Patient Perspective

Migraine – More than a Headache

Introduction

Migraine is a common clinical problem characterized by episodic attacks of head pain and associated symptoms such as nausea, sensitivity to light, sound, or head movement. It is generally thought of as a headache problem, but it has become apparent in recent years that many patients suffer symptoms from migraine who do not have severe headaches as a dominant symptom. These patients may have a primary complaint of dizziness, of ear pain, of ear or head fullness, “sinus” pressure, and even fluctuating hearing loss. Fortunately, treatment regimens long established for the treatment of “classic” migraine headaches are generally effective against these “atypical” symptoms of migraine.

How Common is Migraine?

There are currently more than 48 million Americans with “classic” migraine headaches. In a room with 100 people, nearly 17 are likely to have migraine. This is as common as diabetes and asthma combined. The number of people suffering with atypical forms of migraine is unknown. Females are 3 times more likely to have migraine than males. Although any person can have migraine at any age, migraine is most common between ages 30 and 50. The peak incidence of migraine in females occurs at 35 years of age—at this age, 28% of all females have migraine headaches. The peak incidence of migraine in men occurs at 30 years of age—at this age, about 10% of all males have migraine headaches.

Migraine is a lifelong problem. It may start in childhood and disappear and reappear in new forms throughout an individual’s life. In general, there is a decrease in headache intensity and an increase in the incidence of atypical symptoms of migraine (vertigo, ear pain, bowel symptoms, etc.) as patients mature.  Migraine tends to run in families, so having a relative with migraine makes it more likely that you will have migraine as well.

Surveys show that only 48% of people with migraine headaches have had a diagnosis and are being treated for their headaches. Unfortunately, only 29% of US migraine sufferers are very satisfied with their treatment. This is usually a reflection of a lack of understanding of the nature of migraine and its treatment, or lack of commitment to effective treatments. We hope this material will help you to achieve better control of your migraine symptoms, whatever they are, and improve your quality of life.

How are People with Migraine Different?

Evidence suggests that migraine is an inherited problem of ion channels in the brain. This may result in what is best described as a “sensitive brain”. Most individuals exposed to loud noise, bright light, or excessive motion can adapt to these strong stimuli within minutes, but in the brain of a “migraineur” (migraine patient), the strength of the stimulus continues to grow, and a migraine crisis can occur. This lack of ability to adapt to strong sensory stimulation helps us understand why so many patients have migraine headache or other migraine symptoms that can be provoked by bright light, excessive noise, strong smells, excessive motion, and painful stimuli. 

What Happens During a Migraine Attack?

Abnormal electrical activity may occur in the brain tissues during a migraine attack. Areas of altered activity have been found on brain imaging studies in patients having migraine attacks.  This activity is called “cortical spreading depression,” and it represents a wave of increased activity of nerve cells, followed by decreased activity.  Originally it was thought that blood vessel spasms caused this abnormal activity, but more recently we have learned that this is not the case.  The electrical disturbance is the primary event, which results in blood flow changes.  

The tendency to generate this electrical disturbance is probably enhanced by inheriting certain forms of the ion channels that set the electrical activity in these nerve cells.  Ion channels are like chemical gates – they control the flow of sodium, potassium, and other elements in and out of nerve cells.  Migraine may represent a set of biochemical abnormalities of these gates.  In a sense, individuals with abnormalities are “primed” to generate this abnormal electrical activity.  The addition of something else may push them over the edge and generate the electrical disturbance that underlies migraine attacks.  This is where other triggers come to play a role:  certain foods, weather changes, stress, hormonal changes, sleep disruptions, etc.

The electrical disturbance may cause obvious symptoms.  For example, spreading depression in the vision areas of the brain may result in unusual visual phenomena such as the appearance of spark-like bursts, wavy lines, blind spots, or even complete visual loss in rare cases. Abnormal cortical brain activity over other regions of the cortex can result in temporary confusion, inability to speak, numbness, or even paralysis of any part of the body. These symptoms, which occur due to electrical disturbances at the surface of the brain, typically are brief, lasting no longer than 20 minutes.

