Cover Focus: Headache Management
How to Diagnose and Manage Headaches.

A probing patient history can help you sort through the symptoms.

by Leonid Skorin Jr., O.D., D.O., Dixon, Ill

Almost everyone gets a headache at some point in his or her life. Nine out of 10 have at least one headache in any given year.1 Most people treat themselves. Others, maybe 5 to 15 percent, seek a physician's care.2,3 They account for some 18 million outpatient visits annually to hospitals and healthcare clinics.4 Most of these patients (90 percent) suffer from a vascular headache, a tension headache, or a mixture of the two.5 The others have conditions that lead to inflammation, traction or dilatation of pain-sensitive structures of the head and neck.5

Anytime a patient comes to you complaining of a headache, you're confronted with a wide range of diagnostic possibilities. Most people who seek attention for head pain have some sort of primary headache disorder, whether a migraine, tension-type or cluster headache. Often we're called upon to evaluate someone whose headache is accompanied by visual symptoms or discomfort in or around the eye. Always remember that a headache may be a symptom of a serious underlying condition calling for an immediate diagnostic workup and treatment. These cases often require laboratory and radiographic studies and a neurological consult.

Clinical Evaluation
The single most important tool for evaluating a headache is the patient's history. Since there's no objective way to measure headaches, the diagnosis rests in your ability to extract, dissect and organize relevant features of the patient's presentation.6 One useful approach for obtaining a headache profile is what's called the PQRST symptom analysis.7-9 This approach includes questions about provocative and palliative factors, the quality of the headache, the region in which it occurs, its severity and its temporal characteristics.

• Provocative factors. These include anything that can incite or exacerbate a headache. Medications, body movement, stress, foods, menses or anything the patient reports that influences the pain may be important diagnostic clues. Up to 85 percent of migraine patients report triggering factors for a headache.10 Food triggers occur in 25 percent of migraine sufferers. They include chocolate, cheeses, alcoholic beverages (especially red wine), citrus fruits and foods containing monosodium glutamate, nitrates and aspartate.10,11 Various physical activities, including sex, can trigger a migraine.12

Ingesting alcohol or other vasodilating drugs often precipitates cluster headaches.13 Stress can aggravate tension headaches, which are typically worse at the end of the day. Eyestrain and blurred vision can cause tension-related head pain in patients who do extensive computer work.14 Headaches caused by brain tumors or increased intracranial pressure are worse in the morning. Stooping, coughing, physical activity or sudden head movements may exacerbate them.15

Palliative factors. Certain factors may ameliorate the discomfort of the head pain and associated symptoms. Ask the patient about what he's tried and identify which factors have or haven't helped. Besides medications, ask about other measures such as rest, sleep or relaxation in a quiet darkened room (which is known to help patients with migraine pain11). Rubbing the superficial temporal artery or applying hot or cold compresses can ease migraines.16 Relaxation, rest or sleep can alleviate a tension headache. Cluster headache patients report that sitting upright, rocking in a chair, pacing back and forth or engaging in vigorous movement can lessen the pain.11

If the patient has taken medications, determine the dosage, frequency, efficacy and side effects. The duration of use is also important, since patients must take some drugs for several weeks or months before you know whether they work. The patient may be using the drug incorrectly, either taking too small or too infrequent a dose. Or he may be overusing the medication.11

Quality. The nature of the pain can suggest its origin.  Throbbing or pulsing pain points to a vascular source; burning or aching a muscular cause; sharp or shooting pain a neuritic genesis; a pressure-like sensation a viscus- or chamber-derived origin. A brain tumor headache is usually dull, aching and intermittent, although in some patients it's continuous.15

Region. The location of the pain and its radiation can help in your diagnosis. Migrainous head pain is unilateral in about two-thirds of patients, but in other cases it may be bilateral or holocephalic (involving the whole head).16 Consistent unilateral focal pain may indicate organic disease.9 The "hatband" distribution of head pain usually indicates a tension headache. Pain localized to the eye may be from either an ocular disease or a cluster headache.17,18

Severity. The severity of pain and speed of onset and resolution are important as well. Since most headaches vary in intensity during an attack and from one episode to another, it's useful to ask a patient about the range of pain he experiences during a headache.11

Temporal aspects. Ask about the time of onset and the frequency and duration of the headaches. Most primary headache disorders begin in adolescence or early adulthood.6 Headaches that begin later in life warrant greater suspicion and aggressive evaluation.19

