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)

In a retrospective study 101 patients who underwent surgery for a parotid mass were evaluated. The different diagnostic modalities (sialography, ultrasound, needle biopsy and frozen section) are described and discussed. Eighty-one tumors proved to be benign, of which 56 patients had a pleiomorphic adenoma, ten of them had a recurrent pleiomorphic adenoma, all after an enucleation, which again proved to be an inadequate operation for a parotid mass. The 20 malignant parotid tumors had a poor clinical outcome. Of the 18 patients with a malignant primary parotid tumor three showed a local recurrence and five metastatic disease within five years. The morbidity of parotid surgery is mainly due to post-operative facial nerve weakness (30%), which is mostly reversible, and the Frey syndrome (10%).
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PMID:The management of parotid tumors; a ten-year experience. 357 55

The management of patients undergoing 50 surgical procedures to the parotid gland was reviewed. The overall accuracy of fine needle aspiration cytology was 87%, false-positive and false-negative rates for malignant disease both being 4%. The sensitivity, specificity and accuracy of fine needle cytology for malignant parotid tumours was 66%, 95%, and 91%, respectively, that of benign tumours (pleomorphic adenoma or Warthin's tumour) being 88%, 83% and 87%, respectively. Sensitivity, specificity and accuracy for the remaining (principally inflammatory) parotid diseases was 100%, 95% and 96%, respectively. The predictive value of a positive test for malignant tumours, benign tumours and inflammatory conditions was 66%, 94% and 75%, respectively. The negative predictive value for these conditions was 95%, 71% and 100%, respectively. Facial nerve weakness after parotidectomy occurred in three patients (8.8%), being permanent in two cases (both malignant). Although Frey's syndrome was not recorded in any of the notes, careful follow-up revealed two cases (6%). To date there have been no local recurrences after excision of either benign or primary malignant parotid masses. One patient with squamous cell carcinoma metastatic to the parotid gland died, despite block dissection of the neck and radiotherapy. This small series with a limited follow-up suggests that diseases of the parotid gland can be managed by general surgeons with an interest in this field. Although fine needle aspiration and ultrasonic scan may be helpful, the decision to operate should be made on clinical grounds.
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PMID:An audit of surgery of the parotid gland. 748 74

Local capsular dissection as described by HANCOCK11 for the treatment of parotid pleomorphic adenomas is discussed. The results of 71 primary parotid pleomorphic adenomas are described, including a 5.6% recurrence rate. This method has the advantage that less facial nerve weakness and Frey's syndrome are seen than with superficial or complete parotidectomy. The recurrence rate appeared to be somewhat higher than with most other series.
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PMID:Local capsular dissection of parotid pleomorphic adenomas. 839 67

The effects of intrathecally delivered adenosine agonists on allodynia induced by L5/L6 spinal nerve ligation in rats with lumbar intrathecal catheters were examined. Tactile allodynia was assessed by measuring the threshold for evoking withdrawal of the lesioned hind paw with calibrated von Frey hairs. Intrathecal administration of the A1 adenosine selective agonist, N6-(2-phenylisopropyl)-adenosine R-(-)isomer (R-PIA), produced a dose-dependent (0.3-3 nmol; ED50 = 0.6 nmol) antiallodynic action and evoked a delayed motor weakness at a dosage of 30 nmol. Intrathecal administration of the A2 adenosine selective agonist, CGS 21680 {2-p-(2-carboxyethyl) phenethylamino-5'-N-ethylcarboxamido adenosine hydrochloride}, also produced a dose-dependent reduction in allodynia (2-40 nmol; ED50 = 15 nmol), but this effect was associated at 40 nmol after a short interval with prominent hind limb weakness. Intrathecal pretreatment with A1/A2 adenosine antagonists, caffeine (20 mumol) and 8-sulfophenyltheophylline (60 nmol), blocked antiallodynic actions of R-PIA (1 nmol) and CGS 21680 (40 nmol). Intrathecal pretreatment with the A1 adenosine-selective antagonist, 8-cyclopentyl-1,3-dimethylxanthine (3 nmol), blocked the antiallodynic effect of R-PIA (1 nmol), but even a dose as high as 10 nmol did not block the effect of CGS 21680 (40 nmol). The A2 adenosine-selective antagonist, 3, 7-dimethyl-1-propargylxanthine (3 nmol), prevented the antiallodynic effects of R-PIA (1 nmol) and CGS 21680 (40 nmol). Pretreatment with caffeine (20 mumol), 8-sulfophenyltheophylline (60 nmol) and 3,7-dimethyl-1-propargylxanthine (3 nmol) prevented the motor dysfunction induced by R-PIA (30 nmol) and CGS 21680 (40 nmol), but 8-cyclopentyl-1,3-dimethylxanthine (3 or 10 nmol) did not. Based on these effects, we hypothesize that the antiallodynic effects are mediated through the activation of spinal A1 adenosine receptors and motor dysfunction effects are mediated through A2 adenosine receptors.
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PMID:Pharmacology of the spinal adenosine receptor which mediates the antiallodynic action of intrathecal adenosine agonists. 866 33

