Pain
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Research and treatment of chronic pain over the past 20 or more years have tended to focus on patient coping as the primary behavioral contribution to adjustment. The purpose of the present study was to compare a coping approach to chronic pain with a different behavioral approach referred to as acceptance of chronic pain. These approaches were compared in terms of their ability to predict distress and disability in a sample of patients seeking treatment for chronic pain. ⋯ On the other hand, acceptance of chronic pain was associated with less pain, disability, depression and pain-related anxiety, higher daily uptime, and better work status. Regression analyses examined the independent contributions of coping and acceptance to key adjustment indicators in relation to chronic pain. Results from these analyses demonstrated that acceptance of pain repeatedly accounted for more variance than coping variables.
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Opioids and cannabinoids produce antinociception through both spinal and supraspinal action. Both opioids and cannabinoids also have important peripheral action. Many previous studies indicate that systemically administered cannabinoids enhance antinociceptive properties of opioids. ⋯ Additionally, spinally administered ineffective doses of WIN 55, 212-2 potentiated the antinociceptive effects of topical morphine. These results demonstrate an antinociceptive interaction between topical opioids with topical, and spinal cannabinoids. These observations are significant in using of topical combination of cannabinoid and morphine in the management of pain.
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Neuropathic pain and epileptic seizures bear several similarities, among them is the response to anticonvulsant drugs. It has therefore been hypothesized that epileptiform activity of nociceptive spinal dorsal horn neurons may contribute to paroxysmal forms of neuropathic pain. We used patch-clamp and field potential recordings from young rat spinal cord slices to test if nociceptive dorsal horn structures are indeed able to sustain epileptiform activity. ⋯ During epileptiform activity, previously silent polysynaptic pathways from primary afferent C-fibers to superficial dorsal horn neurons were opened. Stimulation of primary afferents at Adelta- and C-fiber intensity interfered with the epileptiform rhythm, suggesting that both affect the same dorsal horn structures. Similar to neuropathic pain, spinal dorsal horn epileptiform activity was much less reduced by classical analgesics than by anticonvulsant agents.