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Managing Migraines in Active People

Seymour Diamond, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 24 - NO. 12 - DECEMBER 96


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In Brief: Migraine patients who are physically active may find that exercise can provoke a migraine attack or that regular exercise helps reduce the severity of their headaches. After the diagnosis of migraine has been made with a complete history and physical examination, the next steps are to identify the triggers, such as certain foods or changes in sleep schedule, and design an individualized treatment plan. If exercise is a trigger, nondrug measures such as adequate warm-up, nutrition, and hydration during activity are important. Whether the triggers are exercise-related or not, exercise and other general measures may be beneficial adjuncts to the appropriate abortive, pain-relief, or prophylactic drug regimen.

Because migraine is such a common disorder and because many Americans exercise regularly, it's likely that many migraine sufferers lead physically active lives. A migraine patient's exercise habits should be considered in devising a treatment plan, for several reasons. One is that vigorous exercise can trigger a migraine in some patients. A second is that the choice of pharmacologic therapy for migraine may influence the patient's ability to exercise. Finally, as a part of a balanced life-style, exercise may help prevent migraines or limit their severity.

A recent epidemiologic study (1) estimates that the prevalence of migraine in the general population is 23% to 29% of women and 15% to 20% of men. Migraine has a major impact on the economy because of lost work days, lost income, and the money spent on medical care and drugs. Exercise, for some patients, is one more life element compromised by this condition.

Migraine has been defined by the International Headache Society (2) as an "idiopathic, recurring headache disorder manifesting in attacks lasting 4 to 72 hours. Typical characteristics of headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity, and association with nausea, and photo- and phonophobia." Most migraine sufferers report a family history of migraines, and a genetic model has been proposed (3).

Typically, the initial onset of migraine headaches occurs in adolescence or the early 20s—the period when people are most physically active. Migraine can occur in children as young as age 5, with a peak from 10 to 13 years (4). Seventy percent of total migraine sufferers are women, though in children both genders are affected equally.

Migraine Stages

Migraines may be subdivided by the presence or absence of prodromal signs that precede the attack by 10 to 20 minutes. The aura phase, usually consisting of transient, focal neurologic symptoms, is experienced by about 35% of migraine sufferers. Visual disturbances are the most common prodromal signs and include scotomata (blind spots), teichopsia (fortification spectra), photopsia (flashing lights), and visual hallucinations such as metamorphopsia. The aura may also consist of paresthesias, aphasia, vertigo, or ataxia. The symptoms usually resolve before the acute attack.

Patients who have migraine with or without aura may note premonitory signs starting as early as 24 hours before the acute attack. These signs include excessive fatigue or extreme energy, anorexia or increased hunger, constipation or diarrhea, pallor, chills, increased urinary frequency, or fluid retention. Patients may also note changes in mood, such as irritability, depression, euphoria, anxiety, obsessional behavior, or apathy. They may note difficulty in concentrating, excessive yawning, shakiness, or hyperosmia.

Patients who have migraine will describe the pain as throbbing or pulsating, usually severe, and often incapacitating. Migraine is considered a "sick" headache with associated symptoms such as nausea, vomiting, and photophobia. Other complaints associated with an acute attack include phonophobia, osmophobia, diarrhea, dizziness, lightheadedness, chills, and fatigue.

In some patients, attacks involving focal neurologic deficits may persist beyond the headache. Forms of this entity, called complicated migraine, include hemiplegic, ophthalmoplegic, basilar artery, and retinal migraine. These migraine attacks can be frightening for the patient and the treating physician.

The frequency of migraine attacks typically varies from 2 to 8 per month; in some patients they are less frequent. Migraine is not a daily headache. About 60% of female migraine patients report a menstrual relationship to their acute headaches (5). These patients may experience headaches only around the time of menses, such as 2 days immediately before, during the flow, or 2 days postmenses. The duration of migraine attacks also varies, from 4 to 72 hours.

