Migraine-associated vertigo

Migraine associated vertigo is dizziness associated with a migraine headache condition. Migraines causes more vertigo than any other medical condition. When dizziness occurs as a result of migraines this is known as "migraine associated vertigo". Approxmiately 27-42% of migraine patients suffer from associated vertigo.

Epidemiology

'"Migraine causes far more vertigo than any other condition'".

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.

Pathophysiology

The pathophysiology of migraine is not completely understood, nor 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.

Why is vertigo a manifestation 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.

Symptoms and Syndromes Associated with MAV

Vertigo is a vestibular disturbance whereas dizziness is not. Vertigo includes a feeling of rotation and/or illusory sensations of motion. Dizziness is a feeling of light-headedness, giddiness, drowsiness, and/or faintness.

“In patients with migraine-associated vertigo, the first symptoms to appear are typically headache, with vertigo beginning several years later.”

Migraine-associated vertigo 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, and/or light-headedness. Migrainous symptoms during vertigo may occur, such as photophobia, phonophobia, osmophobia, and/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, during the 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.

Cyclic Vomiting is a syndrome in which people suddenly develop vomiting, usually without headache or hearing symptoms.

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.)

Vertigo Syndromes Associated with Migraine

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 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.

Diagnosis

Headache is not required to make the diagnosis of migraine-associated vertigo.. Lembert and Neuhauser propose criteria for definite and probable migraine-associated vertigo.

Definite migraine-associated vertigo: A) Episodic vestibular symptoms of at least moderate severity. B) Current or previous history of migraine according to the 2004 criteria of the HIS (Headache International Society) C) One of the following migrainous symptoms during ≥ 2 attacks of vertigo: migrainous headache, photophobia, phonophobia, visual or other auras. D) Other causes ruled out by appropriate investigations.

Probable migraine-associated vertigo: A) Episodic vestibular symptoms of at least moderate severity. B) One of the following: 1) Current or previous history of migraine according to the 2004 criteria of HIS. 2) Migrainous symptoms during vestibular symptoms. 3) Migraine precipitants of vertigo in more than 50% of attacks: food triggers, sleep irregularities, hormonal change. 4) Response to migraine medications in more than 50% of attacks. C) Other causes ruled out by appropriate investigations.

They add, 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 which awakens the patient.

Treatment

Abortive treatments

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.

Prophylactic Approaches

The Migraine Diet

The first line of prophylactic approach is strict adherence to the “migraine diet.” David Buchholz, M.D., in his Book, Heal Your Headache, gives a comprehensive version of the diet. In short, it is recommended to quit all food triggers for three months, in order to rid the body of all metabolites. These foods 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 is the culprit.

Prophylactic medications

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 CSD and 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.

Tricyclics – amitriptyline/nortriptyline. Hain calls these “messy agents.” They work as central antihistamines, affecting norepinephrine and serotonin receptors.

Supplements

Riboflavin has been rigorously studied and has demonstrated a reduction of migraine days and hours by 44%, although with no reduction in intensity of the headache.