Migraines typically last 4-72 hours. Ones that persist longer than that are called "status migrainosus." Cluster headaches usually last 15 minutes to three hours. Headaches of organic origin don't have a characteristic duration. Headaches that last longer with each new episode require further evaluation.11

Pin down the frequency of the headaches. Changes in the frequency of a headache may signal an intracranial lesion.9 Knowing the frequency of the headache also helps in choosing an appropriate treatment regimen and judging its efficacy.16

Ask about associated symptoms and signs. These include visual or somatic aura (suggesting a migraine); or lacrimation and ipsilateral nasal congestion (suggesting a cluster headache). More than 90 percent of migraine patients have photophobia, while nausea and vomiting occur in up to 30 percent of migraine patients.8

In most cases a detailed history will direct you to the diagnosis of the patient's head pain. Cases that don't fit a benign headache profile merit further evaluation beyond the standard ocular, physical and neurological exams. Examples include: a severe, first-time headache of sudden onset; a headache with a progressive course; any headache accompanied by loss of consciousness or abnormal mental activity; a headache with fever or stiff neck; or any new headache in an elderly patient.20 Consider it a danger signal anytime a headache occurs in a patient with a systemic malignant disease, infection or immunocompromised state.21 These cases require further laboratory and neuroimaging studies.

Migraine Headache
An estimated 23.6 million Americans suffer from migraine headaches.22 Of these, about half get migraines that are moderately to severely disabling.22 Migraine lessens the quality of life and lowers productivity.23,24 The medical costs total about $1 billion annually while indirect costs (due to missed work days, underemployment, reduced productivity) are an estimated $13 billion a year.24 Interestingly, 72-85 percent of migraine patients self-treat.22 That means the true cost of migraine is higher than we think.

Abortive Medications: Analgesics

Drug

Brand Name

Dosage

Aspirin

Bayer

325, 500, 625mg Q4H PRN

Acetaminophen

Tylenol

325, 500mg Q4H PRN

Aspirin, acetaminophen, caffeine

Excedrin Migraine

2 tabs Q6H (max: 8 tabs/day)

Aspirin, butalbital, caffeine

Fiorinal

1-2 tabs Q4H (max: 6 tabs/day)

Acetaminophen, butalbital, caffeine

Fioricet, Esgic

1-2 tabs Q4H (max: 6 tabs/day)

Acetaminophen, butalbital

Phrenilin

1 cap Q4H (max: 6 caps/day)

Isometheptene, dichloraphenazone, Acetaminophen

Midrin

2 caps at onset, then 1 cap QH until relief (max: 5 caps in 12H)


Migraine is a complex syndrome. It consists of a usually benign episodic headache disorder characterized by various combinations of neurological, gastrointestinal and autonomic changes. Visual symptoms often occur.

The most common type of migraine (80 percent) is migraine without aura.10 The other 20 percent of patients experience some sort of aura, although not necessarily with every headache.25,26 Migraine aura consists of neurologic symptoms that typically precede but may accompany the headache.25 Usually the aura develops over 5-20 minutes and lasts less than an hour.27 The headache usually occurs within an hour after the aura stops, but may not develop for several hours, or not at all.29,30 Up to 20 percent of migraine attacks with aura may be unaccompanied by headache, a phenomenon known as migraine equivalent or acephalgic migraine.28 Visual disturbance is the most frequent occurrence in migraine equivalents.30

The most common aura is visual and may have many variants.6,16,31 These include a range of positive visual phenomena such as photopsias (flashes of light, spots, sparks, streaks of light, wavy lines), scintillations (flickering lights) and fortification spectra or teichopsia (jagged zigzag lines).25,32 Up to 79 percent of migraine patients who experience visual aura will see a scintillating scotoma.33 The image can assume different configurations, but patients usually perceive it as a semicircle, crescent or horseshoe-shaped visual defect bordered by moving, shining streaks of light forming acute angles.34 This visual scintillation migrates to the periphery and leaves behind an area of impaired vision.35,36 Other visual phenomena include changes in perception (objects appear smaller, larger or farther away) or distortions of an object's shape, contour or spatial relationship.16,32 Negative visual phenomena include homonymous hemianopic or quadrantic field defects, central scotomas, tunnel vision, altitudinal visual-field defects or complete bilateral blindness.36-38

