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

The purpose of this investigation was to evaluate calcium hydroxide and potassium nitrate individually as densensitizing agents for hypersensitive root surfaces. The apparatus used in the experiment to measure hypersensitivity was (a) a thermo-electric stimulating device to measure hot and cold stimulation quantitatively and (b) a mechanical stimulating device to measure scratch stimulation quantitatively. The conclusions drawn from the study were: 1. Calcium hydroxide was more consistently effective in decreasing sensitivity then was potassium nitrate or the control. 2. Calcium hydroxide as compared to the control was statistically (99% level of significance) more effective in reducing sensitivity to mechanical, hot and cold stimulation immediately and at the conclusion of the experiment (3 months). 3. It appears that calcium hydroxide could be used as a desensitizing agent initially following periodontal surgery to reduce pain from hypersensitive roots in order that proper oral hygiene could be reestablished.
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PMID:Calcium hydroxide and potassium nitrate as desensitizing agents for hypersensitive root surfaces. 26 50

The effects of intrathecally administered normal saline have been studied in patients undergoing graduated spinal anesthesia. The injection of 5 or 10 ml volumes resulted in segmental hypesthesia to pin-scratch and cold stimuli extending from the lower thoracic to the sacral dermatomes. There was also partial sympathetic block evidenced by a diminished psychogalvanic skin reflex. The sites and possible mechanisms of action of saline are discussed; its use as placebo in graduated spinal anesthesia is questioned. It is concluded that normal saline acts as a weak local anesthetic when injected intrathecally.
Pain 1978 Jun
PMID:Local anesthetic effect of intrathecal normal saline. 58 Sep 57

An interesting behavioral syndrome results in animals from the same or similar types of lesions that lead to deafferentation pain in humans; many neurectomized animals begin to scratch, bite, or self-mutilate their denervated limb, a phenomenon termed autotomy. The proposition that this behavior in animals is a response to the chronic pain of peripheral nerve injury has met with considerable controversy. If this issue were resolved, then a better understanding of the neurophysiology of autotomy might help elucidate the mechanisms of the human conditions. To determine the association between deafferentation and the autotomy behavior, we developed a pharmacologically induced functional deafferentation preparation using chronic perineural lidocaine infusion of the sciatic nerve. This 'chronic lidocaine' model's behavior was compared with that of the neurectomy model. While autotomy was noted in 80% of the latter group, no animal undergoing a chronic perineural infusion of lidocaine autotomized. We thus conclude that autotomy is not a response to non-painful sensory deafferentation, but rather that this behavior is a response to pain. We also studied the development of autotomy in a variety of other focal denervation preparations. On the basis of these data, we conclude that autotomy is not due to loss of sensory input on a functional basis nor to an action potential-mediated process. Rather, nerve damage which coincidentally involves sensory loss is necessary and sufficient for the development of this behavior. We suggest that interruption of a humoral feedback process homeostatically operating within the first order sensory neuron with its effect exerted post-synaptically leads to autotomy. The evidence supports the existence of a loss of a transportable, humoral autotomy inhibitory factor.
Pain 1991 May
PMID:Studies in autotomy: its pathophysiology and usefulness as a model of chronic pain. 159 77

