Adolescent Health Care: A Practical Guide

Chapter 22

Headaches

Wendy G. Mitchell

Kiarash Sadrieh

Lawrence S. Neinstein

Recurrent headaches are a frequent problem in adolescents and adults, accounting for numerous physician visits and lost days at work and school. By the age of 15 years, at least 75% of people have experienced at least one headache episode. Most recurrent headaches are not associated with severe organic pathology. In contrast, the single severe acute headache, particularly in a patient without prior headache history, may be due to significant central nervous system (CNS) or systemic disease.

Pain-Sensitive Areas: What Hurts in the Head

In general, the brain parenchyma and dura are insensitive to pain. Pain-sensitive areas include the following:

  1. Intracranial
  2. Cranial nerves (CN) V, IX, and X (most intracranial structures are innervated by CN V)
  3. Dural arteries
  4. Major venous sinuses
  5. Dura at the base of skull
  6. Intracavernous and proximal intracranial portions of the carotid arteries
  7. Extracranial
  8. Skin, fascia, muscles, and blood vessels of the scalp
  9. Upper cervical nerve roots
  10. Muscles of the neck
  11. Sinuses and teeth
  12. Eyes and eye muscles
  13. Ears

Mechanisms of Pain

Vascular Dilation

Distension of pain-sensitive cranial arteries causes headaches. The pain is mediated through the trigeminovascular system, which when depolarized, releases neuropeptides that mediate vasodilation and neurogenic inflammation. This mechanism is involved in migraine headaches and in several headaches associated with fever, systemic infection, metabolic disturbances, and vasodilator drugs. Migraine headaches may be associated with vasoactive agents, including serotonin, bradykinin, norepinephrine, prostaglandins, substance P, neurokinin A, calcitonin gene-related peptide, and histamine. The role of these vasoactive substances may be casual or reactive. There is increasing evidence that migraine is neurally initiated, rather than a direct response of the vascular system, with vascular changes being a secondary phenomena. The “aura” of migraine headaches and the neurological manifestations of complicated migraines may be due to vasoconstriction of intracranial arteries, leading to ischemia in affected areas of the brain.

Muscular Contraction

Increased muscular contraction of the head and neck muscles can lead to a headache. This mechanism of headaches is involved in tension and psychogenic headaches but may be a secondary source of pain in migraines. Patients with a migraine commonly have muscle contraction and tenderness as a result of the headache, rather than as a primary event.

Traction

Traction of pain-sensitive structures intracranially may cause a headache. Examples include mass lesions such as a brain tumor, brain abscess, subdural hematoma, and increased intracranial pressure. Brain tumors rarely cause pain directly unless pain-sensitive CNs are involved, intracranial pressure is increased, or there is traction on the meninges.

Inflammation of Pain-Sensitive Areas

Examples of inflammation of pain-sensitive areas include meningitis (either aseptic or bacterial), sinusitis, dental disease, orbital inflammation, and vasculitic syndromes involving intracranial or extracranial vessels.

Epidemiology

  1. Prevalence
  2. Approximately 40% of children have headaches by age 7 years, 66% by age 12, and 75% of adolescents by

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age 15 years. Most of these headaches are infrequent and nondisabling.

  1. Migraine headaches: Twenty-five percent of migraineurs first develop symptoms during childhood. There is approximately a 4% to 11% prevalence rate among individuals aged 7 years to 11 years and a 8% to 23% prevalence rate among individuals aged 11 years to 15 years and above. However, migraine is commonly underdiagnosed if mild or infrequent, so the prevalence rate may be higher.
  2. Sex: Headaches occur in almost equal prevalence among males and females until puberty. At that time, headaches become more common in females.
  3. Types: Acute headaches are usually associated with a systemic disease such as a viral illness or sinusitis. Most recurrent headaches in adolescents and adults are either vascular headaches (migraines), muscular contraction headaches, or a combination of both. Other causes, such as a brain tumor, are uncommon. Cluster headaches usually start during late adolescence or later but can start as early as 8 years and are far more common in males. Depressive headaches may present in the preadolescent or adolescent years, at times with denial of other depressive symptoms.

Differential Diagnosis and Characteristics

See Table 22.1 for characteristics of headaches.

Acute, Nonrecurrent (First or Worst) Headaches

Although this may be the first attack of episodic, recurrent headaches, it is important to rule out the following serious potentially life-threatening etiologies:

  1. In the Febrile patient
  2. Meningitis: Bacterial, viral, tuberculosis (TB), and other aseptic causes
  3. Brain abscess, epidural empyema, or other intracranial infection
  4. Encephalitis
  5. Sinusitis
  6. Nonspecific headache due to fever
  7. Associated with other infections: Headache is a common symptom in strep throat, influenza, mononucleosis, and rubeola. Patients with human immunodeficiency virus (HIV) or acquired immunodeficiency syndrome (AIDS) frequently complain of headaches.
  8. In the Afebrile patient
  9. Subarachnoid hemorrhage (arteriovenous malformation [AVM], aneurysm with acute bleeding)
  10. Intraparenchymal hemorrhage (AVM, venous angioma, or trauma)
  11. Other (cysticercosis or acute obstructive hydrocephalus)
  12. Headache after a seizure (postictal)
  13. Cerebral ischemia, particularly if other neurological findings or predisposing factors (e.g., sickle cell disease) are present
  14. Severe hypertension
  15. Acute dental disease
  16. Eye or orbit: Acute glaucoma or inflammatory disease of orbit