Abortive Medications: NSAIDs

Drug

Brand Name

Dosage

Ibuprofen

Advil, Motrin

400-800mg at start, then 400-800 in 4H (max: 2.4g/day)

Naproxen sodium

Aleve, Anaprox

825mg at start, can repeat 220-550mg in 3-4H (max: 1-5g/day)

Naproxen

Naprosyn

500mg to start, repeat in 3-4H (max: 1.5g/day)

Indomethacin

Indocin

25-200mg/day or 50mg supp, 1-2 supp at onset

Ketorolac

Toradol

60mg IM at start, then 15-30mg in 6H (max: 180mg/day)

The typical migraine headache consists of unilateral, throbbing or pulsing pain of moderate to severe intensity. It's often accompanied by other symptoms such as nausea, vomiting, anorexia, photophobia and phonophobia.25,27 Migraine sufferers are sensitive to light and sound even when they're headache-free.39

Other migraine variants which have visual phenomena include basilar migraine (bilateral visual field changes, frontal or occipital headache, diplopia, nystagmus, nausea and vomiting), ophthalmoplegic migraine (cranial nerve 3, 4 or 6 involved after headache), and retinal migraine (monocular vision loss lasting 30-60 minutes followed by complete recovery).9,27

 Cluster Headache
Cluster headache is a rare disorder and the only primary headache that occurs more often in men than in women.21 A cluster attack consists of severe unilateral orbital, supraorbital or temporal pain lasting 15 minutes to three hours.27 The headaches may occur once every other day or up to eight times a day.27 They're often associated with conjunctival injection, lacrimation, nasal congestion, rhinorrhea, facial sweating, miosis, ptosis or eyelid edema.9 Raeder's paratrigeminal neuralgia—which has similar findings of pain on one side of the face or head with miosis, ptosis and conjunctival hyperemia—may be a form of cluster headache.40

Cluster headache is considered a primary headache, which means there should be no structural brain changes. Yet recent studies have identified increased gray matter density in an area of the hypothalamus that functional positron emission tomography had previously shown to be activated during cluster attacks.41 This abnormality apparently exists both during attacks and head- ache-free periods.41

Tension Headache
Tension headache, the most common head pain syndrome, affects females more often than males.42 It's characterized by a gradual onset of bilateral, non-throbbing, aching pain over the frontal and temporal regions, often spreading to involve the occipital, posterior cervical and trapezius musculature. The pain often worsens as the day goes on. Reducing stress with relaxation, rest or sleep can help alleviate it.8

Brain Tumor Headache
Thirty percent of patients with primary or metastatic brain tumors have a headache at the time of diagnosis; for many it's the chief presenting complaint.8 What is considered the classic brain tumor headache—severe, worse in the morning and accompanied by nausea and vomiting—occurs in only 17 percent of patients.44 More often the headache is intermittent, dull, aching, unilateral and relatively mild in the beginning.15 Often the headache worsens with a change in body position, coughing or straining, and with time, other neurologic findings and complaints may become evident.8,15,43 Obtain diagnostic imaging for all patients with chronic headache who present with new symptoms or who have abnormal physical findings.

Stroke-Related Headache
Headache is about three times more common in intraparenchymal cerebral hemorrhage than in ischemic stroke.44 Headaches due to intraparenchymal hemorrhage vary widely depending on the hemorrhage location and size. But usually they're ipsilateral, focal and mild to moderate in severity.44 Ischemic disease in the carotid circulation causes a frontal headache 30 percent of the time, usually in the periorbital area or temple on the ipsilateral side.15 Disease in the vertebrobasilar system initiates a posterior headache 59 percent of the time.15

Subarachnoid Hemorrhage
Sudden onset of a severe headache occurs in all patients with acute subarachnoid hemorrhage secondary to ruptured aneurysm or arteriovenous vascular malformation.8 Sometimes called a "thunderclap headache," it's often accompanied by nausea, vomiting and a stiff neck.15 The thunderclap headache can also strike patients who have unruptured aneurysms.11 In some patients a similar but less severe "sentinel" headache due to bleeding may precede the acute headache by several days or even weeks. Diplopia, field defects and loss of consciousness may accompany such headaches.

