We searched Medline for articles in English published between Jan 1, 1980, and Dec 31, 2012, with the search words: “migraine”, “dizziness”, “vertigo”, “vestibular”, “balance”, and “headache”. Terms were expanded using the ‘exp’ (explode) function and the Boolean ‘AND’ function was used to select subsets. Studies of human beings and animals were included. Both original research and review articles were included. Additional citations were obtained by searching for additional articles by first
ReviewVestibular migraine: clinical aspects and pathophysiology
Introduction
Although recurrent vertigo in children was known to be associated with migraine since Basser's description in 1964,1 in 1984 Kayan and Hood2 alerted the clinical community to an important association between vestibular symptoms and migraine in adults. Since that time, appreciation of the role of migraine in the dizzy patient has grown. In fact, although a migrainous aetiology for vestibular symptoms was previously unknown or deemed highly speculative, members of the International Headache Society in collaboration with members of the Barany Society have published diagnostic criteria for a disorder called vestibular migraine.3 As vestibular migraine is rapidly becoming recognised as a common vestibular disorder, and diagnostic criteria have been promulgated, the specialty is poised to make substantial advances in understanding the pathophysiology of this disorder and improving its management. In this Review, we provide an update regarding both the clinical aspects of vestibular migraine and the neurobiological basis for the disorder. Our current understanding of vestibular migraine is rudimentary but continues to evolve. We aim to provide both clinicians and clinician-scientists with the latest relevant information regarding this frequently encountered disorder and with the latest ideas and basic science findings germane to the pathophysiology and rational treatment of vestibular migraine.
Section snippets
Diagnostic criteria
Patients frequently present with a combination of migraine and vestibular symptoms.2 The assessment of these patients needs to address the association between these disorders. That is, are the vestibular symptoms causally related to a migraine subtype; are the vestibular symptoms and the migrainous symptoms simply a chance co-occurrence, or is there some more complex comorbidity association? Currently, the only International Headache Society migrainous disorder that includes vertigo in its
Epidemiology
Vestibular migraine is more prevalent than other vestibular disorders.14 Lempert and Neuhauser15 report a lifetime prevalence of migraine of 16%, a lifetime prevalence of vertigo of 7%, and a comorbidity of 3·2 %, rather than the 1·1% expected by chance alone. Neuhauser and colleagues16 report that vestibular migraine has a 1-year prevalence of 0·89% and accounts for about 10% of patients seen for dizziness and about 10% of patients seen for migraine.17 Hsu and colleagues18 report that the
Symptoms
For most patients, vestibular migraine is an episodic disorder; however, the duration of attacks ranges from seconds to days. Vestibular migraine has a strong female predominance of up to 5 to 1,11 and vestibular migraine often begins several years after typical migraine. Some patients can have a headache-free interval of several years before onset of vestibular migraine. Vestibular migraine might begin in place of headache especially in perimenopausal women.19 Vestibular migraine is more
Genetics
Several studies have investigated the genetics of vestibular migraine. Jen30 concluded that vestibular migraine might be monogenic and heterogeneous. Von Brevern and colleagues31 found no evidence of an association between calcium and sodium channel genes linked to familial hemiplegic migraine and episodic ataxia type 2 and vestibular migraine. Lee and colleagues32 found a region on chromosome 11q that is common in females in a family with vestibular migraine. Bahmad and colleagues33 located a
Related disorders
Several balance disorders are related to vestibular migraine. Ménière's disease, benign paroxysmal positional vertigo, and anxiety are more common in patients with vestibular migraine than would be expected by chance alone. The basis for this high comorbidity remains uncertain but might relate to overlaps between the clinical characteristics of these disorders and those of vestibular migraine, and because vertigo can serve as a migraine trigger.34 Ménière's disease and vestibular migraine
Treatment
Treatment options for patients with vestibular migraine include reduction of triggers, pharmacotherapy, physical therapy, and mitigation of comorbidities. No dedicated evidence base is available and no randomised controlled trials for the treatment of vestibular migraine exist, mainly because of the hitherto lack of diagnostic criteria. Instead, treatments are based on those for migraine headache or are anecdotal. Avoidance of migraine triggers should always be the first avenue of treatment.
Proposed neurobiological bases
Present hypotheses of migraine mechanisms are based on results of combined genetic, in-vitro cell biological, animal model, and clinical studies in human beings.52, 53, 54, 55, 56, 57, 58 This well developed published work provides a conceptual framework for understanding vestibular migraine as a variant produced by the convergence of vestibular information within migraine circuits; therefore, we provide a framework for further development of our understanding of vestibular migraine.
Conclusions and future directions
Vestibular migraine is becoming recognised as a highly prevalent vestibular disorder that is a subtype of migraine. Recently developed diagnostic criteria have helped clinical research, allowing a more complete understanding of the clinical aspects of vestibular migraine. The challenge now is to better understand the pathophysiology of vestibular migraine from both a clinical and basic science perspective to enable improved rational management of this disorder. Recent studies of vestibular
Search strategy and selection criteria
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2023, Sleep MedicineCitation Excerpt :The trigeminal caudal nuclear efferent fibers include the periaqueductal gray, hypothalamus, solitary nucleus, and parabrachial nucleus, several important areas of the central autonomic nerve network. The trigeminal nerve neck complex activation can directly lead to autonomic nervous reflex activation [18,19]. VM is a subtype of migraine, and this study found that in comparison to the controls, the sleep efficiency of the VM group significantly declined, and the arousal index and PSQI were increased, suggesting that the VM patients had inferior sleep quality, which was consistent with previous studies [5].