The electrical disturbance of migraine frequently involves deeper parts of the brain that are important processing centers for the senses.  We believe that these centers become “hypersensitized.”  This means a person having a migraine who senses pain, motion, or sound will tend to have an exaggerated, distorted experience of the pain, motion, or sound that may be so intense that it is difficult to tolerate.  A hallmark of migraine headache – rare but telltale when it happens – is allodynia, the experience of just simply touching the scalp or even the hair as intolerably painful.  Light, sound, motion, or odors can also become intolerable.  The patient may become so sensitive that he or she has no choice but to withdraw to a quiet, dark place and sleep until the episode has passed. 

Another element in migraine is the release of chemicals by the trigeminal nerve.  This nerve supplies sensation to the entire face, scalp, lining of the eyes, nasal cavity and sinuses, teeth and gums, jaw joints, parts of the neck and ears, even shoulders.  This nerve releases inflammatory peptides – short pieces of proteins – into the tissues nearby.  These peptides (CGRP, substance P, etc.) can cause the local blood vessels to become “leaky,” losing their serum into surrounding tissues.  The tissues can even swell and become painful on this basis.  Classic migraine headache may occur when branches of the trigeminal nerve going to the lining of the brain get inflamed, causing painful throbbing headache due to sensitization of the blood vessels around the brain by the inflammatory peptides.  But if branches going to the sinuses are involved instead of those going to the lining of the brain, the symptoms may not seem like classic migraine headache, but instead may be sinus congestion and runny nose.  These patients often feel that they have sinusitis, but scans show no anatomic abnormality of the sinuses.  

Other symptoms of migraine activity in the brain may include retention of fluid, lethargy, nausea, fainting, anxiety, fever, and even (rarely) seizures.

What is a Migraine Trigger?

A migraine trigger is any environmental, dietary, or physiologic factor that can provoke migraine activity in the brain. 

Environmental triggers

Examples of environmental triggers include odors, bright lights, noise, and other excessive sensory stimuli. Painful stimuli that trigger migraine usually occur in the head and neck. The most common of these are neck injury and spasm, temporomandibular joint pain, and sinus inflammation. Forty percent of migraineurs report that they are affected by weather changes such as barometric pressure changes. The mechanism of this trigger is not currently understood.

Food triggers

There are hundreds of potential food triggers for migraine. Comprehensive lists of foods that may contribute to triggering migraine can easily be found on the Web. In general, these foods fall into two main categories: 1) byproducts of food aging and 2) foods with chemicals similar to the neurotransmitters that our brains use.  Byproducts of food aging are found in fermented products like red wine, aged cheeses, and yeast in fresh bread and yogurt. Foods with chemicals similar to our own neurotransmitters that may aggravate migraine are coffee, chocolate, MSG, excessive amounts of n-6 fatty acids, and the nitrites used as preservatives in many of our prepackaged foods. Dietary triggers are generally not the result of allergies but are direct sensitivities to chemicals in foods and beverages.

There is a common misconception that if a person is sensitive to a food item, they will know it, because they will have migraine symptoms within an hour of eating the particular food item. In fact, some effects may come immediately, but some may be delayed for days. Added to this confusion is the reality that many real food triggers may not cause migraine alone, but only in combination with other partial triggers, which together may provoke an attack of migraine headache or symptoms. For example, some migraineurs can eat chocolate or drink red wine alone with no problem, but will suffer a migraine attack if chocolate and red wine are taken together. 

Physiologic triggers

Perhaps the most common trigger of migraine is stress. Patients commonly report increased symptoms when they are fatigued, suffer lack of sleep, or alter their sleep schedule. Many other physiologic stresses can also trigger migraine, such as hunger, exercise, and pain. Some patients suffer migraine from sleeping too much and cannot understand why most of their weekends are ruined by headaches or dizziness. It is not unusual for undiagnosed sleep apnea to trigger migraines.  Migraines are commonly triggered by hormone changes, like the drop in estrogen levels before the menstrual period or after menopause. Through similar mechanisms, oral contraceptives can also be a trigger for symptoms.

