Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162473 (Frey)
 2,599 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Frey's syndrome occurs after parotid gland surgery or injury to the parotid gland and is characterized by gustatory sweating and erythema of the face upon mastication. The syndrome occurs in 50 to 60 per cent of all patients undergoing parotid surgery but the symptoms are only distressing to about 10 per cent of patients undergoing parotidectomy. A case of Frey's syndrome is reported The patient obtained good relief of symptoms with scopolamine cream and atropine cream. Other methods of therapy are discussed along with their limitations. Noninvasive therapy with topical anticholinergic creams is effective and seems appropriate in the control of gustatory sweating.
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PMID:Frey's syndrome. 13 23

Frey's syndrome is distinguished by the appearing of erythema, sensation of hotness, sometimes pain, and transpiration discharge in the preauricular and temporal area when ingestion stars. We present an eleven month old child with this pathology and we review the etiology and clinic manifestations of this syndrome.
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PMID:[Frey syndrome in childhood]. 812 75

The aim of the study was to examine reproducibility of primary and secondary hyperalgesia in a psychophysical model of human inflammatory pain. Mild burns were produced on the crura of 12 volunteers with a 50 x 25 mm thermode (47 degrees C, 7 min). Assessments of (i) cold and warm detection thresholds, (ii) mechanical and heat pain thresholds, (iii) pain to heat (43 degrees C and 45 degrees C, 5 s), (iv) secondary hyperalgesia, and (v) skin erythema were made 1.75 and 0.5 h before, and 0, 1, 2, 4, and 6 h after a burn injury. Sensory thresholds and hyperalgesia to heat and mechanical stimuli were examined by contact thermodes and von Frey hairs, and pain intensity was rated with a visual analog scale (0-100). To describe between-day reproducibility, the subjects were examined three times at intervals of 21 days. Within-day comparisons showed that a 20% change could be detected as significant for all variables with fewer than 12 subjects in a cross-over design (2alpha = 5% and power = 80%). Between-day comparisons demanded up to 25 subjects to detect changes of the same magnitude. The burns caused mild to moderate pain (VAS: mean 29, SD 14) and the subjects (all right-handed) were more sensitive to heat pain on their left side (P < 0.03). Hyperalgesia was induced instantaneously by the burn and outlasted the study period (6 h). However, no spontaneous pain was observed after the injury, and a brief period of hypoesthesia to warm and cold stimuli was induced by the burn. The painful measurements themselves evoked hyperalgesia to heat and mechanical stimuli on the arm, but only to mechanical stimuli on the legs. including secondary hyperalgesia. Hyperalgesia evoked by the measurements was significantly less intense than that induced by injury. Habituation to the painful stimuli was demonstrated by significantly higher pain thresholds and lower pain responses on the second and third day of the study. The burn model is a sensitive psychophysical model of acute inflammatory pain, when cross-over designs and within-day comparisons are used, and the model is suitable for double-blind, placebo-controlled studies of analgesics. In similar models, we recommend that analgesic and placebo are evenly divided between right and left sides and study days.
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PMID:Hyperalgesia in a human model of acute inflammatory pain: a methodological study. 952 Feb 28

The goal of this work is to present our results of the intradermic infiltration with botulinum toxin in patients with Frey syndrome. Sixteen hemifaces in 15 patients were studied. Gustatory stimulation was evoked by sucking on a slice of lemon while measurements were done on both hemifaces, with the normal side being used as a control. Skin temperature and color (erythema) were measured with a digital surface thermometer and a skin chromameter, respectively. Sweat quantity and surface were measured by using the previously described blotting paper and iodine-sublimated paper histogram methods, respectively. Testing was repeated 2 weeks after skin infiltration with botulinum toxin (dilution of 50 U/mL). The interinjection distances were 1 cm, and 0.1 mL (5 U) was infiltrated at each injection site. Frey syndrome complaints disappeared in all patients. Small residual amounts of sweat were measurable. The difference in sweat quantity before and after botulinum toxin infiltration was significant in every patient (P < 0.001). Skin temperature and color measurement gave inconclusive results. In conclusion, Frey syndrome treatment with botulinum toxin is an efficient and well-tolerated technique. Further work should address the optimal injection parameters.
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PMID:Frey syndrome treatment with botulinum toxin. 1082 93

