Articles: neuropathic-pain.
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The aim of this study was to determine the prevalence of neuropathic pain, now recognized as another late complication of leprosy, and its characteristics among leprosy patients. A cross-sectional study was carried out of people treated for leprosy up to at least 5 years ago in a rural area of Ethiopia. Seventy-four patients were interviewed using the Neuropathic Pain Symptom Inventory (NPSI) questionnaire. ⋯ The pain caused a severe or moderate impact on daily life in 75% and 57.7% of cases, respectively, and 92.3% suffered from disrupted sleep. Eighty percent of patients with pain (42/52) took some medication for pain relief. Neuropathic pain is common in patients treated for leprosy and in more than half of them, it causes disruption in their daily life and sleep, limiting their quality of life even more.
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The therapy of neuropathic pain may include the use of co-analgesics, such as antidepressants, however, their desired analgesic effect is associated with significant side effects. An alternative approach to this is their local administration which has been proposed, but there is little data regarding their local co-administration with morphine and the nature of the interaction between morphine and either doxepin or venlafaxine, two antidepressant drugs that have been recently used in neuropathic pain therapies. ⋯ In summary, the results suggest that when amitriptyline (but not doxepin or venlafaxine) is locally co-administered with morphine the effectiveness under neuropathic pain is enhanced, although additional studies are necessary to explain differential mechanisms of interaction of antidepressant drugs with morphine after local administration.
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Neuroscience letters · May 2014
Distinct role of tumor necrosis factor receptor subtypes 1 and 2 in the red nucleus in the development of neuropathic pain.
Previous studies have demonstrated that tumor necrosis factor-alpha (TNF-α) in the red nucleus (RN) plays a facilitated role in the development of neuropathic pain. Here, the protein levels and roles of two different TNF receptors, p55 type 1 (TNFR1) and p75 type 2 (TNFR2), in the RN of rats with spared nerve injury (SNI) were investigated. Immunohistochemistry demonstrated that both TNFR1 and TNFR2 were significantly increased in the RN of rats with SNI compared with sham-operated and normal rats. ⋯ Combined injection of anti-TNFR1-Ab and anti-TNFR2-Ab (500ng for each antibody) into the RN generated a relatively faster and longer analgesic effect compared with single using of anti-TNFR1-Ab or anti-TNFR2-Ab. These results support that TNF-α in the RN plays a crucial role in regulating neuropathic pain, and suggest that the algesic effect of TNF-α is transmitted through both TNFR1 and TNFR2. TNFR1 has equally important role in the early development and later maintenance of neuropathic pain, while TNFR2 is more inclined to play a role in the early development of neuropathic pain.
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Opiate analgesia in the spinal cord is impaired during neuropathic pain. We hypothesized that this is caused by a decrease in μ-opioid receptor inhibition of neurotransmitter release from primary afferents. To investigate this possibility, we measured substance P release in the spinal dorsal horn as neurokinin 1 receptor (NK1R) internalization in rats with chronic constriction injury (CCI) of the sciatic nerve. ⋯ In contrast, DAMGO still inhibited substance P release after inflammation of the hind paw with complete Freund's adjuvant and in naïve rats. This loss of inhibition was not due to μ-opioid receptor downregulation in primary afferents, because their colocalization with substance P was unchanged, both in dorsal root ganglion neurons and primary afferent fibers in the dorsal horn. In conclusion, nerve injury eliminates the inhibition of substance P release by μ-opioid receptors, probably by hindering their signaling mechanisms.