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Headache (cephalalgia) is a common symptom, often associated with disability, but rarely life
threatening. Headaches may be a primary disorder (migraine, cluster, or tension headache) or a
secondary symptom of such disorders as acute systemic or intracranial infection, intracranial
tumor, head injuries, severe hypertension, cerebral hypoxia, and many diseases of the eyes,
nose, throat, teeth, ears, and cervical vertebrae (see Table 168-1). Sometimes no cause is found.

Headaches may result from stimulation of, traction of, or pressure on any of the pain-sensitive
structures of the head: all tissues covering the cranium; the 5th, 9th, and 10th cranial nerves; the
upper cervical nerves; the large intracranial venous sinuses; the large arteries at the base of the
brain; the large dural arteries; and the dura mater at the skull base. Dilation or contraction of
blood vessel walls stimulates nerve endings, causing headache. The cause of most headaches is
extracranial rather than intracranial. Stroke, vascular abnormalities, and venous thromboses are
uncommon causes of headache.


The frequency, duration, location, and severity of the headache; the factors that make it better or
worse; associated symptoms and signs, such as fever, stiff neck, nausea, and vomiting; and
special studies help identify the cause of headache.

Secondary headaches may have specific characteristics. An acute whole-cranial, severe
headache associated with fever, photophobia, and stiff neck indicates an infectious process, such
as meningitis, until proved otherwise. Subarachnoid hemorrhage also causes acute headache
with symptoms and signs of meningeal irritation. Space-occupying lesions often cause subacute,
progressive headache. New-onset headache in an adult > 40 yr always requires thorough
evaluation. With space-occupying lesions, the following may occur: headache on awakening or at
night, fluctuation of headache with postural changes, and nausea and vomiting. Additional
neurologic complaints, such as seizure, confusion, weakness, or sensory changes, may occur
late and are ominous.

Tension headache tends to be chronic or continuous and commonly originates in the occipital or
bifrontal region, then spreads over the entire head. It is usually described as a pressure sensation
or a viselike constriction of the skull. Febrile illnesses, arterial hypertension, and migraine usually
cause throbbing pain that can occur in any part of the head.

Useful tests include CBC, STS, serum chemistry profile, ESR, CSF examination, and, for specific
symptoms, ocular tests (acuity, visual fields, refraction, intraocular pressure) or sinus x-rays. If the
cause of recent, persistent, recurrent, or increasing headache remains in doubt, MRI and/or CT is
appropriate, especially if abnormal neurologic signs are present.


Many headaches are of short duration and require no treatment other than mild analgesics (eg,
aspirin, acetaminophen) and rest.

Treatment of primary headaches is discussed under the specific disorders, below. Alternative
approaches, such as biofeedback, acupuncture, dietary manipulations, and some less
conventional modes, have been advocated for these disorders. None of these treatments has
shown clear-cut benefits in rigorous studies. However, to the extent that an alternative treatment
poses little risk, it may be tried, with the idea that effective headache management is
Treatment of secondary headaches depends on treatment of the underlying disorder. For
meningitis, prompt antibiotic therapy is critical. Subsequently, symptoms can be relieved with
analgesics, including acetaminophen, NSAIDs, or opioid narcotics. Certain disorders require
more specific treatment; eg, temporal arteritis is treated with corticosteroids, and headache due to
benign intracranial hypertension is treated with acetazolamide or diuretics and weight loss.
Subdural hematomas or brain tumors may be treated surgically (see Chs. 175 and 177,

Stress management taught by a psychologist often reduces the incidence of headaches.
However, most patients are helped by an understanding physician who accepts the pain as real,
sees the patient regularly, and encourages discussion of emotional difficulties, whether they are
the cause or the result of chronic headaches. The physician can reassure the patient that no
organic lesion is present and recommend environmental readjustments and the removal of
irritants and stresses. For particularly difficult problems, a team composed of a physician,
psychotherapist, and physiotherapist is most effective in managing chronic headache (see also
Psychogenic Pain Syndromes in Ch. 167).

Tension Headache

Headache that lasts 30 min to 7 days and is nonpulsating, mild to moderate in severity, bilateral,
not aggravated by exertion, and not associated with nausea, vomiting, or sensitivity to light,
sound, or smell.

Tension headache can be thought of as a state of cranial hyperalgesia with reduced endogenous
pain modulation and enhanced pain potentiation. It has many causes; comorbid migraine, mood
disorders, sleep dysfunction, and anxiety states contribute.

Treatment with mild analgesics is helpful: acetaminophen 650 mg po q 4 h, aspirin 300 to 600
mg, or another NSAID, such as ibuprofen or naproxen. For chronic or recurrent headache, many
physicians empirically supplement analgesics with tricyclic antidepressants (eg, amitriptyline 10 to
125 mg/day po) or, occasionally, benzodiazepines (eg, diazepam 2 to 5 mg po qid), but regular
use may cause habituation.

More disabled patients require a multidimensional approach as described above. Recognition of
comorbid illness is essential. Migraine is often associated with chronic tension headaches, so
treatments overlap.