The effects of the intrathecal alpha 2-agonists tizanidine and clonidine and the somatostatin analog octreotide on an experimental rat model of tactile allodynia were investigated to determine the therapeutic potential for treating chronic neuropathic pain. Allodynia was induced by ligating the rat sciatic nerve. The mechanical threshold for paw withdrawal was assessed by applying von Frey hairs to quantify analgesic actions. Mean 50% paw withdrawal thresholds were converted to the percentage of maximum possible effect (%MPE) where %MPE = (postdrug threshold-predrug threshold) divided by (15 g-predrug threshold) x 100. Dose-response curves were plotted for suppression of paw withdrawal 30 minutes after intrathecal injection of various doses of tizanidine, clonidine, and octreotide. Thresholds on the non-lesioned side were greater than 15 g. The lesioned side had baseline thresholds of less than 4.5 g. Dose-response curves were established for the antiallodynia effects of each drug. Tizanidine and clonidine at a 25-micrograms dose increased the threshold to greater than 97% of the MPE, but caused transient hindpaw weakness or sedation. No side effect was observed at a 10-micrograms dose, at which the threshold was 88-96% of MPE. Intrathecal octreotide modestly increased the threshold to only 49-67% of MPE, showing a lesser analgesic effect, although no side effect was observed at a 4-micrograms dose. The antiallodynic effects of intrathecal tizanidine and clonidine were more potent than that of octreotide.
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PMID:Effects of intrathecal nonnarcotic analgesics on chronic tactile allodynia in rats: alpha 2-agonists versus somatostatin analog. 904 98

Chronic non-specific sialadenitis of the parotid gland is an insidious inflammatory disorder which is characterised by intermittent, often painful, swelling of the gland. The disease tends to progress and may lead to the formation of a fibrous mass. The purpose of this paper is to review our experience in the surgical management of patients with chronic non-specific parotid sialadenitis. In a consecutive series of 100 patients treated for benign parotid disease, 19 were found to have chronic non-specific sialadenitis; 10 were male and 9 female. Mean age was 46 years and the mean duration of symptoms was 4.6 years. Sialography was performed in two-thirds of the patients and 17 patients were treated by superficial parotidectomy. Thirteen patients developed temporary facial nerve weakness and three Frey's syndrome. Three patients complained of temporary paraesthesia of the cheek, and two developed painful neuroma of the greater auricular nerve. Although there were two cases of infection of the parotid duct remnant, no recurrence of deep lobe sialadenitis or fistula formation was noted. Histologically, 3 lesions showed mild chronic sialadenitis, the rest had widespread involvement of the gland, and prolonged duration of symptoms was associated with extensive and severe involvement of the gland. Superficial parotidectomy has a very high success rate, with minimal long-term complications, and should be offered early in established cases, to reduce unnecessary morbidity.
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PMID:Chronic non-specific parotid sialadenitis. 992 4

The effect of botulinum toxin A (BTX) was studied on 12 patients with idiopathic craniofacial hyperhidrosis. After confirming the diagnosis by Minor's iodine starch test we first treated one-half of the forehead with an injection of 2.5-4 ng BTX (Dysport) equidistantly intracutaneously. After 4 weeks we assessed the efficacy by another Minor's iodine starch test and then treated the other half. Another 4 weeks later a standardized telephone interview was carried out. After 1-7 days the craniofacial sweating in the area injected had completely ceased in 11 patients and was mildly reduced in the remaining one. The efficacy was confirmed by repeated Minor's iodine starch tests. Mild weakness of frowning was the only side effect, lasting 1-12 weeks and completely resolving in all patients. Although sweating has not yet recurred in most patients at follow-up periods up to 27 months, one patient had a relapse 9 months after treatment. Following reports on palmar and axillary hyperhidrosis and gustatory sweating (Frey's syndrome) this is apparently the first report on the use of BTX in the treatment of idiopathic craniofacial hyperhidrosis. BTX seems a promising new treatment for localized hyperhidrosis.
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PMID:Botulinum toxin for treatment of craniofacial hyperhidrosis. 1115 18