Substance P (SP) injected into intraspinal (i.s.) spaces caused mice to vigorously scratch and bite their skins in an apparent reaction to a perceived cutaneous sensation. The scratching behavior was similar to the reciprocal hindlimb-scratching syndrome (RHS) described for intracranial (i.c.) SP injections. Radiotracer experiments, as well as potency and latency measurements, demonstrated that SP-induced scratching, whether induced by the i.c. or i.s. route, was due to SP receptor stimulation in the cervicothoracic cord. Similarly, biting was due to SP stimulation of the lumbosacral spinal cord. Mice coated with capsaicin, an irritant chemical, scratched and bit the coated areas in a manner similar to animals injected with i.s. SP. Standard analgesics depressed this scratching behavior elicited by topical capsaicin. Non-analgesic drugs, with the exception of amphetamine, did not affect capsaicin-induced pain. It is concluded that i.s. SP induces a painful sensory experience. Some piperazinone derivatives of substance P's C-terminal hexapeptide are shown to specifically antagonize the scratching induced by i.s. SP with little or no effect on motor behavior. These antagonists depressed scratching elicited by topical capsaicin and were analgesic on the hot-plate test. It is concluded that SP is a natural neurotransmitter for pain and that antagonism of endogenous SP systems causes analgesia.
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PMID:Analgesic activities of spinal cord substance P antagonists implicate substance P as a neurotransmitter of pain sensation. 242 37

Behavioural experiments were undertaken to investigate the possible functional significance of opiate receptors located at peripheral endings of primary sensory neurons. The responses of animals to noxious chemical stimuli applied to the ear (ear scratch test) were measured after local pretreatment of these areas with etorphine. Local etorphine administration produced a low dose hyperalgesia and high dose analgesia. Local as opposed to systemic effects of etorphine were inferred from the absence of effects on the contralateral vehicle-treated ear. Systemic administration of naloxone or of a quaternary opiate antagonist (MRZ 2663-BR), which is relatively ineffective in crossing the blood-brain barrier, blocked the low dose hyperalgesic effect of etorphine in the ear scratch test. As a test for the putative hyperalgesic function of peripheral sensory nerve opiate receptors, neonatal rats were treated with capsaicin (50 mg/kg s.c.) to destroy specifically the subpopulation of primary sensory neurons on which the peripheral opiate receptors are thought to be located, without markedly altering pain thresholds. As adults, these neonatally treated rats showed potentiated analgesic responses to systemic morphine, as would be predicted by central 'analgesic' opiate receptors now acting without opposition from peripheral 'hyperalgesic' opiate receptors. These findings suggest that opiate receptors on primary sensory neurons may mediate hyperalgesic functions and that endogenous opioids might normally play a role in the peripheral induction of irritation, inflammation and pain reactions.
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PMID:Hyperalgesia mediated by peripheral opiate receptors in the rat. 300 5

The effect of 900 mg aspirin on persistent itch from chronic dermatoses other than urticaria (eight patients) and other causes (five patients) was measured subjectively using a 10 cm line and objectively as nocturnal scratch using limb meters. There was no change in itch or scratch and it is concluded that aspirin neither affects itch centrally by a pain related mechanism nor affects itch physiologically by cyclo-oxygenase inhibition in the skin.
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PMID:Effect of aspirin on pruritus. 309 11

Twenty four knee prosthesis femoral and tibial components of the 'load angle inlay' design, removed for loosening and pain were examined in the scanning electron microscope, light microscope, and volume loss measured using a simple gauge. In all cases the deformation of the plastic (femoral) component was seen both by increase in the curvature of the inner surface and wear usually on the edge of the bearing surface. Two pairs were subluxed prior to removal from the patient and these not only produced gross deformation of the plastic components, but maximum volume loss of the components examined; the knees exhibited gross instability. The tibial (metal) components stood up remarkably well in all cases, both in wear and deformation which was minimal but sinking and rotation of the plateau did occur for the most part on the external side. Scratch patterns seen on the tibial components were clearly seen and gave an indication of the direction and amount of sliding between the components; in some cases these scratch lines were in more than one direction probably indicative of loosening and instability. Short deep scratches were usually indicative of bone and/or cement particles embedded in the plastic components, abrasive wear was seen on 92 per cent of the femoral components, and cracks were seen on two-thirds, usually parallel and close to the sides.
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PMID:Failure of one design of surface replacement knee arthroplasty due to loosening deformation and wear of the plastic femoral component. 661 74

