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Mindfulness and other behavioral approaches have demonstrated efficacy in treatment of different kinds of chronic pain condition and migraine in particular. Such treatments are of particular utility in the treatment of chronic forms of migraine, also associated to medication overuse headache, in reason of the relevant comorbidity – and bidirectional relationship – between migraine, and two of the most common associated conditions, namely anxiety and depression. Second, in reason of the impact that such treatments may have on behavioral issues that might promote MOH maintenance, including external locus of control and self-efficacy. Although the specific mechanism of action of these approaches has not been clarified yet, the absence of side effects and their effectiveness make these options suitable for different categories of frail patients and also for patients during therapy with medication if we want to improve the efficacy of medications itself. The use of these approaches has to be encouraged for clinicians and for patients to treat at the best pain condition and migraine and to improve the efficacy of the new medication for migraine prevention.
Learn More >We investigated whether sensory attenuation (or failure of) might be an explanation for heightened pain perceptions in individuals with chronic pain. N = 131 (50% chronic pain) individuals underwent a single experimental session, which included the force-matching task and several self-reported symptom and psychological measures. Individuals matched a force delivered to their finger, either by pressing directly on their own finger with their other hand (direct) or by using potentiometer to control the force through a torque motor (slider). All participants overestimated the target force in the direct condition reflecting the sensory attenuation phenomenon. No differences in the magnitude of sensory attenuation between chronic pain and control groups were observed (direct: Z = - 0.90, p = 0.37 and slider: Z = - 1.41, p = 0.16). An increased variance of sensory attenuation was observed in chronic pain individuals (direct: F(1, 129) = 7.22, p = 0.008 and slider: F(1, 129), p = 0.05). Performance in the slider condition was correlated with depressive symptoms (r = - 0.24, p = 0.05), high symptom count (r = - 0.25, p = 0.04) and positive affect (r = 0.28, p = 0.02). These were only identified in the chronic pain individuals. Overall, our findings reveal no clear differences in the magnitude of sensory attenuation between groups. Future research is needed to determine the relevance of sensory attenuation in neuro-cognitive models related to pain perception.
Learn More >Spinal cord injury (SCI) is a devastating condition for patients, affecting nearly 2.5 million people globally. Multiple side effects of SCI have resulted in a terrible life experience for SCI patients, of which neuropathic pain has attracted the most scientific interest. Even though many efforts have been made to attenuate or eliminate neuropathic pain induced by SCI, the outcomes for patients are still poor. Therefore, identifying novel diagnosis or therapeutic targets of SCI-induced neuropathic pain is urgently needed. Recently, multiple functions of long non-coding RNA (lncRNA) have been elucidated, including those in SCI-induced neuropathic pain. In this study, lncRNA small nucleolar RNA host gene 12 (SNHG12) was found to be upregulated in the dorsal root ganglion (DRGs) of rats with spare nerve injury (SNI). By constructing SCI rat models, we found that lncRNA SNHG12 expression was increased in the DRGs, and mainly distributed in the cytoplasm of PC12 cells. Paw withdrawal threshold (PWT), paw withdrawal latency (PWL), and enzyme linked immunosorbent assay (ELISA) results indicated that lncRNA SNHG12 knockdown attenuated SNI-induced neuropathic pain, and decreased the expression levels of interleukin (IL)-1β, IL-6, and tumour necrosis factor α (TNF-α) in the DRGs. Bioinformatics analysis, RNA pull-down, chromatin immunoprecipitation (ChIP), and luciferase reporter gene assays showed that lncRNA SNHG12 regulates the RAD23 homologue B, nucleotide excision repair protein (RAD23B) expression, through targeting micro RNA (miR)-494-3p. Furthermore, the study indicated that Kruppel-Like Factor 2 (KLF2) could regulate lncRNA SNHG12 expression in PC12 cells. This study identified a novel KLF2/lncRNA SNHG12/miR-494-3p/RAD23B axis in SNI-induced neuropathic pain, which might provide a new insight for developing novel diagnosis, or therapeutic targets of SCI-induced neuropathic pain in the future.
Learn More >The noradrenergic neurons of locus coeruleus (LC) project to the spinal dorsal horn (SDH), and release norepinephrine (NE) to inhibit pain transmission. However, its effect on pathological pain and the cellular mechanism in the SDH remains unclear. This study aimed to explore the analgesic effects and the anti-neuroinflammation mechanism of LC-spinal cord noradrenergic pathway (LC:SC) in neuropathic pain (NP) mice with sciatic chronic constriction injury.
Learn More >Potassium (K ) channels have been demonstrated to play a prominent involvement in nociceptive processing. Kir7.1, the newest members of the Kir channel family, has not been extensively studied in the CNS, and its function remains largely unknown. The present study investigated the role of spinal Kir7.1 in the development of pathological pain.
Learn More >The prophylactic treatment of migraine includes anticonvulsant drugs such as valproic acid and topiramate. However, these substances are often poorly tolerated by migraine patients. So far levetiracetam has hardly been studied as an episodic migraine prophylactic agent in adults.
Learn More >To investigate previous treatment and clinical characteristics in migraine and tension-type headache patients at their first visit to a tertiary headache center.
Learn More >CGAR, a Phase 3b open-label study, evaluated the long-term safety of galcanezumab in patients with cluster headache who completed one of two Phase 3 double-blind studies in chronic or episodic cluster headache.
Learn More >Inequitable variability in healthcare practice negatively affects patient outcomes. Children of color may receive different analgesic medications in the perioperative period, resulting in different outcomes.
Learn More >Maxadilan, a potent vasodilator peptide, selectively activates the PAC receptor, a promising target for migraine therapy. Therefore, maxadilan has been suggested as a tool to study the pharmacodynamics (PDs) of PAC receptor antagonists. The objectives of this first-in-human study were to: (1) determine the safety, tolerability, dose response, and time course of the dermal blood flow (DBF) changes after intradermal (i.d.) injections of maxadilan in the human forearm, and (2) assess the inter-arm and inter-period reproducibility of this response. This was a single-center, open-label study in healthy subjects, comprising three parts: (1) dose-response (n = 25), (2) response duration (n = 10), and (3) reproducibility (n = 15). DBF measurements were performed using laser Doppler imaging (LDI) up to 60 min postinjection, or up to 5 days for the response duration assessments. To assess reproducibility, the intraclass correlation coefficient (ICC) and sample sizes were calculated. The i.d. maxadilan (0.001, 0.01, 0.1, 0.9, 3, and 10 ng) produced a well-tolerated, dose-dependent increase in DBF, with a half-maximal effective concentration fitted at 0.0098 ng. The DBF response to 0.9 ng maxadilan was quantifiable with LDI up to 72 h postinjection. The inter-period reproducibility of the DBF response was better upon 0.9 ng (ICC > 0.6) compared to 0.01 ng (ICC < 0.4) maxadilan. However, irrespective of the study design or maxadilan dose, a sample size of 11 subjects is sufficient to detect a 30% difference in DBF response with 80% power. In conclusion, intradermal maxadilan provides a safe, well-tolerated, and reproducible PD biomarker for PAC receptor antagonists in vivo in humans.
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