European journal of pain : EJP
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Endogenous pain inhibitory mechanisms are known to reduce pain intensity, but whether they influence the size and distribution of pain referral is unclear. This study aimed to determine if referred pain is reduced by applying a remote, conditioning painful stimulus. ⋯ The current results indicate a link between endogenous inhibition and pain referral. Descending inhibitory control effects on pain referral support a spinal mechanism involved in pain referral. Future studies should investigate whether the spatial characteristics of referred pain (e.g. size, frequency of affected body regions and distribution away from the primary nociceptive stimulus) can useful to evaluate the efficiency of endogenous pain modulation.
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Review Meta Analysis
The effect of experimental and clinical musculoskeletal pain on spinal and supraspinal projections to motoneurons and motor unit properties in humans: a systematic review.
Numerous studies have examined the influence of pain on spinal reflex excitability, motor unit behaviour and corticospinal excitability. Nevertheless, there are inconsistencies in the conclusions made. This systematic review sought to understand the effect of pain on spinal and supraspinal projections to motoneurons and motor unit properties by examining the influence of clinical or experimental pain on the following three domains: H-reflex, corticospinal excitability and motor unit properties. ⋯ This is a comprehensive systematic review and meta-analysis which synthesizes evidence on the influence of pain on spinal and supraspinal projections to motoneurons and motor unit properties considering measures of the H-reflex, corticospinal excitability and motor unit behaviour. The H-reflex is largely not influenced by the presence of either clinical or experimental pain. Whilst inhibitory effects on corticospinal excitability and motor unit behaviour were evident under experimental pain conditions, more variable responses were observed for people with painful musculoskeletal disorders.
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Randomized Controlled Trial
Anti-Nociceptive Effects of Oxytocin Receptor Modulation in Healthy Volunteers - a Randomized, Double-Blinded, Placebo-Controlled Study.
There is increasing evidence for oxytocin as a neurotransmitter in spinal nociceptive processes. Hypothalamic oxytocinergic neurons project to the spinal dorsal horn, where they activate GABA-ergic inhibitory interneurons. The present study tested whether the long-acting oxytocin-analogue carbetocin has anti-nociceptive effects in multi-modal experimental pain in humans. ⋯ This study provides evidence of the anti-nociceptive effect of intravenous administration of the oxytocin agonist carbetocin in healthy male volunteers.
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Neuropathic pain (NP) after spinal cord injury (SCI) is a disabling condition, without an effective treatment. Hyperexcitability of N-methyl-D-aspartate (NMDA) receptors and oxidative stress have been reported to be associated with pain development. Amantadine, an NMDA receptor antagonist, has been proposed as a potential therapy for NP. However, its use has not been tested for NP after SCI. ⋯ This study suggests that acute treatment with amantadine decreases hypersensitivity threshold and frequency of hypersensitivity response in a dose-dependent manner, in rats with SCI, by decreasing oxidative stress. Since amantadine is an easily accessible drug and has fewer adverse effects than current treatments for hypersensitivity threshold and frequency of hypersensitivity response, amantadine could represent a safe and effective therapy for the treatment of neuropathic pain. However, further research is required to provide evidence of the effectiveness and feasibility.
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Neuropathic pain (NeP) medications have several side effects that affect NeP patients' quality of life. Betanin, the most common betacyanin pigment, has been shown to have potent antioxidant and anti-inflammatory properties in vivo; thus, it has potential as a healthcare treatment. In this study, we focused on betanin (red beetroot extract) as a potential therapy for NeP. ⋯ This article supports findings of the effect of betanin on NeP and provides a potential therapeutic candidate for NeP. Furthermore, elucidating the underlying mechanism of the effect of betanin on microglial activation could assist the development of new treatments for chronic pain.