Previous reports of extensive lipid accumulation within neurons of the autonomic nervous system in Fabry disease suggest an anatomicopathologic basis for the peculiar pain, diminished sweating, and gastrointestinal symptoms experienced in this disorder. To further assess autonomic function in Fabry disease, noninvasive clinical tests were performed on 10 patients. Diminished sweating was found in each; the loss was approximately uniform proximally and distally, suggesting sweat gland dysfunction rather than autonomic neuropathy. Impaired pupillary constriction with pilocarpine, and reduced saliva and tear formation were found in half the patients. Disordered intestinal mobility was demonstrated in the oldest patients. In all cases, the cutaneous flare response to scratch and intradermal histamine was diminished, and pruritus was not experienced. Signs of autonomic dysfunction are present in Fabry disease and correlate with the known lipid deposition in autonomic neurons.
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PMID:Fabry disease: impaired autonomic function. 680 89

The studies described herein characterize animal behavioral models for conjunctival and cutaneous itch. Histamine was used as the reference stimulus for model development because it is firmly established as a pruritogen in both conjunctiva and skin. Itching evokes the desire to scratch in human subjects, so hind limb scratching at the afflicted area was used to identify pruritogenic stimuli. Under optimized environmental conditions, hind limb scratching behavior yielded substantial and highly reproducible responses. The conjunctival itch-scratch response was delineated from pain and foreign body sensations by using appropriate stimuli. Examination of a large and diverse variety of autocoids revealed that only histamine, platelet-activating factor (PAF) and arachidonic acid and its cyclooxygenase metabolite prostaglandin E2 possessed meaningful pruritogenic activity. PAF-induced ocular pruritus did not involve histamine release, according to studies with appropriate antagonists. Thus PAF-induced ocular pruritus was unaffected by the histamine H1-receptor antagonist pyrilamine but was substantially attenuated by the PAF antagonists WEB 2086 and CV-6209 and was virtually abolished by E-6123. Similar itch-scratch behaviors were quantified in hairless guinea pig skin following the application of cowhage or the iontophoretic administration of histamine and PAF. Findings from these newly developed itching models suggest that PAF could be an important mediator of the pruritic sensation by activating a population of nerve endings responsible for encoding the itch sensation.
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PMID:Characterization of a behavioral model for peripherally evoked itch suggests platelet-activating factor as a potent pruritogen. 785 91

The therapeutic utility of cyclooxygenase (CO) inhibitors, such as ketorolac, in reducing the inflammatory events associated with allergic conjunctivitis is not unexpected since prostanoids (PG) elicit conjunctival redness (PGD2, PGE2, PGF2 alpha), edema (PGD2, TxA2), eosinophil infiltration (PGD2, PGJ2) and mucous cell discharge (PGD2, PGJ2, TxA2). Recently, topically administered ketorolac has also been reported to alleviate the itching associated with allergic conjunctivitis. This was viewed as intriguing since CO inhibitors are not regarded as useful for treating itching dermatoses and PGs do not elicit itching when applied to the skin. In order to investigate the antipruritic activity of ketorolac, we developed a model for reproducibly measuring ocular surface itch responses. The model involves itch-scratch responses to pruritogens applied locally to the ocular surface. Painful and foreign body stimuli do not produce an itch-scratch response. Unlike reported skin studies, PGE2 was a potent itch-producing substances in the conjunctiva. PGD2 was weakly pruritogenic but PGF2 alpha and the TxA2-mimetic U-46619 were inactive. The PG precursor arachidonic acid was also a potent pruritogen and its effects were inhibited by ketorolac pretreatment. Ketorolac also dose-dependently inhibited the itching associated with experimental allergic conjunctivitis. It appears that PGs are potent itch-producing substances in the conjunctiva and the anti-itch efficacy of ketorolac in allergic conjunctivitis appears to involve inhibition of conjunctival PG biosynthesis from arachidonic acid.
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PMID:The pruritogenic and inflammatory effects of prostanoids in the conjunctiva. 859 Feb 66


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