Vestibular migraine (VM) is becoming an increasingly recognized cause of episodic vertigo. It is defined as vertigo or dizziness caused by migraine (1) or recurrent vertigo as a symptom of migraine (2). The terminology for vestibular migraine is varied and has not been uniform. Migraine associated vertigo, migrainous vertigo, migraine variant, benign recurrent vertigo, and migraine-related vestibulopathy have all been used and applied to roughly the same patient population. “Vestibular Meniere’s disease” is considered to be a migraine equivalent. The pathophysiological relationship between migraine and vertigo is poorly understood. It is unclear if the vertigo might be an aura like the visual aura of spreading depression, part of the headache event like photophobia, caused by transient alterations in the vestibular labyrinth, or due to another process (3). In our clinic, the term migraine variant is often used as a general term to describe vertigo due to migraine that is associated with or without an actual headache. Most patients with VM do not experience headache with their episodes of vertigo. These spontaneous episodes can last for seconds to days and are associated with the typical migraine headache symptoms such as light sensitivity (photophobia), noise sensitivity (phonophobia), visual scotomas (black or white spots), or migraine aura. Common migraine triggers such as stress, abnormal sleeping patterns, dietary triggers, and hormonal fluctuations may bring on an episode of vertigo.
Vestibular migraine is a clinical diagnosis and is made after other possible causes have been ruled out. Neuhauser et al proposed two separate diagnostic categories: definite VM and probable VM (4). The diagnostic criteria are as follows (4):
Definite Vestibular Migraine:
Comment: Vestibular symptoms are rotational vertigo or another illusory self or object motion. They may be spontaneous or positional. Vestibular symptoms are “moderate” if they interfere with but do not prohibit daily activities and “severe” if patients cannot continue daily activities.
Probable Vestibular Migraine:
According to these diagnostic criteria, Neuhauser et al reported that the frequency of definite VM was 7% in a group of 200 consecutive dizziness clinic patients, and 9% in a group of 200 migraine patients (4).
A long-term evaluation of the clinical criteria for definite and probable VM performed by Radtke et al showed that approximately 9 years after initial diagnosis 85% of patients had a confirmed diagnosis of definite VM and that 14 of 28 patients initially classified as probable VM met criteria for definite VM (5). This indicated high reliability and validity of the proposed diagnostic criteria for VM.
When evaluating patients with episodic vertigo it is important to see the patient when they are “dizzy” or in an acute vertigo attack. All of our dizzy patients are told that they can be added on to our schedule as an “urgent add-on” with worsening symptoms. This allows for better description of symptoms and ultimately a more accurate diagnosis. Seeing patients during their episodes, using infrared video oculography, and obtaining serial hearing tests are essential in helping to determine the cause of vertigo attacks that last for seconds to days.
Imaging studies such as an MRI brain with and without contrast with attention to the internal auditory canals, CT scans of the temporal bone, further vestibular studies (VNG, VEMP, rotatory chair), and labs are ordered appropriately on a case-by-case basis in order to aid diagnosis and evaluate for other possible causes of dizziness and vertigo.
Treatment of VM essentially mirrors that of migraine headaches. Improvement of vertigo symptoms after treatment with migraine abortive medication (Sumavel, Treximet, Maxalt, Relpax, Imitrex, Cambia etc.) may help in determining the diagnosis of VM.
Depending on the response to abortive medication, frequency, and severity of VM attacks, preventative medication may be indicated. Treatment of VM is based more upon clinical preference and experience than actual clinical studies. Typically, we start with dietary modification with a low tyramine diet. Adequate hydration with 2-liter mixture of 2/3 water and 1/3 electrolyte beverage is also recommended. If there is no improvement, migraine preventative medications are used. These medications include Topamax, Namenda (a non-specific glutamate antagonist), amitriptyline or nortriptyline, propranolol, and verapamil. Other preventative medications that have been used in the treatment of VM include venlafaxine and valproic acid.
The patient’s comorbid conditions are also factored in when prescribing preventative medication for VM. Topamax is recommended in obese individuals, as weight loss is a common side effect. Namenda is a generally well-tolerated medication with minimal side effect for those patients with “hypersensitivity” to medication. Amitriptyline and nortriptyline may be considered in VM accompanied by depression. Propranolol has shown good efficacy in prevention of migraine headache and has additional benefit in patients with hypertension. Verapamil has been less effective in studies (6).
Baier et al performed a retrospective study assessing the treatment of VM with migraine prophylactic medications versus patients without treatment. In the treatment group, the primary medications used were beta-blockers and to a lesser degree valproic acid, Topamax, butterbur root extract and lamotrigine (7). Patients with prophylactic medication experienced a decrease in frequency (80%), duration (65%), and intensity (68%) of episodic vertigo attacks while the untreated group showed only a decrease in intensity of attacks (7).
According to the American Migraine Study II, the prevalence of migraine in the United States in 1999 was 18.2% among females and 6.5% among males, which was similar to the results from the American Migraine Study conducted in 1989. At that time the prevalence was 17.6% in females and 5.7% in males (8).
VM effects more than 1% of the general population (2). By comparison, the prevalence of Ménière’s disease in the United States is 190 per 100,000 or 0.19 %, which would make VM more common than Meniere’s disease (9).
Although VM episodes can last from seconds to days, the typical length of episodes seen in our clinic are hours to days. VM needs to be distinguished from Meniere’s disease, which is another cause of vertigo that can last for hours to days. As noted above, there may be a link between Meniere’s disease and migraine. The lifetime prevalence of migraine with or without aura was higher in Ménière’s disease patients (56%) when compared to controls (25%) (10). Furthermore, 45% of the patients with Ménière’s disease always experienced at least one migrainous symptom with Ménière attacks and the frequent occurrence of migrainous symptoms during Ménière attacks suggests a pathophysiologic link between the two diseases (10).
In our clinic, because of the suggested pathophysiological link between Meneire’s disease and migraine, patients with a diagnosis of Meniere’s disease are treated with migraine prophylactic and abortive medications along with low sodium diet and diuretic therapy. However, patients with a diagnosis of VM are not treated as if they have Meniere’s disease.
The following paper studies the link between Meniere's disease and migraine: