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Volume 2, Issue 4, Pages 209-212 (December 2004)


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Managing migraine: A women’s health issue

Kersti Bruining, MD (FAAN)aCorresponding Author Informationemail address

Three out of four migraine sufferers are women. Despite medical advances, migraines are underdiagnosed and undertreated—in fact, fewer than half of all sufferers seek a physician’s help. On the plus side, successful management of this debilitating condition is gratifying for physicians and patients alike.

Article Outline

Abstract

What else do we know about migraine?

Recognizing a migraine for what it is

Migraine: the great masquerader?

The role of imaging studies

The origins of migraine

Managing migraines: setting goals

Identifying migraine triggers

Treatment: acute and prophylactic

References

Web-based resources on migraine

Copyright

There are 28 million migraine sufferers in the United States, and 21 million of them are women. The oneyear prevalence of migraine is 18% in women, and 6.5% in men, according to a population-based study reaching 20,000 households.1

What else do we know about migraine? 

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Prevalence of migraine is highest in the 25 to 55 age range. It rises through early adult life, peaks in approximately the mid-30s, then begins to decline.

Prevalence at all postpubertal ages is greater among women, though at the peak age of occurrence the female:male ratio is 3:1.

Interestingly, at prepubertal ages the rate of onset of migraine is slightly higher in boys than in girls.

Half of all persons suffering from migraine develop headaches before age 20, with the headaches often beginning in the early childhood years.

Migraine headaches have a significant adverse impact on quality of life. Between half and three-quarters of headache sufferers say they are less productive at work, in school, and at home, and that the headaches force them to miss family and social events.1

Sadly, fewer than half of all migraine sufferers consult a physician.2 The overwhelming majority of those who do seek help turn to their primary care physician.3

Key points 

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Half of all persons suffering from migraine develop headaches before age 20. Prevalence peaks in the mid-30s, then starts to decline.

Recurrent headaches that are moderate to severe in intensity are considered migraines until proved otherwise.

A rapidly decreasing estrogen level is substantially more likely to result in a migraine than a gradually decreasing level.

Fewer than half of all migraine sufferers consult a physician.

Migraines are easily triggered by variations in cycles of sleeping, eating, exposure to caffeine, and stress levels. A migraineur is most able to limit headache frequency by maintaining a “nearly boring” regular routine.

A goal of 50% reduction in headache frequency and severity can be reasonably attained by preventive treatment.

Recognizing a migraine for what it is 

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The International Headache Society criteria for migraine and other headaches, published in 1988 and updated in 2004,4 remain the standard (Table 1). Not all migraine sufferers meet the IHS criteria, however. Several other important diagnostic considerations help make migraine easier to identify (Table 2). Overall, headache specialists widely believe that recurrent headaches that are moderate to severe in intensity are migraines until proved otherwise.

TABLE 1.

International Headache Society criteria for migraine

Five or more attacks lasting between 4 and 72 hours

Two or more of the following features:
Unilateral

Pulsating

Moderate or severe intensity

Aggravated by routine physical activity


One or more of the following:
Nausea and/or vomiting

Photophobia and phonophobia


Not attributable to another disorder

TABLE 2.

Migraine: Key diagnostic points

41% of migraine patients report bilateral pain

50% of migraine headaches are nonpulsatile

Nausea is extremely common, but vomiting occurs in less than one-third of patients

Migraine with aura (previously known as classical migraine) is migraine with an accompanying neurologic disturbance. The disturbance may occur either before or during the migraine. The most common disturbance is visual—for example, the image of sparkling lights or a loss of a portion of the vision, known as scotoma. Table 3 summarizes features typically associated with migraine, including its predictable perimenstrual flare-ups.5

TABLE 3.

Features commonly associated with migraine

Predictable perimenstrual occurrence of headache

Characteristic triggers (see Table 6)

Improvement with sleep

Positive family history of migraine

Childhood precursors (motion sickness, episodic vomiting, or episodic vertigo) or osmophobia (or aversion to strong odors) during the migraine

Stereotypical symptoms occurring shortly before the migraine, such as yawning, stiff neck, craving for sweets

Migraine: the great masquerader? 

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Migraine is frequently mistaken for other types of disorders.

Tension headache is a much less distinctive and poorly understood type of headache, and is frequently mimicked by underlying diseases. Tension-type headache and migraine have many overlapping features. In fact, there is current debate whether tension-type headache is a distinct entity or simply a mild form of migraine.

Migraines are also commonly mistaken for sinus headaches, primarily because the pain of both conditions may localize in the region surrounding the eyes and frontal and maxillary sinuses. Migraine pain is considered a referred pain from the trigeminal nerve pathways. Many patients report that changes in weather trigger headaches; they assume that the headaches are related to sinus pathology and don’t recognize that weather changes may be a trigger for migraine. Up to 50% of migraine sufferers also report nasal congestion and tearing with their migraines. Diagnostically important is their fact that both the pain and these nasal symptoms generally resolve within hours rather than many days, as might be expected with acute sinusitis.6

The role of imaging studies 

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The diagnosis of migraine is based on clinical criteria. After a systematic review of the efficacy of diagnostic testing, the American Academy of Neurology has recommended that neither CT scan nor MRI of the brain is likely to increase the diagnostic yield or to uncover pathologic entities in patients whose symptoms are consistent with migraine (Table 4).7 Thus, the routine use of imaging studies in patients whose headaches fit the broad definition of recurrent migraine is not warranted.