Treatment of Migraine

It seems easy to take pain medications or abortive medications such as narcotics or triptans to suppress symptoms, but when taken frequently, these can worsen the problem by causing rebound symptoms more intense than the original attack. It is unfortunately common that patients get themselves into a vicious cycle, resulting in decreased functioning at work and at home with the expected emotional consequences before preventative treatment is sought.  The best treatment results will be obtained by those patients who work to understand what migraine is and how migraine is affecting their lives. This allows a teamwork approach with the physician and better outcomes. 

The mainstay of treatment for migraine headache and atypical migraine symptoms is trigger identification and avoidance. This requires education about migraine triggers and the use of a migraine diary in which the patient is asked to record their symptoms, the probable trigger for that particular episode, and treatments that helped. Unlike many environmental and physiologic triggers, dietary triggers can be avoided. In general, an attempt to improve lifestyle by reducing stress, improving sleep habits, and adding regular exercise are beneficial. When done maximally, many patients will obtain near complete freedom from their migraines with this treatment alone. 

We generally recommend an initial dietary trial that avoids only the most common migraine triggers. “The Dizzy Cook” website is a good resource for recipes that avoid typical triggers. If good results are not achieved within a few weeks, a comprehensive diet which eliminates all potential migraine triggers is recommended. It may take 6-10 weeks for a patient suffering from severe and debilitating migraine symptoms to respond, but most do. After an improvement in symptoms is achieved, suspected foods can be added to the diet – but slowly, and one at a time, to see whether they are an important trigger for that patient. Despite the difficulty of this kind of a trial, we have found that even the most severely affected migraineurs tend to respond and are generously rewarded for their efforts.

Recent clinical studies have found that altering the composition of fats in the daily diet can improve migraine symptoms. Specifically, increasing dietary eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) while limiting linoleic acid can lead to decreased frequency and severity of headaches. An example of such a diet would include consumption of at least 4 ounces of fish every day, 2 teaspoons of ground flaxseed, while limiting linoleic acid to 1.8% of total caloric intake. Linoleic acid is commonly found in corn oil blends. An alternative to this would be blends of macadamia nut oil, extra virgin olive oil, and regular butter. One example of a recent trial can be found here.

At times, symptoms may be so constant that individual events and their triggers cannot be easily identified. In these cases, it may be helpful to give medications to elevate the threshold above which migraine triggering in the brain occurs. These may be medications originally used for blood pressure control, depression, or seizures which have been found to be easily tolerated and very good at preventing frequent migraine attacks. These include beta blockers, antidepressants, antiseizure medications, calcium channel blockers, and tricyclic antidepressants,. When these are successful, the breakthrough attacks which do occur are usually easily attributed to some particular trigger or aggravating factor, which can then be avoided. It may take 6-8 weeks to respond to a medication, and it is not uncommon for a patient to have to try more than one medication. Patients requiring medications to elevate migraine threshold can realistically expect a 50-80% reduction in symptom intensity and frequency. 

When traditional migraine preventative medications fail, there is a growing list of options. OnabotulinumtoxinA (Botox) injections to the head and neck have been shown to reduce migraine intensity and number of headache days (four or more continuous hours of headache) for patients with chronic migraine (≥15 days/four weeks). Unfortunately, Botox is not as effective for preventing episodic migraine. 

There has also been growing pharmaceutical interest in blocking the effects of calcitonin gene-related peptide (CGRP), a neuropeptide which contributes to migraine symptoms. There are currently two types of drugs that can do this. The first kind are molecules that bind to the CGRP receptor in turn preventing CGRP from binding and having its effects. These drugs typically ended in “gepant” such as ubrogepant (tradename Ubrelvy), rimegepant (Nurtec), and atogepant (Qulipta). Some of the gepants can be used for acute treatment and some can be used for prevention of episodic migraine.  The second, newer class are the CGRP monoclonal antibodies, which bind directly to CGRP thereby preventing it from binding to its receptor and causing symptoms. These drugs typically end in “mab”. The FDA has approved the use of erenumab (Aimovig), eptinezumab (Vyepti), fremanezumab (Ajovy), and galcanezumab (Emgality) for the preventative treatment of episodic and chronic migraine. These are typically given as injections once or twice a month.

