Abstract and Introduction
Vestibular migraine is an underdiagnosed but increasingly recognized neurological condition that causes episodic vertigo associated with other features of migraine. It is now thought to be the most common cause of spontaneous (non-positional) episodic vertigo, affecting up to 1% of the population. A meta-analysis of preventative treatments for vestibular migraine was published in 2021, but the authors were unable to establish a preferred treatment strategy due to low quality of evidence and heterogeneity of study design and outcome reporting. Therefore, there remains a clinical need for pragmatic management guidelines specific to vestibular migraine using the available evidence. Here, we provide a practical review utilizing a systematic qualitative assessment of the evidence for abortive and preventative interventions in adults. The overall evidence base for vestibular migraine treatment is of low quality. Nevertheless, we provide practical treatment recommendations based on the available evidence and our experience to help guide clinicians treating patients with vestibular migraine. We also discuss how future clinical trials could be designed to improve the quality of evidence in this condition.
Vestibular migraine (VM) is an underdiagnosed but increasingly recognized condition that causes episodic vertigo, often accompanied by headache. A condition first clearly described by Boenheim in 1917, it is now thought to be the most common cause of spontaneous (non-positional) episodic vertigo, affecting between 1% and 2.7% of the general population,[2,3] 11% of patients in specialized dizziness clinics and 13% of patients in headache clinics. Previously known variously as 'migrainous vertigo', 'migraine-associated vertigo', 'migraine-associated dizziness', 'migraine-anxiety-associated dizziness' and 'migraine-related vestibulopathy', vestibular migraine has been accepted by the International Classification of Headache Disorders (ICHD) as the unifying term that identifies both the vestibular and migrainous symptoms.
The clinical presentation of vestibular migraine is diverse. Episodes of dizziness usually last between 5 min and 72 h, although shorter and longer episodes have been reported. Vestibular symptoms can mimic benign paroxysmal positional vertigo, and prominent auditory symptoms with overlap with Ménière's disease have been reported.[8,9] Episodes are often, but not invariably, accompanied by other symptoms of migraine, including migrainous headache, photophobia, phonophobia and visual aura. Neurological examination is classically unremarkable, but during acute attacks can reveal spontaneous or positional nystagmus in the majority of patients,[7,10–13] and some studies have reported mild abnormalities of semicircular canal function and eye movements interictally.[7,10,14–18] The current diagnostic criteria, first proposed by Neuhauser et al. and ratified by the International Headache Society and the committee for the International Classification of Vestibular Disorders (ICVD) of the Bárány Society, mandate a history of migraine and the temporal overlap of vestibular and migrainous symptoms in at least 50% of episodes, and allow for the possibility of probable vestibular migraine (see Table 1). Importantly for a disease without an objective diagnostic gold standard, these criteria have been shown to be reliable on repeated assessments over a 9-year period.
The pathophysiology of vestibular migraine is incompletely understood. As with migraine, there is a significant female preponderance[4,19] for reasons not well explained. Both environmental and genetic factors are likely to be important,[20,21] and recent familial studies have suggested possible loci of interest at 5q35, 11q (with reduced penetrance in men) and 22q12. One proposed mechanism for episodes is hypoperfusion of the inner ear during migrainous attacks secondary to vasospasm resulting in vertiginous symptoms, a theory that is supported by the occasional association of migraine with sudden sensorineural hearing loss and the observation that migraine is a risk factor for stroke;[26,27] however, cochlear symptoms are certainly not a universal feature. Alternatively, episodes may be due to sensitization and activation of the trigeminovascular system leading to release of the pro-inflammatory neuropeptides substance P and calcitonin gene-related peptide (CGRP), which has connections with brain areas associated with processing of nociceptive information as well as thalamic and vestibular-associated cortices. Neuroimaging studies support the hypothesis that there are specific abnormalities in the structure and activity of the vestibulo-thalamo-cortical pathway in vestibular migraine.[29,30]
Due to a paucity of data on the management of vestibular migraine specifically, treatment recommendations have generally been extrapolated from studies on other forms of migraine. Pharmacological options for acute migraine include paracetamol, non-steroidal anti-inflammatory drugs (NSAIDs), antiemetics and triptans. Prophylactic treatment options include beta-blockers (propranolol, metoprolol), calcium channel blockers (for example, flunarizine), antiepileptic drugs (topiramate, sodium valproate), antidepressants (amitriptyline, nortriptyline, venlafaxine), antiserotonergic drugs (pizotifen), antihypertensives (candesartan, lisinopril) and monoclonal antibodies against CGRP (erenumab, fremanezumab, galcanezumab). Supplements (co-enzyme Q10, magnesium and riboflavin), greater occipital nerve block, botulinum toxin, external trigeminal nerve stimulation (eTNS), single transcranial magnetic stimulation and non-invasive vagus nerve stimulation (nVNS) are recommended by the British Association for the Study of Headache. Acupuncture may be helpful for some patients. A Cochrane review in 2015 that set out to identify effective pharmacological agents for the prevention of vestibular migraine failed to identify any completed study that met the strict inclusion criteria required for Cochrane reviews. A review and meta-analysis of preventive treatments for vestibular migraine was published in 2021, but the authors were unable to establish a preferred treatment strategy due to low quality of evidence and heterogeneity of study design and outcome reporting.
As current migraine treatment guidelines are based on work that did not assess the efficacy of interventions to control vestibular symptoms, there remains a clinical need for pragmatic management guidelines specific to vestibular migraine using the available evidence. Considering this, we felt that performing another meta-analysis would not be of practical utility given such a small number of appropriate studies. Equally, a narrative review would likely include publications at risk of serious bias due to poor study quality and significant heterogeneity. Thus, while others have provided comprehensive systematic reviews and meta-analyses of vestibular migraine treatment,[33,34] here we sought to offer a practical, clinically oriented review utilizing a systematic qualitative assessment of the evidence for each treatment option, upon which we offer treatment recommendations.
Brain. 2022;145(11):3741-3754. © 2022 Oxford University Press