Articles: neuropathic-pain.
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Postherpetic neuralgia (PHN) is a neuropathic sequelae in 8% to 27% of individuals with prior varicella zoster virus infection and herpes zoster resulting in retrograde demyelination, neurotoxic reactive oxygen species levels, and proinflammatory cytokine activation of microglia. Pain management strategies are well documented, but not always effective. Laser therapy has shown utility in nerve injury-related pain disorders and was considered a potentially efficacious intervention. ⋯ Theoretically, laser therapy induced tissue changes in this case occurring at and below the skin surface altering inflammatory and excitatory peripheral mechanisms noted to take place in the PHN patient. Peripheral nociceptor firing must be brought back to normal thresholds to resolve such chronic neuropathic pain and inhibit the possible central sensitization component. Anti-inflammatory cytokines, growth factors, nitric oxide, adenosine triphosphate (ATP), and other mechanisms stimulated by laser therapy as noted in medical literature may be central to the favorable response seen in this patient. Controlled clinical trials of class 4 laser therapy in the PHN patient population with similar doses would be beneficial to determine if this is an effective treatment option in PHN.
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Nerve injury sometimes leads to chronic neuropathic pain associated with neuroinflammation in the nervous system. In the case of chronic neuropathic pain, the inflammatory and algesic mediators become predominant and result in pain hypersensitivity following nervous system damage. It is well known that urinary trypsin inhibitor (ulinastatin, UTI) has an anti-inflammatory activity. Recently, the neuroprotective action of UTI on the nervous system after ischemic injury has been reported. Thus, we evaluated the neuroprotective effect of ulinastatin in a rat model of neuropathic pain. ⋯ Ulinastatin, which was administered for 3 days after SNL, increased the paw withdrawal threshold and it could have a neuroprotective effect in the rat model of neuropathic pain.
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Pharmacol. Biochem. Behav. · Oct 2013
Activation of mTOR in the spinal cord is required for pain hypersensitivity induced by chronic constriction injury in mice.
The mammalian target of rapamycin (mTOR) is known to regulate cell growth, and it also participates in pain transmission as has been recently verified in inflammatory and neuropathic pain models. The targeting of mTOR represents a new strategy for the control of chronic pain. In the present study, we investigated the effect of mTOR in the expression of PSD95 and NR2B-PSD95 or GluA2-PSD95 interaction ratio in a chronic constriction injury (CCI) mice model. ⋯ These data suggest that the mTOR pathway is activated in the spinal dorsal horn in CCI-induced neuropathic pain, and the intrathecal injection of rapamycin can reduce mechanical allodynia. Our findings indicate that spinal mTOR is an important component of CCI-induced neuropathic pain, and mTOR may be a potential target for chronic pain therapy.
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Neuropathic pain (NP) develops as a consequence of a lesion or disease affecting the somatosensory pathways in the peripheral or central nervous system, and occurs in many neurological diseases (eg, peripheral neuropathy, radiculopathy, spinal cord injury, stroke and multiple sclerosis). It affects 6%-8% of the general population and its impact on quality of life, mood and sleep exceeds the burden of its causative pathology. A peculiar feature of NP is the coexistence of negative and positive symptoms and signs, reflecting loss-of-function and gain-of-function of the somatosensory system, respectively. ⋯ In recent years, a redefinition, diagnostic algorithm, and some guidelines on diagnosis and treatment of NP have been published. This review offers an updated overview on the definition, pathophysiology, clinical evaluation, diagnosis and treatment of NP and focuses on some of the most frequent NP conditions. We intend to help overcome uncertainties on NP and bridge the gap between evidence based medicine and the real clinical world.
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Experimental neurology · Oct 2013
Burn injury-induced mechanical allodynia is maintained by Rac1-regulated dendritic spine dysgenesis.
Although nearly 11 million individuals yearly require medical treatment due to burn injuries and develop clinically intractable pain, burn injury-induced pain is poorly understood, with relatively few studies in preclinical models. To elucidate mechanisms of burn injury-induced chronic pain, we utilized a second-degree burn model, which produces a persistent neuropathic pain phenotype. Rats with burn injury exhibited reduced mechanical pain thresholds ipsilateral to the burn injury. ⋯ Heat hyperalgesia testing produced variable results, as expected from previous studies of this model of second-degree burn injury in rats. Administration of Rac1-inhibitor, NSC23766, attenuated dendritic spine dysgenesis, decreased mechanical allodynia and electrophysiological signs of burn-induced neuropathic pain. These results support two related implications: that the presence of abnormal dendritic spines contributes to the maintenance of neuropathic pain, and that therapeutic targeting of Rac1 signaling merits further investigation as a novel strategy for pain management after burn injury.