Management of vestibular migraine

1. Therapeutic Advances in Neurological Disorders 
May 2011 vol. 4 no. 3 183-191
2. Alexandre R. Bisdorff, Centre Hospitalier Emile Mayrisch, rue Emile Mayrisch, Esch-sur-Alzette, 4003 Luxembourg    alexbis@pt.lu

Vestibular Migraine is considered to be the second most common cause of vertigo and the most common cause of spontaneous episodic vertigo. The duration of attacks varies from seconds to days, usually lasting minutes to hours, and they mostly occur independently of headaches. Long-lasting individual attacks are treated with generic antivertiginous and antiemetic drugs. Specific antimigraine drugs are unlikely to be very effective for rescue. The mainstay of the management of vestibular migraine is prophylactic medication. To date, there are no controlled trials available; the body of knowledge builds on case series and retrospective or observational studies. Most drugs are also used for the prevention of migraine headaches. The choice of medication should be guided by its side effect profile and the comorbidities of patients. Betablockers such as propanolol or metoprolol are preferred in patients with hypertension but in the absence of asthma. Anticonvulsants include topiramate when patients are obese, valproic acid and lamotrigine. Lamotrigine is preferred if vertigo is more frequent than headaches. Calcium antagonists include verapamil and flunarizine. If patients have anxiety, tricyclic antidepressants such as amitryptiline or nortryptiline or SSRIs and benzodiazepines such as clonazepam are recommended. Acetazolamide is effective in rare genetic disorders related to migraine-like episodic ataxia; however, its place in vestibular migraine is still to be established. Nonpharmacological measures such as diet, sleep, hygiene and avoidance of triggers are recommended as they are for migraine. Vestibular rehabilitation might be useful when there are complications such as loss of confidence in balance or visual dependence.

Cluster Headache: Diagnosis and Treatment

	Semin Neurol 2010; 30(2): 175-185 DOI: 10.1055/s-0030-1249226
© Thieme Medical Publishers

Spreading depression: from serendipity to targeted therapy in migraine prophylaxis

CURRENT REVIEW: CLINICAL SCIENCE

Spreading depression: from serendipity to targeted therapy in migraine prophylaxis

C Ayata

Stroke and Neurovascular Regulation Laboratory, Department of Radiology, and Stroke Service and Neuroscience Intensive Care Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.

Correspondence to Cenk Ayata, 149 13th Street, Room 6408, Charlestown, MA 02129, USA. e-mail: cayata@partners.org
Cephalalgia. Volume 29 Issue 10, Pages 1095 - 1114

Published Online: 7 Sep 2009

Copyright © 2009 International Headache Society

ABSTRACT

Despite the relatively well-characterized headache mechanisms in migraine, upstream events triggering individual attacks are poorly understood. This lack of mechanistic insight has hampered a rational approach to prophylactic drug discovery. Unlike targeted abortive and analgesic interventions, mainstream migraine prophylaxis has been largely based on serendipitous observations (e.g. propranolol) and presumed class effects (e.g. anticonvulsants). Recent studies suggest that spreading depression is the final common pathophysiological target for several established or investigational migraine prophylactic drugs. Building on these observations, spreading depression can now be explored for its predictive utility as a preclinical drug screening paradigm in migraine prophylaxis.

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DIGITAL OBJECT IDENTIFIER (DOI)

10.1111/j.1468-2982.2009.01982.x

Cortical spreading depression—new insights and persistent questions

CURRENT REVIEW: BASIC SCIENCE

Cortical spreading depression—new insights and persistent questions

A Charles & KC Brennan

Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA

Correspondence to Andrew Charles, 635 Charles Young Drive Suite 575, Los Angeles, CA 90095, USA. Tel. +1-310-794-1870, fax +1-310-206-6906, e-mail acharles@ucla.edu
Cephalalgia Volume 29 Issue 10, Pages 1115-1124

Published Online: 7 Sep 2009

Copyright © 2009 International Headache Society

ABSTRACT

Since its original extensive description by Leao in 1944, thousands of publications have characterized the phenomenon of cortical spreading depression (CSD). Despite the attention that CSD has received over more than six decades, however, many fundamental questions regarding its initiation, propagation, functional consequences, and relationship to migraine and other human disorders remain unanswered. Advances in genetics and cellular imaging have led to important insights into the basic mechanisms of CSD, with increasing attention focused on specific neuronal ion channels, neurotransmitters and neuromodulators. In addition, there is growing recognition that astrocytes and the vasculature may play an active, rather than simply a passive or reactive role in CSD. Several recent descriptions of CSD in humans in the setting of brain injury provide definitive evidence that this phenomenon can occur and have important functional consequences in the human brain. Although the exact role of CSD in migraine has yet to be conclusively established, there is strong evidence that the investigation of CSD in animal models can provide meaningful information about migraine that can be translated into the clinical setting. This review will briefly address the extensive work that has been done on CSD over more than half a century, but focus primarily on more recent studies with a particular emphasis on relevance to migraine.

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DIGITAL OBJECT IDENTIFIER (DOI)

10.1111/j.1468-2982.2009.01983.x