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      An update on migraine: current understanding and future directions

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          Abstract

          Migraine is a common brain disorder with high disability rates which involves a series of abnormal neuronal networks, interacting at different levels of the central and peripheral nervous system. An increase in the interest around migraine pathophysiology has allowed researchers to unravel certain neurophysiological mechanisms and neurotransmitter involvement culminating in the recent development of novel therapies, which might substantially change the clinical approach to migraine patients. The present review will highlight the current aspects of migraine pathophysiology, covering an understanding of the complex workings of the migraine state and the brain regions responsible for them. We will further discuss the therapeutic agents which have appeared in the most recent years for migraine care, from calcitonin gene-related peptide (CGRP) receptor antagonists, gepants; through serotonin 5-HT 1F receptor agonists, ditans, and CGRP or CGRP receptor monoclonal antibodies to invasive and non-invasive neuromodulation techniques.

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          Pathophysiology of Migraine: A Disorder of Sensory Processing.

          Peter J Goadsby, Philip Holland, Margarida Martins-Oliveira … (2017)
          Plaguing humans for more than two millennia, manifest on every continent studied, and with more than one billion patients having an attack in any year, migraine stands as the sixth most common cause of disability on the planet. The pathophysiology of migraine has emerged from a historical consideration of the "humors" through mid-20th century distraction of the now defunct Vascular Theory to a clear place as a neurological disorder. It could be said there are three questions: why, how, and when? Why: migraine is largely accepted to be an inherited tendency for the brain to lose control of its inputs. How: the now classical trigeminal durovascular afferent pathway has been explored in laboratory and clinic; interrogated with immunohistochemistry to functional brain imaging to offer a roadmap of the attack. When: migraine attacks emerge due to a disorder of brain sensory processing that itself likely cycles, influenced by genetics and the environment. In the first, premonitory, phase that precedes headache, brain stem and diencephalic systems modulating afferent signals, light-photophobia or sound-phonophobia, begin to dysfunction and eventually to evolve to the pain phase and with time the resolution or postdromal phase. Understanding the biology of migraine through careful bench-based research has led to major classes of therapeutics being identified: triptans, serotonin 5-HT1B/1D receptor agonists; gepants, calcitonin gene-related peptide (CGRP) receptor antagonists; ditans, 5-HT1F receptor agonists, CGRP mechanisms monoclonal antibodies; and glurants, mGlu5 modulators; with the promise of more to come. Investment in understanding migraine has been very successful and leaves us at a new dawn, able to transform its impact on a global scale, as well as understand fundamental aspects of human biology.
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            Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model.

            Hayrunnisa Bolay, Uwe Reuter, Andrew Dunn … (2002)
            Although the trigeminal nerve innervates the meninges and participates in the genesis of migraine headaches, triggering mechanisms remain controversial and poorly understood. Here we establish a link between migraine aura and headache by demonstrating that cortical spreading depression, implicated in migraine visual aura, activates trigeminovascular afferents and evokes a series of cortical meningeal and brainstem events consistent with the development of headache. Cortical spreading depression caused long-lasting blood-flow enhancement selectively within the middle meningeal artery dependent upon trigeminal and parasympathetic activation, and plasma protein leakage within the dura mater in part by a neurokinin-1-receptor mechanism. Our findings provide a neural mechanism by which extracerebral cephalic blood flow couples to brain events; this mechanism explains vasodilation during headache and links intense neurometabolic brain activity with the transmission of headache pain by the trigeminal nerve.
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              CGRP and its receptors provide new insights into migraine pathophysiology.

              Tony Ho, Lars Edvinsson, Peter J Goadsby (2010)
              Over the past 300 years, the migraine field has been dominated by two main theories-the vascular theory and the central neuronal theory. The success of vasoconstrictors such as ergotamine and the triptans in treating acute migraine bolstered the vascular theory, but evidence is now emerging that vasodilatation is neither necessary nor sufficient to induce a migraine attack. Attention is now turning to the core migraine circuits in the brain, which include the trigeminal ganglia, trigeminal nucleus, medullary modulatory regions, pons, periaqueductal gray matter, hypothalamus and thalamus. Migraine triggers are likely to reflect a disturbance in overall balance of the circuits involved in the modulation of sensory activity, particularly those with relevance to the head. In this Review, we consider the evidence pointing towards a neuronal mechanism in migraine development, highlighting the role of calcitonin gene-related peptide (CGRP), which is found in small to medium-sized neurons in the trigeminal ganglion. CGRP is released during migraine attacks and can trigger migraine in patients, and CGRP receptor antagonists can abort migraine. We also examine whether other drugs, such as triptans, might exert their antimigraine effects via their actions on the neuronal circuit as opposed to the intracranial vasculature.
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                Author and article information

                Contributors
                Peter J. Goadsby: +44-203-299-3106 , peter.goadsby@kcl.ac.uk
                Journal
                Journal ID (nlm-ta): J Neurol
                Journal ID (iso-abbrev): J. Neurol
                Title: Journal of Neurology
                Publisher: Springer Berlin Heidelberg (Berlin/Heidelberg )
                ISSN (Print): 0340-5354
                ISSN (Electronic): 1432-1459
                Publication date (Electronic): 20 March 2017
                Publication date PMC-release: 20 March 2017
                Publication date (Print): 2017
                Volume: 264
                Issue: 9
                Pages: 2031-2039
                Affiliations
                [1 ]ISNI 0000 0001 2322 6764, GRID grid.13097.3c, Headache Group, Department of Basic and Clinical Neuroscience, , King’s College London, ; London, UK
                [2 ]ISNI 0000 0004 0391 9020, GRID grid.46699.34, NIHR-Wellcome Trust King’s Clinical Research Facility, , King’s College Hospital, ; London, UK
                Article
                Publisher ID: 8434
                DOI: 10.1007/s00415-017-8434-y
                PMC ID: 5587613
                PubMed ID: 28321564
                SO-VID: 4d01f093-99a8-45fa-9aa2-5161ccda7e5a
                Copyright © © The Author(s) 2017
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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.

                History
                Date received : 11 January 2017
                Date accepted : 20 February 2017
                Categories
                Subject: Neurological Update
                Custom metadata
                issue-copyright-statement © Springer-Verlag GmbH Germany 2017

                ScienceOpen disciplines: Neurology
                Keywords: migraine,pathophysiology,treatment,cgrp,neuromodulation
                Data availability:
                ScienceOpen disciplines: Neurology
                Keywords: migraine, pathophysiology, treatment, cgrp, neuromodulation

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