We present a retrospective series of 23 consecutive parotidectomies, over a 10-year period (1989-1999) for 22 patients with chronic sialadenitis unresponsive to conservative measures. There were 10 male and 12 female patients. Mean age was 52 years (range 12-72), and mean duration of symptoms 4.5 years (range 8 months-30 years). All patients had preoperative sialography and 2 had computed tomography to exclude a neoplasm. A complete superficial parotidectomy with preservation of the main duct was done in all cases. Fifteen patients developed temporary facial nerve weakness postoperatively and 7 developed Frey's syndrome. There were no cases of permanent facial nerve palsy. Nineteen patients reported complete resolution of their symptoms and 3 patients had mild persisting symptoms that did not necessitate any further treatment. Histologically there was evidence of sialadenosis in one case and benign lymphoepithelial lesion in another; the others showed evidence of chronic sialadenitis of varying degrees of severity. Fifteen patients had postoperative sialograms, of which 11 showed evidence of some filling of residual parotid gland parenchyma and in 8 patients there was filling of a normal-looking accessory lobe. In this series, superficial parotidectomy with preservation of the main duct was safe and effective, with minimal long-term complications, for most patients with chronic parotid sialadenitis that was unresponsive to conservative measures and, in some patients, it allowed some preservation of function. The potential damage to the facial nerve and the cosmetic problems associated with a total or near-total parotidectomy were avoided.
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PMID:Clinical and radiological evidence to support superficial parotidectomy as the treatment of choice for chronic parotid sialadenitis: a retrospective study. 1237 2

A series of 31 consecutive parotidectomies was evaluated. FNAC could differentiate tumour from non tumour in 72.8% of cases. For actual histology, FNAC was correct in 66.6%. Frozen section was correct in differentiating between benign, malignant and inflammatory conditions in all cases. Eighty-eight percent of frozen section histology concurred with final histology. The immediate postoperative period had 13 cases of facial nerve dysfunction, but only 3 cases had residual weakness. The branch most commonly affected was the mandibular branch (92.3%). Two patients had Frey's syndrome and one had a traumatic neuroma. FNAC and CT scans improve preoperative planning, providing histological evidence and the extent of the lesion.
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PMID:An audit of parotidectomy in Singapore: a review of 31 cases. 1456 49

Intrathecal administration of serotonin type 2 (5-HT(2)) receptor agonists, alpha-methyl-5-hydroxytryptamine maleate (alpha-m-5-HT) or (+/-)-1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride (DOI), produces antiallodynic effects in a rat model of neuropathic pain. In the present study, we examined the antiallodynic effects of intrathecally administered agents which are selective for 5-HT(2C) receptors. Allodynia was produced by tight ligation of the left L5 and L6 spinal nerves, and was measured by applying von Frey filaments to the left hindpaw. Administration of the 5-HT(2C) receptor agonist, 6-chloro-2-(1-piperazinyl)-pyrazine (MK212; 3-100 microg), 1-(m-chlorophenyl)-piperazine (mCPP; 30-300 microg), or 1-(m-trifluoromethylphenyl)-piperazine (TFMPP; 30-300 microg), produced antiallodynic effects in a dose-dependent manner with no associated motor weakness. The ED(50) values of MK212, mCPP, and TFMPP were 39.2, 119.9, and 191.9 microg, respectively. Intrathecal pretreatment with the selective 5-HT(2C) receptor antagonist RS-102221 (30 microg) diminished the effects of the highest doses of 5-HT(2C) receptor agonists. The preferential 5-HT(2A) receptor antagonist ketanserin (30 microg) did not reverse the effects. In contrast to 5-HT(2C) receptor agonists, the antiallodynic effects of intrathecally administered alpha-m-5-HT (30 microg) and DOI (100 microg) were reversed by ketanserin, but not by RS-102221. These results indicate that 5-HT(2C) receptors have a role in spinal inhibition of neuropathic pain, and the effects produced by intrathecal administration of 5-HT(2C) receptor agonists are mediated by a mechanism different from that of alpha-m-5-HT or DOI, which seem to produce their effects through 5-HT(2A) receptors.
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PMID:Antiallodynic effects of intrathecally administered 5-HT(2C) receptor agonists in rats with nerve injury. 1510 20


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