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

Percutaneous radiofrequency neurotomy has been used in the treatment of pain from the cervical zygapophysial joints, but the results have been modest and not compelling. Several factors might account for its apparent poor success rate, including inadequate patient selection, inaccurate surgical anatomy, and technical errors. In an effort to overcome these confounders, we used comparative local anesthetic blocks to preoperatively, definitively diagnose cervical zygapophysial joint pain and developed an amended operative technique based on formal anatomical studies. An audit was conducted of our experience with 19 patients to determine whether there was sufficient merit in the amended procedure to justify a randomized, double-blind, controlled trial. The duration of complete pain relief was the principal outcome measure. Side effects and complications were also monitored. Of the 10 patients who underwent third occipital neurotomy for the treatment of C2-C3 zygapophysial joint pain, only 4 obtained long-lasting relief. The other six patients reported an early return of their pain and constituted technical failures; the third occipital nerve was inadequately coagulated and recovered in the immediate postoperative period. Of the 10 patients who underwent lower cervical medial branch neurotomy, 7 obtained complete pain relief for clinically useful periods and were able to resume their activities of daily living and employment. After procedures at all levels, a brief period of postoperative pain was experienced by the patients and ataxia was a side effect of third occipital neurotomy. There were no cases of postoperative infection or anesthesia dolorosa. Given the high technical failure rate of third occipital neurotomy, we recommend that this procedure be abandoned until the technical problems can be overcome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Percutaneous radiofrequency neurotomy in the treatment of cervical zygapophysial joint pain: a caution. 759 4

An unusual case of a Yorkshire terrier with a dermoid sinus associated with multiple spinal/costal malformations is described. The dog presented with ataxia and pain in the dorsal thoracic region. Diagnostic characterisation of the lesions was obtained with radiography, myelography and computed tomography. After surgical removal of the sinus, the dog showed marked clinical improvement over a two-year period.
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PMID:Dermoid sinus and spinal malformations in a Yorkshire terrier: diagnosis and follow-up. 760 60

In a double blind study, eight horses were treated intravenously at seven-day intervals with detomidine at doses of 10, 20 and 40 micrograms/kg, or with romifidine at doses of 40, 80 and 120 micrograms/kg, or with a placebo solution. Their sedative and analgesic effects were evaluated by objective measurements and by a clinician at 15-minute intervals for three hours and the horses' instability in stocks, locomotor ataxia and heart rate were recorded simultaneously. The administration of both drugs at all doses resulted in sedation. The sedation achieved with romifidine was significantly shallower and shorter-lived than with detomidine at the recommended doses (P < 0.05). The results obtained with the highest dose of romifidine were in some cases significantly inferior and shorter-lived than those obtained with the medium dose (P < 0.05). Detomidine at the 10 micrograms/kg dose was similar in its effects to the two highest doses of romifidine. At all doses detomidine had analgesic properties against the effects of electrical pain stimulation at the withers, the coronary bands on the front and hind legs, and in the perianal region, which were dose-dependent in depth and duration, whereas romifidine was devoid of any analgesic effect. Instability and ataxia were more pronounced with detomidine than with romifidine but the effects were only slight to moderate and not regarded as a hindrance to procedures for which sedation is needed. Bradycardia was evident with both drugs at all doses; its severity and duration was related to the sedative properties of the drugs and was dose related. No other side effects were observed.
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PMID:Sedative and analgesic effects of detomidine and romifidine in horses. 760 8

This study compared the antinociceptive properties of systemic administration of selective, non-peptidergic antagonists at neurokinin (NK1 and NK2) receptors to those of other classes of antinociceptive agent. (All doses are in mg/kg.) In mice, the NK1 antagonist, CP 99,994, preferentially (inhibitory dose50 (ID50) = 4.4) inhibited the late phase (LP) as compared to the early phase (EP) (16.1) of formalin-induced licking (FIL). A high dose (17.6) elicited ataxia in the rotarod test. Acetic acid-induced writhing was reduced at intermediate doses (10.0) whereas the tail-flick (TF) response to thermal and mechanical stimuli was inhibited only at high doses (22.7 and 17.7, respectively). Modulation of stimulus intensity did not modify the influence of CP 99,994 upon the response to heat. A similar pattern of data was acquired with RP 67,580, although this NK1 antagonist more potently inhibited writhing (2.8). In contrast, RP 68,651, the inactive isomer of RP 67,580, neither reduced the LP of FIL nor modified writhing indicating that these actions of RP 67,580 were stereospecific. Three further NK1 antagonists, SR 140,333, WIN 51,708 and WIN 62,577, likewise inhibited the LP of FIL and failed to modify the TF response at non-ataxic doses. Further, SR 140,333 (0.5) and WIN 51,708 (1.4) were potent ligands in the writhing procedure. The NK2 antagonist, SR 48,966, mimicked NK1 antagonists in preferentially inhibiting the LP (7.7) as compared to the EP (26.9) of FIL. Further, only at doses higher than those evoking ataxia (20.9) did SR 48,968 modify the TF response (36.5 and 32.0 for heat and pressure, respectively). However, it differed to NK1 antagonists in being inactive in the writhing test (> 40.0). In comparison to these NK1 and NK2 antagonists, the mu-opioid agonists (morphine and fentanyl) and kappa-opioid agonists (enadoline and U 69,593) equipotently inhibited all nociceptive responses at doses not provoking ataxia. While the glycine B receptor partial agonist, (+)-HA 966, selectively blocked the LP of FIL and did not evoke ataxia, the NMDA receptor channel blocker, (+)-MK 801, elicited antinociception only at doses close to those provoking ataxia. Finally, the NSAIDs, indomethacin and ibuprofen, the BK2 antagonist, Hoe 140 and the nitric oxide synthase (NOS) inhibitors, L-NAME and 7 nitroindazole, inhibited the LP (but not the EP) of FIL and (except for L-NAME) also reduced writhing: in contrast, they did not evoke ataxia and were inactive in the TF procedures.(ABSTRACT TRUNCATED AT 400 WORDS)
Pain 1995 May
PMID:Antinociceptive profiles of non-peptidergic neurokinin1 and neurokinin2 receptor antagonists: a comparison to other classes of antinociceptive agent. 765 44