If after maximizing the benefits of trigger identification and avoidance and medications to elevate the threshold of migraine, breakthrough headaches are still occurring, medications to abort acute attacks may be prescribed, specifically the triptans. There are triptans that can help improve migraine symptoms both deep in the brain and those painful symptoms associated with sensitized blood vessels around the brain.  Because they can cause rebound, they should not be used more than a few times a month. Doctors’ opinions may vary on this.

Some patients will have occasional severe headaches which can be aborted effectively with triptans without the risk of rebound. These patients should always be on the lookout for an increase in headache frequency and intensity that are the first signs of rebound. Long term treatment of acute headaches with narcotics generally leads to increasing medication needs and must be considered very cautiously, especially in patients with histories of chemical dependency.

Migraine and other related disorders

Migraine and Meniere’s Disease

There is increasing interest among ENT physicians in the connection between migraine and Meniere’s disease. Meniere’s disease is a disorder of the inner ear characterized by episodic fullness, tinnitus (ringing), hearing loss, and vertigo whose cause is poorly understood. It has classically been associated with a pattern of fluid buildup in a portion of the inner ear.  While the prevalence of migraine in the US population is 17%, the prevalence of migraine in patients with Meniere’s disease is 56%, and the prevalence of migraine in patients with bilateral Meniere’s disease is 85%. 

It has been found that the tiny blood vessels in the inner ear are innervated by branches of the trigeminal nerve that innervate the intracranial blood vessels.  We have already seen how this nerve releases peptides in migraine that can cause inflammation of local blood vessels.  Interestingly, experiments have shown that electrical stimulation of the trigeminal nerve has caused blood vessels in the inner ear to become “leaky” as well.  Could it be that this leads to fluid changes in the inner ear, which could affect it severely enough to cause a problem like Meniere’s disease?  This is presently speculative, but we find that many patients with migraine and Meniere’s disease who are treated effectively for migraine have experienced an improvement in their Meniere’s symptoms. 

Migraine and Vertigo

Many epidemiological studies show a link between migraine and vertigo. More than twenty-five percent of migraineurs experience vertigo, and the prevalence of migraine among those with dizziness is 60% more than that of migraine among the general population. Patients who experience dizziness, vertigo, or other vestibular symptoms in addition to migraine may be diagnosed with vestibular migraine. It is thought that the same underlying causes of migraine may also cause vestibular symptoms.

We typically find that patients with vestibular migraine have had classic migraine headaches at some point in the past or have a family history of migraine. However, many patients seen in the balance clinic have had headache-free intervals of up to several years before vertigo begins. In fact, some patients may present without a history of headache. Such patients may instead suffer from other migraine symptoms such as photophobia or phonophobia. The asynchronous presentation of vertigo and headache may cause difficulty in diagnosing this disorder. 

Patients with vestibular migraine may experience episodes of vertigo lasting minutes to days. The vertigo episodes can be spontaneous or caused by a certain head position. This can produce confusion in distinguishing vestibular migraine from benign positional vertigo. Patients can also report vertigo that can be triggered by complex or large visuals or head motion. Often, such patients report motion sensitivity and head motion-induced dizziness (not necessarily vertigo). 

Fortunately, many anti-migraine medications have the same beneficial effects for vestibular symptoms as they do for migraine headaches, reducing the frequency and severity of spells. Medications that affect the CGRP pathway are currently under investigation for their use in patients experiencing vertigo and migraine. Physical therapy may also help manage vestibular symptoms however there is little conclusive evidence. 

