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Query: UMLS:C0423716 (Neuropathic pain)
 1,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effectiveness of intrathecal opioid therapy when applied to different pain mechanisms, in particular neuropathic and nociceptive pain conditions, was studied retrospectively in 43 patients suffering from cancer pain. On the basis of clinical and radiological data, the pain mechanisms were categorized as nociceptive (n = 23) and neuropathic (n = 20). The average duration of treatment of nociceptive pain was 5 months, of neuropathic pain only 2.5 months. The initial median reduction of pain with intrathecal opioid therapy was 77.8% for nociceptive and 61.1% for neuropathic pain. Long-term results with patients suffering nociceptive pain showed a continuing good median pain reduction of 66.7%. Patients suffering from neuropathic pain showed poor long-term results (11.1% median pain reduction). Neuropathic pain in the extremities reacted least to the application of intrathecal opioids. Optimal results were obtained for nociceptive pain in the trunk area of the body.
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PMID:The significance of intrathecal opioid therapy for the treatment of neuropathic cancer pain conditions. 1141 61

Neuropathic pain, a debilitating pain condition, is a common consequence of damage to the nervous system. Optimal treatment of neuropathic pain is a major clinical challenge because the underlying mechanisms remain unclear and currently available treatments are frequently ineffective. Emerging lines of evidence indicate that peripheral nerve injury converts resting spinal cord glia into reactive cells that are required for the development and maintenance of neuropathic pain. However, the mechanisms underlying reactive astrogliosis after nerve injury are largely unknown. In the present study, we investigated cell proliferation, a critical process in reactive astrogliosis, and determined the temporally restricted proliferation of dorsal horn astrocytes in rats with spinal nerve injury, a well-known model of neuropathic pain. We found that nerve injury-induced astrocyte proliferation requires the Janus kinase-signal transducers and activators of transcription 3 signalling pathway. Nerve injury induced a marked signal transducers and activators of transcription 3 nuclear translocation, a primary index of signal transducers and activators of transcription 3 activation, in dorsal horn astrocytes. Intrathecally administering inhibitors of Janus kinase-signal transducers and activators of transcription 3 signalling to rats with nerve injury reduced the number of proliferating dorsal horn astrocytes and produced a recovery from established tactile allodynia, a cardinal symptom of neuropathic pain that is characterized by pain hypersensitivity evoked by innocuous stimuli. Moreover, recovery from tactile allodynia was also produced by direct suppression of dividing astrocytes by intrathecal administration of the cell cycle inhibitor flavopiridol to nerve-injured rats. Together, these results imply that the Janus kinase-signal transducers and activators of transcription 3 signalling pathway are critical transducers of astrocyte proliferation and maintenance of tactile allodynia and may be a therapeutic target for neuropathic pain.
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PMID:JAK-STAT3 pathway regulates spinal astrocyte proliferation and neuropathic pain maintenance in rats. 2137 95