Temporal Arteritis

Abortive Medications: Selective Serotonin Agonists

Drug

Brand Name

Dosage

Sumatriptan

Imitrex

Oral: 25-50mg, subcutaneous: 6mg, nasal spray: 20mg

Zolmitriptan

Zomig

Oral: 2.5-5mg

Naratriptan

Amerge

Oral: 2.5mg

Rizatriptan

Maxalt, Maxalt MLT

Oral: 5-10mg, sublingual: 5-10mg


Headache can also result from temporal arteritis, an occlusive inflammatory process causing an ischemic optic neuropathy. This disease of the elderly can result in severe, sudden, unilateral or bilateral vision loss. Other symptoms include temporal or occipital headache (up to 80 percent of patients), pain and tenderness of the scalp, face or oral mucosa, jaw claudication, depression, fatigue and loss of appetite.45 Clinical signs include a pallid swollen disc, central retinal artery occlu- sion or branch retinal artery occlusion.45 Workup for temporal arteritis includes an erythrocyte sedimentation rate, C-reactive protein and a temporal artery biopsy.46

Pseudotumor Cerebri
Pseudotumor cerebri is a condition of increased intracranial pressure. The diagnosis is based on these four criteria:46,47

  • The intracranial pressure is elevated above 200-250mm water.
  • The composition of the cerebrospinal fluid must be normal.
  • All neuroimaging studies must be normal.
  • All symptoms and signs should be those of elevated intracranial pressure alone.

The headache of pseudotumor cerebri is similar to a vascular headache, yet it presents like those seen with brain tumors. It is often pounding, intermittent and gradually increasing in intensity.8 Other findings may include transient visual obscurations, diplopia, dizziness, tinnitus and papilledema. Neuroimaging is mandatory to rule out an intracranial tumor. MRI is preferable, especially if you suspect a lesion of the brainstem or posterior fossa.48

Sinus Headache
Migraine and tension headaches are often confused with sinus headaches because the pain occurs in the same place. The pain of sinusitis comes from engorged and inflamed nasal structures. The headache that accompanies it usually has a deeper, dull, aching quality with a heaviness and fullness. Rarely is there nausea and vomiting.11

All sinusitis pain is not the same. Maxillary sinusitis pain occurs most often in the cheek, the gums and the teeth of the upper jaw. Ethmoid sinusitis pain is felt between the eyes, and the eye itself may be tender with increased pain upon eye movement. Frontal sinusitis pain strikes mainly in the forehead. Sphenoid sinusitis pain affects the vertex, but can also be more generalized; it's aggravated by standing, walking, bending or coughing. It often interferes with sleep, and narcotics bring little relief.11,27

Headache Treatment
To manage headache successfully, you first need to identify the type of headache you're dealing with. Since many headaches stem from some triggering factor, recognizing and avoiding these triggers is a critical part of any treatment regimen.10 Lifestyle changes, relaxation, biofeedback, acupuncture and other behavioral interventions may help.49

Prophylactic Medications

Category

Drug

Brand Name

Beta-blockers

Propranolol
Metoprolol
Timolol
Nadolol
Atenolol

Inderal
Lopressor
Blocadren
Corgard
Tenormin

Calcium channel blockers

Verapamil
Nifedipine
Nimodipine

Calan, Isoptin
Procardia
Nimotop

Antidepressants

Amitriptyline
Nortriptyline
Imipramine
Desipramine
Doxepin

Elavil, Endep
Pamelor, Aventyl
Tofranil, Presamine
Norpramin, Pertofrane
Sinequan, Adapin

Serotonin antagonists

Methysergide

Sansert

Anticonvulsants

Divalproex
Valproic acid

Depakote
Depakene

Recently we've seen many new medications for migraine. While there's still no cure, most patients can get relief through a combination of stress management, avoidance of headache triggers and preventive or acute drug therapy.

The pharmacological treatment of migraine divides into abortive and prophylactic measures. Most patients with migraine need only abortive treatment. These medications include analgesics, antiemetics, anxiolytics, NSAIDs, ergots, steroids, tranquilizers, narcotics and selective serotonin agonists.16,50,51 They can treat many mild-to-moderate headaches with analgesics or NSAIDs.