Migraine and Otalgia (Ear pain)

Up to 40% of migraineurs report ear pain that lasts anywhere from seconds to months on end. Ear pain has many causes, including infection and Eustachian tube problems in the ear, TMJ, and referred pain from the extensive lining of the throat. Migraineurs who present to the doctor with ear pains frequently complain that their ears are hypersensitive to touch, to wind, and to cold. When an otolaryngologist has ruled out all these other causes of ear pain in a patient with a history of migraine, migraine treatment is often effective in eliminating the pain. 

Migraine and Sinus Pressure

A great deal of confusion exists among patients and their physicians regarding the source of symptoms of facial pressure. While facial pressure is indeed a cardinal symptom of “true” sinusitis, up to 45% of migraine patients report attack-related “sinus” symptoms, including tearing, runny nose, and nasal congestion. In migraine, these symptoms may be caused by a release of peptides by the trigeminal nerve branches going to the mucous membranes in the nasal cavity and sinuses. These symptoms may last only a few minutes or hours during the migraine episode. Sinus symptoms caused by colds or sinus infections tend to last for days. 

Sinus pain, which feels like pressure, is also commonly associated with migraine, and may be the only “headache” experienced in a migraine. In migraine, symptoms tend to last minutes to hours rather than for days, as in sinus infections.

Where can I Learn More about Migraine?

Several websites provide valuable information.  Dr. Timothy Hain maintains an excellent website on vertigo and imbalance disorders at www.dizziness-and-balance.com.  A website specifically devoted to migraine-associated vertigo can be found at www.mvertigo.org.  

Cover of book: Heal Your Headache: The 1-2-3 ProgramIn addition, we typically recommend that patients read the book, Heal your Headache the 1-2-3 Program by David Buchholz, MD. This book provides a comprehensive diet plan composed completely of foods that do not trigger migraine. It is much easier to follow this diet than to be suspicious of every food that you have in your cabinet at home or that you see in the supermarket. It also teaches and emphasizes the concepts of rebound and the additive character of migraine triggers. Patients who have severe migraine-related vertigo may not be able to read a whole book because of their condition. They will benefit greatly from reading the book together with a family member who can help them to stay on track and to understand all the concepts in the book. 

Those patients who do love to read and who have very atypical manifestations of migraine often find great comfort in the experiences of Oliver Sacks, MD, in his book, Migraine. Dr. Sacks is an extremely insightful neurologist with a gift for writing and who himself had migraines beginning at age 2. He has collected an astonishing series of patient stories with both common and extremely unusual symptoms, all attributable to migraine mechanisms. 

Treatment Guidelines for Physicians

For treatment we first encourage a strict migraine control diet, eliminating common migraine culprits including chocolate, wines, caffeine, certain cheeses, monosodium glutamate (MSG) as well as less frequently recognized problem foods containing yeast (yogurt, sourdough, freshly made bread), nuts, nut products, citrus fruits, tomatoes, onions, alcoholic beverages, and artificial sweeteners.  Glutamate can occur in foods not only through the addition of MSG, but also by hydrolyzing (breaking down) proteins Labels that include “hydrolyzed casein,” “hydrolyzed yeast extract,” etc., are likely to include glutamate.

We also encourage a regular sleep schedule and aerobic exercise program. Patients are also counseled to avoid vasoconstrictive medications such as psuedoephedrine, and to minimize the use of triptans, which may cause rebound symptoms. 

When patients follow these guidelines and still have migraine-associated symptoms, we emphasize prophylactic medications in preference to the “quick fix” agents such as fiorinal, triptans, narcotics, or steroids.  Effective prophylactic medications are chosen based on the patient’s other medical problems and tolerance of side effects.  Some suggested regimens follow:

Beta-blockers

Propranolol LA 60 mg/d increasing as needed up to 240 mg/d.  Reactive airway disease (e.g., asthma) and diabetes are usually contraindications.  Depression may be worsened by beta-blockers.  Nadolol has fewer such CNS side effects; it is started at 20 mg/d and increased every 2-4 weeks as needed up to 120 mg/d. Metoprolol may be a cheaper alternative and starts at 50 mg BID increasing as needed up to 200 mg.

