Vestibular migraine: Clinical aspects and pathophysiology

Department of Otolaryngology, University of Pittsburgh, Pittsburgh, PA 15213, USA. Electronic address: .
The Lancet Neurology (Impact Factor: 21.9). 07/2013; 12(7):706-15. DOI: 10.1016/S1474-4422(13)70107-8
Source: PubMed


Vestibular migraine is becoming recognised as a distinct clinical entity that accounts for a high proportion of patients with vestibular symptoms. A temporal overlap between vestibular symptoms, such as vertigo and head-movement intolerance, and migraine symptoms, such as headache, photophobia, and phonophobia, is a requisite diagnostic criterion. Physical examination and laboratory testing are usually normal in vestibular migraine but can be used to rule out other vestibular disorders with overlapping symptoms. The pathophysiology of vestibular migraine is incompletely understood but plausibly could include neuroanatomical pathways to and from central vestibular structures and neurochemical modulation via the locus coeruleus and raphe nuclei. In the absence of controlled trials, treatment options for patients with vestibular migraine largely mirror those for migraine headache.

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    ABSTRACT: - Diagnostic criteria for vestibular migraine have recently been formulated.- The diagnosis of vestibular migraine is based on a history of migraine and episodes of vertigo, not necessarily accompanied by the well-known headache.- If, during an attack of vertigo, headache is absent, the association with migraine is often not made.- In the event of frequent attacks of vertigo, prophylactic pharmacotherapy can be given, just as in migraine without dizziness.
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    ABSTRACT: Awareness of the importance of migraine in patients with symptoms of vestibular dysfunction is increasing. This article gives an overview of the multiple facets of the link between migraine and vestibular dysfunction. The vestibular and the headache community have published a consensual definition of vestibular migraine, which is an important step to promote research on the topic and the awareness of clinicians. Vestibular migraine is considered the most common cause of spontaneous recurrent vertigo. So far, the evidence for vestibular migraine has been mainly epidemiological, but the recent follow-up of a cohort over 9 years could show the robustness of the diagnosis over time.Additionally, migraine and vestibular dysfunction have multiple potential interactions and links through a range of comorbidities such as Menière's disease, benign paroxysmal positional vertigo, anxiety and motion sickness, which go beyond the diagnostic entity of vestibular migraine. The further refinement and wider acceptance of the diagnostic entity of vestibular migraine is an important development as it is one the most common vestibular disorders. But the relationship between migraine and vestibular dysfunction is complex and has many aspects beyond vestibular migraine.
    Current opinion in neurology 12/2013; 27(1). DOI:10.1097/WCO.0000000000000061 · 5.31 Impact Factor
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    ABSTRACT: Vestibular migraine (VM) is one of the most common causes of the episodic vestibular syndrome. It occurs in patients with previous or current history of migraine who experience recurrent episodes of vestibular symptoms with migrainous features during the attacks. The pathophysiology of VM is poorly understood and several hypotheses have been proposed. Probably various mechanisms are involved resulting in both peripheral and central vestibular dysfunction participate. A smart clinical characterization of the attacks is essential to establish a proper diagnosis and planning a correct approach. The diagnosis should be made on the basis of the clinical history. Now, diagnostic criteria of VM are well defined. Occasionally, diagnosis of VM cannot be easy because of variety of confusing clinical manifestations, such as positional nystagmus or hearing loss causing misdiagnosis. There is not a well-established therapy for VM. It is assumed that management of VM is similar to migraine, in both acute crisis and preventive therapy. The role of neuroleptics, H1 receptor antagonists, benzodiazepines, steroids and triptans in the acute attacks, and dietary changes and lifestyle modifications, anticonvulsants, antidepressants, beta-blocking drugs, and calcium antagonists, as well as vestibular rehabilitation, in VM prevention have been revised. Preventive treatment for VM is not well supported by prospective, randomized, placebo-controlled clinical trials. Several drugs have been shown to be effective in some studies, but the clinical evidence is limited. Large randomized clinical trials are needed.
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