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Migraine
is a chronic, episodic primary headache. Symptoms typically last
4 to 72 h and may be severe. Pain is often but not always unilateral,
throbbing, worse with exertion, and accompanied by autonomic symptoms
(eg, nausea; sensitivity to light, sound, or odors). Fortification
spectra and other transient focal neurologic deficits occur in a
few patients, usually just before the headache. Diagnosis is clinical.
Treatment is with serotonin 1B,1D receptor agonists, antiemetics,
and analgesics. Preventive regimens include lifestyle modifications (eg,
of sleeping habits or diet) and drugs (eg, β-blockers,
amitriptyline, valproate, topiramate).
Epidemiology
and Pathophysiology
Migraine is the most common cause of recurrent moderate to severe headache; lifetime prevalence is 18% for women and 6% for men in the US. It most commonly begins during puberty or young adulthood, waxing and waning in frequency and severity over the ensuing years and usually diminishing after age 50. Studies show familial aggregation of migraine.
Migraine is thought to be a neurovascular pain syndrome with altered central neuronal processing (activation of brain stem nuclei, cortical hyperexcitability, and spreading cortical depression) and involvement of the trigeminovascular system (triggering neuropeptide release, which produces painful inflammation in cranial vessels and the dura mater).
The triggering mechanism for specific attacks is often unclear. However, many potential migraine triggers have been identified; they include drinking red wine, skipping meals, excessive afferent stimuli (eg, flashing lights, strong odors), weather changes, sleep deprivation, stress, and hormonal factors. Head trauma, neck pain, or temporomandibular joint dysfunction sometimes triggers or exacerbates migraine.
Fluctuating estrogen levels are a potent migraine trigger. Many women have onset of migraine at menarche, severe attacks during menstruation (menstrual migraine), and worsening during menopause. For most women, migraines remit during pregnancy (but sometimes there is an exacerbation during the 1st or 2nd trimester). Oral contraceptives and other hormone therapy occasionally trigger or worsen migraine and have been associated with stroke in women who have migraine with aura.
Symptoms and Signs
In some patients, some migraine attacks are preceded or accompanied by a neurologic aura (prodrome) lasting minutes to an hour (migraine with aura). Most commonly, auras involve visual symptoms (fortification spectra—eg, binocular flashes, arcs of scintillating lights, bright zigzags, scotomata). Paresthesias and numbness (typically starting in one hand and marching to the ipsilateral arm and face), speech disturbances, and transient brain stem–thalamic dysfunction are less common than visual auras. Some patients have attacks of migraine aura with little or no headache.
Pain varies from moderate to severe, and attacks last from hours to days, typically resolving with sleep. The pain can be bilateral or unilateral, most often in a frontotemporal distribution, and is described as aching, squeezing, or sometimes throbbing.
Migraine is more than a headache. Autonomic symptoms such as nausea (and occasionally vomiting), photophobia, sonophobia, and osmophobia are prominent. Patients report difficulty concentrating during attacks. Routine physical activity usually aggravates migraine headache; this effect, plus the photophobia and sonophobia, encourages most patients to lie in a dark, quiet room during attacks. Severe attacks can be incapacitating, disrupting family and work life.
Attacks vary significantly in frequency and severity. Many patients have several types of headache, including milder attacks without nausea or photophobia; these attacks may resemble tension headache.
Rare forms of migraine include basilar artery migraine, with combinations of vertigo, ataxia, visual field loss, sensory disturbances, focal weakness, and altered level of consciousness. Abdominal migraine (periodic syndrome), which affects children with a family history of migraine, is characterized by 2-h bouts of abdominal pain, flushing or pallor, nausea, and vomiting. These children often develop typical migraines later in life.
Diagnosis
Diagnosis is based on characteristic symptoms and a normal physical (including neurologic) examination. Typical cases without worrisome findings (see Headache: Testing) do not require CNS imaging.