Anticonvulsants

Topiramate has been shown to be a very effective migraine prophylactic agent.  It is started at 25 mg daily and increased weekly to a goal of 100-200 mg twice daily.  Patients often report cognitive slowing (“brain fog”) when they start this medication, but this usually resolves over a few weeks with this plan for a slow increase in the dose.  The main side effect at higher doses is a tingling sensation.  Rarely, patients can develop kidney issues – metabolic acidosis or kidney stones.  If there is a history of stones, regular monitoring of the urine may be necessary. 

Depakote is also an effective prophylactic agent but does not need to be titrated. 250-500 mg BID is well tolerated and can come in an extended-release formulation. It has a black box warnings for hepatotoxicity and pancreatitis so be mindful of administration in patients who drink excessive amounts of alcohol or who have prior liver or pancreatic disease.

Sodium valproate 250-500 mg BID is usually well tolerated, but liver function tests and platelets should be monitored.  Gabapentin is usually well tolerated.  It is started at a low dose of 300 mg a day, with weekly escalating doses to a first target dose of 300 mg three times a day (900 mg total).  Then it can be increased gradually to another target dose of 1800 mg total a day (in 3 divided doses), or until side effects (usually sedation) appear. It has the inconvenience of frequent dosing, but with a low adverse effect profile.  Dosing adjustments are necessary for renal insufficiency, and the medication should not be used in children under 12 years old.  

Calcium channel blockers

Diltiazem CD 120 mg/d increasing as tolerated to 240-480 mg total/d, often in two divided doses.  Constipation and hypotension are the most common side effects, but this is often the best-tolerated regimen.

Antidepressants

Nortriptyline starting at LOW doses (10 mg/d) and slowly increasing to 50-100 mg at night.  Higher doses (100-200 mg) may occasionally be needed.  Levels can help guide therapy.  Dry mouth, weight gain, and sedation are the most common side effects.  Patients with poor sleep often benefit the most from these agents.  

Selective serotonin reuptake inhibitor (SSRI) agents have less proven benefit in migraine control.  We have found mixed agents helpful, such as venlafaxine (Effexor).  The full starting dose of Effexor XR 37.5 mg can have prominent serotonergic effects, including, on occasion, panic attacks.

But the Effexor XR 37.5mg capsules can be opened, and the dose divided in into two or three parts.  Each part can be placed in a closed gelatin capsule and taken as a low starting dose once daily for a week.  The dose can be gradually increased to the full 37.5 mg.  As the dose is increased, the drug has greater effects on blocking norepinephrine reuptake, which may be the salient effect on migraine.  So patience is necessary as a long time may be needed to reach a fully therapeutic dose.  Heart rate and blood pressure should be monitored, as these can be dose-limiting.

All patients are cautioned that migraine symptoms often do not respond quickly to these interventions.  Great patience is required of the patient and physician as 6-8 weeks of diet changes or the full dose of any new medication may be needed before benefits are seen.

Anxiety, depression, and even panic attacks are frequent accompanying diagnoses in these patients.  These diagnoses should be recognized and discussed.  The choice of a prophylactic medication may also be influenced by these other conditions.

One of the best resources for migraine therapeutics currently available is Lawrence Robbins’ Management of Headache and Headache Medications. It very clearly outlines strategies for first line, second line, and combination therapy for migraine and other headache types in an easy-to-use handbook format. 

By Drs. Michael Teixido and John Carey. Updated June 2022 by Pavan Krishnan, pre-doctorate research fellow at Johns Hopkins