Targeting the Triggers

A number of migraine triggers have been identified. Some patients are particularly sensitive to foods containing vasoactive substances, such as tyramine, and should avoid chocolate, aged cheese, pickled foods, processed meats, fermented sausage, or cultured dairy products (sour cream, yogurt). Patients who routinely consume excessive caffeine may also precipitate a migraine attack if they miss the caffeine-containing beverage or medication. The artificial sweetener aspartame, used extensively in low-calorie foods (diet soda and sugar-free desserts, candy, and gum), has been identified as a migraine trigger (6). Monosodium glutamate (MSG), used as a flavor enhancer in common prepared foods and fast foods, has long been identified with the "Chinese restaurant" syndrome. Though the syndrome has recently been discounted by a US Food and Drug Administration committee, my personal observation is that MSG can trigger acute headaches in about 20% of all migraine patients. These patients should be attentive to the ingredients used in their food.

Alcohol is a well-known migraine provocateur, with red wine being the most common (7). Because red wine does not contain significant levels of tyramine, the complex flavonoid phenols have been suggested as the culprits because they are present in smaller amounts in white than in red wines (8).

Patients who have migraines tend to be sensitive to any changes in their daily lifestyle. Stress, fatigue, oversleeping, or skipped or missed meals can all help precipitate a migraine. At the Diamond Headache Clinic, we advise patients to maintain a strict schedule for meals and sleep. Many patients will complain of a weekend or holiday headache that can be linked to sleeping past their usual wake-up time and missing the first cup of coffee or orange juice. We recommend that patients rise at the same time each day, drink or eat, then return to bed if they desire. With the stress of busy lifestyles and the quest for achieving and maintaining a desirable weight, individuals may skip or delay a meal. The mechanism by which hunger or hypoglycemia triggers a headache is unknown. A regular meal schedule is encouraged for those who are sensitive to missed meals (9).

When Exertion Is a Trigger

Any form of exertion—straining at stool, coughing, sneezing, orgasm, or strenuous exercise—can trigger headache in sensitive individuals. Patients who present with migraine triggered by exertion should be thoroughly evaluated to rule out an organic disorder, including arteriovenous malformation, Arnold-Chiari malformation, pheochromocytoma, and aneurysm; however, the cause of exertional headaches is usually benign and can be easily treated. Patients who present with exertional migraine should undergo a complete neurologic examination and computed tomography. Magnetic resonance imaging with gadolinium may be indicated. The criteria for ordering neuroradiologic scanning are listed in table 1.


Table 1. Criteria for Ordering Neuroradiologic Scanning in Patients With Migraine

Suspicion of cerebellar hemorrhage or infarct

Stroke in progress or completed stroke with emergency use of anticoagulants

History and examination suggestive of intracerebral hemorrhage or mass lesion

Acute signs of increased intracranial pressure

Patients at risk for cerebral abscess who require lumbar puncture

Blunt head trauma with signs of increased intracranial pressure

Depressed skull fracture

Open skull fracture

Penetrating head injury

Head injury with Glasgow coma rating less than 9

Exertional migraine has been linked to many factors, such as excessive fatigue, lack of adequate warm-up before exercise, dehydration, relative hypoglycemia, and exercise at high altitude. This form of headache may be triggered by moderately intense but prolonged activity and may present in patients who exert themselves in hot, humid weather. The headache may be aggravated by exposure to cold and by dyspnea (10). Headaches associated with exercise at high altitudes may occur 6 to 96 hours after exposure. Patients describe the pain of exertional headaches as throbbing and aggravated by maneuvers that increase intracranial pressure, such as coughing, running, straining at stool, Valsalva's maneuver, or orgasm.

Effort migraine usually occurs immediately after the exertion and lasts from 5 minutes to 24 hours. The majority of patients have a personal or family history of migraine. Prodromal symptoms without headache pain can also occur after exercise (11).

Cases of Exertional Migraine

An interesting description of effort migraine was written by Jokl (12), who experienced a headache immediately after running a mile relay in a university track championship. During his freshman year in medical school he ran the anchor leg on the mile relay team at the German track championships, finishing in a personal best of under 50 seconds in the team's victory. A few minutes after the race he developed nausea, headache, prolonged weakness, and vomiting that lasted 15 minutes and quickly subsided.

Another report (13) focused on several runners at the Olympic Games in Mexico City in 1968. Despite the high conditioning of the athletes, they experienced scotomata, unilateral retroorbital pain, nausea, and vomiting. These episodes occurred after longer running events but not after sprints. In addition to the high altitude, heat and humidity contributed to the athletes' discomfort.

