The journal of headache and pain
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Research in migraine points towards central-peripheral complexity with a widespread pattern of structures involved. Migraine-associated neck and shoulder muscle pain has clinically been conceptualized as myofascial trigger points (mTrPs). However, concepts remain controversial, and the identification of mTrPs is mostly restricted to manual palpation in clinical routine. This study investigates a more objective, quantitative assessment of mTrPs by means of magnetic resonance imaging (MRI) with T2 mapping. ⋯ Our approach enables the identification of mTrPs and their quantification in terms of T2 mapping even in the absence of qualitative signal alterations. Thus, it (1) might potentially challenge the current gold-standard method of physical examination of mTrPs, (2) could allow for more targeted and objectively verifiable interventions, and (3) could add valuable models to understand better central-peripheral mechanisms in migraine.
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Observational Study
Pain-related avoidance and endurance behaviour in migraine: an observational study.
The role of avoidance and endurance behaviour is well established in chronic musculoskeletal pain, but less is known about its significance in migraine. ⋯ This indicates that improvement in headache frequency and disability can be achieved in the absence of changes in avoidance or endurance behaviour. However, because of its significant link to headache-related disability, avoidance behaviour (especially social avoidance) should be investigated as a potential additional target of migraine therapy.
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The present study aimed to preliminary explore the abnormal neuromagnetic activation in female migraine patients between attacks using magnetoencephalography (MEG) and pattern reversed visual evoked magnetic fields (PR-VEFs). ⋯ The findings presented in the current study, suggested that interictal cortical activation following a visual stimulus was low in female migraine patients. The low pre-activation was detected in the visual cortex using VEF and MEG in both low and high-frequency band. Our results add to the existing evidence that cortical interictal excitability change may be relative to the pain-module mechanism in migraine brains. Thus, our data improved the apprehension of the cortical disorder of migraine in the high-frequency domain.
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Practice Guideline
European headache federation guideline on the use of monoclonal antibodies acting on the calcitonin gene related peptide or its receptor for migraine prevention.
Monoclonal antibodies acting on the calcitonin gene-related peptide or on its receptor are new drugs to prevent migraine. Four monoclonal antibodies have been developed: one targeting the calcitonin gene-related peptide receptor (erenumab) and three targeting the calcitonin gene-related peptide (eptinezumab, fremanezumab, and galcanezumab). The aim of this document by the European Headache Federation (EHF) is to provide an evidence-based and expert-based guideline on the use of the monoclonal antibodies acting on the calcitonin gene-related peptide for migraine prevention. ⋯ Monoclonal antibodies acting on the calcitonin gene-related peptide are new drugs which can be recommended for migraine prevention. Real life data will be useful to improve the use of those drugs in clinical practice.
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Recent technical advances in genetics made large-scale genome-wide association studies (GWAS) in migraine feasible and have identified over 40 common DNA sequence variants that affect risk for migraine types. Most of the variants, which are all single nucleotide polymorphisms (SNPs), show robust association with migraine as evidenced by the fact that the vast majority replicate in subsequent independent studies. However, despite thorough bioinformatic efforts aimed at linking the migraine risk SNPs with genes and their molecular pathways, there remains quite some discussion as to how successful this endeavour has been, and their current practical use for the diagnosis and treatment of migraine patients. ⋯ A major issue is to what extent one can rely on bioinformatics to pinpoint the actual disease genes, and from this the linked pathways. In this Commentary, we will provide an overview of findings from GWAS in migraine, current hypotheses of the disease pathways that emerged from these findings, and some of the major drawbacks of the approaches used to identify the genes and pathways. We argue that more functional research is urgently needed to turn the hypotheses that emerge from GWAS in migraine to clinically useful information.