Articles: neuropathic-pain.
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Phosphodiesterase 2A (PDE2A) is an evolutionarily conserved enzyme that catalyzes the degradation of the cyclic nucleotides, cyclic adenosine monophosphate, and/or cyclic guanosine monophosphate. Recent studies reported the expression of PDE2A in the dorsal horn of the spinal cord, pointing to a potential contribution to the processing of pain. However, the functions of PDE2A in spinal pain processing in vivo remained elusive. ⋯ Our findings indicate that PDE2A contributes to the processing of inflammatory pain in the spinal cord.
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Anesthesia and analgesia · Aug 2014
Comparative StudyNovel Use of Perineural Pregabalin Infusion for Analgesia in a Rat Neuropathic Pain Model.
The anticonvulsant drugs pregabalin and gabapentin are often used systemically to treat some forms of chronic neuropathic pain. However, many patients report side effects serious enough to cause discontinuation of the drug. Here we present evidence that pregabalin may block neuropathic pain when applied to the site of nerve injury in a rat neuropathic pain model. ⋯ Perineural pregabalin administration produced superior analgesia compared with that of systemic pregabalin in this neuropathic pain model. Perineural pregabalin treatment may provide a useful alternative to systemic pregabalin treatment for neuropathic pain.
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Practice Guideline Comparative Study
The appropriate use of neurostimulation of the spinal cord and peripheral nervous system for the treatment of chronic pain and ischemic diseases: the Neuromodulation Appropriateness Consensus Committee.
The Neuromodulation Appropriateness Consensus Committee (NACC) of the International Neuromodulation Society (INS) evaluated evidence regarding the safety and efficacy of neurostimulation to treat chronic pain, chronic critical limb ischemia, and refractory angina and recommended appropriate clinical applications. ⋯ Appropriate neurostimulation is safe and effective in some chronic pain conditions. Technological refinements and clinical evidence will continue to expand its use. The NACC seeks to facilitate the efficacy and safety of neurostimulation.
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Experimental neurology · Aug 2014
ReviewNeuroinflammatory contributions to pain after SCI: roles for central glial mechanisms and nociceptor-mediated host defense.
Neuropathic pain after spinal cord injury (SCI) is common, often intractable, and can be severely debilitating. A number of mechanisms have been proposed for this pain, which are discussed briefly, along with methods for revealing SCI pain in animal models, such as the recently applied conditioned place preference test. During the last decade, studies of animal models have shown that both central neuroinflammation and behavioral hypersensitivity (indirect reflex measures of pain) persist chronically after SCI. ⋯ Nociceptor activity is known to drive central neuroinflammation in peripheral injury models, and nociceptors appear to be an integral component of host defense. Thus, emerging results suggest that spinal and systemic effects of SCI can activate nociceptor-mediated host defense responses that interact via neuroinflammatory signaling with complex central consequences of SCI to drive chronic pain. This broader view of SCI-induced neuroinflammation suggests new targets, and additional complications, for efforts to develop effective treatments for neuropathic SCI pain.