General Principles
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Headache is one of the most common disorders and symptoms reported to primary care, the emergency department, and team physicians.
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Complaints of headache account for 1%–4% of primary care office and emergency department visits.
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In the general population, the prevalence of headache in a 1-year period is >90%, and the lifetime prevalence is 93%–99%.
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Headaches are one of the most commonly reported pain complaints among children and adolescents.
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In a population study of adolescents aged 11–21 years, >90% had experienced headaches, regardless of the type, over 1 year.
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Among children aged 4–17 years in the United States, 6.7% had frequent headache pain over a 12-month period.
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Various studies on athletes have shown a headache prevalence of 35%–50% related to participation in their sport.
Causes of Headache
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The exact cause of many headaches is a source of much debate and likely differs for each specific type of headache. Physiologic changes in the head and brain that consist of, but are not limited to, changes in neurotransmitter regulation, vascular dilation and constriction, and cranial nerve irritation that cause activation of pain signals are all contributors to the development of headache. Cyclical hormonal changes and genetic predisposition are also thought to play an important role.
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Tension-type headache (TTH), migraine, and cluster headaches combine to make up >90% of headaches experienced by the general population.
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Adults mostly experience TTHs, whereas children are more likely to have migraine headaches.
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Among children aged 3–18 years who visit pediatric neurologic clinics, vascular/migrainous headaches account for 52%, chronic headaches/TTHs for 21%, and unclassified headaches for 19%. Remainders are mixed tension-migraine, psychogenic, or posttraumatic.
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Of headache-caused emergency department visits:
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Migraine and TTHs account for 25%–55% of visits.
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Headache associated with systemic illness accounts for 33%–39% of visits.
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Headache caused by a serious neurologic condition (subarachnoid hemorrhage, intracranial mass, meningitis, or hemorrhage) accounts for 1%–16% of visits.
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Classification of Headache Disorders
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In 1988, the International Headache Society (IHS) created its first classification of headache disorders. This classification was updated and revised in 2003 and then again in 2013.
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Headache has many causes. The IHS classification gives a physician a logical approach to make a rapid and accurate differential diagnosis.
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Headache disorders are classified as primary, secondary, or those caused by cranial neuralgias.
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Primary headaches are those that have no underlying cause; there are three main types: migraine headache, TTH, and cluster headache (trigeminal autonomic cephalalgias).
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Secondary headaches are those that may be attributed to certain underlying pathologic conditions, i.e., infectious, neoplastic, vascular, psychiatric, traumatic, drug-induced, or homeostatic changes.
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Cranial neuralgia headaches are those that are initiated by compression, distortion, or irritation of specific cranial nerves and subsequently cause pain in the area that those nerves innervate.
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The athletic population suffers from the same headache disorders as the general population but may also have a predisposition to suffer from other headache disorders and subtypes because of the effects of exercise and because of participation in their specific sports.
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Sports-/exercise-related primary headaches are exercise-/effort-induced migraine and primary exertional headaches.
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Sports-/exercise-related secondary headaches are acute and chronic posttraumatic headache (PTH), cervicogenic headache, high-altitude headache, and diving headache.
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Sports-/exercise-related cranial neuralgia headaches are external compression headache and cold-stimulus headache.
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Assessing Headache in the General and Athletic Population
Like all other medical evaluations, the assessment of headache begins with a thorough history and physical examination. Most patients will have a completely normal general physical and neurologic examination, so obtaining a detailed history is critical. After history and physical examination have been completed, a further investigation may be warranted, depending on the history and physical findings. This investigation may include laboratory workup, imaging, and/or diagnostic procedures.
Headache History
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When was the first onset of headache?
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What is the frequency?
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Where is the location and is there any radiation of pain?
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What is the character of the pain? (dull, throbbing, sharp)
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What is the intensity of the pain?
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Are there any associated symptoms?
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Nausea/vomiting
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Photophobia/phonophobia
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Confusion
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Blurry vision
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Gait disturbances
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Were there any medications taken?