In a review from Japan, it is reported that a 51-year-old woman with no history of migraine experienced several unilateral headaches associated with nausea that occurred during or immediately after swimming (14). The pain was relieved by rest. Physical and neurologic examinations were negative. The physicians suggested that the pathophysiology could be attributed to changes in intracranial pressure and constriction of the intracranial blood vessels because of swimming. These changes also led to a secondary cerebral hypoxia, and eventually the headache. The authors concluded that the possible link between swimming and headache merited further study.

In another report, a 48-year-old woman complained of severe migraine onset within 1 hour of completing a rigorous exercise bout (15). The woman had a history of headaches, but reported she had experienced no acute attacks during 5 years of taking aerobics classes. However, in the preceding year, the headaches occurred after each exercise session. After considering all factors and undergoing neuroradiologic testing, the patient realized that these exercise-related headaches started after she switched from oral estrogen to an estrogen patch. When the patient exercised, her circulation increased, which hastened the absorption of the estrogen, resulting in a typical migraine attack.

Exercise as Therapy?

Persons who have a migraine headache seek a dark, quiet room, and the headaches are often relieved by rest. The severity of the headache and associated symptoms usually prevents the patient from participating in daily activities, including exercise, whether strenuous or mild. For some patients, however, exercise can help prevent or relieve migraines.

An anecdotal report (16) detailed the case of a 43-year-old former professional dancer who participated in a regular aerobic exercise program and noted that exercise helped abort acute migraine attacks. At the onset of the prodromal phase, if the opportunity afforded itself, the dancer would go for a run, which would eliminate the visual aura symptoms and prevent the headache. The author warned about generalizing this measure for all migraine sufferers, and noted that a high level of fitness may first be necessary to duplicate these results. The author also reported that the subject had a long history of participation in exercise without migraine.

Exercise may be recommended in a multidisciplinary treatment regimen. To promote healthy behavior, activities such as walking, jogging, or other exercise may be indicated. At the Diamond Inpatient Headache Unit, patients are encouraged to participate in an exercise program supervised by the physical therapy department.

In one study (17), 11 migraine sufferers participated in a 6-week cardiovascular exercise program. By the end of the program, the patients' cardiovascular fitness had improved and they reported that their migraine attacks were less painful. The authors thought that two factors might have contributed to the improvement. The patients might have had certain expectations for the study, and cardiovascular exercise might have improved their mood and response to stressful stimuli. The researchers acknowledged that the results should not be generalized and that researchers should determine if longer exercise programs maintain positive outcomes.

Treatment Options

Migraine treatment can be divided into four kinds of measures: nonpharmacologic, abortive, pain relief, and prophylactic. Table 2 (see below) details the pharmacologic options for managing migraine headaches.

Nonpharmacologic measures. Nondrug strategies for managing migraines include avoiding possible triggers. Maintaining strict schedules for sleep and meals can prevent headaches related to fatigue and hunger. A balanced lifestyle is extremely important for active patients. If exercise is considered a migraine precipitant, patients should be encouraged to warm up adequately before working out. A competitive swimmer was able to reduce her headaches by quantitative warm-ups before each race (18). Progressive relaxation exercises and biofeedback techniques may be helpful for active individuals. Using these nondrug modalities before exercise might prevent effort migraine or, at least, decrease the severity of an acute headache.

Abortive therapy. In abortive therapy, the patient takes the medication at the first sign of a headache. The agent of choice for migraine abortive therapy is sumatriptan succinate. Sumatriptan is a specific 5-hydroxytryptamine1 receptor (5-HT1) subtype agonist that provides the beneficial effect of 5-HT without its side effects. Sumatriptan may be administered subcutaneously or orally and is considered an effective, safe agent in migraine abortive therapy. For patients who experience a headache immediately after exercise and are not able to take a medication immediately, sumatriptan is particularly useful because it can be used at any time during an attack. It is contraindicated in patients who have coronary artery disease, Prinzmetal's angina, or uncontrolled hypertension.

The ergot preparations have long been used as migraine abortive agents. Their efficacy depends on use early in an attack. For patients experiencing migraine with aura, the agent should be used during the prodromal phase. In the United States, ergotamine is available sublingually or in combination with caffeine in oral and rectal preparations. The sublingual form may be preferred because of its rapid onset of action. Ergotamine is not available in the United States for parenteral administration, but an ergotamine derivative, dihydroergotamine mesylate (DHE), administered subcutaneously, has been used effectively in migraine abortive therapy. The ergot preparations cannot be used daily; a 4-day hiatus must be maintained between days of use to prevent rebound headaches. Ergots cannot be used concomitantly with sumatriptan.

