European journal of pain : EJP
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Conditioned pain modulation (CPM) is a validated measure of the function of endogenous pain inhibitory pathways. Placebo effects reflect top-down inhibitory modulation of pain. CPM and placebo effects are both influenced by expectations, albeit to varying degrees, and are related to neurotransmitter systems such as the endogenous opioid system, and it can be speculated that CPM responses are positively associated with the magnitude of placebo effects. Yet, no studies have tested this. ⋯ Conditioned pain modulation and placebo effects are endogenous pain-modulating phenomena that are influenced by some of the same mechanisms. This study suggests that CPM and placebo effects in neuropathic pain are independent phenomena that may be mediated by different mechanisms.
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The therapeutic influence of somatotopic matching between pain topography and motor cortex stimulation site for neuropathic pain (NP) remains controversial. ⋯ Strict somatotopic targeting of rTMS does not appear warranted for the treatment of upper limb or face NP. Since the hand motor area is easier to target and provides better results, it might be privileged for both types of pain.
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(1) To develop a checklist to assess the representation of biopsychosocial lower back pain (LBP) online information; (2) to analyse publicly accessed online LBP information from a Google search for the degree that psychosocial contributors are described alongside the traditional biomedical approach to explaining LBP; (3) whether websites use information on pain biology to educate on LBP; (4) any inaccurate or false information regarding the mechanisms of LBP and; (5) the amount of websites certified by established benchmarks for quality health information. ⋯ The online LBP information retrieved from a Google search needs to be guided by information more sensitive to the psychosocial contributors to pain and disability. This study also highlights the presence of inaccurate information that implied pain as a measure of tissue damage or as an input to the nervous system.
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Recent evidence has shown that chronic back pain (CBP) can lead to functional alterations in the circuitry underlying the cognitive control of pain. Thought suppression (TS) is a common type of cognitive control of pain. Previous research has shown that TS has paradoxical effects that may increase the awareness of pain. Pain-related TS may also increase individuals' attention to pain, which may also increase pain sensation, but thus far, the relationship between pain-related TS and structural brain alterations is unknown. ⋯ The link between pain-related thought suppression and brain morphology may provide a new perspective on the understanding of cognitive control of pain in chronic low back pain, which may help improve cognitive behavioural therapy.
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Chemotherapy-induced peripheral neuropathic pain (CIPNP) is a serious dose-limiting neurotoxic effect of cancer drug treatment. The underlying mechanism(s) of this debilitating condition, which lacks effective drug treatment, is incompletely understood. However, neural-immune interactions, involving increased expression and release of cytokines, are believed to be involved. Here, we examined, in the paclitaxel rat model of CIPNP, whether plasma levels of 24 cytokines/chemokines change after paclitaxel treatment, and whether blocking of signalling of some of those cytokines would reverse/attenuate behavioural signs of CIPNP. ⋯ This study demonstrates that paclitaxel-treated rats exhibit, in addition to indices of mechanical and cold hypersensitivity, a behavioural sign of spontaneous pain, the principal compliant of patients with neuropathic pain. This was accompanied by upregulation in plasma levels of key cytokines/chemokines (IL-1α, IL-1β, IL-6, TNF-α, INF-γ and MCP-1) 31 days post-treatment. However, it is noteworthy that cytokine release, rather than nerve injury per se, may be causative of NP in this model of CIPNP. Nevertheless, our findings that pharmacological blockade of TNF-α, IL-1β and MCP-1 attenuated both evoked and spontaneous pain suggest that strategies that target inhibition of these cytokines may be effective in treating CIPNP.