Hyperalgesia on intradermal capsaicin application can be attenuated by systemic application of local anesthetics. We tested whether low doses of local anesthetics applied pre- or post-traumatically can reduce heat trauma-induced primary and secondary hyperalgesia in humans. Six healthy volunteers consented to the randomized, double-blind, and cross-over designed study. In each subject, a first-degree burn injury was induced three times (corresponding to a pre-traumatic, post-traumatic and control group) at an interval of at least 3 weeks. Heat was applied by a computer-controlled Peltier thermode (47 degrees C, 5 min). In the pre-traumatic group, lidocaine infusion was commenced 30 min prior to heat trauma, and in the post-traumatic group immediately after heat trauma for a total infusion time of 60 min each. Volunteers rated pain on a visual analogue scale (VAS) between threshold and tolerance maximum (0-100% VAS). Primary hyperalgesia was quantified by determining mechanical (von Frey hairs) and thermal (Peltier thermode) pain thresholds. Secondary hyperalgesia was quantified by determining the area in which normally unpleasant von Frey hairs evoked pain or tenderness. Baseline thermal and mechanical pain thresholds did not differ between groups. Heat application always resulted in a first-degree burn injury including both primary and secondary hyperalgesia. The former remained by and large stable for about 4 h whereas the latter continuously increased within the first 2 h. Lidocaine did not affect primary hyperalgesia, irrespective of pre- or post-traumatic application, but substantially reduced the development of secondary hyperalgesia on pre-traumatic, and for tendency on post-traumatic infusion (treatment groups did not differ significantly). Burn injury-induced erythema was smallest in the pre-traumatic group and largest in the control group; however, the level of significance was not reached. Plasma concentrations of lidocaine were always higher than 1.5 microg/ml 30 min after bolus application of lidocaine and reached a peak of 2-3 microg/ml after about 1 h. Thus, local anesthetics at concentrations that do not block nerve conduction substantially affect ongoing central changes in pain processing that are induced by a real tissue trauma. A significant preemptive effect could not be demonstrated. The anti-hyperalgesic effect of lidocaine is likely based on action of central (spinal) sites, but peripheral sites may also be addressed.
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PMID:Effect of pre- or post-traumatically applied i.v. lidocaine on primary and secondary hyperalgesia after experimental heat trauma in humans. 1106 17

Primary hyperalgesia to mechanical and thermal stimuli are major clinical symptoms of inflammatory pain and can be induced experimentally by ultraviolet-B (UV-B) irradiation in humans. We set-up a pig model in order to have more options for pharmacological intervention on primary hyperalgesia. Pig skin was irradiated with a dose one- to threefold higher than the minimum erythema dose (MED) and investigated for mechanical and heat responsiveness 24 and 48 h post UV-B treatment. C-fiber activation upon mechanical and thermal stimulation was assessed indirectly by extent of the axon reflex erythema (flare) measured by laser Doppler imaging. Mechanical stimulation with von Frey filaments (100 mN) induced flare responses in UV-B treated skin at 24 and 48 h, but no effect was measured in normal untreated skin. Increased mechanical stimulation (600 mN) elicited a small flare response in normal skin in an area of 1.8 cm(2) on average that was extending about 2.5 cm(2) in the UV-B irradiated sites. Thermal stimuli provoked in normal pig skin flare areas of approximately 2 cm(2) (45 degrees C, 10 s) and 4.5 cm(2) (47 degrees C, 10 s) which increased to about 3.5 cm(2) (45 degrees C) and 5.5 cm(2) (47 degrees C) following UV-B irradiation at 24 and 48 h. No significant differences of mechanically or thermally induced hypersensitivity were seen between 24 and 48 h after irradiation. We conclude that UV-B induced mechanical and heat sensitization of primary afferent nociceptors can be assessed in pig skin, providing a new human-like model of primary hyperalgesia. Sensitization of primarily mechano-insensitive (silent) nociceptors, which are underlying the flare response in humans, most probably contributes to the observation presented here.
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PMID:Nociceptor sensitization to mechanical and thermal stimuli in pig skin in vivo. 1761 Nov 31

Frey syndrome is characterized by erythema, flushing, and gustatory sweating in the preauricular area. It most commonly occurs after parotid surgery. A 21-year-old man who had a wide local excision, sentinel node biopsy, and superficial parotidectomy for a right temple superficial spreading melanoma and who subsequently developed gustatory sweating in the preauricular area is described. The presentation, diagnosis, pathogenesis, and treatment options of Frey syndrome are reviewed.
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PMID:Frey syndrome in a patient with facial melanoma: auriculotemporal syndrome presenting with gustatory sweating following wide local excision, sentinel node biopsy, and superficial parotidectomy. 2279 76

