were treated with empirical antifungal treatment, 28 of the 37 patients (76%) died from fungal infection at a median time of 17 d from the onset of clinical symptoms. Nine patients were cured by antifungal therapy plus, in five cases, radical surgery procedures. An analysis of factors influencing outcome demonstrated that the resolution of chemotherapy-induced neutropenia and prolonged treatment with amphotericin B and, if feasible, radical surgical debridement treatment, were significantly correlated with recovery from infection. Mucormycosis, a rare filamentous fungal infection that occurs most frequently in neutropenic acute leukaemia patients, is characterized by a high mortality rate. Extensive and aggressive diagnostic and therapeutic procedures are essential to improve the prognosis in these patients.
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PMID:Mucormycosis in patients with haematological malignancies: a retrospective clinical study of 37 cases. GIMEMA Infection Program (Gruppo Italiano Malattie Ematologiche Maligne dell'Adulto). 937 50

The local release of pro-inflammatory neuropeptides in the periphery has been associated with the development of neurogenic inflammation. However, there is an increasing number of reports demonstrating tissue-dependent differences regarding the mechanisms engaged by these neuropeptides to initiate and maintain the inflammatory response in the target tissue. Since skin is often involved in tissue injury, the present studies were designed to develop a model for assessing cutaneous peptide secretion as a marker for neurogenic inflammation in skin tissue. Calcitonin gene-related peptide (CGRP), as one of several neuropeptides known to be involved in neurogenic inflammation, was chosen to study capsaicin-induced effects on peripheral neurosecretion. The corial surface of the hairy skin of a rat hindlimb was superfused in vitro, and the basal and capsaicin-evoked peripheral release of immunoreactive CGRP (iCGRP) was measured using a radioimmunoassay. The main objectives of these studies were to characterize the various properties of this release including dose-dependency, exocytosis and receptor-mediation as well as the effects of acute and long-term capsaicin desensitization. Capsaicin significantly and dose-dependently increased the release of iCGRP at concentrations ranging from 3 to 300 microM. Omission of calcium ions or treatment with the competitive capsaicin receptor antagonist capsazepine completely inhibited the capsaicin-induced iCGRP release. Superfusion of the skin with 100 microM capsaicin following a conditioning stimulation with capsaicin at concentrations ranging from 0.3 to 100 microM led to an acute, dose-dependent desensitization of the CGRP response. In addition, chronic desensitization following the neonatal injection of capsaicin completely abolished the acute iCGRP response to capsaicin. The method described here should prove to be a valuable tool for the evaluation of the processes regulating the peripheral, cutaneous release of pro-inflammatory neuropeptides. This strategy, therefore, may lead to a better understanding of the mechanisms involved in the development and maintenance of neurogenic inflammation, particularly in the skin.
Pain 1997 Nov
PMID:Peripheral CGRP release as a marker for neurogenic inflammation: a model system for the study of neuropeptide secretion in rat paw skin. 941 6

Effect of weight bearing of the hindlimbs on the assessment of mechanically-induced hindlimb withdrawal threshold was determined in intact rats and in rats with various pathophysiological conditions causing allodynia or hyperalgesia. Hindlimb withdrawal was elicited by applying a series of calibrated monofilaments to the plantar or the dorsal surface of the paw. During testing the rat was either in a restraint tube with hindlimbs hanging semi-extended without weight bearing or it was standing on a metal grid (bearing its own weight). In intact rats, the withdrawal thresholds were significantly lower when the stimulus site was the dorsal hairy skin rather than the plantar glabrous skin. Also, thresholds were significantly lower when the hindlimbs were not bearing weight. Following carrageenan-induced unilateral inflammation of the plantar paw or a tibial nerve cut there was a marked threshold decrease to test stimuli applied to plantar or dorsal paw, respectively, ipsilateral to the pathological condition in standing rats. However, when the hindlimbs were not weight bearing the unilateral threshold decrease was markedly attenuated (carrageenan-treated rats) or completely abolished (tibial cut). In contrast, in rats with a unilateral spinal nerve ligation the threshold decrease ipsilateral to the nerve lesion was highly significant independent of the weight bearing of the hindlimbs. The results indicate that weight bearing of hindlimbs is an important confounding factor in the assessment of tactile allodynia in rats.
Pain 1998 Jan
PMID:Weight bearing of the limb as a confounding factor in assessment of mechanical allodynia in the rat. 951 60


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