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Effects of onabotulinumtoxinA treatment in patients with and without allodynia: results of the COMPEL study.

OnabotulinumtoxinA is effective in treating chronic migraine (CM), but there are limited data assessing how allodynia affects preventive treatment responses. This subanalysis of the 108-week, multicenter, open-label COMPEL Study assessed the efficacy and safety of onabotulinumtoxinA in people with CM with and without allodynia.

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Cerebrovascular reactivity as a determinant of deep white matter hyperintensities in migraine.

To evaluate the association between the cerebrovascular reactivity to carbon dioxide (CO-CVR) and the deep white matter hyperintensity (WMH) burden in patients with migraine.

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Adherence to Behavioral Therapy for Migraine: Knowledge to Date, Mechanisms for Assessing Adherence, and Methods for Improving Adherence.

In other disease states, adherence to behavioral therapies has gained attention, with a greater amount of studies discussing, defining, and optimizing adherence. For example, a meta-analysis formally discussed adherence in 25 studies of CBT for 11 different disorders, with only 6 of the 25 omitting addressing or defining adherence. Many studies have discussed the use of text messages, graph-based adherence rates, and email/telephone reminders to improve adherence. This paper examined the available literature regarding adherence to behavioral therapy for migraine as well as adherence to similar therapies in other disease states. The goal of this research is to apply lessons learned from adherence to behavioral therapy for other diseases in better understanding how we can improve adherence to behavioral therapy for migraine.

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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.

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Quantitative magnetic resonance imaging of the upper trapezius muscles – assessment of myofascial trigger points in patients with migraine.

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.

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The market for migraine drugs.

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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.

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A TREK to Translate Genetics to Mechanisms of Migraine.

In this issue of Neuron, Royal et al. (2018) find that a mutant form of the TRESK ion channel linked to migraine undergoes alternative translation to produce an inhibitory protein that blocks TREK channels, leading to neuronal hyperexcitability and migraine in rodents.

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Episodic Migraine Comorbidities: Avoiding Pitfalls and Taking Therapeutic Opportunities.

Migraine is a common neurologic disorder. This article will discuss a few factors that influence migraine (mostly episodic) and its treatment, such as sleep, obstructive sleep apnea (OSA), obesity, and affective disorders, as well as autoimmune diseases. Practitioners must be aware of these coexisting conditions (comorbidities) as they affect treatment. It is noted in literature that both the quantity (too much or too few hours) and the quality (OSA related) of sleep may worsen migraine frequency. An associated risk factor for OSA, obesity also increases migraine frequency in episodic migraine cases. A bidirectional relationship with migraine along with depression and anxiety is debated in the literature. Retrospective cohort studies are undecided and lack statistical significance, but prospective studies do show promising results on treatment of anxiety and depression as a means of improving migraine control. Finally, we address the topic of autoimmune diseases and migraine. While few studies exist at this time, there are cohort study groups looking into the association between rheumatoid arthritis, hypothyroidism, and antiphospholipid antibody. There is also evidence for the link between migraine and vascular diseases, including coronary and cerebral diseases. We suggest that these comorbid conditions be taken into account and individualized for each patient along with their pharmaceutical regimen. Physicians should seek a multifactorial treatment plan including diet, exercise, and healthy living to reduce migraine frequency.

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Novel hypotheses emerging from GWAS in migraine?

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. Although existing genetic information seems to favour involvement of vascular mechanisms, but also neuronal and other mechanisms such as metal ion homeostasis and neuronal migration, the complexity of the underlying genetic pathophysiology presents challenges to advancing genetic knowledge to clinical use. 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.

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