Infectious arthritis caused by Candida spp was diagnosed in 2 horses. Source of infection was by direct inoculation in 1 horse and was presumed to be hematogenous in the other horse. On microbial culturing of synovial fluid and synovial membrane specimens, the organisms were isolated in both horses. In both horses, the joint infections resolved after i.v. administration of amphotericin B and joint drainage; however, 1 horse was eventually euthanatized because of signs of cervical pain and progressively worsening ataxia. Fungal organisms isolated on microbial culturing of joint specimens in horses, although uncommon, should not be dismissed as contaminants, particularly if the same organism is recovered from more than 1 specimen. Successful resolution of fungal arthritis may be achieved with appropriate antifungal treatment, combined with joint drainage.
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PMID:Amphotericin B treatment of Candida arthritis in two horses. 775 Dec 43

A 12-year-old Standard-bred mare and a 21-year-old Quarter Horse gelding were treated for signs of abdominal pain and sweating. The mare also had muscle fasciculations, azotemia, and ataxia, and was euthanatized after signs of pain became refractory to analgesics. The gelding died when ventricular tachycardia developed during general anesthesia for exploratory celiotomy. Adrenal pheochromocytomas (bilateral in the mare), associated with retroperitoneal and intra-abdominal hemorrhage, were found on postmortem examination. Pheochromocytoma should be considered in older horses with signs of abdominal pain and sweating. Further consideration of pheochromocytoma should be afforded in older horses in which muscle fasciculations, ataxia, azotemia, and intraperitoneal hemorrhage are recognized. Identification, by per rectum palpation, of retroperitoneal swelling in the dorsal aspect of the abdomen also should alert the diagnostician to the possibility of a ruptured pheochromocytoma.
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PMID:Pheochromocytoma in two horses. 775 37

Sensory neuropathies are rare but unique peripheral neuropathies that involve only the peripheral sensory system. The diagnosis is made by both clinical and electrophysiological findings. Sensory neuropathies occur predominantly in women. The symptoms begin in the arms more often than the legs and occur asymmetrically. Pain and severe sensory ataxia in varying degrees are the main presenting symptoms. Definable causes of sensory neuropathies are hereditary, paraneoplastic, immunological, metabolic, infectious, and drug-induced disorders. In our experience, however, nearly half of all sensory neuropathies have been idiopathic. The clinical course of these sensory neuropathies is variable. The symptoms clearly worsened in 25% of our patients, but in the rest remained unchanged for many years, resulting in a poor functional prognosis because of intractable pain and ataxia. Most sensory neuropathies are resistant to any treatment. We review the electrophysiological features, laboratory findings, and nerve biopsy results in our patients and discuss in detail the potential underlying diseases included in the differential diagnosis.
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PMID:Causes and diagnosis of sensory neuropathies: a review. 786 Jul 19

