Articles: hyperalgesia.
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Recent literature suggests that the withdrawal of remifentanil (RF) infusion can be associated with hyperalgesia in clinical and nonclinical settings. We performed a systematic review and a meta-analysis of randomized controlled trials with cross-over design, to assess the effect of discontinuing RF infusion on pain intensity and areas of hyperalgesia and allodynia in healthy volunteers. Nine studies were included. ⋯ The area of hyperalgesia was larger after RF withdrawal (SMD: 0.55; 95% CI: 0.27-0.84; P = 0.001; I 2 = 0%). The area of allodynia did not vary between treatments. These findings suggest that the withdrawal of RF induces a mild but nonclinically relevant degree of hyperalgesia in HVs, likely linked to a reduced pain threshold.
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Brainstem areas involved in descending pain modulation are crucial for the analgesic actions of opioids. However, the role of opioids in these areas during tolerance, opioid-induced hyperalgesia (OIH), and in chronic pain settings remains underappreciated. We conducted a revision of the recent studies performed in the main brainstem areas devoted to descending pain modulation with a special focus on the medullary dorsal reticular nucleus (DRt), as a distinctive pain facilitatory area and a key player in the diffuse noxious inhibitory control paradigm. ⋯ However, the upregulation of MOR and DOR, at the rostral ventromedial medulla, in inflammatory pain models, suggests therapeutic avenues to explore. Mechanistically, the rationale for the diversity and complexity of alterations in the brainstem is likely provided by the alternative splicing of opioid receptors and the heteromerization of MOR. In conclusion, this review emphasizes how important it is to consider the effects of opioids at these circuits when using opioids for the treatment of chronic pain and for the development of safer and effective opioids.
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Observing someone experience pain relief or exacerbation after an intervention may induce placebo hypoalgesia or nocebo hyperalgesia. Understanding the factors that contribute to these effects could help in the development of strategies for optimizing treatment of chronic pain conditions. We systematically reviewed and meta-analyzed the literature on placebo hypoalgesia and nocebo hyperalgesia induced by observational learning (OL). ⋯ Overall, the meta-analysis demonstrates that OL can shape placebo hypoalgesia and nocebo hyperalgesia. More research is needed to identify predictors of these effects and to study them in clinical populations. In the future, OL could be an important tool to help maximize placebo hypoalgesia in clinical settings.
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Curr Pain Headache Rep · Nov 2023
ReviewNeurovascular Compression-Induced Intracranial Allodynia May Be the True Nature of Migraine Headache: an Interpretative Review.
Surgical deactivation of migraine trigger sites by extracranial neurovascular decompression has produced encouraging results and challenged previous understanding of primary headaches. However, there is a lack of in-depth discussions on the pathophysiological basis of migraine surgery. This narrative review provides interpretation of relevant literature from the perspective of compressive neuropathic etiology, pathogenesis, and pathophysiology of migraine. ⋯ Vasodilation, which can be asymptomatic in healthy subjects, may produce compression of cranial nerves in migraineurs at both extracranial and intracranial entrapment-prone sites. This may be predetermined by inherited and acquired anatomical factors and may include double crush-type lesions. Neurovascular compression can lead to sensitization of the trigeminal pathways and resultant cephalic hypersensitivity. While descending (central) trigeminal activation is possible, symptomatic intracranial sensitization can probably only occur in subjects who develop neurovascular entrapment of cranial nerves, which can explain why migraine does not invariably afflict everyone. Nerve compression-induced focal neuroinflammation and sensitization of any cranial nerve may neurogenically spread to other cranial nerves, which can explain the clinical complexity of migraine. Trigger dose-dependent alternating intensity of sensitization and its synchrony with cyclic central neural activities, including asymmetric nasal vasomotor oscillations, may explain the laterality and phasic nature of migraine pain. Intracranial allodynia, i.e., pain sensation upon non-painful stimulation, may better explain migraine pain than merely nociceptive mechanisms, because migraine cannot be associated with considerable intracranial structural changes and consequent painful stimuli. Understanding migraine as an intracranial allodynia could stimulate research aimed at elucidating the possible neuropathic compressive etiology of migraine and other primary headaches.
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Review Meta Analysis
Exercise-induced hypoalgesic effects of different types of physical exercise in individuals with neck pain: a systematic review and meta-analysis.
To evaluate the exercise-induced hypoalgesic (EIH) effects of different types of physical exercise in individuals with neck pain. ⋯ Isometric and ROM exercises exerted hypoalgesia at local and remote sites. A larger EIH effect following submaximal aerobic exercises was exerted at the remote testing site compared with the local site.