For patients who cannot take ergotamine or who have migraine attacks lasting more than 1 day, a combination agent containing isometheptene mucate, dichloralphenazone, and acetaminophen may be indicated. Isometheptene mucate has cerebral vasoconstrictor effects similar to those of the ergot preparations. Nonsteroidal anti-inflammatory drugs (NSAIDs) have been effective in migraine abortive therapy because they inhibit inflammation and prostaglandin formation. The phenothiazines—chlorpromazine and prochlorperazine—are often effective as migraine abortive agents in emergency departments because of their dopaminergic and adrenergic effects. These agents can also relieve the gastrointestinal effects of migraine. However, their sedative effects may not be appropriate for patients who are eager to return to vigorous activity.

Pain relief. Despite valiant efforts to abort migraine attacks, pain relief measures may be required. Narcotic analgesics should be avoided in patients who have frequent attacks because of the addiction potential. An excellent alternative is the NSAID ketorolac tromethamine, which is available for parenteral administration. Transnasal butorphanol tartrate also has been effective in relieving the pain of migraine. Phenothiazines may be used to relieve the associated symptoms of a migraine attack. Metoclopramide hydrochloride, believed to enhance the absorption of oral medications, has limited sedative action and may be used in combination with an analgesic or with DHE.

Prophylactic treatment. Migraine prophylaxis is indicated for patients experiencing more than two attacks per month, or if the severity and the associated symptoms significantly affect the patient's daily life. In active individuals, special consideration must be given to the effect these agents may have on performance and to the effects that exercise may have on the absorption of these agents.

The only agents approved by the US Food and Drug Administration for the prophylactic treatment of migraine are propranolol hydrochloride, timolol maleate, methysergide maleate, and divalproex sodium. Propranolol and timolol are nonselective beta blockers and are contraindicated in patients who have asthma, chronic obstructive pulmonary disease, congestive heart failure, or atrioventricular conduction disturbances. These drugs must be used with caution in patients who also take insulin, oral hypoglycemics, or monoamine oxidase (MAO) inhibitors. Other beta blockers may be used, including nadolol. Metoprolol tartrate, a cardioselective beta blocker, may be used in patients who do not tolerate nonselective beta blockers (propranolol, timolol, and nadolol). In many individuals, beta blockers cause a decrease in heart rate and in exercise tolerance. During maximal exercise, these agents may also lower blood pressure and oxygen uptake. The benefits of aerobic exercise may be compromised if pulse measurements are used to determine conditioning; beta blockers will mask an increased pulse rate and patients may overexert.

Methysergide maleate is a vasoconstrictor that inhibits the inflammatory mechanisms of serotonin. Long-term use has been linked to cardiac, pulmonary, and retroperitoneal fibrotic syndromes. Methysergide should never be used for more than 6 consecutive months without a 4- to 6-week hiatus. During methysergide therapy, the patient should be regularly evaluated and an intravenous pyelogram ordered at the end of a 6-month therapeutic interval to rule out retroperitoneal fibrosis. In active individuals, methysergide can cause muscle cramping, weakness, and arthralgias. Divalproex sodium has recently been approved by the FDA for the treatment of migraine. It has demonstrated efficacy in patients who have migraines that are refractory to other treatments and those who have concomitant seizure or bipolar disorders.

Other agents are used in migraine prevention but have not received FDA approval for this indication. Calcium channel blockers, particularly verapamil hydrochloride and nimodipine, have been effective in migraine prophylaxis. Nimodipine has the highest marked selectivity for the cerebral vasculature, but may not be indicated in active individuals because it can cause muscle pain and fatigue. Verapamil hydrochloride is considered effective because of its antiplatelet actions and is not reported to be detrimental to active people.

Clonidine hydrochloride, an alpha-adrenergic blocker, has demonstrated efficacy in migraine, particularly in patients who have diet-related attacks.

