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Not be neglected: Galen’s description of critical headache.

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The etiological roles of miRNAs, lncRNAs, and circRNAs in neuropathic pain: A narrative review.

Non-coding RNAs (ncRNAs) are involved in neuropathic pain development. Herein, we systematically searched for neuropathic pain-related ncRNAs expression changes, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular non-coding RNAs (circRNAs).

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Body Composition does not influence Conditioned Pain Modulation and Exercise Induced Hyperalgesia in Healthy Males and Females.

Obese individuals report a higher susceptibility to chronic pain. Females are more likely to have chronic pain and excess adipose tissue. Chronic pain is associated with dysfunctional pain modulatory mechanisms. Body composition differences may be associated with pain modulation differences in males and females. The purpose of this study was to investigate body composition (lean vs fat mass) differences and pain modulatory functioning in healthy males and females.

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Risankizumab improved health-related quality of life, fatigue, pain, and work productivity in psoriatic arthritis: Results of KEEPsAKE 1.

Psoriatic arthritis (PsA) is a heterogeneous disease that impacts many aspects of social and mental life, including quality of life. Risankizumab, an antagonist specific for interleukin-23 (IL-23), is currently under investigation for the treatment of adults with active PsA. This study evaluated the impact of risankizumab versus placebo on health-related quality of life (HRQoL) and other patient-reported outcomes (PROs) among patients with active PsA and inadequate response or intolerance to conventional synthetic disease-modifying antirheumatic drugs (csDMARD-IR) in the KEEPsAKE 1 trial.

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Sounding out pain.

A circuit for sound-induced analgesia has been found in the mouse brain.

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Sound induces analgesia through corticothalamic circuits.

Sound-including music and noise-can relieve pain in humans, but the underlying neural mechanisms remain unknown. We discovered that analgesic effects of sound depended on a low (5-decibel) signal-to-noise ratio (SNR) relative to ambient noise in mice. Viral tracing, microendoscopic calcium imaging, and multitetrode recordings in freely moving mice showed that low-SNR sounds inhibited glutamatergic inputs from the auditory cortex (ACx) to the thalamic posterior (PO) and ventral posterior (VP) nuclei. Optogenetic or chemogenetic inhibition of the ACx→PO and ACx→VP circuits mimicked the low-SNR sound-induced analgesia in inflamed hindpaws and forepaws, respectively. Artificial activation of these two circuits abolished the sound-induced analgesia. Our study reveals the corticothalamic circuits underlying sound-promoted analgesia by deciphering the role of the auditory system in pain processing.

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Regional and neuraxial anaesthesia techniques for spinal surgery: a scoping review.

Whilst general anaesthesia is commonly used to undertake spine surgery, the use of neuraxial and peripheral regional anaesthesia techniques for intraoperative and postoperative analgesia is an evolving practice. Variations in practice have meant that it is difficult to know which modalities achieve optimal outcomes for patients undergoing spinal surgery. Our objective was to identify available evidence on the use of regional and neuraxial anaesthesia techniques for adult patients undergoing spinal surgery.

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Altered cortical trigeminal fields excitability by spreading depolarization revealed with functional ultrasound imaging combined with electrophysiology.

Spreading depolarization (SD), usually termed cortical spreading depression has been proposed as the pathophysiological substrate of migraine aura and as an endogenous trigger of headache pain. The links between neurovascular coupling and cortical craniofacial nociceptive activities modulated by SD were assessed by combining local field potential (LFPs) recordings in the primary somatosensory cortex (S1) with functional ultrasound (fUS) imaging of S1 and caudal insular (INS) cortices of anesthetized male rats. A single SD wave triggered in the primary visual cortex elicited an ipsilateral, quadriphasic hemodynamic and electrophysiological response in S1 with an early phase consisting of concomitant increases of relative cerebral blood volume (rCBV) and LFPs. A transient hypoperfusion was then correlated with the beginning of the neuronal silence, followed by a strong increase of rCBV while synaptic activities remained inhibited.LFPs and rCBV recovery period was followed by a progressive increase in S1 and INS baseline activities and facilitation of cortical responses evoked by periorbital cutaneous receptive fields stimulation. Sensitization of cortical ophthalmic fields by SD was bilateral, occurred with precise spatiotemporal profiles and was significantly reduced by pre-treatment with a NMDA antagonist. Combined high-resolution assessing of neurovascular coupling and electrophysiological activities has revealed a useful preclinical tool for deciphering central sensitization mechanisms involved in migraine attacks.A crucial unsolved issue is whether visual aura and migraine headache are parallel or sequential processes. Here we show that a single spreading depolarization (SD) wave triggered from the primary visual cortex is powerful enough to elicit progressive, sustained increases of hemodynamic and sensory responses to percutaneous periorbital noxious stimuli recorded in S1 and Insular ophthalmic fields. Sensitization of cortical ophthalmic fields by SD was bilateral, occurred with precise spatiotemporal profiles and was significantly reduced by pre-treatment with a NMDA antagonist. Combined high-resolution assessing of neurovascular coupling and electrophysiological activities has revealed a useful preclinical tool for deciphering central sensitization mechanisms involved in migraine attacks.

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Real-time monitoring of cannabis and prescription opioid co-use patterns, analgesic effectiveness, and the opioid-sparing effect of cannabis in individuals with chronic pain.

Despite a rapid expansion of cannabis use for pain management, how cannabis and prescription opioids are co-used and whether co-use improves analgesia and promotes reduction of opioid use in the daily lives of individuals with chronic pain is poorly understood. Based upon ecological momentary assessment (EMA), the present study examined (1) how pain and use of opioids and/or cannabis in the previous moment is associated with individuals' choice of opioids and/or cannabis in the next moment, (2) the effects of co-use on pain severity and pain relief, and (3) whether daily total opioid consumption differs on days when people only used opioids vs. co-used. Adults with chronic pain (N=46) using both opioids and cannabis who were recruited online completed a 30-day EMA. Elevated pain did not increase the likelihood of co-use in subsequent momentary assessments. Switching from sole use of either opioids and cannabis to co-use was common. Neither co-use nor sole use of either cannabis or opioids were associated with reductions in pain in the next moment. However, participants reported the highest daily perceived pain relief from co-use compared to cannabis and opioid use only. Post-hoc analysis suggested recall bias as a potential source of this discrepant findings between momentary vs. retrospective assessment. Lastly, there was no evidence of an opioid-sparing effect of cannabis in this sample. The present study shows preliminary evidence on cannabis and opioid co-use patterns, as well as the effects of co-use on pain and opoid dose in the real-world setting.

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Potentiation of morphine antinociception and inhibition of diabetic neuropathic pain by the multi-chemokine receptor antagonist peptide RAP-103.

We determined the ability of the multi-chemokine receptor (CCR2/CCR5/CCR8) antagonist RAP-103 to modulate pain behaviors in an acute model of surgical pain, with and without an added opioid (morphine), and by itself in a chronic model of Streptozotocin (STZ)-induced diabetic peripheral neuropathy (DPN).

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