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      The Burden of Migraine in Adults with Atrial Septal Defect: A Nationwide Cohort Study

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          Abstract

          We aimed to investigate migraine diagnoses in a hospital setting, use of prescription migraine medicine and levels of serotonin in patients with atrial septal defect. Using Danish national registries to identify all patients born before 1994 diagnosed with atrial septal defect between 1959 and 2013, thus including 2277 patients and a gender and age matched comparison cohort of 22756. Plasma serotonin was measured in 136 patients with a small, unclosed, atrial septal defects and 18 controls. Patients with atrial septal defect had an increased risk of receiving a migraine diagnosis (HR 3.4 (95% CI: 2.6–4.6)) and receiving migraine medicine (HR 1.8 (95% CI: 1.2–2.5)). Ten years after closure, 93% of those using migraine medicine pre-closure, were still receiving this. The risk of having very high plasma serotonin levels was increased in patients with atrial septal defect compared with the control group, but there was no difference in the median values between the two groups. Migraine and use of migraine medicine were increased in atrial septal defect patients. The use of medicine was not diminished by closure of the defect. Plasma serotonin was severely elevated in 18% of the patients with atrial septal defect.

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          Serotonin and migraine: biology and clinical implications.

          Migraine is the most frequent neurological disorder in the adult population worldwide, affecting up to 12% of the general population and more frequent in women ( approximately 25%). It has a high impact on our society due to its disabling nature and, therein, reduced quality of life and increased absenteeism from work. Headache is the primary clinical manifestation and it has been associated with 'a hereditary or predisposed sensitivity of neurovascular reactions to certain stimuli or to cyclic changes in the central nervous system' (1). Amongst the many neurotransmitters in the brain, the serotonergic (serotonin, 5-HT) system from the brainstem raphe nucleus has been most convincingly implicated in migraine pathophysiology. The documented changes in 5-HT metabolism and in the processing of central 5-HT-mediated responses during and in between migraine attacks have led to the suggestion that migraine is a consequence of a central neurochemical imbalance that involves a low serotonergic disposition. Although the exact cascade of events that link abnormal serotonergic neurotransmission to the manifestation of head pain and the accompanying symptoms has yet to be fully understood, recent evidence suggests that a low 5-HT state facilitates activation of the trigeminovascular nociceptive pathway, as induced by cortical spreading depression. In this short review, we present and discuss the original and most recent findings that support a role for altered serotonergic neurotransmission in the manifestation of migraine headache.
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            Percutaneous Closure of Patent Foramen Ovale in Patients With Migraine: The PREMIUM Trial.

            Migraine is a prevalent and disabling disorder. Patent foramen ovale (PFO) has been associated with migraine, but its role in the disorder remains poorly understood.
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              Serotonin and migraine: a reconsideration of the central theory

              The 5-hydroxytryptamine (5-HT) has been implicated in migraine pathophysiology for the past 50 years. A low central 5-HT disposition associated with an increase in 5-HT release during attack is the most convincing change of 5-HT metabolism implicated in migraine. Peripheral studies on plasma/platelet have not generally shown low 5-HT levels. Studies on 5-HT reactivity showed hypersensitivity, also expressed as reduced tachyphylaxis (habituation), which successively was evidenced as the most characteristic marker of an altered sensory neurotransmission. Even the gender and seasonal variations of 5-HT parameters seem to agree with a low 5-HT turnover with receptoral hypersensitivity. The interpretation of the effects of some serotonergic drugs and recent neuroimaging studies give major evidence for this cascade of events. Although the exact mechanism that links abnormal 5-HT neurotransmission to the manifestation of head pain has yet to be fully understood, a deficit on 5-HT descending pain inhibitory system is still probably today the most implicated in migraine pathophysiology. This short review focuses and discusses the alteration of peripheral and central 5-HT parameters in migraine patients.
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                Author and article information

                Contributors
                Camilla@nyboe.nu
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                15 May 2019
                15 May 2019
                2019
                : 9
                : 7410
                Affiliations
                ISNI 0000 0004 0512 597X, GRID grid.154185.c, Department of Cardiothoracic and Vascular Surgery, , Aarhus University Hospital, ; Aarhus, Denmark
                Article
                43895
                10.1038/s41598-019-43895-z
                6520354
                31092873
                4d7aab90-887d-4068-a77e-f71b2cd550ba
                © The Author(s) 2019

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 23 October 2018
                : 3 May 2019
                Funding
                Funded by: FundRef https://doi.org/10.13039/501100004954, Augustinus Fonden (Augustinus Foundation);
                Award ID: 14-2326
                Award Recipient :
                Funded by: FundRef https://doi.org/10.13039/100007605, Aarhus Universitet (Aarhus University);
                Categories
                Article
                Custom metadata
                © The Author(s) 2019

                Uncategorized
                congenital heart defects,epidemiology
                Uncategorized
                congenital heart defects, epidemiology

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