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  48. Barbanti P, Fabbrini G, Pesare M, Cerbo R. Neurovascular symptoms during migraine attacks. [abstract] Cephalalgia. 2001;21(4):295.
  49. Kaniecki R. Migraine headache exacerbation with sumatriptan injection: a sign of supratherapeutic dosing? [abstract] Cephalalgia. 2001;21(4):413.
  50. Kayan A, Hood JD. Neuro-otological manifestations of migraine. Brain. 1984;107:1123.
  51. Wladislavosky-Waserman P, Facer G et al. Meniere’s disease: a 30-year epidemiologic and clinical study in Rochester, MN, 1951-1980. Laryngoscope. 1996;94:1098-1102.
  52. Vass Z, Dai CF et al. Co-localization of the vanilloid capsaicin receptor and substance P in sensory nerve fibers innervating cochlear and vertebro-basilar arteries. Neuroscience. 2004;124:919-927.
  53. Buchholz D. Heal your Headache the 1-2-3 Program. Workman Publishing Company, New York, NY. 2002.
  54. Sacks O. Migraine. Vintage Books, New York, NY. 1992.
  55. Robbins L. Management of Headache and Headache Medications, 2nd Edition. Springer-Verlag, New York, NY. 2000. 
  56. Burch R, Rizzoli P, Loder E. The Prevalence and Impact of Migraine and Severe Headache in the United States: Figures and Trends From Government Health Studies. Headache. 2018;58(4):496-505. doi:10.1111/head.13281
  57. Ramsden C E, Zamora D, Faurot K R, MacIntosh B, Horowitz M, Keyes G S et al. Dietary alteration of n-3 and n-6 fatty acids for headache reduction in adults with migraine: randomized controlled trial BMJ 2021; 374 :n1448 doi:10.1136/bmj.n1448
  58. Diener HC, Dodick DW, Aurora SK, Turkel CC, DeGryse RE, Lipton RB, Silberstein SD, Brin MF; PREEMPT 2 Chronic Migraine Study Group. OnabotulinumtoxinA for treatment of chronic migraine: results from the double-blind, randomized, placebo-controlled phase of the PREEMPT 2 trial. Cephalalgia. 2010 Jul;30(7):804-14. doi: 10.1177/0333102410364677. Epub 2010 Mar 17. PMID: 20647171
  59. Gazerani P. Migraine and Diet. Nutrients. 2020;12(6):1658. Published 2020 Jun 3. doi:10.3390/nu12061658
  60. https://vestibular.org/article/diagnosis-treatment/types-of-vestibular-disorders/vestibular-migraine/

The following website compiles many of the references related to migraine associated vertigo and has an active forum on the subject:

www.mvertigo.org

Vitamins and Dietary Supplements

Certain vitamins and food supplements may provide a benefit in terms of headache prevention. Many unsubstantiated claims can be found on the internet and at health food stores. The best evidence exists for the agents below (published peer reviewed, randomized controlled trials, albeit small ones in some cases). Side effects are typically mild.

  • B2/Riboflavin – up to 400mg / day
  • Magnesium – up to 400mg 2x / day (diarrhea possible)
  • Coenzyme Q10 – up to 100mg 3x / day (expensive) 

Note: There are a few companies that package more than one of the above vitamins / supplements into a single pill for convenience. One such product is “Migravent”, info. available at www.migravent.com; another is “MigreLief”, info. available at www.migrelief.com.

  • Melatonin – There is some weaker evidence that melatonin, a hormone that helps regulate sleep, may help headaches if 3–6 mg is taken an hour or so before bedtime. Significant side effects are rare. Probably most useful in treating cluster headaches.

The following are used in Europe more commonly, but are less regulated or reliable in the US:

  • Butterburr (Petasites hybridus) extract, Petadolex brand (pyrrolizidine alkaloid free), 50–75mg twice a day with food (expensive)
  • Feverfew (Parthenium integrifolium) 50mg+ per day (inexpensive)

We do not specifically endorse any brand name item, nor do we have any financial interest in any of these products.

Migraine Diet

(Thanks to Dr. Jason Rosenberg and the Johns Hopkins Headache Center for this compilation, which we have modified from our experience.) 

 Food may play a significant role in the frequency of migraine. Although some migraine patients find that eating certain foods will provoke symptoms every single time, the effect of diet may be less obvious. In general, the more “trigger” foods you consume, the more symptoms you may have. The hope is that by avoiding these possible triggers, the better off you will be. Eating regularly timed meals, avoiding hunger, avoiding dehydration, and avoiding skipping meals is probably more important than the specific foods you do or do not eat. Try following this list as strictly as possible for at least two months. If it helps, you may gradually add back your favorite foods one at a time, keeping track of your headaches as you do so.

