Pain
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Randomized Controlled Trial
Transcranial direct current stimulation as a treatment for patients with fibromyalgia: a randomized controlled trial.
Previous studies suggest that transcranial direct current stimulation (tDCS) over the primary motor cortex (M1) reduces chronic pain levels. In this randomized controlled trial, we investigated the effects of 5 consecutive 20-minute sessions of 2-mA anodal tDCS directed to the M1 in 48 patients (45 females) with fibromyalgia. Changes in pain, stress, daily functioning, psychiatric symptoms, and health-related quality of life were measured. ⋯ Fibromyalgia-related daily functioning improved in the active tDCS group compared with the sham group. The stimulation was well tolerated by the patients, and no significant difference in the adverse effects between the groups was observed. The results suggest that tDCS has the potential to induce statistically significant pain relief in patients with fibromyalgia, with no serious adverse effects, but small effect sizes indicate that the results are unlikely to reflect clinically important changes.
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Randomized Controlled Trial
Intrathecal clonidine and adenosine: effects on pain and sensory processing in patients with chronic regional pain syndrome.
Chronic pain may be accompanied by hyperalgesia and allodynia, and analgesic interventions may reduce these hypersensitivity phenomena. Preclinical data suggest that intrathecal clonidine and adenosine reduce hypersensitivity, but only clonidine reduces pain; therefore, we tested the effects of these interventions in patients with chronic pain. Twenty-two subjects with pain and hyperalgesia in a lower extremity from complex regional pain syndrome were recruited in a double-blind crossover study to receive intrathecal clonidine, 100 μg, or adenosine, 2 mg. ⋯ The percentage change in pain report did not correlate with the percentage change in areas of hyperalgesia (P = 0.09, r = 0.08) or allodynia (P = 0.24, r = 0.24) after drug treatment. Both intrathecal clonidine and adenosine acutely inhibit experimentally induced and clinical hypersensitivity in patients with chronic regional pain syndrome. Although these drugs do not differ in analgesia by the primary outcome measure, their difference in effect on pain scores over time and lack of correlation between effect on pain and hypersensitivity suggest that analgesia does not parallel antihyperalgesia with these treatments.
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Attentional bias to pain among family caregivers of patients with pain may enhance the detection of pain behaviors in patients. However, both relatively high and low levels of attentional bias may increase disagreement between patients and caregivers in reporting pain behaviors. This study aims to provide further evidence for the presence of attentional bias to pain among family caregivers, to examine the association between caregivers' attentional bias to pain and detecting pain behaviors, and test whether caregivers' attentional bias to pain is curvilinearly related to patient and caregiver disagreement in reporting pain behaviors. ⋯ Importantly, caregivers' attentional bias to pain was significantly positively associated with reporting pain behaviors in patients above and beyond pain severity. It is reassuring that attentional bias to pain was not related to disagreement between patients and caregivers in reporting pain behaviors. In other words, attentional bias does not seem to cause overestimation of pain signals.
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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.
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Review Meta Analysis
Postoperative pain treatment after total hip arthroplasty: a systematic review.
Treatment of postoperative pain should rely on results from randomized controlled trials and meta-analyses of high scientific quality. The efficacy of a particular intervention may depend on the type of surgical procedure, which supports the reporting of "procedure-specific" interventions. The aim of this systematic review was to document the procedure-specific evidence for analgesic interventions after total hip arthroplasty (THA). ⋯ Intrathecal opioids increased pruritus, and lumbar plexus block reduced nausea and pruritus. The GRADE-rated quality of evidence ranged from low to very low throughout the analyses. This review demonstrated, that some analgesic interventions may have the capacity to reduce mean opioid requirements and/or mean pain intensity compared with controls, but the available randomized placebo-controlled trials does not allow a designation of a "best proven intervention" for THA.