Pain
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Comparative Study
Results availability for analgesic device, complex regional pain syndrome, and post-stroke pain trials: comparing the RReADS, RReACT, and RReMiT databases.
Evidence-based medicine rests on the assumption that treatment recommendations are robust, free from bias, and include results of all randomized clinical trials. The Repository of Registered Analgesic Clinical Trials search and analysis methodology was applied to create databases of complex regional pain syndrome (CRPS) and central post-stroke pain (CPSP) trials and adapted to create the Repository of Registered Analgesic Device Studies databases for trials of spinal cord stimulation (SCS), repetitive transcranial magnetic stimulation (rTMS), and transcranial direct current stimulation (tDCS). We identified 34 CRPS trials, 18 CPSP trials, 72 trials of SCS, and 92 trials of rTMS/tDCS. ⋯ Results availability is higher 12 months after study completion but remains below 60% for peer-reviewed publications. Recommendations to increase results availability include supporting organizations advocating for transparency, enforcing existing results reporting regulations, enabling all primary registries to post results, stating trial registration numbers in all publication abstracts, and reducing barriers to publishing "negative" trials. For all diseases and treatment modalities, evidence-based medicine must rigorously adjust for the sheer magnitude of missing results in formulating treatment recommendations.
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Patients with knee osteoarthritis demonstrate decreased pressure pain thresholds (PPTs), facilitated temporal summation (TS) of pain, and decreased conditioned pain modulation (CPM) compared with healthy controls. This study aimed to correlate preoperative PPTs, TS, and CPM with the development of chronic postoperative pain after total knee replacement (TKR) surgery. Knee pain intensity (visual analog scale [VAS]: 0-10), PPTs, TS, and CPM were collected before, 2 months, and 12 months after TKR. ⋯ Preoperative TS level correlated to 12-month postoperative VAS (R = 0.240, P = 0.037). Patients who developed moderate-to-severe pain had pronociceptive changes compared with patients who developed mild pain postsurgery. Preoperative TS level correlated with the postoperative pain intensity and may be a preoperative mechanistic predictor for the development of chronic postoperative pain in patients with osteoarthritis after TKR.
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Neuropathic pain is one of the most difficult consequences of spinal cord injury (SCI). The clinical correlates of the underlying mechanisms responsible for neuropathic pain are not well understood, although methods such as quantitative somatosensory testing (QST) or brain imaging have been used to further a mechanism-based understanding of pain. Our previous SCI study demonstrated a significantly lower glutamate-glutamine/myo-inositol ratio (Glx/Ins) in the anterior cingulate cortex in persons with severe neuropathic pain compared with those with less severe neuropathic pain or pain-free, able-bodied controls, suggesting that a combination of decreased glutamatergic metabolism and glial activation may contribute to the development of severe neuropathic pain after SCI. ⋯ A cluster analysis including SCI participants resulted in 1 group (n = 19) with significantly (P < 0.001) greater pain intensity (6.43 ± 1.63; high neuropathic pain [HNP], and lower Glx/Ins [1.22 ± 0.16]) and another group (n = 35) with lower pain intensity ratings (1.59 ± 1.52, low neuropathic pain [LNP], and higher Glx/Ins [1.47 ± 0.26]). After correcting for age, QST indicated significantly greater somatosensory function in the HNP group compared with the LNP group. Our results are consistent with research suggesting that damage to, but not abolition of, the spinothalamic tract contributes to development of neuropathic pain after SCI and that secondary inflammatory processes may amplify residual spinothalamic tract signals by facilitation, disinhibition, or sensitization.