Pain
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The neural mechanisms whereby placebo conditioning leads to placebo analgesia remain unclear. In this study we aimed to identify the brain structures activated during placebo conditioning and subsequent placebo analgesia. We induced placebo analgesia by associating a sham treatment with pain reduction and used fMRI to measure brain activity associated with three stages of the placebo response: before, during and after the sham treatment, while participants anticipated and experienced brief laser pain. ⋯ However, during altered pain experience only aMCC, post-central gyrus and posterior cingulate demonstrated altered activity. The common frontal cortical areas modulated during anticipation in both the placebo conditioning and placebo analgesia phases have previously been implicated in placebo analgesia. Our results suggest that the main effect of placebo arises from the reduction of anticipation of pain during placebo conditioning that is subsequently maintained during placebo analgesia.
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Chronic alcohol consumption produces a painful peripheral neuropathy for which there is no reliable successful therapy, which is mainly due to lack of understanding of its pathobiology. Alcoholic neuropathy is characterized by spontaneous burning pain, hyperalgesia (an exaggerated pain in response to painful stimuli) and allodynia (a pain evoked by normally innocuous stimuli). Chronic alcohol intake is known to decrease the nociceptive threshold with increased oxidative-nitrosative stress and release of proinflammatory cytokines coupled with activation of protein kinase C. ⋯ TNF-alpha and IL-1beta levels were also significantly increased in both serum and sciatic nerve of ethanol-treated rats. Treatment with alpha-tocopherol and tocotrienol for 10 weeks significantly improved all the above-stated functional and biochemical deficits in a dose-dependent manner with more potent effects observed with tocotrienol. The study demonstrates the effectiveness of tocotrienol in attenuation of alcoholic neuropathy.
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Meta Analysis
Treatment of fibromyalgia syndrome with gabapentin and pregabalin--a meta-analysis of randomized controlled trials.
The efficacy of gabapentin (GPT) and pregabalin (PGB) in the treatment of fibromyalgia syndrome (FMS) was assessed. We screened MEDLINE, PsycINFO, SCOPUS, www.clinicaltrials.org, the Cochrane Library (through October 2008), and the reference sections of original studies on GPT/PGB in FMS. Randomized controlled trials (RCTs) on the treatment of FMS with GPT and PGB were analyzed. ⋯ There was strong evidence for a reduction of pain (SMD -0.28, 95% CI -0.36, -0.20; p<0.001), improved sleep (SMD -0.39, 95% CI -0.48, -0.39; p<0.001), and improved health-related quality of life (HRQOL) (SMD -0.30, 95% CI -0.46, -0.15; p<0.001), but not for depressed mood (SMD -0.12, 95% CI -0.30, 0.06; p=0.18). There was strong evidence for a non-substantial reduction of fatigue (SMD -0.16, 95% CI -0.23, -0.09, p<0.001) and of anxiety (SMD -0.18, 95% CI -0.27, -0.10; p<0.001). The external validity of the studies was limited because patients with severe somatic and mental disorders were excluded.