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Are there any alleviating or exacerbating factors?
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Is there a prior history of headache?
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Is there a family history of headache?
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Has there been a change in the headache characteristics? (if prior history is positive)
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Is there a history of other medical issues?
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What medications is the athlete taking?
Physical Examination
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Assess for level of consciousness, orientation, alertness, mini-mental status, and overall affect.
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Check vital signs to rule out hypertension.
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Evaluate head, eyes, ears, nose, and throat to assess for papilledema. Check for central nervous system abnormalities, including cranial nerve testing, ptosis, pupil reactivity, and head trauma.
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Conduct musculoskeletal evaluation to assess for nuchal rigidity, temporomandibular joint problems, cervical spine range of motion, areas of scalp tenderness, and neck tenderness.
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Conduct neurologic examination to assess for motor, sensory, and reflex response; also include evaluation of gait.
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Check for evidence of systemic illness (assess abnormalities in the cardiovascular, respiratory, and gastrointestinal [GI] systems).
Additional Investigation
Laboratory evaluation: To rule out metabolic issues. Laboratory examinations that may aid in diagnosis are erythrocyte sedimentation rate, complete blood count, liver function tests, thyroid function tests, antinuclear antibodies, antiphospholipid antibodies, and drug screening. Appropriate tests must be conducted as indicated by the history and physical examination.
Imaging tests: Possibilities include cervical spine films, CT (with or without contrast), MRI, EEG, and MR angiography. Selection of tests should be individualized.
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Cervical spine radiography (flexion/extension views) in patients with trauma/neck pain, possible fracture, and instability.
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CT scan with contrast for patients with new-onset exertional headache.
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Some experts do not advocate CT unless neurologic examination is abnormal.
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May not be helpful for suspected posterior fossa lesions
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CT better for acute bleeding and bony fractures; detects surgical lesions as well as MRI scan
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MRI has greater tissue contrast resolution than CT.
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Better to perform MRI >48 hours after trauma and in patients with arteriovenous malformations (AVMs) or tumor
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Study of choice when looking for lesions in the posterior fossa
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Less radiation exposure compared with CT
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According to the Quality Standards Subcommittee of American Academy of Neurology, routine use of brain imaging is not warranted for adults with recurrent headaches that have been defined as migraines with no recent change in pattern, no history of seizure, and no other focal neurological signs or symptoms.
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Diagnostic procedure: Lumbar puncture (LP) to rule out subarachnoid hemorrhage from aneurysm; detects minor leaks, which occur in 39% of patients who later have ruptures. CT scans are negative in 55% of patients with minor leaks.
General Considerations
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Consider the same diagnostic evaluation in athletes as in nonathletes, except in cases of trauma with an increased risk of intracranial bleed.
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Workup should be complete when diagnosis is in question. This may include, but is not limited to, evaluation for drug abuse, hypertension, vascular lesions, neoplasms, intracranial bleeding, and psychiatric issues.
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Be cognizant of “red flags” within the history or physical examination that should prompt further neurologic evaluation in the form of either imaging or other diagnostic procedures ( Box 39.1 ).
Box 39.1
Red Flags in the Evaluation of Headache
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Headache onset after the age of 50 years
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Sudden onset of severe headache
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Change in headache pattern
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Headache associated with systemic illness and fever
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Headache associated with neck stiffness
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Headache with focal neurologic deficits
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Presence of papilledema
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Headache in the setting of moderate/severe trauma
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Alteration of consciousness or amnesia
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Early morning nausea and vomiting without headache
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Occurrence of seizure(s) after headache
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Primary Headache Disorders
See Table 39.1 .
