Migraine-associated vertigo is vertigo associated with a migraine, either as a symptom of migraine or as a related but distinct neurological disorder; when referred to as a disease unto itself, it is also termed vestibular migraine or migraine-related vestibulopathy. Migraine causes more vertigo than any other medical condition. Approximately 27-42% of migraine patients suffer from associated vertigo.
The vertigo itself is a feeling of spinning or other motion when the sufferer is not actually moving. It is often accompanied by nausea and may lead to vomiting. As a symptom of migraine, it may also be accompanied by other migraine symptoms either before, during, or after the episode of vertigo. In some patients, however, the vertigo is the only symptom of migraine.
In a recent study, the prevalence of migraine and vertigo was 1.6 times higher in 200 dizziness clinic patients than in 200 age and sex-matched controls from an orthopaedic clinic. Among the patients with unclassified or idiopathic vertigo, the prevalence of migraine was shown to be elevated. In another study, migraine patients reported 2.5 times more vertigo and also 2.5 motes dizzy spells during headache-free periods than the controls. This demonstrates a causal relationship between migraine with vertigo and dizziness.
MAV may occur at any age with a female:male ratio of between 1.5 and 5:1. Familial occurrence is not uncommon. In most patients, migraine headaches begin earlier in life than MAV with years of headache-free periods before MAV manifests. 
According to medical practices treating migraines, 27-42% of patients report episodic vertigo. About 36% of these experience vertigo during headache-free intervals. The remainder experience vertigo preceding onset or during the headache itself.
The pathophysiology of migraine is not completely understood, therefore, neither is that of migraine-associated vertigo. However, both central and peripheral defects have been observed.
According to the latest theory, the process starts with a patient who has a hyperexcitable brain. Add to that, environmental events which push the individual’s brain past a threshold, leading to electrical changes (cortical spreading depression (CSD), which causes aura. CSD also stimulates the trigeminal nucleus caudalis (TNC), and causes the release of inflammatory neuropeptides (CGRP) which produce vasodilation and sensitization (allodynia) in the trigeminal nerve circuit. Pain and sensitization lead to a positive feedback loop.
As to why vertigo can be a symptom of migraine, John Carey, M.D. of Johns Hopkins, presented the following hypothesis at the Spring 2008 Conference on Migraine-Associated Vertigo: “The blood vessels of the cochlea and vestibular labyrinth are innervated by branches of V1 of the trigeminal nerve.” This causes plasma extravasation with substance P in the stria vascularis and cochlear tissues.
According to Hain, an asymmetric release of neuropeptides result in the sensation of vertigo; if the release is symmetric, the patient feels an increased sensitivity to motion due to an increased vestibular firing rate during head movements. It has also been suggested that CGRP and other neuropeptides produce a prolonged hormone-like effect as these diffuse into the extracellular fluid. “This may explain the prolonged symptoms in some patients with migraine-associated vertigo, as well as the typical progression of persistent spontaneous vertigo followed by benign positional vertigo and then motion sensitivity.”
Brantberg, Trees & Baloh proposed in 2005 that there are multiple migraine-associated vertigo syndromes and multiple genes and environmental factors underlying them. Their study showed that typical migraine headaches progressed over time into attacks of vertigo and about half of the patients had visual aura. Only half of the patients had ever had a headache simultaneous with an attack of vertigo.
Vertigo is a medically recognized term for the symptom of vestibular disturbance. It may include a feeling of rotation or illusory sensations of motion or both. The general term dizziness is used by nonmedical people for those symptoms but often refers to a feeling of light-headedness, giddiness, drowsiness, or faintness, all of which must be differentiated from true vertigo, since the latter symptoms might have other causes.
Migraine-associated vertigo, as a symptom, may manifest as episodic rotational vertigo (with or without nausea and vomiting), positional vertigo, constant imbalance, movement-associated dysequilibrium, illusory self or object motion, head motion intolerance, or light-headedness. Other migrainous symptoms may occur, such as photophobia, phonophobia, osmophobia, or visual or other auras. There is usually minimal or no nystagmus, which differentiates it from other peripheral vestibular syndromes. If nystagmus does present, it is often directed vertically. Tinnitus and hearing loss may occur. Symptoms may appear during the prodrome or precursor stage of the attack, during the headache (if the patient gets headache), or often during headache-free intervals.