Common diagnostic errors include not realizing that migraine often causes bilateral pain and is not always described as throbbing. Autonomic and visual symptoms of migraine often lead to a misdiagnosis of sinus headache or eyestrain. A dangerous error is to assume that any headache in patients known to have migraine represents another migraine attack. A thunderclap headache or change in the previous headache pattern may indicate a new, potentially serious disorder.
In older patients, migraine with aura can be mistaken for a transient ischemic attack, especially when the aura occurs without headache. In younger patients, several unusual disorders can mimic migraine with aura: dissection of the carotid or vertebral artery, antiphospholipid antibody syndrome, cerebral vasculitis, moyamoya disease, CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), and MELAS (mitochondrial encephalopathy, lactic acidosis, and strokelike episodes) syndrome.
Prognosis
and Treatment
For some patients, migraine is an infrequent, tolerable inconvenience. For others, it is a devastating malady resulting in frequent periods of incapacity, loss of productivity, and severely impaired quality of life. Consequently, treatment is stratified based on frequency, duration, and severity of attacks. A thorough explanation of the disorder helps patients understand that although migraine cannot be cured, it can be controlled, enabling them to better participate in treatment.
Patients are urged to keep a written headache diary to document the number and timing of attacks, possible triggers, and response to treatment. Identified triggers are eliminated when possible (see also the practice guideline for patient
education concerning treatment of primary headache from the National Headache Foundation). Behavioral interventions (biofeedback, stress management, psychotherapy) are used when stress is a major trigger or when analgesics are being overused.
Acute migraine
headache:
(See also the practice guideline for the treatment
of acute migraine headache from the National Headache Foundation.) Mild to moderate attacks are treated with NSAIDs or acetaminophen . Analgesics containing opioids, caffeine, or butalbital are helpful for infrequent, mild attacks but are prone to being overused, sometimes leading to rebound headache and daily headache syndrome.
In patients whose mild attacks often evolve into incapacitating migraine or whose attacks are severe from the onset, triptans are used. Triptans are selective serotonin 1B,1D receptor agonists. They are not analgesic per se but specifically block the release of vasoactive neuropeptides that trigger migraine pain. Triptans are most effective when taken at the onset of attacks. They are available in oral, intranasal, and sc forms (see Table 2: Headache: Drugs for Migraine and Cluster Headaches ); sc forms are more effective but have more adverse effects. Combining a triptan with an antiemetic at the onset of attacks is effective when nausea is prominent.
IV dihydroergotamine with a dopamine antagonist antiemetic (eg, metoclopramide 10 mg IV, prochlorperazine 5 to 10 mg IV) is helpful for aborting very severe, persistent attacks. The antiemetic alone may relieve mild attacks.
Triptans and dihydroergotamine can cause coronary artery constriction and are thus contraindicated in patients with coronary artery disease or uncontrolled hypertension; they must be used with caution in older patients and in patients with vascular risk factors.
A good response to dihydroergotamine or a triptan should not be interpreted as diagnostic for migraine because these drugs may relieve headache due to subarachnoid hemorrhage and other structural abnormalities.
Opioids should be a last resort (rescue drug) for severe headache when other measures are ineffective.
Prevention
(See also the practice guideline for the preventive
treatment of migraine headache from the National Headache Foundation.) Daily preventive therapy is warranted when frequent migraines interfere with activity despite acute treatment. For patients who use analgesics frequently, particularly those with rebound headache, preventive drugs (see Table 2: Headache: Drugs for Migraine and Cluster Headaches) should be combined with a program for stopping overused analgesics. Choice of drug can be guided by coexisting disorders: eg, a small bedtime dose of amitriptyline for patients with depression or insomnia; a β-blocker for patients with hypertension or coronary artery disease; or topiramate , which can induce weight loss, for obese patients.
Periodic injections of small doses of botulinum toxin type A into the scalp reduces the number and severity of migraine attacks in some patients unresponsive to other preventive treatments.
Last full review/revision November 2005
Content last modified March 2008
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