| Migraine | Cluster | Tension-Type | |
|---|---|---|---|
| Onset | Peaks in adolescence | 30′ s or 40′ s | Variable; ≥20′ s |
| Frequency | 1–2 attacks/mo, often with menses | ≥1 attacks/day for 6–8 wk | Episodic: <15 days/mo Chronic: >15 days/mo |
| Location | Unilateral more common than bilateral; frontotemporal or orbital | 100% unilateral Generally orbitotemporal | Bifrontal, bioccipital, neck |
| Quality | Throbbing or intense pressure | Nonthrobbing, penetrating, boring | Squeezing, pressing, aching |
| Duration | 4–72 h, usually 12–24 h | 30 min–2 h, usually 45–90 min | Episodic: several hours Chronic: all day |
| Prodrome | Changes in mood, energy, appetite | May include brief, mild burning in eye and internal nares | None |
| Aura | Up to 60 min, usually 20 min; ‘often’ visual | None | None |
| Associated Symptoms | Nausea, vomiting, photophobia | Ipsilateral ptosis-miosis, conjunctival injection, tearing, stuffed and running nose | Episodic: loss of appetite, light or sound sensitivity Chronic: light or sound sensitivity, nausea |
| Behavior | Go to dark, quiet room | Frenetic pacing, rocking | Generally not affected or mild decrease in function |
Migraine Headache
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Definition: Migraine is a chronic, idiopathic neurologic disorder characterized by episodic headaches of high intensity that may be preceded by, accompanied with, or followed by other associated symptoms ( Figs. 39.1 and 39.2 ).
Figure 39.1
Mechanisms of migraine.
Figure 39.2
Migraine pathophysiology.
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Associated symptoms
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Premonitory (prodrome) symptoms: Occur hours up to 1–2 days before development of migraine headache. These symptoms are often thought of as a warning of an impending migraine.
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Fatigue
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Difficulty concentrating
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Yawning
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Change in appetite
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Change in sleep patterns
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Change in mood
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Aura: A set of reversible focal neurologic symptoms that occur at the beginning of a migraine headache or just before its onset. Auras typically last for <60 minutes. Visual symptoms are most common.
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Visual changes (scintillating scotoma, visual field deficits, and blurry vision)
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Sensory disturbances (pins and needles sensation and numbness)
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Speech disturbances (dysphasia)
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Motor deficits (rare)
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Resolution (postdrome) symptoms: These are symptoms that follow the headache and may include certain premonitory symptoms.
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Exhaustion
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Exhilaration
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Depression
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Nausea
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Scalp tenderness
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Migraine headache is divided into two major subtypes by the IHS.
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Migraine without aura
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Migraine with aura (10%–15% of migraines)
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Migraine headaches are typically unilateral but can be bilateral. Bilateral migraine is more likely to occur in children/adolescents than adults. They also tend to have a pulsating nature, moderate-to-severe intensity, exacerbation by activity, and an association with nausea, vomiting, photophobia, and phonophobia.
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IHS diagnostic criteria for migraine are enlisted in Box 39.2 .
Box 39.2
Ihs Diagnostic Criteria for Migraine Without Aura
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At least five attacks fulfilling criteria B–D
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Headaches lasting for 4–72 hours
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Headache has at least two of the following characteristics:
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unilateral location
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pulsating quality
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moderate or severe pain intensity
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aggravated by physical activity
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During headache, at least one of the following is present:
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nausea and/or vomiting
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photophobia and phonophobia
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Cannot be attributed to another disorder
Modified from Headache Classification Subcommittee of the International Headache Society (IHS). The International Classification of Headache Disorders. 3rd edition (beta version). Cephalalgia. 2013;33(9):629-808.
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Typical age of onset is in adolescence.
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18% of women and 6% of men report headaches that meet the definition of migraine. The female-to-male ratio is 3 : 1.
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A survey of 791 male and female NCAA division I basketball players showed a total prevalence rate of 2.9% (0.9% of males, 4.4% of females).
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70% of females who suffer from migraines note a relationship between their menstrual cycles and migraine attacks.
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Migraine without aura: highest incidence during first 3 days of menses
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Severe, debilitating forms of migraine include status migrainous, in which migraine lasts for >72 hours, and chronic migraine, in which migraines occur for ≥15 days per month.