Antidepressants, including tricyclic agents and MAO inhibitors, have long been recognized as beneficial in migraine prophylaxis. Some tricyclics, such as protriptyline hydrochloride, have been linked to resting tachycardia. Active individuals may not be able to tolerate the anticholinergic effects, such as dry mouth, blurred vision, and urine retention. In children with migraine, the agent of choice is cyproheptadine hydrochloride, which blocks histamine and serotonin receptors. In adults who have migraine, the effects of cyproheptadine have been equivocal.

NSAIDs have demonstrated efficacy in migraine prophylaxis. These agents do not affect athletic performance but have been known to cause fatigue as well as gastrointestinal complaints.

Prophylactic treatment for skiers and others who have headaches at higher altitudes may include a diuretic, such as acetazolamide or furosemide, or a corticosteroid. The agent should be started immediately before traveling to the higher altitudes. If this procedure does not help, the patient may need to return to a lower altitude.

Freedom for Fitness Pursuits

For active migraine patients, it is essential that accurate diagnosis and appropriate therapy be undertaken to maintain the patient's exercise routines. If exertion continues to trigger headaches, neuroradiologic evaluation may be indicated to rule out organic disease. However, the right combination of nondrug and drug therapies usually removes migraine as an obstacle to patients' full, active lifestyles.


Table 2. Pharmacologic Treatments for Migraine and Side Effects That May Impair Exercise

Agent Dose Route Effect on Exercise

Abortive

Sumatriptan succinate* 6 mg, may repeat after 1 hr, up to 12 mg/24 hr SC None

Sumatriptan succinate* 25 mg, may repeat in 2 hr, can increase with each attack, up to 100 mg Oral None

Ergotamine tartrate* 2 mg, may repeat every 30 min, up to 6 mg/24 hr, 10 mg/wk Sublingual None

Ergotamine tartrate with caffeine* 1 mg, 100 mg; may repeat every 30 min, up to 6 tab/24 hr, 10 tab/wk Oral Caffeine may act as a stimulant

Ergotamine tartrate with caffeine* 2 mg, 100 mg; may repeat in 1 hr, up to 2 tab/day, 5 tab/wk Rectal None

Dihydroergotamine mesylate* 0.5 to 1.5 mg IM, IV, SC None

Isometheptene mucate with dichloralphenazone and acetaminophen 65 mg, 100 mg, 325 mg; 2 tabs at onset, may repeat 1 tab every hour up to 5 tab/24 hr Oral None

Aspirin 900 mg Oral None

Naproxen sodium 825 mg, may repeat 275-550 mg every 30-60 min, up to 1,375 mg/24 hr Oral None

Flurbiprofen 50-100 mg, may repeat every 6 hr Oral None

Etodolac 300 mg 3 times a day Oral None

Mefenamic acid 500 mg Oral None

Diclofenac sodium 50-75 mg 2 to 4 times a day Oral None

Chlorpromazine hydrochloride 25-50 mg, may repeat every 6 hr Oral Sedation

Chlorpromazine 100 mg, may repeat every 6 hr Rectal Sedation

Chlorpromazine hydrochloride 25-50 mg, may repeat every 6 hr IM Sedation

Prochlorperazine 25-50 mg, may repeat every 6 hr Oral Sedation

Prochlorperazine 25 mg, may repeat every 6 hr Rectal Sedation

Prochlorperazine 10 mg, may repeat every 6 hr IM Sedation


Pain Relieving

Aspirin 500 mg twice a day Oral None

Ketoprofen 12.5-25 mg twice a day Oral None

Naproxen sodium 275-550 mg twice a day Oral None

Ibuprofen 200-400 mg every 4 hr Oral None

Ketorolac tromethamine 10 mg 4 times a day Oral None

Ketorolac tromethamine 60 mg twice a day IM None

Butorphanol tartrate 1 mg, may repeat within 60-90 min; two-dose sequence may be repeated every 3-4 hr Nasal Possible aberrant psychological profile