The latest abortive agents, such as the selective serotonin agonists and dihydroergotamine (Migranal), can treat the entire migraine complex, including the nausea, vomiting, photophobia and phonophobia. They're also effective against prolonged attacks, although patients should take these early on.50

Prophylactic therapy is indicated under certain conditions: if attacks occur more than three times a month; if they last more than 48 hours; if they're severe; if the patient can't cope; if treatment of an acute attack is inadequate or causes serious side effects; or if attacks occur after prolonged aura.52 The major medication groups include beta-adrenergic blockers, antidepressants, calcium channel antagonists, serotonin antagonists, anticonvulsants and NSAIDs. The choice of drug depends on its side-effect profile and any coexistent conditions.49 Administer prophylactic medication as monotherapy whenever possible.53 Still, these agents are seldom more than 55-65 percent effective.52 That means abortive medication may be necessary whenever a patient on prophylactic therapy gets a "breakthrough" headache.

Dr. Skorin is a member of the Review of Optometry Editorial Review Board and a frequent contributor.

1. Silberstein SD, Lipton RB. Headache epidemiology: emphasis on migraine. Neurol Clin 1996;14:421-434.
2. Kumar KL, Cooney TG: Headaches. Med Clin North Am 1995;79:261-286.
3. Trachtenbarg DE. Tension headaches. Postgrad Med 1994;95:44-56.
4. Soloman GD. Evolution of the measurement of quality of life in migraine. Neurology 1997;48 (Suppl 3):S10-S15.
5. Dalessio D, Silberstein S. Wolff's Headache. New York: Oxford University Press, 1993.
6. Cady RK. Diagnosis of headache. In: Cady RK, Fox AW, eds. Treating The Headache Patient. New York: Marcel Dekker Inc., 1995:101-122.
7. DeGowin RL. The medical history. In: DeGowin RL, ed. Bedside Diagnostic Examination, 5th ed. New York: Macmillan, 1987.
8. Finkel AG, Mauer JD, Lundeen TF. Headache and facial pain. In: Bailey BJ, ed. Head and Neck Surgery—Otolaryngology, 2nd ed. Philadelphia: Lippincott-Raven, 1998:287-304.
9. Skorin L. Headache: Diagnosis and Treatment. In: Onofrey BE, ed. Clinical Optometric Pharmacology and Therapeutics. Philadelphia: J. B. Lippincott, 1996:1-29.
10. Selby G, Lance JW. Observations on 500 cases of migraines and allied vascular headache. J Neurol Neurosurg Psychiatry 1960;23:23-32.
11. Silberstein SD, Lipton RB, Goadsby PJ. Headache in Clinical Practice. St. Louis: Mosby-Year Book, 1998.
12. Skorin L. When orgasm causes headache pain.  Rev Optom 1992;129:71.
13. Kudrow L. Cluster headache and paroxysmal hemicrania. In: Samuels MA, Feske S, eds. Office Practice of Neurology. New York: Churchill Livingstone, 1996:1129-1132.
14. Sheedy JE. Vision problems at video display terminals: a survey of optometrists. J Am Optom Assoc 1992;63:687-692.
15. Skorin L. Nonprimary headaches. In: Onofrey BE, Skorin L, Holdeman NR, eds. Ocular Therapeutics Handbook: A Clinical Manual. Philadelphia: Lippincott-Raven, 1998:531-536.
16. Davidoff RA. Migraine: Manifestations, Pathogenesis and Management. Philadelphia: FA Davis, 1995.
17. Gallagher RM. Drug Therapy for Headache. New York: Marcel Dekker, 1991.
18. Kudrow L, Kudrow D. Cluster headache and variant syndromes. In: Cady RK, Fox AW, eds. Treating the Headache Patient. New York: Marcel Dekker, 1995:193-210.
19. Silberstein SD. Evaluation and emergency treatment of headache. Headache 1992;32:396-407.
20. Edmeads J. Headache. 4th ed. Dorval, Quebec: Sandoz Canada, 1992.
21. Capobianco DJ, Cheshire WP, Campbell JK. An overview of the diagnosis and pharmacologic treatment of migraine. Mayo Clin Proc 1996;71:1055-1066.
22. Stewart WF, Lipton RB, Celentano DD, et al. Prevalence of migraine headache in the United States: relation to age, income, race and sociodemographic factors. JAMA 1992;267:64-69.