TABLE 4.

Diagnostic testing using CT and MRI of the brain

In patients with typical recurrent migraine, neither CT nor MRI is warranted

CT or MRI is warranted in patients with:
Recent significant change in headache pattern

Focal neurologic symptoms or signs

History of seizures


When imaging is warranted in non-migraine headache, consensus expert opinion is that MRI is more sensitive than CT

Imaging studies are called for when headaches do not meet clinical diagnostic criteria for migraine, that is, in patients in whom the headache pattern has suddenly changed, and in patients who have focal neurologic symptoms or signs or seizures. The use of EEG testing is not warranted unless the patient’s symptoms suggest seizures.8

The origins of migraine 

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Our understanding of migraine pathophysiology has burgeoned in recent years. Migraines are now known to be a genetically based disorder. The gene loci of migraines have been identified in an extremely rare form of the disease known as hemiplegic migraine. These loci have been found to be the result of an ion channelopathy.9

The genetic tendency toward migraines also makes individuals more sensitive to a variety of environmental triggers. A migraineur is most able to limit headache frequency by maintaining a “nearly boring” regular routine. Specifically, migraines are easily triggered by variations in cycles of sleeping, eating, exposure to caffeine, stress levels, and the like.

Migraine is felt to be neurovascular in origin. While the pathogenesis of migraine pain is not fully understood, a number of components seem to be involved. First, the ion channels within the brainstem nuclei become activated. This results in cerebral blood vessel dilation with pain, with further activation of the trigeminal nerve. Brain stem pathways that normally modulate sensory input are affected. The trigeminal nerve communicates with the spinal tract of the trigeminal nerve, leading to neck pain. The trigeminal nerve also communicates with other portions of the brain via interneuronal synapses, leading to the experience of migraine.10

Managing migraines: setting goals 

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The management of migraine starts with a therapeutic partnership between the patient and physician. It can be tremendously helpful to teach the patient that migraines are genetically based and the result of neurovascular disturbances in the brain (Table 5). Offering the patient strategies for identifying and avoiding certain headache triggers is important (Table 6). Reinforcing behavioral management strategies—including regular sleep, meals, exercise, moderate caffeine use, and stress management—plays an important role in headache control. Flag that key word: The patient should be educated to expect control of this chronic condition, rather than a cure.

TABLE 5.

Basic principles of migraine management

Establish a therapeutic partnership with the patient

Provide patient education
Explain the nature of the disorder (genetic, neurovascular)

Review common triggers and how to avoid them (see Table 6)

Emphasize important behavioral management strategies: “Boringly regular” lifestyle (regular sleep, meals, exercise)


Stress management

Caffeine use only in moderation and only early in the day

TABLE 6.

Common migraine triggers

Sleep deprivation or excess

Missed or delayed meals

Hormonal changes, most notably rapid drops in estrogen levels

Stress and anxiety

Physical exertion

Environmental factors

Headache pharmacotherapy includes both acute and preventive measures. The goal of acute treatment is to stop pain and prevent progression of the headache and its associated features. The goal of preventive treatment is to decrease migraine frequency and severity. The goal of a 50% reduction in headache frequency and severity can be reasonably attained by preventive treatment. That objective can be substantially exceeded with a combination of trigger and lifestyle management and effective medication for acute migraine episodes.

Identifying migraine triggers 

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Most patients who episodically have migraines can identify certain triggers (Table 6). Common triggers include changes in daily sleep or meal schedules. Environmental factors such as noise, bright lights, and fumes often trigger migraines in susceptible individuals. Decreasing estrogen levels are also associated with migraines; a rapidly decreasing estrogen level is substantially more likely to result in a migraine than a gradually decreasing level. Changes in progesterone, on the other hand, have not been shown to be associated with migraine.11, 12, 13

Some people are susceptible to certain foods that predictably trigger migraines. Eliminating the suspected food from the diet for 2– 3 weeks is the most effective way to test this potential trigger. Diets purporting to reduce migraines are not generally helpful.

Treatment: acute and prophylactic 

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Acute migraine treatment may consist of nonspecific pain relievers, including nonsteroidal anti-inflammatory drugs, opioids, or analgesics. Medications that specifically address the neurovascular changes occurring in migraine include the triptans and ergotamine products, and dihydroergotamine. The triptans and ergotamines are serotonin agonists, though ergotamine-containing compounds are not as selective in their effects.