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Common migraine triggers include aspartame, caffeine (use or withdrawal), estrogens, monosodium glutamate, nicotine, nitrates, progesterone, alcohol, cheese, chocolate, menstruation, missed meals, perfume, red grapes, sleep (too much or too little), stress, changes in environment/weather, and exercise.
Treatment Options
Overview: Abortive treatment is appropriate if headaches occur once or twice per month, particularly if predicted by aura. It is more effective if used as early as possible, and a large single dose is more effective than multiple smaller doses.
Nonsteroidal anti-inflammatory drugs (NSAIDs): Chronic use should be avoided, particularly in those with a history of peptic ulcer disease, gastritis, and renal insufficiency. Specific medication and initial dosages:
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Ibuprofen: 1200 mg PO (peak effect at 1 hour)
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Naproxen: 500–825 mg PO (peak effect at 2 hours)
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Indomethacin: 50 mg PO
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Ketorolac: 30–60 mg IM, with additional 30 mg in 8 hours if necessary
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Dihydroergotamine (DHE-45): Is available in parenteral form and is typically given with an antiemetic
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DHE-45: 1.0 mg IV/IM/SQ, given 30 minutes after metoclopramide 5 mg or prochlorperazine 5 mg; may be repeated in 1 hour (90% effective)
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DHE-45 (nasal): 1.0 mg of intranasal puffs, repeating in 15 minutes
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Favorable side-effect profile when compared to ergotamine (minimal cardiovascular effects and nausea; no rebound headache; nausea/vomiting, GI upset, and muscle cramping have been reported)
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DHE-45 is a vasoconstrictor and is therefore contraindicated in patients with cerebrovascular, cardiovascular, or peripheral vascular disease. It is also contraindicated in patients with severe hypertension, ischemic heart disease, renal or hepatic disease, sepsis, recent infection, or those who may be pregnant.
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Triptans: This class of medication causes vasoconstriction and blocks pain pathways within the brainstem. They are selective 5-hydroxytryptamine (5-HT) receptor agonists and are specifically used to treat migraines. All medications belonging to this class have similar side-effect profiles (nausea, dizziness, chest pressure, asthenia, and dry mouth). They also carry the same precautions in that they should be avoided if possible in those with cardiovascular disease, peripheral vascular disease, hypertension, and hepatic dysfunction.
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Sumatriptan (Imitrex): 5-HT1D receptor agonist; the first triptan developed, it is available in injectable, oral, and intranasal spray forms
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Injectable dosage: 4–6 mg SC initially; may repeat in 1 hour (maximum of two 6-mg injections in 24 hours); recommended initial dose is 6 mg
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Oral dosage: 25–100 mg initially; may repeat dosage in 2 hours (maximum of 200 mg in 24 hours). The recommended initial dose is 50 mg because it is more efficacious than 25 mg and has fewer side effects than 100 mg without loss in efficacy.
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Nasal spray dosage: 5–20 mg initially; may repeat in 2 hours (maximum of 40 mg in 24 hours); recommended initial dose is 20 mg
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Tfelt-Hanson showed that 6 mg of the injectable form was more efficacious than 100 mg of the oral form and also had the fastest onset of action of all forms. The intranasal form has the same efficacy and a faster onset of action than the oral form, but limited therapeutic effects are seen for the first 30 minutes.
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DHE versus SC sumatriptan: DHE less effective at 2 hours (73% vs. 85%), but no difference after 2 hours; headache recurred in 45% of sumatriptan-treated patients and 17.7% of DHE-treated patients.