TABLE 22.1
Headache Presentations

Type of Headache

Onset

Location

Pain Quality

Common migraine

Gradual

Unilateral or bilateral

Throbbing, pulsating

Classic migraine

Gradual

Unilateral

Throbbing, pulsating

Muscle contraction

Variable, usually afternoon

Occipital, bilateral, frontal, bandlike

Steady pressure, dull

Cluster

2 a.m. to 3 a.m., abrupt

Unilateral, orbital, or temporal

Burning, boring, excruciating

Mass lesions

Gradual or sudden, but usually recent

Focal or general

Varied, often dull ache

Pseudotumor (benign increased intracranial pressure)

Variable

Vertex or diffuse

Dull

Depressive

Prolonged, constant

Generalized

Dull, unvarying

Recurrent Headaches (Episodic, Complete Recovery between Episodes)

  1. Muscle tension headaches: There is currently debate in the neurological literature that primary muscle tension headaches exist, other than in situations of direct neck trauma. Many headache experts consider “tension headaches” to be mostly misdiagnosed vascular headaches. Characteristics are as follows:
  2. Bandlike, bilateral, steady pain, occipital more than temporal
  3. Lacking the following: Throbbing, nausea, vomiting, photophobia, and associated neurological symptoms
  4. Often gradual in onset and related to stress or fatigue
  5. May be caused by minor trauma to neck muscles, whiplash, and muscle strain

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  1. May be caused by temporomandibular (TMJ) joint dysfunction
  2. Migraine: Also known as vascular headache
  3. Migraine with aura or “classic migraine”: 10% to 15% Characteristics are as follows:
  • “Aura” of sensory disturbances: Visual changes, numbness, tingling, dizziness, vertigo, and syncope are common.
  • Throbbing, unilateral, and usually frontal or temporal pain occurs.
  • Anorexia, nausea, and vomiting are frequent accompanying symptoms.
  • Phonophobia and photophobia are common.
  • Sleep often relieves migraine symptoms.
  • Family history is often positive for migraines. Although a parent may not describe his or her headaches as migraines, more careful history of family members' headache patterns often reveals vascular headaches.
  • A childhood history of motion sickness or cyclic vomiting is common.
  • Pattern of headaches varies over time. Exacerbations or onset may be precipitated by puberty, college, or other life stresses.
  • In some subjects, episodes may be precipitated by certain foods, including chocolate, tyramine-containing cheeses, red wines, and foods containing monosodium glutamate (MSG), nitrates, or nitrites.
  • History of relief with triptans or ergot compounds is supportive of diagnosis.
  1. Migraine without aura or “common migraine”: 80% to 90%
  • Characteristics are as previous migraine, but lacking aura
  • May be bilateral and variable in pain distributions
  1. Variant migraine: 5% to 10%
  • Hemiplegic migraine: Often familial and presents with hemiplegia, aphasia, or speech disturbances, followed by headache and associated symptoms as stated earlier. Headache is generally contralateral to hemiplegia. Headache may be less symptomatic than hemiplegia. Some are related to specific channelopathies. For example, genetic abnormalities in the CACNL1A4gene (a calcium channelopathy) may present as familial hemiplegic migraine.
  • Confusional migraine: More common in younger children but may continue into the teen years. A period of confusion and disorientation is usually followed by vomiting, deep sleep, and waking up feeling well. Headache may not be reported by the children and is generally not prominent.
  • Abdominal migraine: Episodic abdominal pain with nausea or vomiting, followed by or accompanied by a headache. However, the headache may be minimal or absent, and vomiting is the most prominent symptom. Aura may precede pain. Relief of episodes by sleep or antimigraine therapies supports diagnosis.
  • Basilar migraine: Dizziness, vertigo, syncope, and dysarthria are common, and precede variable headache and vomiting. Headache may be minimal or even absent. Common in adolescent girls.
  • Ophthalmoplegic migraine: Abnormal eye movements, sometimes with near-complete ophthalmoplegia and diplopia, are followed by more typical migraine symptoms.
  1. Cluster headaches: Found in <5% of children and adolescents
  2. Male predominance.
  3. Steady burning or pain; usually localized behind one eye; sudden onset; extremely severe but brief.
  4. Rhinorrhea, lacrimation, and conjunctival injection on the same side is common.
  5. Horner syndrome ipsilaterally during attack is common.
  6. During clusters, multiple daily episodes occur, often in early morning hours, awakening patient from sleep.
  7. Differential diagnosis includes occult dental disease, acute glaucoma, and tic douloureux. It must be noted that several rare metabolic disorders may mimic a migraine, including mitochondrial diseases such as MELAS (mitochondrial myopathy, encephalopathy lactacidosis, and strokelike episodes syndrome); and several organic acidurias. If metabolic disease is suspected, blood for lactate, pyruvate, and ammonia and urine for organic acids should be collected for tests during the episodes. CADASIL, a familial disorder with slowly progressive vasculopathy and leukoencephalopathy, may present during adolescence with migraine headaches, usually hemiplegic.

Chronic Headaches (Variable but Essentially Continuous or Increasing Since Onset)

  1. Intracranial mass lesions
  2. Although many patients with brain tumors have headaches, very few patients with headaches have brain tumors.
  3. Headaches due to brain tumors are usually accompanied by other neurological symptoms such as vomiting, diplopia, gait abnormalities, weakness, neuroendocrine abnormalities, or personality and behavioral changes.
  4. Headaches may be increasing in severity and frequency, and may occur nocturnally.
  5. Findings from neurological examination and funduscopic examination are often abnormal.
  6. Hydrocephalus (with or without mass)
  7. May be relatively constant, often worse in the morning.
  8. Aqueductal stenosis may present in adolescents, even if congenital.
  9. Head may be large, but this is not universal.
  10. Pain is usually dull, vertex, and not very severe.
  11. Pain may be increased by straining, bowel movements, coughing, or bending.
  12. Postlumbar puncture headaches or spontaneous “low pressure” headaches due to cerebrospinal fluid (CSF) leak
  13. Headache is positional, often abruptly relieved by recumbency.
  14. Headache, nausea, and vomiting may be severe if the patient is upright.
  15. Primary treatment is 1 to 2 days of recumbency.
  16. If severe and not relieved in several days, epidural blood patch provides relief in approximately 90% of cases caused by lumbar puncture, but may cause some lower back discomfort.
  17. Salt and fluid loading and abdominal binders are of limited efficacy.

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  1. Occasionally, spontaneous or posttraumatic occult CSF leaks may present identically, particularly in patients with Marfan syndrome. Opening pressure on a spinal tap is extremely low.
  2. Pseudotumor cerebri (also called benign intracranial hypertension): Increased intracranial pressure without mass effect
  3. Papilledema is common. Visual fields may be abnormal, including enlarged blind spot or constricted peripheral fields.
  4. Visual obscuration (transient dimming or loss of vision with straining or position change) may be present. CN palsies, more frequently of CN VI and VII, may be associated.
  5. Pain is usually dull and vertex.
  6. Pseudotumor cerebri is more common in females and obese patients.
  7. May be caused by excessive vitamin A or vitamin D intake, rapid steroid taper, certain immunosuppressants such as cyclosporin, or tetracycline or minocycline intake (for acne or other indications), or isotretinoin (Accutane).
  8. There is a risk of permanent visual loss if untreated. A patient with headache and papilledema should be treated as an emergency to prevent potential visual loss.
  9. Treatment: Lumbar puncture (postimaging) may be both diagnostic and therapeutic. A careful measurement of opening pressure with the patient in a relaxed position is necessary for diagnosis. Reduction of CSF pressure to 200 mm water or 50% of opening pressure is helpful. Serial lumbar punctations may be needed. Acetazolamide may be useful in some patients provided they tolerate adequate doses of the medication. Corticosteroids are often effective but very difficult to wean without recurrent symptoms. Rarely, a lumboperitoneal shunt needs to be placed. Optic nerve sheath fenestration may be necessary to relieve pressure on the optic nerve.
  10. “Transformed migraine”: Migraine attacks may go from episodic to chronic, essentially continuous, pain.
  11. Excessive use (usually approximately >14 tablets/week) of symptomatic medication (analgesics, triptans, or ergots) may contribute to transformation to chronic daily headache.
  12. Other migrainous symptoms are usually present but may only be present in retrospect.
  13. Depressive headaches
  14. “All day, all the time, every day, no relief.”
  15. Other overt depressive symptoms may be absent.
  16. Excessive disability (school absenteeism and social isolation) is common.
  17. Family history is often positive for affective disorders.
  18. Often responsive to antidepressant medications and supportive psychotherapy.
  19. Posttraumatic (head trauma)
  20. Headaches usually have mixed migrainous and “tension” quality.
  21. Onset within a few days of head trauma, continuing for weeks to months, but diminishing gradually over time.
  22. Minor head trauma may precipitate episodic migraines.
  23. Local extracranial disease.
  24. Chronic sinusitis
  25. Dental disease, including TMJ joint dysfunction
  26. Glaucoma
  27. Other orbital inflammatory lesions
  28. Vasculitis involving extracranial vessels (rare in adolescents)
  29. HIV or AIDS
  30. Chronic or recurrent headaches are common.
  31. May be due to HIV, other coexisting infections (intracranial, sinus, or ear), or treatment, including antiretroviral agents.
  32. Pregnancy
  33. Early pregnancy may be associated with headache, nausea, and vomiting.
  34. Pregnancy may exacerbate migraines.
  35. Chronic meningitis or other inflammatory conditions
  36. CNS sarcoidosis may present with meningeal or parenchymal involvement.
  37. TB, fungal, or recurrent or chronic “aseptic” meningitis may present with sustained or recurrent headaches.
  38. Headaches due to substance or drug abuse
  39. Both drug use and drug withdrawal may cause headaches.
  40. Small amounts of alcohol cause intense flushing and headaches in genetically prone individuals, usually of Asian origin.
  41. Alcohol withdrawal causes headaches. Be particularly alert for recurrent morning headaches due to daily alcohol consumption.
  42. Cocaine increases blood pressure and may cause headaches.
  43. Excessive (or even therapeutic) doses of over-the-counter (OTC) stimulants such as ephedrine, pseudoephedrine, caffeine, or “kava” may cause headaches.
  44. Inhalants may cause prominent headache symptoms.
  45. Amphetamines and withdrawal from amphetamines cause headache, as do other stimulants such as “ecstasy”.
  46. Headaches due to obstructive sleep apnea
  47. Headaches are often worst upon awakening.
  48. History of snoring is common.
  49. History of pauses or gasps during sleep is generally elicited only after asking the parent to observe breathing pattern during sleep.
  50. Large tonsils and adenoids and “mouth breathing” are often apparent on physical examination.
  51. Headaches due to other medical conditions: Headaches may be intermittent or continuous. Hypoxia, hypercarbia, significant hypertension, severe anemia, uremia, and dialysis all cause intermittent or continuous headaches in some patients. In addition, multiple medications used for other medical conditions, particularly chemotherapy, antiretroviral therapy, and agents used in organ transplant recipients cause headache. This is particularly important in treating adolescents with other chronic conditions such as cystic fibrosis, chronic pulmonary disease, renal failure, sickle cell anemia, cancer, organ transplantations, or cyanotic congenital heart disease. Treatment is generally aimed at the underlying condition and symptomatic relief of pain. Treatment options may be severely limited by the underlying condition in patients with migraine coexisting with other chronic illnesses.

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TABLE 22.2
International Headache Society Criteria for Migraine with Aura

From Headache Classification Subcommittee of the International Headache Society. The international classification of headache disorders (2nd edition). Cephalagia 2004;8(Suppl 1):9.

1.  At least two attacks that fulfill criteria B

2.  Migraine aura fulfilling the following:

1.  Aura consisting of at least one of the following, but no motor weakness:

1.  Fully reversible visual symptoms including positive features (e.g., flickering lights, spots, or lines) and/or negative features (i.e., loss of vision)

2.  Fully reversible sensory symptoms including positive features (i.e., pins and needles) and/or negative features (i.e., numbness)

3.  Fully reversible dysphasic speech disturbance

2.  At least two of the following:

1.  Homonymous visual symptoms and/or unilateral sensory symptoms

2.  At least one aura symptom develops gradually over 5 min and/or different aura symptoms occur in succession over 5 min

3.  Each symptom lasts 5 to 60 min

3.  Not attributed to another disorder

Diagnosis

In the evaluation of the patient with headaches, the history is (nearly) everything. The rest is the examination.

(See Tables 22.2 and 22.3 for International Headache Society [IHS] criteria for migraines.)

TABLE 22.3
International Headache Society Criteria for Migraine without Aura

From Headache Classification Subcommittee of the International Headache Society. The international classification of headache disorders (2nd edition). Cephalagia 2004;8(Suppl 1):9.

1.  At least five attacks that fulfill criteria in B to D

2.  Headache attacks that last 4–72 hr (untreated or unsuccessfully treated)

3.  Headache has at least two of the following characteristics:

1.  Unilateral site

2.  Pulsating quality

3.  Moderate to severe intensity

4.  Aggravation by or causing avoidance of routine physical activity (e.g., climbing stairs)

4.  During headache, at least one of the following symptoms:

1.  Nausea or vomiting (or both)

2.  Photophobia and phonophobia

5.  Not attributed to another disorder

The history must include the following:

  1. Onset: Age at first episode; events or illnesses surrounding onset; temporal pattern of headaches (time of day, day of week, and season); frequency.
  2. Pattern and chronology of pain: Have the patient describe a typical headache episode in detail.
  3. Prodrome
  4. Location
  5. Quality (pounding, dull, sharp, or sticking)
  6. Change in quality or location as headache progresses
  7. Associated autonomic symptoms (sweating, pallor, flushing, and palpitations)
  8. Nausea, vomiting, and anorexia
  9. Duration and diurnal variation
  10. Severity and limitation of activities
  11. Response to medications and sleep
  12. Preceding and accompanying symptoms, particularly visual or other neurological symptoms.
  13. Precipitants of specific episodes or precipitants at onset of headaches.
  14. Stress: Family, school, and peers
  15. Illnesses
  16. Foods/diet/eating pattern: Nitrate or nitrite-containing foods (cured meats), MSG, chocolate, nuts, cheeses, and other specific suspect foods; skipping meals (true food “allergies” causing migraine are rare)

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  1. Medications: Intake of OTC medications (particularly decongestants or diet pills)
  2. Exertion and orgasm
  3. Caffeine intake or withdrawal
  4. Alcohol intake
  5. Toxic exposures, particularly lead and hydrocarbons
  6. Physical exposures: Bright or flashing lights, temperature changes, and strong odors
  7. Other associated illnesses or symptoms, including HIV risks. Changes in menstrual pattern or galactorrhea may suggest pituitary lesion or pregnancy.
  8. Medications (prescribed and OTC).
  9. Analgesics
  10. Birth control pills
  11. Other medications used for headaches (acute or prophylactic)
  12. Tetracycline, minocycline, medications for acne
  13. Vitamin consumption, particularly fat-soluble vitamins (e.g., vitamins A, D, and E), unusual diets, and supplements.
  14. Substance abuse.
  15. Depression or mood disorders.
  16. School phobia or school avoidance and other secondary gains.
  17. Behavior between attacks: Any recent personality change or change in school performance.
  18. Family history.
  19. Migraines or other headaches
  20. Epilepsy
  21. Affective disorders
  22. Other neurological conditions
  23. Other criteria for migraines: Raskin (1995) identified additional clinical features that suggest the benign nature of a migraine attack. These exceed the IHS criteria (Tables 22.2 and22.3) of migraine and consist of the following factors: (a) precipitation by menstruation (although the second edition of the IHS classification report does provide criteria formenstrual migraineand menstrual-related migraine), (b) amelioration with sleep, (c) amelioration during pregnancy, (d) appearance after sustained exertion, and (e) triggers such as alcohol, odors, foods, or changes in the weather.

Physical Examination

The physical examination should include a good general physical examination plus a careful neurological examination. If possible, the patient should be examined both during a typical episode and when free of symptoms. Pertinent physical findings include the following:

  1. Vital signs: Elevated blood pressure or temperature.
  2. Eyes, ears, nose, and throat: Sinus tenderness, acute or chronic otitis, poor dentition, and refractive error, TMJ pain, or dysfunction.
  3. General physical examination: Café au lait spots, depigmented macular lesions suggesting tuberous sclerosis, signs of systemic illness, and galactorrhea.
  4. Neck: Nuchal rigidity, spasm or tenderness of cervical neck muscles, or “trigger points.”
  5. Funduscopic and visual examination: Papilledema, narrowing of vessels, optic atrophy; visual fields, and visual acuity.
  6. Neurological examination: Head circumference, mental status, CNs, motor and sensory examination, gait, reflexes, and coordination.

Laboratory Tests

In patients with recurrent headaches separated by periods of complete recovery, laboratory and radiological work-ups are seldom indicated in the presence of normal physical examination findings. Laboratory and radiological work-ups should be guided by the history and physical examination results; for example, sinus films may be indicated if facial tenderness or nasal discharge suggest sinusitis. Neuroimaging (computed tomography or magnetic resonance imaging) is indicated if it is an acute severe or increasing headache, if it is an abnormal result on neurological examination, if papilledema is present, or if the head circumference is above the 95th percentile without other explanation. Neuroimaging is notgenerally needed for long-standing recurrent headaches with complete clearing of symptoms between episodes in the face of normal neurological and funduscopic examination results. Other evaluation is guided by physical findings and history. For example, in an adolescent with morning headaches, snoring, and large tonsils, a sleep study to rule out obstructive sleep apnea may be appropriate.

In contrast, an acute severe headache in a patient with no prior headache history must be considered more closely, as underlying systemic or CNS pathology may be life threatening. Neuroimaging and lumbar puncture should be considered to aid in the diagnosis of an acute condition and may be necessary on an emergency basis.

Therapy

  • Rule 1A: Not having a headache is better than getting rid of it once it occurs. Rule 1B: Not taking pills every day is better than taking pills. Look for precipitants, particularly avoidable ones.
  • Rule 2: Take the preferred abortive medication at the onset of the headache, the earlier the better.
  • Rule 3: Do not underestimate the role of reassurance.
  • Adolescents and parents are often more concerned that the headache is caused by a brain tumor than by the discomfort of the headache itself. Once the adolescent is reassured, treatment beyond simple analgesics may be neither necessary nor desired by the patient.

General strategies for headache management are as follows:

  1. Headache diary: The patient should be encouraged to understand the causes and precipitants for headaches. Keeping a headache diary can be therapeutic itself, even if no specific precipitants are ever identified. The diary is kept for a variable period, usually until at least three typical headache episodes have occurred or up to 3 months if no attacks occur while keeping the diary. The adolescent (with the help of a parent) maintains a detailedrecord of headaches, medication intake, and results, as well as activities, foods, stresses, sleep pattern, and physical environment. The following items can be important in uncovering the precipitating factors in recurrent headaches:

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  1. Foods: Chocolate, nuts, cola, caffeine-containing beverages, and cheeses. (Best to record all food intake in the diary.)
  2. Food additives: MSG, nitrates, and nitrites. Nitrates and nitrites are present in nearly all cured meats such as hot dogs, bacon, sausage, ham, and lunch meats. MSG is not always clearly listed on food labels. Foods commonly high in MSG include dried soups and noodles, dried flavoring packets for taco or spaghetti sauces, and some snack foods.
  3. Physical stimulants: Exposure to bright lights; rapidly moving or strobe lights (or strobe effect when driving); temperature changes; exercise; and sexual activity.
  4. All medications, including OTC medications and birth control pills, for headache and any other conditions.
  5. Alcohol or other substance intake.
  6. Obvious allergic symptoms (rashes, asthma, and allergic rhinitis).
  7. Stresses: School, tests, and emotional stressors.
  8. Sleep pattern: Deviations from usual pattern, particularly excessive sleep, may precipitate headaches.
  9. Treatment of tension headaches
  10. A brief period of relaxation or a nap often brings relief.
  11. Simple physical measures: Massage or stretching exercises of the neck muscles or warm or cold compresses may help, particularly with relaxation. Biofeedback is occasionally effective but is expensive and requires a very motivated patient and family. Other means of physical relaxation (i.e., yoga, meditation) may be helpful in motivated individuals.
  12. Simple analgesics (e.g., acetaminophen, nonsteroidal anti-inflammatory drugs [NSAIDs], and aspirin), if not used excessively, are often effective.
  13. Combined analgesic-sedative drugs (butalbital [Fiorinal] or other combinations) should be used sparingly, if at all.
  14. Mixed tension-vascular headaches, if very frequent and disabling, may be treated on a prophylactic basis with low-dose tricyclic antidepressants, usually amitriptyline.
  15. Migraine headaches

Things to do on a trial basis for all patients with migraines include the following:

  1. Wear sunglasses, brimmed hat, or visor whenever in bright sun. Sunglasses need not be expensive, but should be “100% ultraviolet (UV) protective”. In many communities, a “doctor's note” is needed to allow a hat or sunglasses to be worn during outdoor activities at school.
  2. Avoid strobe lights or strobelike conditions.
  3. Try a diet eliminating MSG and nitrates or nitrites.
  4. Stabilize caffeine intake (same amount every day) or wean off completely.
  5. Try eliminating all alcohol intake.
  6. Try stabilizing sleep pattern to approximately the same amount of sleep daily (i.e., avoid sleep deprivation during the school week followed by “sleeping in” on weekend).
  7. Medications for acute episodic migraine treatment (classic, common, or variant) in patients with relatively infrequent headaches
  8. Simple analgesics, taken as soon as possible at the onset of the episode (e.g., acetaminophen or NSAIDs such as ibuprofen) often abort the migraine, without the need for stronger medications. American

Academy of Neurology (AAN) Practice Parameters recommend ibuprofen as safe and effective. They state that the acetaminophen is probably effective and should be considered. Caffeine (either as a tablet, combined with analgesic, or as a beverage) may potentiate the effect of the analgesic.

  1. Antiemetic, either orally, rectally, or parenterally: Promethazine (Phenergan), chlorpromazine (Thorazine), metoclopramide (Reglan), or prochlorperazine (Compazine) combined with or followed by an analgesic is very helpful if nausea or vomiting is prominent. Use of a sedating antiemetic will often allow oral analgesics to be tolerated, promote sleep, and relieve nausea and vomiting.
  2. Sedative-analgesic combinations: Small doses of a short-acting sedative such as barbiturate with acetaminophen or aspirin are reasonable if headaches are infrequent and relieved by sleep. Multiple preparations and brands are available.
  3. Triptans: Several triptans are available, all selective serotonin receptor agonists. Various preparations (regular tablets, orally dissolvable tablets, nasal sprays, and injections) are marketed. They cannot be mixed (i.e., do not use more than one particular triptan in a given 24-hour period). They should also not be mixed with ergot preparations. They are contraindicated in hemiplegic migraines. Generally, if one triptan does not work, switching to another may not help. If one type works but has unacceptable side effects, or duration of action is too short, another may be better tolerated.
  • Sumatriptan (Imitrex), a specific serotonin agonist is administered by subcutaneous injection, nasal spray, or orally.
  • –Self-injection: The “self-injection” syringes are available only in a 6-mg dose, which may be too high for a smaller adolescent. Fractional doses (2–3 mg) may be used from unit-dose vials using a regular syringe and needle. Because subjective sensory phenomena may be very worrisome to the patient, the first dose should generally be given under direct medical supervision. If successful and well tolerated, the adolescent or the parents may be instructed in administration at home, particularly if episodes are infrequent but very severe.
  • –Oral: Oral sumatriptan is available as 25- and 50- mg tablets. The adult dose is 25 to 50 mg, given once or twice. Onset of action is in approximately 1 hour, and relief may be long standing if the event is interrupted.
  • –Nasal spray: Sumatriptan nasal spray is particularly effective for those patients with nausea and vomiting, and can be used at home or school. Nasal sumatriptan is recommended by the AAN for acute migraine treatment. The nasal spray is available in 5- and 20-mg single-dose dispensers. Adolescents generally respond to 10 to 20 mg. The spray generally causes a metallic taste, which lasts for 30 to 60 minutes. Using the spray with the head tilted forward, then compressing the nostrils for a few minutes may partially prevent this effect, which is quite noxious to some patients.
  • Zolmitriptan, another serotonin agonist that has been used in adults, is particularly useful for

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cluster headaches. It comes in 2.5- and 5-mg tablets (maximum dose, 10 mg/24 hours). It also has similar adverse effects such as paresthesias, heaviness, nausea, and tightness.

