Migraine-Associated Vertigo

Introduction

The clinical association of migraine and vertigo or dizziness has been given many names in the literature, including migraine-associated vertigo, migraine-associated dizziness, vestibular migraine, migrainous vertigo, migraine-related vestibulopathy, basilar artery migraine, and others. According to Stewart and associates, 17% of the female population and 6% of males experience severe migraine headaches. Because about one-third of persons with migraine experience dizziness, the prevalence of migraine combined with vertigo or dizziness is expected to be about 3% of the population. “Vestibular migraine” is the most recent nomenclature for the combination of migraine and vertigo. If the criteria for vestibular migraine recommended by the International Headache Society are used, prevalence has been estimated to be roughly 1% of the population. It is clear that the combination of migraine and dizziness is common in the general population.

Research studies concerning “vestibular migraine” usually employ criteria proposed by Neuhauser and Lempert, which entail a complex decision tree. These criteria are well suited to research endeavors. In this review we will use a looser definition better suited to practicing clinicians—namely, headaches with migrainous characteristics combined with dizziness or vertigo, and refer to this more pragmatically defined entity as “migraine-associated vertigo” or MAV.

The literature concerning migraine in general is immense and even that regarding MAV is substantial; therefore, an exhaustive review is impractical. In addition, other reviews have been published recently. Here we will focus on the salient features of MAV, concentrating on points of interest to the clinician.

It is important to understand that the diagnosis of “migraine” means only that the patient endorses a particular set of symptoms, as delineated by the International Headache Society. There is no biomarker for migraine, and the diagnosis of migraine is not nearly as specific or certain as diagnosing a brain tumor with imaging, or a hypothyroid state with blood testing. It is to be hoped that as we better understand the molecular biology and genetics of migraine symptoms, we will be able to categorize migraine into headache variants, associated with objective markers and individualized treatments.

Pathophysiology of Migraine-Associated Vertigo

The pathophysiology of migraine remains poorly understood and probably is variable as well. In this discussion, we will use the mechanistic framework that migraine sufferers are more sensitive to many types of sensory input, and that when there is an overload of sensory input, a threshold is surpassed, triggering a cortical event followed by brainstem events causing even more sensory signaling to occur, generally resulting in a severe headache and a transient “shutdown” of the individual.

There is good evidence that the brain of many persons with migraine is hyperexcitable. Persons with migraine are generally more likely to experience discomfort from bright light, loud sound, smells, motion, and many other sensory inputs that are not disturbing to nonmigraineurs. Migraine sufferers are frequently extraordinarily sensitive to sensory stimuli during their headaches but also are often more sensitive at baseline, independent of their migraine headaches. As an example, patients with migraines often give a history of motion sickness. Studies find that 45% of children with migraines and 50% of adults with migraines report a history of being highly susceptible to motion sickness. In other words, sensory sensitivity accompanying migraines may be “hardwired.”

If we attempt to become more specific about mechanism, research and clinical data suggest involvement of many processes—vascular, electrical, and biochemical processes. Research on migraine aura, such as the “cortical spreading depression of Leão” and changes in blood flow in the occipital cortex demonstrated in migraines with certain visual auras, implicates both vascular dysregulation and abnormal electrical activity. The response of migraine to serotonin agonists such as triptans implicates biochemical dysfunction of trigeminal brainstem circuits. The vasodilator peptide, calcitonin gene-related peptide (CGRP), is found in cell bodies of trigeminal neurons. CGRP probably modulates vascular nociception and has been heavily implicated in the headache of migraine. There may be a positive feedback loop in which sensory overload triggers cortical circuitry that causes release of CGRP, which increases painful input. Triptans, acting as 5-HT1B/D agonists, block these responses.

In MAV the same general mechanisms have been proposed. The fact that patients with MAV often have nystagmus implicates dysfunction at the level of the brainstem (particularly the vestibular nuclei), although another obvious possibility is cortical dysfunction affecting the purported vestibular cortex.

Common Historical Features of Migraine-Associated Vertigo

MAV, by any name, is broadly defined and almost “anything goes” with respect to symptoms and timing, as long as one combines a “migrainous” headache and dizziness. A study of MAV found that the most common vestibular symptom was rotational vertigo (70%), followed by intolerance of head motion (48%) and positional vertigo (42%). Less common symptoms include a sensation of motion sickness, floating, rocking, tilting, a sensation of walking on an uneven surface, and lightheadedness. The chronology is similarly variable. Neuhauser found the most common duration to be 5–60 minutes (33%), followed by 1–24 hours (21%), seconds to 5 minutes (18%) and more than 24 hours (2%). There are also reports of symptoms lasting months to years. Onset can be gradual or abrupt. Cutrer proposed that the mechanism of short vertigo attacks was aura, while longer attacks were due to processes resembling central sensitization.

Vertigo or dizziness and migraine headaches need not be simultaneous for patients to qualify for a potential diagnosis of MAV. Neuhauser reported that during symptoms of MAV, 45% of patients consistently have migraine headache, 48% of patients sometimes have migraine headache, and 6% of patients never have migraine headache. During an MAV incident, 70% of patients have photophobia and 64% have phonophobia.

Some patients identify triggers for MAV that are similar to triggers for other migraines, including dietary factors (caffeine, chocolate, alcohol, aged cheeses, monosodium glutamate, nitrites), weather-related triggers (low pressure, storm fronts, changes of season), and internal states (physical exertion, dehydration, sleep deprivation, menses). The time lapse between trigger exposure and symptom onset is usually on the order of minutes to hours but is occasionally more delayed.

Patients with MAV commonly report unusual discomfort from motion and visual input including both bright light and “busy” visual environments. “Motion sickness” symptoms, punctuated by dizziness attacks, may occur with or without headache.

Patients with migraine or MAV can have hearing complaints, especially tinnitus and phonophobia, but these are almost always transient and nonprogressive. Transient synchronous bilateral reduction of hearing is unusual but almost unique to migraine. One study of patients with both migraine and dizziness reported that 66% describe phonophobia, 63% describe tinnitus, 32% describe hearing loss, and 11% describe fluctuating hearing loss and aural fullness. In patients with MAV and hearing symptoms, hearing often fluctuates in both ears at the same time. This, of course, differentiates MAV from Meniere’s disease or labyrinthitis.