Motion sickness occurs more frequently in migraine patients (30-50%) than in controls. . Benign Paroxysmal Vertigo Syndrome of Children is an example of migraine-associated vertigo in which headache does not occur. Basilar migraine consists of two or more symptoms (vertigo, tinnitus, decreased hearing, ataxia, dysarthria, visual symptoms in both hemifields or both eyes, diplopia, bilateral paresthesias, paresis, decreased consciousness and/or loss of consciousness) followed by throbbing headache. Auditory symptoms are rare. However, a study showed a fluctuating low-tone sensorineural hearing loss in more than 50% of patients with BAM with a noticeable change in hearing just before the onset of a migraine headache. The attacks of vertigo are usually concurrent with the headache and the family history is usually positive. The diagnostician must rule out: TIAs, and paroxysmal vestibular disordered accompanied by headache.
There is also a familial vestibulopathy, familial Benign Recurrent Vertigo (fBRV), where episodes of vertigo occur with or without migraine headache. Testing may show profound vestibular loss. The syndrome responds to Acetazolamide. Familial Hemiplegic Migraine (FHM) has been linked to mutations in the calcium channel gene. (Ophoff et al. 1966 cf. Lempert et al.) 
BPPV Migraine is commonly associated with benign paroxysmal positional vertigo (BPPV), the most common vestibular disorder in patients presenting with dizziness. The two may be linked by genetic factors or by vascular damage to the labyrinth.
Ménière’s disease There is an increased prevalence of migraine in patients with Ménière’s disease and migraine leads to a greater susceptibility of developing Ménière’s disease. But they can be distinguished. Migraine-associated vertigo may go on for days, weeks, months, even years, whereas Ménière’s disease never goes on longer than 24 hours.
Motion sickness is more prevalent in patients with migraine.
Psychiatric syndromes Dizziness and spinning vertigo are the second most common symptom of panic attacks, and they can also present as a symptom of major depression. Migraine is a risk factor for developing major depression and panic disorder and vice versa.
Lembert and Neuhauser propose criteria for definite and probable migraine-associated vertigo.
A diagnosis of definite migraine-associated vertigo includes a case history of
A diagnosis of probable migraine-associated vertigoincludes a case history of episodic vestibular symptoms of at least moderate severity and one of the following:
They add that, in patients with a clear-cut history, no vestibular tests are required. Other historical criteria which are helpful in making the diagnosis of migraine-associated vertigo are vertiginous symptoms throughout the patient’s entire life, a long history of motion intolerance, sensitivity to environmental stimuli, illusions of motion of the environment, and vertigo that awakens the patient.
Treatment of migraine-associated vertigo is the same as the treatment for migraine in general.
The vasoconstrictors DHE, ergotamine, isometheptene constrict blood vessels of the brain. Triptans, such as rizatriptan (Maxalt), eletriptan (Relpax), sumatriptan (Imitrex), zolmitriptan (Zomig), and naratriptan (Amerge) bind to serotonin receptors, reducing pain by blocking TNC and reducing secondary sensitization.
It is recommended to quit all food triggers for three months as a trial preventative approach. Proposed migraine trigger substances include caffeine, chocolate, MSG, processed meats and fish, fermented dairy products, nuts, alcohol and vinegar, citrus fruits, dried fruits along with some other fruits, some vegetables, especially onions, yeast, and aspartame. The three major substances thought to be causative triggers are histamine, phenylethylamine, and tyramine.
If after three months, there is no clear improvement, the patient will move on to prophylactic medications. If, however, there is significant help with the removal of trigger foods, the job is to add back foods, one at a time, to find out which, if any, is the culprit (or are the culprits).
According to Hain, the mechanisms of most of the prophylactic medications are not well understood, but they all work about 75% of the time and take weeks to months to work.  He categorizes prophylactic medications as follows:
CSD blockers: Anticonvulsants. These probably raise the threshold for CSDand include the following: Topiramate (Topamax) is about 75% effective. Side effects include, but are not limited to, weight loss, hair loss, speech disturbance, difficulty in word-finding and tingling in the hands and feet. Other anticonvulsants used include: gabapentin (Neurontin), divalproex sodium (Depakote) and levetiracetam (Keppra).
Mysterious mechanism agents: Beta blockers and L-channel calcium channel blockers Beta blockers are 75% effective though the mechanism of action is unclear. Any beta blocker will work: propranolol, metoprolol, or atenolol. Side effects include fatigue, slow pulse and hypotension. It takes one month for them to work.
L-channel calcium channel blockers including: Verapamil is 75% effective. The mechanism is not well understood, although it possibly blocks TNC or possibly relates to the calcium channel gene. It takes two weeks to work. The main side effect is constipation.
Neurochemical modulators: Antidepressants Venlafaxine (Effexor) is 80% effective. The mechanism is not very clear. Effexor is an SNRI and SSRI. It is very useful in managing the sensory amplifications seen in migraine. It is inexpensive. The side effects are minor. However, high doses have a difficult withdrawal syndrome.