We report a 65-year-old woman with progressive multiple cranial neuropathy. She had been suffered from bronchial asthma since 1979 for which prednisolone had been prescribed. She noted an onset of pain around her nose in October, 1989, which extended into the periorbital regions bilaterally. In February, 1990, she was treated with stellate ganglion block and trigeminal nerve block; these treatments partially alleviated her pain. In May of 1991, she noted a difficulty in swallowing solid foods. In November of the same year, she developed right facial paresis; two weeks later, she noted numbness in her left face, and was hospitalized to our service on December 16, 1991. On admission, she was afebrile and general physical examination was unremarkable except for piping rales in her both lung fields. On neurologic examination, she was alert and oriented to all spheres; higher cerebral functions were intact. In the cranial nerves, her olfactory sense was lost bilaterally; her vision was markedly diminished bilaterally only to recognize hand movements; the optic fundi appeared normal; the pupils were isocoric and reacted to light promptly. The extraocular muscles were moderately weak to most of the directions more on the left; no nystagmus was present. Facial sensation was diminished bilaterally; the jaw deviated to right; right facial paresis of peripheral type was present; her hearing was diminished bilaterally more on the right. The movement of the soft palate was diminished on the right side; dysphagia was present; her voice was horse; the gag reflex was diminished. The sternocleidomastoid muscle was weak bilaterally; the tongue appeared normal. Examination of gait was differed because of headache, however, no apparent motor weakness was present. No ataxia or involuntary movement was noted. Deep reflexes were normally elicited and symmetric. Plantar response was flexor. Sensation in the extremities was intact. Kernig's sign was positive at 70 degree leg extension; eyeball tenderness was also present bilaterally, however, no nuchal stiffness was noted. Following abnormalities were present in the laboratory examination: WBC 11,400/microliters, ESR 50 mm/hr, CRP 6.1 mg/dl. The lumbar CSF was under a normal pressure containing 29 WBC/microliters (neutrophils 7, lymphocytes 20, others 2), 67 mg/dl of protein, and 53 mg/dl of sugar; cultures for acid-fast bacilli as well as for other bacteria were negative; no malignant cells were found. A cranial CT scan revealed an isodensity mass in the orbit and ill-defined low density areas in the white matters of the frontal lobes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 65-year-old woman with headache, facial pain, and progressive multiple cranial neuropathy]. 787 85

In this study, we examined whether activation of 5-HT1A receptors elicits antinociception in response to acute noxious chemical, thermal and mechanical stimuli in mice. In the writhing test, both agonists (e.g., 8-OH-DPAT, S 14671 and WY 50,324) and partial agonists (e.g., buspirone and gepirone) elicited a pronounced antinociception. However, antagonists (e.g., (-)-alprenolol and WAY 100,135) also induced antinociception and, at lower (inactive) doses, failed to modify the action of agonists. In addition, the separation between doses required for induction of antinociception as compared to those required for induction of ataxia (in the rotarod test) was variable and low for both agonists (median: 1.9) and partial agonists (median: 1.3), although it was somewhat greater for antagonists (> or = 3.3). In the hot-plate test, only certain agonists (e.g., 8-OH-DPAT) and partial agonists (e.g., gepirone) elicited antinociception and their actions were not attenuated by 5-HT1A antagonists which, themselves, were inactive in this paradigm. The 5-HT1C/2 antagonist, ritanserin, the 5-HT3 antagonist, ondansetron, the dopamine D2 receptor antagonist, raclopride, and the alpha 1-adrenoceptor antagonist, prazosin, were also ineffective in modifying the antinociception evoked by 5-HT1A agonists and partial agonists in the hot-plate test. In contrast, their actions were strongly attenuated by the alpha 2-adrenoceptor antagonist, idazoxan. In the tail-flick tests to noxious heat and noxious pressure, 5-HT1A receptor agonists, partial agonists and antagonists generally failed to induce antinociception. Moreover, modulation of stimulus intensity (from very weak to very intense) did not reveal any influence upon the latency to respond. In conclusion, in the writhing test, the data provide no evidence for a specific antinociceptive effect of the activation of 5-HT1A receptors. Further, in the hot-plate test, for those 5-HT1A agonists and partial agonists which induce antinociception, alpha 2-adrenoceptors rather than 5-HT1A receptors are implicated in their actions. Finally, in reflexive tests, irrespective of stimulus quality or intensity, 5-HT1A agonists and partial agonists do not mediate antinociception. These data suggest that the activation of 5-HT1A receptors does not, under these conditions of acute noxious stimulation, elicit antinociception.
Pain 1994 Jul
PMID:Serotonin and pain: evidence that activation of 5-HT1A receptors does not elicit antinociception against noxious thermal, mechanical and chemical stimuli in mice. 797 Aug 39

The tachykinin receptor antagonists (3aR,7aR)-7,7-diphenyl-2(1-imino-2-(2-methoxyphenyl/ethyl)++ +perhydroisoindole) (RP 67580) and (+)-(2S-3S)-3-(2-methoxybenzylamino)-2-phenylpiperidine (CP-99,994), which act selectively at neurokinin (NK)1 receptors, inhibited the early phase of formalin-induced pain in mice. Although (+)-(1-hydroxy-3-aminopyrrolidine-2-one) ((+)-HA966), a partial agonist at glycine B receptors, was inactive alone, it potentiated the actions of RP 67580 (but not its inactive stereoisomer, RP68651) and CP-99,994. In its presence, the dose-response curve for RP 67580 was dose-dependently shifted to the left. In contrast, (+)-HA966 did not modify the induction of ataxia by RP 67580 and CP-99,994. These data suggest that co-administration of partial agonists at glycine B receptors may improve the antinociceptive potency and 'therapeutic window' of tachykinin NK1 receptor antagonists.
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PMID:The glycine B receptor partial agonist, (+)-HA966, enhances induction of antinociception by RP 67580 and CP-99,994. 801 34


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