  • Rizatriptan, 5- and 10-mg oral disintegrating tablets. This form is useful for adolescents who cannot or will not swallow a pill during a migraine.
  • Naratriptan comes as 1- and 2.5-mg tablets. Has not shown significant efficacy for adolescent migraines. It is longer acting and may be useful in adolescents in whom sumatriptan is effective but has recurrent headaches when a dose wears off.
  1. Ergot derivatives are much less commonly used since the introduction of triptans. Ergotamine must be used at the onset of symptoms. Medication should be available to the adolescent at all times, including school. Sublingual, oral, rectal, or inhaled preparations are available, with multiple brand names. Cafergot combines ergotamine and caffeine. Other preparations mostly contain only ergotamine, usually ergotamine tartrate, 1 to 2 mg/dose.
  2. Dihydroergotamine (DHE) is available for either intravenous or intramuscular injection or as a nasal spray: DHE-45, given intravenously 10 to 15 minutes after a parenteral dose of antiemetic (commonly metoclopramide [Reglan] or chlorpromazine [Thorazine]), may provide rapid relief of migraine symptoms, even several hours after onset. Several small doses may be given under direct supervision in an emergency department or office. DHE nasal spray (Migranal) may be used at home or school and is sometimes effective in adolescents who do not tolerate or respond to triptans. Do not use DHE for hemiplegic migraines.
  3. Inhaled high-flow oxygen may relieve cluster headaches rapidly. Patients with cluster headaches often carry a small tank of oxygen with them at all times and become psychologically dependent on the availability of this treatment modality if it is effective at relieving their severe attacks of pain.
  4. Chlorpromazine (Thorazine) (10 mg intravenously single dose) has been reported to relieve migraine pain rapidly.
  5. Intravenous valproic acid (Depacon) has been used with success as an abortive medication in adolescent migraines. Doses of 1,000 mg to 1,500 mg were efficacious in one series. However, there have been no randomized, controlled studies to date.

Warning: If headaches are frequent (i.e., more than twice a week), beware of analgesic or ergot overuse syndromes. This may convert intermittent migraines to chronictransformed” migraines.

  1. Prophylactic treatment: Adolescents with severe recurrent attacks causing significant school absenteeism or functional limitations should be considered for prophylactic treatment. Prophylactic treatment is generally indicated in migraines accompanied by significant neurological deficits (e.g., hemiplegic migraines), even if the episodes are infrequent. Prophylactic treatment may be preferred even in patients responsive to NSAIDs, triptans, or other agents, due to the inability to carry medications to school. Continue treatment until the headache pattern has markedly improved for approximately 6 months, then consider a trial of tapering-off medication. Current AAN Practice Parameters state that there is insufficient evidence to recommend any drug approved in the United States for migraine prophylaxis.

They do find that flunarizine, a calcium channel blocker not available in the US, is probably effective for migraine prophylaxis in adolescents. There is anecdotal evidence for a number of prophylactic medications, however.

  1. β-Blockers: Propranolol is effective in approximately 70% of adolescents with severe migraines, although there have been few well-controlled studies. The initial dose is 40 to 80 mg, divided twice daily (b.i.d.) or three times a day (t.i.d.). A slow-release preparation of propranolol may allow for once daily dosing. Higher doses (up to 240 mg/day) may be used. The effect is not immediate. Usually, a gradual decrease in headache frequency is seen over several weeks to months. Side effects include fatigue, depression, and decreased exercise tolerance, particularly at high doses. Severe asthma, insulin-dependent diabetes, and depression are contraindications. Other β-blockers (e.g., atenolol, nadolol, timolol, and metoprolol) may also be effective.
  2. Tricyclic antidepressants (amitriptyline, imipramine, desipramine): Amitriptyline (Elavil) is useful for prophylaxis of migraines or mixed tension-vascular headaches. The initial daily dose is 10 to 25 mg at bedtime, increased gradually as needed to 75 to 100 mg/day. Side effects include sedation, dry mouth, arrhythmias, hypotension, and decreased tolerance of warm environments. At higher doses, electrocardiogram should be monitored.
  3. Low-dose aspirin or NSAIDs (e.g., ibuprofen and naproxen) used in chronic low doses may effectively prevent migraine attacks. NSAIDs may be particularly effective in menstrual migraines if started a day or two before expected symptomatic periods.
  4. Cyproheptadine (Periactin): The usual dose is 2 to 4 mg t.i.d. A major side effect is sedation. Significant weight gain occasionally occurs.
  5. Anticonvulsants: Valproic acid (Depakote), low-dose phenobarbital, topiramate (Topamax), levetiracetam (Keppra), and possibly phenytoin (Dilantin) have been reported to prevent migraines. The dose used often is lower than that necessary for seizure control. Divalproex sodium (Depakote) is currently approved by the Food and Drug Administration for migraine prophylaxis at a dose of 500 mg/day. Topiramate has been shown to be effective in a randomized controlled trial of patients aged 12 to 65 years. The best responses were to doses of 100 mg/day and 200 mg/day. The main adverse effects were paresthesias, fatigue, and nausea. Studies in children show cognitive disturbances as the main side effect.
  6. Calcium channel blockers (e.g., verapamil and nimodipine) have been used with limited success for migraine prophylaxis. Flunarizine (not available in the United States) has demonstrated significant headache reduction in a double-blind placebo-controlled trial.
  7. Clonidine (Catapres) has occasionally been reported to be useful.
  8. Methysergide (Sansert): Significant risks make this a last choice in most circumstances. It should not be used continuously for more than 6 months, because of risk of retroperitoneal and pericardial fibrosis. Close follow-up is essential. However, this is