Prophylactic

Propranolol hydrochloride** 60-160 mg/day Oral Mild sedation, bradycardia

Timolol maleate** 10-20 mg/day Oral Mild sedation, bradycardia

Nadolol** 20-120 mg/day Oral Mild sedation, bradycardia

Metoprolol tartrate 100-200 mg/day Oral Mild sedation, bradycardia

Atenolol 25-100 mg/day Oral Mild sedation, bradycardia

Verapamil hydrochloride 120-480 mg/day Oral Possible bradycardia

Nimodipine 30 mg 3 or 4 times a day Oral Possible bradycardia

Nicardipine hydrochloride 20-30 mg 2 or 3 times a day Oral Possible bradycardia

Amitriptyline 10-150 mg/day Oral Dry mouth

Doxepin hydrochloride 10-150 mg/day Oral Dry mouth

Phenelzine sulfate 15-60 mg/day Oral None

Aspirin 81 mg/day Oral None

Ketoprofen 50-75 mg 2 or 3 times a day Oral None

Naproxen 250-750 mg/day Oral None

Naproxen sodium 250-750 mg/day Oral None

Fenoprofen calcium 600 mg 3 times a day Oral None

Flurbiprofen 50-100 mg 3 times a day Oral None

Indomethacin 25-50 mg 3 times a day Oral None

Piroxicam 20 mg every morning Oral None

Nabumetone 500-750 mg twice a day Oral None

Diclofenac sodium 50 mg once or twice a day Oral None

Clonidine hydrochloride 0.1 mg 3 times a day Oral None

Methysergide maleate 2 mg 3 times a day Oral None

Divalproex sodium 250-2,000 mg/day Oral None

* A 4- to 5-day hiatus must be maintained between days of use to avoid rebound headache.
** Contraindicated in patients who have asthma or chronic bronchitis
SC = subcutaneous, IM = intramuscular, IV = intravenous

References

  1. Stewart WF, Lipton RB, Celentano DD, et al: Prevalence of migraine headache in the United States: relation to age, income, race, and other sociodemographic factors. JAMA 1992;267(1):64-69
  2. International Headache Society: Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain: Headache Classification Committee of the International Headache Society. Cephalalgia 1988;8(suppl 7):1-96
  3. Peroutka SJ: The genetic evaluation of migraine: the future is now. Headache Qrtly 1994;5(3):199-200
  4. Rothner AD: Headache syndromes in children and adolescents: diagnosis and management, in Diamond S, Dalessio DJ (eds): The Practicing Physician's Approach to Headache, ed 5. Baltimore, Williams & Wilkins, 1992, p 207
  5. Edelson RN: Menstrual migraine and other hormonal aspects of migraine. Headache 1985;25(7):376-79
  6. Koehler SM, Glaros A: The effect of aspartame on migraine headache. Headache 1988;28(1):10-14
  7. Hannah P, Glover V, Sandler M: Tyramine in wine and beer, letter. Lancet 1988;1(8590):879
  8. Pradalier A, Ollat H: Migraine and alcohol. Headache Qrtly 1991;2(3):177-186
  9. Davidoff RA: Migraine: Manifestations, Pathogenesis, and Management. Philadelphia, FA Davis, 1995
  10. Meyer JS, Dalessio DJ: Headache associated with chemicals, toxins, systemic infections, and metabolic disorders (toxic vascular headache), in Dalessio DJ, Silberman SD (eds): Wolff's Headache and Other Head Pain, ed 6. New York City, Oxford University Press, 1993, pp 209-234
  11. Thompson JK: Exercise-induced migraine prodrome symptoms. Headache 1987;27(5):250-251
  12. Jokl E: Indisposition after running. Med Dello Sport 1965;5:363
  13. Jokl E: Olympic medicine and sports cardiology. Ann Sports Med 1984;1(4):127-169
  14. Indo T, Takahashi A: Swimmer's migraine. Headache 1990;30(8):485-487
  15. North K, Davies L: Postexercise headache in menopausal women. Lancet 1993;341(8850):972
  16. Darling M: The use of exercise as a method of aborting migraine. Headache 1991;31(9):616-618
  17. Lockett DM, Campbell JF: The effects of aerobic exercise on migraine. Headache 1992;32(1);50-54 [published erratum in Headache 1992;32(4):187]
  18. Lambert RW Jr, Burnet DL: Prevention of exercise-induced migraine by quantitative warm-up. Headache 1985;25(6):317-319

Dr Diamond is director of the Diamond Headache Clinic and the Diamond Inpatient Headache Unit at Columbus Hospital in Chicago. He is adjunct professor of pharmacology and molecular biology at Finch University of Health Sciences/Chicago Medical School in North Chicago, Illinois. Address correspondence to Seymour Diamond, MD, Diamond Headache Clinic, 467 W Deming Pl, Suite 500, Chicago, IL 60614-1726.


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