The journal of pain : official journal of the American Pain Society
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Randomized Controlled Trial
Anodal transcranial direct current stimulation reduces secondary hyperalgesia induced by low frequency electrical stimulation in healthy volunteers.
The aim of the study was to determine whether transcranial direct current stimulation (tDCS) reduced pain and signs of central sensitization induced by low frequency electrical stimulation in healthy volunteers. Thirty-nine participants received tDCS stimulation under 4 different conditions: anodal tDCS of the primary motor cortex (M1), anodal tDCS of the dorsolateral prefrontal cortex (DLPFC), anodal tDCS over M1 and DLPFC concurrently, and sham tDCS. Participants were blind to the tDCS condition. ⋯ Overall, these findings suggest that anodal tDCS over M1 suppresses pain, and that anodal tDCS over DLPFC modulates secondary hyperalgesia (a sign of central sensitization) in healthy participants. PERSPECTIVE: Anodal transcranial current stimulation (atDCS) at the left motor cortex and the dorsolateral prefrontal cortex increased the electrically-evoked pain threshold and reduced secondary hyperalgesia in healthy participants. Replication of this study in chronic pain populations may open more avenues for chronic pain treatment.
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Dorsal root ganglion stimulation (DRGS) is a neuromodulation therapy for chronic pain that is refractory to conventional medical management. Currently, the mechanisms of action of DRGS-induced pain relief are unknown, precluding both our understanding of why DRGS fails to provide pain relief to some patients and the design of neurostimulation technologies that directly target these mechanisms to maximize pain relief in all patients. ⋯ Here, we summarize the leading hypotheses of the mechanisms of DRGS-induced analgesia, and propose areas of future study that will be vital to improving the clinical implementation of DRGS. PERSPECTIVE: This article synthesizes the evidence supporting the current hypotheses of the mechanisms of action of DRGS for chronic pain and suggests avenues for future interdisciplinary research which will be critical to fully elucidate the analgesic mechanisms of the therapy.
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Randomized Controlled Trial
Producing clinically meaningful reductions in disability: A causal mediation analysis of a patient education intervention.
Patient education is recommended as first-line care for low back pain (LBP), although its efficacy for providing clinically meaningful reductions in disability has been questioned. One way to improve treatment effects is to identify and improve targeting of treatment mechanisms. We conducted a pre-planned causal mediation analysis of a randomized, placebo-controlled trial investigating the effectiveness of patient education for patients with acute LBP. 202 patients who had fewer than six-weeks' duration of LBP and were at high-risk of developing chronic LBP completed two, one-hour treatment sessions of either intensive patient education, or placebo patient education. 189 participants provided data for the outcome self-reported disability at three-months and the mediators, pain self-efficacy, pain catastrophizing, and back beliefs at one-week post treatment. ⋯ Considering the mediator-outcome relationship, patient education would need to induce an 8 point difference on the pain self-efficacy questionnaire (0-60); an 11 point difference on the back beliefs questionnaire (9-45); and a 21 point difference on the pain catastrophizing scale (0-52) to achieve a minimally clinically important difference of 2 points on the Roland Morris Disability Questionnaire (0-24). PERSPECTIVE: Understanding the mechanisms of patient education can inform how this treatment can be adapted to provide clinically meaningful reductions in disability. Our findings suggest that adapting patient education to better target back beliefs and pain self-efficacy could result in clinically meaningful reductions in disability whereas the role of pain catastrophizing in acute LBP is less clear.
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Determining the mechanistic causes of complex biopsychosocial health conditions such as low back pain (LBP) is challenging, and research is scarce. Cross-sectional studies demonstrate altered excitability and organization of the somatosensory and motor cortex in people with acute and chronic LBP, however, no study has explored these mechanisms longitudinally or attempted to draw causal inferences. Using sensory evoked potential area measurements and transcranial magnetic stimulation derived map volume we analyzed somatosensory and motor cortex excitability in 120 adults experiencing acute LBP. ⋯ These data provide evidence that low somatosensory cortex excitability in the acute stage of LBP is a cause of chronic pain. PERSPECTIVE: This prospective longitudinal cohort study design identified low sensorimotor cortex excitability during the acute stage of LBP in people who developed chronic pain. Interventions that target this proposed mechanism may be relevant to the prevention of chronic pain.
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Gut dysbiosis, defined as pathogenic alterations in the distribution and abundance of different microbial species, is associated with neuropathic pain in a variety of clinical conditions, but this has not been explored in the context of neuropathy in people with HIV (PWH). We assessed gut microbial diversity and dysbiosis in PWH and people without HIV (PWoH), some of whom reported distal neuropathic pain (DNP). DNP was graded on a standardized, validated severity scale. ⋯ Two candidate pathways for these associations, involving microbial pro-inflammatory components and microbially-produced anti-inflammatory short chain fatty acids, are discussed. Future studies might test interventions to re-establish a healthy gut microbiota and determine if this prevents or improves DNP. PERSPECTIVE: The association of neuropathic pain in people with HIV with reduced gut microbial diversity and dysbiosis raises the possibility that re-establishing a healthy gut microbiota might ameliorate neuropathic pain in HIV by reducing proinflammatory and increasing anti-inflammatory microbial products.