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Relaxation, biofeedback, and cognitive behavioral therapy are evidence-based behavioral therapies for migraine. Despite such efficacy, research shows that only about half of patients initiate behavioral therapy recommended by their headache specialists.
We aimed to evaluate associations of human leukocyte antigen variants with migraine or headache in hospital and population-based settings.
Consistent associations between the severity of neuropathic pain and cutaneous innervation have not been described. We collected demographic and clinical data, McGill Pain Questionnaires (MPQ) and skin biopsies processed for PGP9.5 and CGRP immunohistochemistry from patients with bortezomib-induced peripheral neuropathy (BiPN; n=22), painful diabetic neuropathy (PDN; n=16), chronic idiopathic axonal polyneuropathy (CIAP; n=16) and 17 age-matched healthy volunteers. Duration of neuropathic symptoms was significantly shorter in patients with BiPN in comparison with PDN and CIAP patients. BiPN was characterized by a significant increase in epidermal axonal swellings and upper dermis nerve fiber densities (UDNFD) and a decrease in subepidermal nerve fiber densities (SENFD) of PGP9.5-positive fibers and of PGP9.5 containing structures that did not show CGRP labeling, presumably non-peptidergic fibers. In PDN and CIAP patients, intraepidermal nerve fiber densities (IENFD) and SENFD of PGP9.5-positive and of non-peptidergic fibers were decreased in comparison with healthy volunteers. Significant unadjusted associations between IENFD and SENFD of CGRP-positive, i.e. peptidergic, fibers and the MPQ sensory-discriminative, as well as between UDNFD of PGP9.5-positive fibers and the MPQ evaluative/affective component of neuropathic pain, were found in BiPN and CIAP patients. No significant associations were found in PDN patients. Cutaneous innervation changes in BiPN confirm characteristic features of early, whereas those in CIAP and PDN are in line with late forms of neuropathic pathology. Our results allude to a distinct role for non-peptidergic nociceptors in BiPN and CIAP patients. The lack of significant associations in PDN may be caused by mixed ischemic and purely neuropathic pain pathology.
To evaluate the long-term safety and tolerability of ubrogepant for the acute treatment of migraine.
We investigated if parental multi-site chronic pain increases the risk of adult offspring developing additional chronic pain sites, and if offspring body mass index (BMI) and leisure time physical activity modify this association. We used longitudinal data on 7,654 offspring linked with their parents who participated in the population-based HUNT Study (Norway) in 1995-97 and 2006-08. Logistic regression was used to estimate odds ratios (ORs) with 95% confidence interval (CI). One-third of offspring (n=2,573) developed additional chronic pain sites. Having both parents with 1-2 chronic pain sites increased the risk of developing additional pain sites compared to having parents free of chronic pain (OR=1.33; 95% CI 1.05-1.68), with larger effects observed when both parents had ≥3 chronic pain sites (OR=1.46; 95% CI 1.17-1.82). These associations were largely driven by maternal pain, i.e., there was no association between paternal chronic pain and risk of additional pain sites in offspring. The parent-offspring transfer of additional pain sites (when both parents had ≥3 pain sites) strengthened when offspring were obese (OR=2.56; 95% CI 1.75-3.75) or physically inactive (OR=1.73; 95% CI 1.33-2.27). In conclusion, parental multi-site chronic pain increases the risk of offspring developing additional chronic pain sites, particularly those with obesity or inactivity. Perspective: This longitudinal analysis investigated the parent-offspring transmission of multi-site chronic pain, and whether lifestyle behaviours in offspring modify this association. The findings suggest that having parents with multi-site chronic pain increases the risk of offspring developing additional chronic pain sites, particularly if offspring are obese or inactive.
To test the hypotheses that insufficient duration, high fragmentation, and poor sleep quality are temporally associated with migraine onset on the day immediately following the sleep period (day 0) and the following day (day 1).
Patients suffering from fibromyalgia syndrome (FMS) are heterogenous. They often present with sensory abnormalities and comorbidities.
The SARS-Cov-2 pandemic requires special attention on its psychological effects and the impact on patients with chronic pain.
Our study aimed to identify differentially methylated CpGs/regions and their enriched genomic pathways associated with underlying chronic musculoskeletal pain in older individuals. We recruited cognitively healthy older adults with ( = 20) and without ( = 9) self-reported musculoskeletal pain and collected DNA from peripheral blood that was analyzed using MethylationEPIC arrays. We identified 31,739 hypermethylated CpG and 10,811 hypomethylated CpG probes (s ≤ 0.05). All CpG probes were clustered into 5966 regions, among which 600 regions were differentially methylated at ≤ 0.05 level, including 294 hypermethylated regions and 306 hypomethylated regions (differentially methylated regions). Ingenuity pathway enrichment analysis revealed that the pain-related differentially methylated regions were enriched across multiple pathways. The top 10 canonical pathways were linked to cellular signaling processes related to immune responses (i.e. antigen presentation, programed cell death 1 receptor/PD-1 ligand 1, interleukin-4, OX40 signaling, T cell exhaustion, and apoptosis) and gamma-aminobutyric acid receptor signaling. Further, Weighted Gene Correlation Network Analysis revealed a comethylation network module in the pain group that was not preserved in the control group, where the hub gene was the cyclic adenosine monophosphate-dependent transcription factor ATF-2. Our preliminary findings provide new epigenetic insights into the role of aberrant immune signaling in musculoskeletal pain in older adults while further supporting involvement of dysfunctional GABAergic signaling mechanisms in chronic pain. Our findings need to be urgently replicated in larger cohorts as they may serve as a basis for developing and targeting future interventions.