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a very effective modality for patients with refractory, frequent migraines.

  1. Lithium carbonate has been reported to be an effective prophylactic medication for chronic cluster headaches.
  2. Combinations of high-dose riboflavin (vitamin B2) and magnesium may prevent migraine in some patients. A commercial preparation of magnesium oxide, riboflavin, and the herb feverfew is sold as a food supplement.
  3. “Transformed migraines,” chronic migraines, rebound headache if severe and disabling.
  4. Intravenous DHE, usually combined with metoclopramide or chlorpromazine, is given over 2 to 4 days on an adjusted q8h schedule. This requires hospitalization, dose supervision, and dose titration over the first few doses.
  5. Short courses of high-dose corticosteroids may end the episode. Usually, high-dose prednisone (2 mg/kg/day) or dexamethasone (Decadron) is used for approximately 5 days, followed by a rapid taper.
  6. Withdrawal of chronic (overused or daily use) nonnarcotic and narcotic analgesics, triptans, and ergots is essential. This may require hospitalization for detoxification.
  7. Psychological supportive therapy, relaxation therapies, and physical exercise programs are often essential to improve the health status of teens with chronic daily headaches.

Prognosis

Guidetti and Galli (1998) studied the evolution of headaches in children and adolescents and found that 34% remitted, 45% improved, 6% worsened, and the condition remained unchanged in 15%. Up to 40% to 50% of childhood-onset migraines may remit during adolescence or young adulthood. Adolescence-onset migraines often continue into adulthood. However, adolescents should be reassured that even people with a strong tendency to have migraines do not have frequent attacks throughout life. Patterns of occurrence are highly variable. The goal is to avoid any offending agents, use effective medication in appropriate doses, and lead a functional lifestyle.

Web Sites

For Teenagers and Parents

http://www.headaches.org/. Web site of the National Headache Foundation.

http://familydoctor.org/x502.xml. The American Academy of Family Physicians handout on headaches.

http://www.ninds.nih.gov/disorders/headache/headache.htm. National Institutes of Health site on headaches.

http://www.achenet.org/. American Council for Headache Education.

http://www.aan.com/professionals/practice/pdfs/Headache_Peds_Patients.pdf. AAN Headache Information.

http://www.emedicinehealth.com/migraine_headache_in_children/article_em.htm Emedicine patient information.

For Health Professionals

http://www.familydoctor.org/flowcharts/502.html. Flowcharts on headaches from the American Academy of Family Physicians.

http://www.emedicine.com/neuro/topic528.htm.

http://www.emedicine.com/neuro/topic529.htm. Emedicine

http://www.neuropat.dote.hu/pain.htm. Internet Handbook of Neurology.

http://www.ahsnet.org/. American Headache Society—Publisher's of Headache.

References and Additional Readings

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Annequin D, Tourniaire B, Massiou H. Migraine and headache in childhood and adolescence. Pediatr Clin North Am 2000;47:617.

Brandes JL, Saper JR, Diamond M, et al. Topiramate for migraine prevention: a randomized controlled trial. JAMA 2004;291(8):965.

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Deleu D, Hanssens Y. Current and emerging second generation triptans in acute migraine therapy: a comparative review. J Clin Pharmacol 2000;40:687.

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Guidetti V, Galli F. Evolution of headache in childhood and adolescence: an 8-year follow-up. Cephalgia 1998;18(7): 449.

Hamalainen ML, Hoppu K, Santavuori P. Sumatriptan for migraine attacks in children: a double-blind, randomized, placebo-controlled, crossover study. Neurology 1997;48: 1100.

Hamalainen ML, Hoppu K, Valkeila E, et al. Ibuprofen or acetaminophen for the acute treatment of migraine in children: a double-blind, randomized, placebo-controlled, crossover study. Neurology 1997;48:103.

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Lewis DW, Yonker M, Winner P, The treatment of pediatric migraine. Pediatr Ann 2005;34(6):448.

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Ojaimi J, Katsabanis S, Bower S, et al. Mitochondrial DNA in stroke and migraine with aura. Cerebrovasc Dis 1998;8:102.

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