Pain
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Persistent postsurgical pain is a prevalent but underacknowledged condition. The aim of this study was to assess the prevalence, sensory qualities, and postoperative determinants of persistent pain at 3 to 4years after total knee replacement (TKR) and total hip replacement (THR). Patients completed a questionnaire with included the Western Ontario and McMaster Universities Index of Osteoarthritis (WOMAC) Pain Scale, PainDetect Questionnaire, Short-Form McGill Pain Questionnaire, and questions about general health and socioeconomic status. ⋯ In conclusion, this study found that persistent postsurgical pain is common after joint replacement, although much of the pain is mild, infrequent, or an improvement on preoperative pain. The association between the number of pain problems elsewhere and the severity of persistent postsurgical pain suggests that patients with persistent postsurgical pain may have an underlying vulnerability to pain. A small percentage of patients have severe persistent pain after joint replacement, and this is associated with depression and the number of pain problems elsewhere.
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Spinal cord injury (SCI) commonly results in the development of neuropathic pain, which can dramatically impair the quality of life for SCI patients. SCI-induced neuropathic pain can be manifested as both tactile allodynia (a painful sensation to a non-noxious stimulus) and hyperalgesia (an enhanced sensation to a painful stimulus). The mechanisms underlying these pain states are poorly understood. ⋯ Furthermore, both intrathecal gabapentin treatment and blocking SCI-induced Ca(v)α2δ-1 protein upregulation by intrathecal Ca(v)α2δ-1 antisense oligodeoxynucleotides could reverse tactile allodynia in SCI rats. These findings support that SCI-induced Ca(v)α2δ-1 upregulation in spinal dorsal horn is a key component in mediating below-level neuropathic pain states, and selectively targeting this pathway may provide effective pain relief for SCI patients. Spinal cord contusion injury caused increased calcium channel Ca(v)α2δ-1 subunit expression in dorsal spinal cord that contributes to neuropathic pain states.