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      The Intimate Relationship between Vestibular Migraine and Meniere Disease: A Review of Pathogenesis and Presentation

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      Publication date (Electronic):
      Journal: Behavioural Neurology
      Publisher: Hindawi Publishing Corporation

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          Abstract

          Vestibular migraine (VM) has only recently been recognized as a distinct disease entity. One reason is that its symptoms overlap greatly with those of other vestibular disorders, especially Meniere disease (MD). The pathophysiology of neither VM nor MD is entirely elucidated. However, there are many theories linking migraine to both disorders. We reviewed the current understanding of migraine, VM, and MD and described how VM and MD are similar or different from each other in terms of pathophysiology and presentation, including hypotheses that the two share a common etiology and/or are variants of the same disease.

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          Vestibular migraine: diagnostic criteria.

          Thomas Lempert, Jes Olesen, Joseph Furman … (2012)
          This paper presents diagnostic criteria for vestibular migraine, jointly formulated by the Committee for Classification of Vestibular Disorders of the Bárány Society and the Migraine Classification Subcommittee of the International Headache Society (IHS). The classification includes vestibular migraine and probable vestibular migraine. Vestibular migraine will appear in an appendix of the third edition of the International Classification of Headache Disorders (ICHD) as a first step for new entities, in accordance with the usual IHS procedures. Probable vestibular migraine may be included in a later version of the ICHD, when further evidence has been accumulated. The diagnosis of vestibular migraine is based on recurrent vestibular symptoms, a history of migraine, a temporal association between vestibular symptoms and migraine symptoms and exclusion of other causes of vestibular symptoms. Symptoms that qualify for a diagnosis of vestibular migraine include various types of vertigo as well as head motion-induced dizziness with nausea. Symptoms must be of moderate or severe intensity. Duration of acute episodes is limited to a window of between 5 minutes and 72 hours.
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            Pathophysiology of migraine.

            Daniela Pietrobon, Michael A. Moskowitz (2013)
            Migraine is a collection of perplexing neurological conditions in which the brain and its associated tissues have been implicated as major players during an attack. Once considered exclusively a disorder of blood vessels, compelling evidence has led to the realization that migraine represents a highly choreographed interaction between major inputs from both the peripheral and central nervous systems, with the trigeminovascular system and the cerebral cortex among the main players. Advances in in vivo and in vitro technologies have informed us about the significance to migraine of events such as cortical spreading depression and activation of the trigeminovascular system and its constituent neuropeptides, as well as about the importance of neuronal and glial ion channels and transporters that contribute to the putative cortical excitatory/inhibitory imbalance that renders migraineurs susceptible to an attack. This review focuses on emerging concepts that drive the science of migraine in both a mechanistic direction and a therapeutic direction.
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              Chaos and commotion in the wake of cortical spreading depression and spreading depolarizations.

              Daniela Pietrobon, Michael A. Moskowitz (2014)
              Punctuated episodes of spreading depolarizations erupt in the brain, encumbering tissue structure and function, and raising fascinating unanswered questions concerning their initiation and propagation. Linked to migraine aura and headache, cortical spreading depression contributes to the morbidity in the world's migraine with aura population. Even more ominously, erupting spreading depolarizations accelerate tissue damage during brain injury. The once-held view that spreading depolarizations may not exist in the human brain has changed, largely because of the discovery of migraine genes that confer cortical spreading depression susceptibility, the application of sophisticated imaging tools and efforts to interrogate their impact in the acutely injured human brain.
              Article 0 comments Cited 145 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Behav Neurol
                Journal ID (iso-abbrev): Behav Neurol
                Journal ID (publisher-id): BN
                Title: Behavioural Neurology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 0953-4180
                ISSN (Electronic): 1875-8584
                Publication date (Print): 2016
                Publication date (Electronic): 29 August 2016
                Volume: 2016
                Electronic Location Identifier: 3182735
                Affiliations
                Department of Otolaryngology, Head and Neck Surgery, Loma Linda University Medical Center, Loma Linda, CA, USA
                Author notes

                Academic Editor: Kadriye Agan

                Author information
                http://orcid.org/0000-0002-8637-661X
                Article
                DOI: 10.1155/2016/3182735
                PMC ID: 5019886
                PubMed ID: 27651559
                SO-VID: 00b4a550-efeb-4f66-b4a7-2e9b33105060
                Copyright © Copyright © 2016 Y. F. Liu and H. Xu.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 7 May 2016
                Date accepted : 7 August 2016
                Categories
                Subject: Review Article

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