23. Von Korff M, Stewart WF, Simon DJ, et al.  Migraine and reduced work performance.
Neurology 1998;50:1741-1745.
24. Hu XH, Markson LE, Lipton RB, et al. Burden of migraine in the United States. Arch Intern Med 1999;159:813-818.
25. Lipton RB, Rapoport AM. Migraine with and without aura. In: Samuels MA, Feske S,
eds. Office Practice of Neurology. New York: Churchill Livingstone, 1996:1105-1111.
26. Rapoport AM. The diagnosis of migraine and tension-type headache, then and now.
Neurology 1992;42(Suppl 2):11-15.
27. Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988;8(Suppl 7):1-96.
28. Jensen K, Tfelt-Hansen P, Lauritzen M, et al. Classic migraine, a prospective recording of symptoms.  Acta Neurol Scand 1986;73:359-362.
29. Blau JN. Classical migraine: Symptoms between visual aura and headache onset. Lancet
1992;340:355-356.
30. Whitty CWM. Migraine without headache.  Lancet 1967;2:283-285.
31. Campbell JK: Manifestations of migraine. Neurol Clin 1990;8:841-855.
32. Skorin L: Visual hallucinations: Perception as deception. Rev Optom 1993;130:30-32.
33. Manzoni GC, Farina S, Lanfranchi M, et al. Classic migraine: clinical findings in 164
patients. Eur Neurol 1985;24:163-169.
34. Richards W. The fortification illusions of migraines. Sci Am 1971;224:88-96.
35. Fisher CM. Late-life migraine accompaniments—further experience. Stroke 1986;17:1033-1042.
36. Fisher CM. Late-life migraine accompaniments as a cause of unexplained transient ischemic attacks. Can J Neurol Sci 1980;7:9-17.
37. O'Connor PJ. Acephalgic migraine. Ophthalmology 1981;88:999-1003.
38. Sjaastad O. Transitory, isolated global blindness and headache: the possible relationship to migraine.  Funct Neurol 1986;1:467-471.
39. Main A, Dowson A, Gross M. Photophobia and phonophobia in migraineurs between attacks.  Headache 1997;37:492-495.
40. Skorin L. Ocular, neurologic exams reveal Raeder's neuralgia. Rev Optom 1990;127:106-115.
41. May A, Ashburner J, Buchel C, et al. Correlation between structural and functional changes in brain in an idiopathic headache syndrome. Nat Med 1999;5:836-838.
42. Oleson J, Schoene J, eds. Tension-Type Headache: Classification, Mechanisms and Treatment. New York: Raven Press, 1993.
43. Forsyth PA, Posner JB. Headaches in patients with brain tumors: a study of 111 patients.
Neurology 1993;43:1678-1683.
44. Gorelick PB, Hier DB, Caplan LR, et al.  Headache in acute cerebrovascular disease. Neurology 1986;36:1445-1450.
45. Skorin L. Temporal arteritis. In: Onofrey BE, Skorin L, Holdeman NR, eds. Ocular
Therapeutics Handbook: A Clinical Manual.  Philadelphia, Lippincott-Raven, 1998:552-555.
46. Alexander LJ, Skorin L, Bartlett JD: Neuro-Ophthalmic Disorders. In: Bartlett JD,
Jaanus SD, eds. Clinical Ocular Pharmacology, 3rd ed.  Boston: Butterworth-Heinemann, 1995:515-559.
47. Skorin L. Pseudotumor cerebri. In: Onofrey BE, Skorin L, Holdeman NR, eds.
Ocular Therapeutics Handbook: A Clinical Manual.  Philadelphia: Lippincott-Raven,
1998:549-552.
48. Skorin L. Superiority of MRI in identifying tumors of the brainstem and posterior fossa.
Ocular Surgery News 1993;11:10-11.
49. Silberstein SD, Lipton RB. Overview of diagnosis and treatment of migraine. Neurology 1994;44(Suppl 7):S6-S16.
50. Tepper SJ. Migraine: latest options for acute therapy. Consultant 1998;38:1163-1175.
51. Moore KL, Noble SL. Drug treatment of migraine: Part I. Acute therapy and drug-rebound headache. Am Fam Physician 1997;56:2039-2054.
52. Dieuer HC, Limmroth V. The treatment of migraine. Rev Contemp Pharmacother 1994;5:271-284.
53. Noble SL, Moore KL. Drug treatment in migraine: Part II. Preventive therapy. Am Fam
Physician 1997;56:2279-2286.

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