This experimental, translational, experimental pain, single-center, randomized, double-blind, single-dose, 3-treatment, 3-period cross-over proof-of-concept volunteer trial studied the efficacy of a novel TRPV1 antagonist (V116517) on capsaicin- and UV-B-induced hyperalgesia. Heat and pressure pain thresholds, von Frey stimulus-response functions, and neurogenic inflammation were assessed together with safety. Each treatment period was 4 days. The 3 single oral treatments were 300 mg V116517, 400 mg celecoxib (a COX-2 inhibitor), and placebo. The heat pain detection and tolerance thresholds were increased significantly (P < 0.0001) by V116517. Heat pain detection and tolerance thresholds showed significantly less capsaicin hyperalgesia after V116517 (P = 0.004 and P < 0.0001, respectively). Celecoxib reduced UV-B-provoked pressure pain sensitization (P = 0.01). Laser Doppler flowmetry and erythema index after UV-B were significantly (P < 0.0001) reduced by celecoxib. Stimulus-response function in capsaicin-treated areas showed significant differences between both celecoxib and placebo and between V116517 and placebo. The body temperature showed no change, and no side effects were reported for any of the treatments. The TRPV1 antagonists and the COX-2 inhibitor showed different antihyperalgesic profiles indicating different clinical targets. In addition, the preclinical profile of V116517 in rat models of UV-B and capsaicin-induced hypersensitivity was compared with the human experimental data and overall demonstrated an alignment between 2 of the 3 end points tested. The TRPV1 antagonist showed a potent antihyperalgesic action without changing the body temperature but heat analgesia may be a potential safety issue.
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PMID:A randomized, double-blind, positive-controlled, 3-way cross-over human experimental pain study of a TRPV1 antagonist (V116517) in healthy volunteers and comparison with preclinical profile. 2716 61

Causes of facial rashes and erythema in infants are many but rarely only happen during feeding times which are commonly and sometimes wrongly attributed to food allergy. There is a rare condition called Auriculotemporal nerve syndrome that is characterized by recurrent episodes of gustatory facial flushing and sweating along the cutaneous distribution of Auriculotemporal nerve: the so-called Frey syndrome. This condition is most frequently observed in adults usually after parotid surgery. It is rare in children and is mostly attributed to forceps assisted delivery. It can also be misinterpreted as food allergy. Here we report a case of an infant with Frey syndrome without any history of perinatal trauma, which was considered initially as food allergy and highlights the importance of distinguishing it from food allergy.
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PMID:Recurring Facial Erythema in an Infant. 2784 66

Freshwater stingray accidents cause an immediate, intense, and unrelieved pain which is followed by edema, erythema and necrosis formation. Treatment for stingray envenomation is based on administration of analgesic, antipyretic and anti-inflammatory drugs. Concerning pain control, it is prescribed to immerse punctured limb on hot water to alleviate pain. There are no studies demonstrating specific targets on which stingray venom acts to promote pain. Therefore, the aim of this work was to investigate some mechanisms of Potamotrygon motoro venom (PmV) that contribute to nociception induction. Evaluating spontaneous pain behavior in mice injected i.pl. with PmV, it was seen that PmV induced both neurogenic and inflammatory pain. PmV also induced hyperalgesia in both mice and rats, evaluated through electronic von Frey and rat paw pressure test, respectively. Partial inhibition of hyperalgesia was observed in mice treated with cromolyn or promethazine, which indicated that mast cell and histamine via H1 receptor participate in the inflammatory pain. To search for some targets involved in PmVinduced hyperalgesia, the participation of TRPV1, calcium channels, neurokinins, CGRP, and norepinephrine, was evaluated in rats. It was seen that PmV-induced hyperalgesia occurs with the participation of neurokinins, mainly via NK1 receptor, CGRP, and calcium influx, through both P/Q and L-type voltage-dependent calcium channels, besides TRPV1 activation. The data presented herein indicate that PmV causes hyperalgesia in rodents which is dependent on the participation of several neuroinflammatory mediators.
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PMID:Potamotrygon motoro stingray venom induces both neurogenic and inflammatory pain behavior in rodents. 2980 62


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