Category Foods to Avoid, Reduce, or Limit Foods that are OK
Caffeine No more than 2 servings / day. Do not vary the amount or timing from day to day. Coffee, tea, colas, Mountain Dew, Sunkist, certain medications (Anacin, Excedrin) Decaffeinated coffee, herbal or green tea, caffeine-free sodas, fruit juice (see below)
Snacks / Desserts Chocolate, nuts (peanuts, especially), peanut butter, seeds Fruits listed below, sherbet, ice cream, cakes, pudding, Jello, sugar, jam, jelly, honey, hard candy, cookies made w/o chocolate or nuts
Alcohol Avoid all, especially: ales, Burgundy, chianti, malted beers, red wine, sherry, vermouth.  Note: some medications contain alcohol (Nyquil) Non-alcoholic beverages
Dairy Aged cheeses: Brie, blue, boursault, brick, Camembert, cheddar, Emmentaler, gouda, mozzarella, Parmesan, Provolone, Romano, Roquefort, stilton, Swiss, etc. Buttermilk, chocolate milk, sour cream. Eggs and yogurt should be limited to 2-3 times per week Other cheeses: American, cottage, cream cheese, farmer, ricotta, Velveeta.

Milk, Egg substitute

Cereals & Grains Fresh breads and yeast products, fresh bagels, fresh doughnuts, yeast extracts, brewer’s yeast, sourdough(*freezing bread may inactivate yeast) Commercial breads (white, wheat, rye, multi-grain, Italian), English Muffins, crackers, rye, toast, bagels, potatoes, rice, spaghetti, noodles, hot or dried cereals, oatmeal
Meats Aged, canned, cured, or processed meats (bologna, pepperoni, salami, other pre-packaged deli meats), pickled meats or fish, salted or dried meats or poultry, hot dogs, sausages, jerky Fresh / unprocessed meats, poultry, fish, lamb, pork, veal, lamb, tuna
MSG (monosodium glutamate) Avoid glutamate in all its multiple forms: MSG, “natural flavoring,” “flavor enhancer,” etc. Soy sauce, foods containing “hydrolyzed protein products” or “autolyzed yeast”, canned soups, bouillon cubes, Accent, meat tenderizers, seasoned salts. Pickled, preserved or marinated foods Salt and other spices, butter, margarine, cooking oil, white vinegar, salad dressing (small amounts)
Sweeteners Aspartame (Equal, Nutrasweet) (somewhat controversial) Sucrose (sugar), high fructose corn syrup, sucralose (Splenda), saccharin (Sweet ’n Low) 
Vegetables Pole or broad beans, lima beans, Italian beans, lentils, snow peas, fava beans, Navy beans, pinto beans, pea pods, sauerkraut, garbanzo beans, onions, olives, pickles Asparagus, beets, broccoli, carrots, corn, lettuce, pumpkins, spinach, squash, string beans, tomatoes– all those not listed
Fruit Avocados, figs, papaya, passion fruit, raisins, red plums. Limit bananas and citrus fruit & juice (orange, lemon, lime, grapefruit, tangerines) to ½ cup per day Apples, berries, peaches, pears, prunes, fruit cocktail
Mixed Dishes Beef stroganoff, cheese blintzes, frozen meals / TV diners, lasagna, macaroni and cheese, pizza

Note that tyramine, nitrites, nitrates, and MSG are found in many foods and may be difficult to avoid. Learn to read labels.

While there are few consistent scientific studies of the effect of food on headaches, there is a general consensus about which foods may be important to avoid. The above list is drawn from various sources including the National Headache Foundation, journal articles, websites and books (such as David Buchholz’s Heal Your Headache: The 1-2-3 Program for Taking Charge of Your Pain). © 2006 Jason Rosenberg, MD