Common animal models for spasticity and pain

Abstract

Abstract-Animal models of spasticity and pain have allowed for the elucidation of possible mechanisms and the evaluation of potential therapeutic interventions for these serious clinical problems. Each model mirrors the clinical appearance of many features of the syndrome, but few reproduce the myriad patient reports of either intensity or relevant contributing factors, especially in models of chronic neuropathic pain. Often these models have been used to predict the potency and efficacy of pharmacologic agents that work in human pain states. Pain models have relied on measurements of the shifts in behavioral hypersensitivity to tactile and thermal stimuli, tests that are not used quantitatively in human patients. Even with the multiple peripheral and central models of spasticity and pain used in animals, only a few actually test human conditions: namely, diabetic neuropathy, chemotherapy, and immunotherapy for tumors. However, all these models have allowed for the comparison of certain behavioral, cellular, biochemical, and molecular mechanisms with human patient populations. Here we review the few extant models of spasticity, nerve injury, and central injury models of pain, and describe their features and use.

Buprederm™, a New Transdermal Delivery System of Buprenorphine: Pharmacokinetic, Efficacy and Skin Irritancy Studies

“…Therefore, antinociceptive activity of Bupredermi was evaluated using chemical and thermal models of acute pain, acetic acid-induced writhing test and the tail flick test. Such thermal tail-flick tests are most widely and reliably used for revealing the potency of opioid analgesics, useful for predicting analgesic effects in humans (69)(70).…”

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“…The writhing test can predict effective analgesic doses for agents that can be used in humans (Dubinsky et al, 1987;Eaton, 2003). The mediators involved in the genesis of the nociception observed in the writhing test are the eicosanoids and sympathomimetic amines, the release of which is preceded by the release of the nociceptive cytokines TNF-a, IL-1b, and IL-8 (Duarte et al, 1988;Ribeiro et al, 2000a;Thomazzi et al, 1997).…”

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“…Because DiPOA has a higher selectivity for mu over kappa, as compared with morphine, this may contribute to the lack of efficacy in the PSN model. Secondly, both the CCI and SNL models involve a more substantial inflammatory component as compared with the PSN model (Lindenlaub and Sommer, 2000;Eaton, 2003), which may account for the efficacy of peripherally applied opioid agonists observed using these models. Finally, the time point in these studies was 14 days postsurgery or less; at this time, there may be a significant inflammatory component due to the surgery.…”