Cluster Headache

Headache that lasts 15 to 180 min, is severe, is unilateral, is located periorbitally and/or
temporally, occurs up to 8 times per day, and is associated with at least one of the following:
tearing, red eye, stuffy nose, facial sweating, ptosis, or miosis.

Men have cluster headache more often than women. Triggers include alcohol, sleep, and
barometric pressure change. The pathophysiology is unknown but may be similar to that of
migraine (see above).

Diagnosis is based on symptoms and the exclusion of intracranial pathology. Treatment is
prophylactic, abortive, or analgesic. The calcium channel blocker verapamil and the serotonin
antagonist methysergide are used for prophylaxis. Sumatriptan and ergots are used for abortive
treatment. Indomethacin is uniquely effective for cluster headache.

Headache that lasts 4 to 72 h, is throbbing, is moderate to severe in intensity, is unilateral,
becomes worse with exertion, and is associated with nausea, vomiting, or sensitivity to light,
sound, or smell.

Only three or four of the above criteria must be present for accurate diagnosis.

About 24 million Americans have migraines. Migraines may occur at any age but usually begin
between ages 10 and 40, more often in women than in men. Headaches often partially or
completely remit after age 50. More than 50% of patients have a family history of migraine.

Etiology and Pathophysiology

The cause is unknown, and the pathophysiology is not fully understood. Changes in brain and
scalp arterial blood flow occur, but whether vasodilation and vasoconstriction are a cause or an
effect of the migraine is unclear. Cortical spreading depression (fundamental changes in the brain
cortex in which a crest of hyperpolarization is followed by depolarization) may induce neurogenic
inflammation, with vasodilation, activated WBCs and permeable capillaries. The inflammation
leads to irritation of perivascular trigeminal sensory fibers. A cascade of events follows, causing
changes in blood flow and the severe headache. Intracranial vascular malformations are a rare
cause of migraine-like headaches.

The mechanism for migraines is not well defined, but several triggers are recognized. Cycling
estrogen, a significant trigger, may explain why there are three times as many women with
migraines as men. Evidence of estrogen's role as a trigger includes the following: During puberty,
migraine becomes much more prevalent in females than in males; migraines are particularly
difficult to control in the premenopausal period; and oral contraceptives and estrogen
replacement therapy often make migraine worse. Other triggers include insomnia, barometric
pressure change, and hunger. The association of diet and migraine is usually overstated. No
prospective study has proved an association.

Symptoms, Signs, and Diagnosis

Migraine may be preceded by a short prodromal period of depression, irritability, restlessness, or
anorexia and may be associated with an aura (in 10 to 20% of occurrences). An aura usually
precedes the headache by no more than 1 h but is often concurrent. An aura is a transient,
reversible neurologic visual, somatosensory, motor, or language deficit. Most persons report
visual auras, including flashing lights, scintillating scotoma, and fortification spectrums.

Symptoms usually follow a pattern in each patient, except unilateral headaches may not always
occur on the same side. The patient may have attacks daily or only once every several months.
Diagnosis is based on the symptom patterns when there is no evidence of intracranial pathologic
changes. Migraine is more probable when the patient has a family history of migraine or of visual
prodromata. No diagnostic tests are useful, except to exclude other causes.


Treatment depends on the frequency of attacks and the presence of comorbid illness. In general,
treatment can be classified as prophylactic, abortive, or analgesic (see Table 168-2).

If a person has more than one migraine a week, long-term prophylaxis should be considered. -
blockers, calcium channel blockers, tricyclic antidepressants, or anticonvulsants may be used.
The choice is empiric but is guided by the presence of comorbid illness. For example, if
hypertension coexists, -blockers or calcium channel blockers would be most efficient. If
depression or sleep dysfunction coexists, tricyclic antidepressants should be tried first.

Abortive drugs are used for acute treatment. A new class of drugs that activate serotonin
receptors (5-hydroxytryptamine [5-HT] 1B/1D agonists) block neurogenic inflammation and can
abort migraine pain in about 70% of patients. Sumatriptan, the prototype, is available in oral and
subcutaneous injection forms. Subcutaneous dosing is more effective but has more adverse
effects, which include flushing, nausea, esophageal constriction, and, rarely, coronary artery
constriction. Caution is advised in prescribing sumatriptan to men > 55 yr, postmenopausal
women, or persons with a history of heart disease. The next generation of 5-HT 1B/1D agonists
(eg, eletriptan, naratriptan, rizatriptan, zolmitriptan) promises to increase the benefits and reduce
the adverse effects. Ergot alkaloid derivatives, such as ergotamine tartrate and
dihydroergotamine, in oral and parenteral preparations can be used effectively. Dopamine
antagonist antiemetics, such as metoclopramide and prochlorperazine, are effective, even if
nausea is not prominent.

Analgesics should be used sparingly. They are effective in some patients but cause rebound
headache with dose escalation in others. NSAIDs are probably best for mild to moderate
headaches. Opioids should be avoided except under special circumstances and strict guidelines.

Table 168-1 secondary headache
Anti-migraine treatment

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