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Other efficacious triptans include: Naratriptan (Amerge) , Frovatriptan (Frova), Rizatriptan (Maxalt), Eletriptan (Relpax), Zolmitriptan (Zomig), and Almotriptan (Axert)
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Others:
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Midrin contains isometheptene (sympathomimetic amine vasoconstrictor), dichloralphenazone (sedative), and acetaminophen. Consider it in patients unable to use ergots. Dosage: 2 tablets PO; may take 1 tablet every 1 hour after initial dose until improvement (maximum of 5 tablets per attack)
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Butalbital combinations (Fiorinal or Fioricet) may also be used. Special concerns may arise regarding abuse potential and sedation. Dosage: 2 tablets PO; may repeat (in 4 hours maximum of 6 tablets in 24 hours)
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Intranasal butorphanol: Mixed agonist-antagonist opioid analgesic; used for severe attacks; one puff equals 5 mg morphine
Dosage: 1 spray; may repeat in 1 hour
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Intranasal lidocaine 4% solution provided rapid relief (within 5 minutes) of headache, nausea, and photophobia in a prospective, double-blind, placebo-controlled trial. Relapse was common.
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Intravenous antiemetic medications (chlorpromazine, prochlorperazine, and metoclopramide) have shown some efficacy as monotherapy in the treatment of migraine. Practical use of such medications outside of the emergency department setting is low.
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First-Line Choice in Athletes
Overview: Because of the efficacy, ease of administration, and relatively quick onset of action, athletes should use oral or injectable forms of triptans for first-line therapy of moderate migraines. Nasal DHE may be another good option secondary to ease of administration. For mild migraines, NSAIDs in any form should be tried initially.
Prophylactic treatment: Indicated in patients with ≥4 attacks per month or attacks lasting several days that cause severe disability
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Beta-blockers are agents of choice.
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Only two are FDA approved: propranolol and timolol, which lack intrinsic sympathomimetic activity (ISA)
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Long-acting form of propranolol increases compliance and is useful in patients with coexisting hypertension, angina pectoris, or thyrotoxicosis.
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Contraindicated in patients with asthma, chronic obstructive pulmonary disease, congestive heart failure, atrioventricular conduction problem, or prescription for monoamine oxidase inhibitors
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Other beta-blockers used despite lack of FDA approval: nadolol, metoprolol, and atenolol
Metoprolol is a selective beta-blocker that can be used in patients with concomitant pulmonary disease.
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Beta-blockers and athletes: Negative effects on aerobic performance cause some concern for use in athletes. Moreover, beta-blockers are banned in certain sports and by certain athletic rules committees because they may provide an unfair advantage.
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Calcium channel blockers: Nimodipine, a selective cerebrovascular vasoconstrictor, and verapamil have been shown to be useful in migraine prophylaxis.
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NSAIDs: Various NSAIDs may be used with varying degrees of efficacy. They are more efficacious for menstrual migraines and should be started 2–3 days before menses (see later discussion).
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Antidepressants (tricyclic): Amitriptyline and clomipramine are used most often. Efficacy is attributed to antidepressant and analgesic actions. They are particularly effective in patients with coexisting migraine and TTH. They are sedating and hence should be used at bedtime.
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Antiepileptics: Valproate, topiramate, and gabapentin are used most often. Only valproate and topiramate are FDA approved for this indication. They are category C and D drugs, respectively, so there should be a concern for use in premenopausal female athletes; ensure birth control. There are no known adverse effects on exercise, although certain antiepileptics are sedating.
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Menstrual migraine treatment: “Miniprophylaxis” may be achieved with the use of NSAIDs or long-acting triptans (frovatriptan and naratriptan) when initiated 2–3 days before menstruation and continued until 3 days after. Hormonal treatment can be used to prevent estrogen withdrawal, which contributes to the development of menstrual migraine. Treatment strategies include the use of extended- and regular-cycle oral contraceptive pills with supplemental estrogen during the inactive pill week, and the use of supplemental estrogen alone during menstruation.
Tension-Type Headache
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Definition: TTHs are headaches of mild to moderate intensity that can be either episodic with varying frequency or chronic with episodic headaches being much more common. Pain is usually bilateral, and patients often report it being “vice-like.” The most significant examination finding is pericranial tenderness to palpation ( Fig. 39.3 ).
