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Clinical pain

Ellingsen T, Buus A, Moller BK, Stengaard-Pedersen K. In vitro migration of mononuclear cells towards synovial fluid and plasma from rheumatoid arthritis patients correlates to RANTES synovial fluid levels and to clinical pain parameters. Scand J Rheumatol 2000 29(4) 216-221. [Pg.193]

Endogenous opioids and opioid receptors inhibit pain responses 932 CLINICAL PAIN 932... [Pg.927]

Clinical pain is characterized by the presence of spontaneous pain or hypersensitivity to pain-provoking stimuli 932... [Pg.927]

Clinical pain is characterized by the presence of spontaneous pain or hypersensitivity to pain-provoking stimuli. Hypersensitivity includes pain produced by low-intensity stimuli that normally only elicit an innocuous sensation (allodynia), or an exaggerated response to a noxious stimulus (hyperalgesia). There are two distinct forms of clinical pain, the pain that occurs after tissue injury or inflammatory diseases (inflammatory pain) and the pain associated with a lesion or disease of the nervous system (neuropathic pain). Although the mechanisms responsible for the initiation and maintenance of these pains differ, they are both characterized by heightened... [Pg.932]

Watkins, L. R. and Maier, S. F. Glia a novel drug discovery target for clinical pain. Nat. Rev. DrugDiscov. 2 973-985,2003. [Pg.937]

Kayser, V., Besson, J. M., Guilbaud, G. Evidence for a noradrenergic component in the antinociceptive effect of the analgesic agent tramadol in an animal model of clinical pain, the arthritic rat, Eur. J. Pharmacol. 1992, 224, 83-88. [Pg.282]

Compounds with moderate p-affinities are very potent in a variety of pain models in mice and rats. In addition to antinociceptive efficacy in models of acute pain (tail flick, writhing) these compounds inhibit acute and persistent inflammatory pain (Randall Selitto, formalin test). Furthermore, they show strong inhibition of acute visceral pain (colorectal distension) and of tactile and cold allodynia in models of neuropathic pain (spinal nerve ligation (Chung), chronic constriction injury (Bennett)). The data suggest these compounds to be potential candidates for the management of clinical pain indications. Somatic and visceral pain with and without inflammatory conditions as well as neuropathic pain might be addressed with this approach. [Pg.361]

Clinical investigations to date have focussed on effects of adenosine in experimentally-induced pain as well as clinical pain states. These studies have shown that adenosine administration reduces pain primarily in situations that involve enhanced excitability and nociceptive transmission in the CNS. Since centrally-mediated enhanced excitability is considered to be an important factor in chronic pain conditions, adenosine-induced pain relief in patients with neuropathic pain suggests that adenosine and adenosine analogs are of special importance for future research. [Pg.484]

Pain has been a human problem since the beginning of time but the last decade has seen an explosion of information about the transmitters, receptors and channels involved in the transmission and modulation of noxious messages generated in peripheral tissues. This has lead to the identification of a number of potential new targets for analgesic therapy. We now have more experimental drugs available, which allows us to study the roles of transmitters and receptors in physiological events. There are now numerous animal models for clinical pain states such as inflammation and neuropathies, and these models have shown that several transmitter systems which have minor actions in acute pains can play important roles in more persistent pains. [Pg.609]

This ability to test drugs in contexts other than acute pain models has arisen from good communication between bench scientists, clinicians and industry. Until recently investigations into the mechanisms of clinical pain syndromes all relied on animal studies using acute stimuli. The symptoms of pain arising from nerve injury, neuropathic pain, such as allodynia, spontaneous pain, hyperalgesia, sensory deficits and in some cases a sympathetic component are simply not seen in the older acute models. There are now several animal models which mimic peripheral and central neuropathic states. The same is true for inflammation. [Pg.609]

One additional point of consideration when interpreting the above studies is to note that in pre-clinical models, retigabine and to a lesser extent ICA-27243 also affect locomotor activity. However, in general there is a separation between the MED for efficacy in pain models and the lowest dose which shows locomotor side-effects, supporting the hypothesis that Kv7 agonists are effective in pre-clinical models of pain independent of inhibiting motor function. These results in conjunction with those reported in studies on sensory neurons indicate that Kv7 activation inhibits nociceptive neuronal firing and behavioral endpoints in pre-clinical pain models. [Pg.37]

All clinical pain studies are using a visual-analogue scale. We are so incredibly bad at treating pain. The terribly sad situation with pain is illustrated by the following. To enroll in a study for a new pain drug, a patient has to have pain graded by himself or herself at level 4 or higher on a scale of 1 to 10, where zero is no pain and 10 is unbearable pain. [Pg.38]

Results from the rat paw lick model seem to correlate well with clinical painfulness experience and the muscle irritation test with certain antibiotic formula-tions. However, because rat paw lick results from a wide variety of drug formulations have not been published, these correlations may hold only for a certain subset of painful formulations. A formulation could cause pain but yet not cause muscle damage upon intramuscular injection. Additionally, some formulations are painful upon intravenous injection. [Pg.1410]

Keywords Endo cannabinoid Spinal cord Periaqueductal gray Supraspinal Peripheral CBI CB2 THC Hyperalgesia Clinical pain... [Pg.510]

The varying results obtained with tryptophan in different types of clinical pain probably reflect the fact that pain includes many physiological phenomena, which act through many different mechanisms. Tryptophan has been shown to have a therapeutic effect most frequently with chronic pain associated with deafferentation or neural damage. [Pg.191]


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See also in sourсe #XX -- [ Pg.932 ]




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