A recent U.S.-funded meta-analysis of acute migraine therapies permits the categorization of treatments.14 Drugs considered to have substantial empirical and clinical benefit include those listed together in the meta-analysis as well as others that have been introduced recently. All of the currently available triptans—sumatriptan (Imitrex), naratriptan (Amerge), zolmitriptan (Zomig), rizatriptan (Maxalt), almotriptan (Axert), frovatriptan (Frova), and eletriptan (Relpax)—are in this group, as are naproxen, ibuprofen, prochlorperazine, and butorphanol nasal spray (Stadol NS).

Prophylactic migraine treatments are used in persons whose headaches are especially frequent (2–3 days a week or more), especially disabling, and in whom acute treatments are either contraindicated or ineffective. Preventive treatments are drawn from several medication categories, including betablockers, tricyclic antidepressants, and antiepileptic drugs, among others. Many patients with headaches of this frequency could benefit from a neurologic consultation to help in management.

In summary, migraine headaches are common and disabling. They are the result of a neurovascular process, a genetically based phenomenon. Highly effective treatments are available to reduce the disability of this condition, making its treatment gratifying to both the patient and physician. □


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Figure 1. The neurovascular theory of migraine. Brainstem pathways that normally modulate sensory input become dysfunctional. Ion channels within the brainstem nuclei are activated, dilating cerebral blood vessels, causing pain and further activating nerves, particularly the trigeminal complex. The trigeminal nerve communicates with other portions of the brain via interneuronal synapses, causing the experience of migraine.


References 

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1. 1 Lipton RB , Steward WF , Diamond S , et al.   Prevalence and burden of migraine in the United States (data from the American Migraine Study II) . Headache . 2001;41(7):646–657 . MEDLINE | CrossRef

2. 2 Lipton RB , Scher AI , Kolodner K , et al.   Migraine in the United States (epidemiology and patterns of health care use) . Neurology . 2002;58(6):885–894 . MEDLINE

3. 3 Lipton RB , Stewart WF , Simon D , et al.   Medical consultation for migraine (results from the American Migraine Study) . Headache . 1998;38:87–96 . MEDLINE

4. 4 Headache Classification Committee of the International Headache Society . the international classification of headache disorders . Cephalalgia . 2004;24:1–160 . CrossRef

5. 5 Pryse-Phillips WEM , Dodick DW , Edmeads JG , et al.   Guidelines for the diagnosis and management of migraine in clinical practice . Can Med Assoc J . 1997;156:1273–1287 .

6. 6 Barbanti P , Fabbrini G , Pesare M , et al.   Unilateral cranial autonomic symptoms in migraine . Cephalalgia . 2002;22:256–259 . MEDLINE | CrossRef

7. 7 Frishberg BM, Rosenberg JH, Matchar DB, et al. Evidence-based guidelines in the primary care setting. Neuroimaging in patients with nonacute headache. US Headache Consortium. www.aan.com/professionals/practice/pdfs/g10088.pdf, accessed November 12, 2004

8. 8 American Academy of Neurology Practice Parameter . Evidence-Based Guidelines for Migraine Headache (an evidence-based review) . 2000; Report of the Quality Standards Subcommittee of the American Academy of Neurology. .

9. 9 Ophoff RA , Terwindt GM , Vergouwe GM , et al.   Familial hemiplegic migraine and episodic ataxia type-2 are caused by mutations in the Ca2+ channel gene CACNL1A4 . Cell . 1996;87:543–552 . MEDLINE | CrossRef

10. 10 Goadsby PJ , Lipton RB , Ferrari MD , et al.   Migraine (current understanding and treatment) . N Engl J Med . 2002;346:257–270 . CrossRef

11. 11 Somerville BW . The role of progesterone in menstrual migraine . Neurology . 1971;21:853–859 . MEDLINE

12. 12 Somerville BW . The role of estradiol withdrawal in the etiology of menstrual migraine . Neurology . 1972;22: 355–35. .

13. 13 Somerville BW . Estrogen withdrawal migraine. I Duration of exposure required and attempted prophylaxis by premenstrual estrogen administration . Neurology . 1975;25:239–244 . MEDLINE

14. 14 Matchar DB, Young WB, Rosenberg JH, et al: Evidence-based guidelines for migraine headache in the primary care setting. Pharmacological management of acute attacks. US Headache Consortium. www.aan.com/professionals/practice/pdfs/gl0087.pdf, accessed November 12, 2004.

Web-based resources on migraine 

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American Academy of Neurology www.aan.com

American Headache Society www.ahsnet.org

Headache Assessment Quiz www.headachequiz.com

International Headache Society www.i-h-s.org

National Headache Foundation www.headaches.org

a Neurologist, Private Practice, Traverse City, MI, Clinical Assistant Professor, Department of Neurology & Ophthalmology, Michigan State University, College of Osteopathic Medicine, East Lansing, MI

Corresponding Author Information1213 West Front Street, Traverse City, MI 49684

PII: S1546-2501(04)00226-9

doi:10.1016/j.sram.2004.11.009


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