Migraine is a relatively common disorder. Population-based studies have yielded remarkably consistent 1-year period prevalence estimates of approximately 6% in men and 15–18% in women.9,10 Most studies find that migraine is approximately three times more common in women than in men.9,10
Headache diagnosis is usually based on the retrospective reporting of attack characteristics. The results of general medical and neurologic examinations, as well as laboratory studies, are usually normal and serve to exclude other, more ominous, causes of headache in migraineurs.
The migraine attack can be divided into four phases:
Although most people experience more than one phase, most do not experience all four phases.13 No one phase is absolutely required for a diagnosis of migraine.
The epilepsy attack also has premonitory, aura, attack, and postictal phases. The similarity in terminology does not imply similarity in mechanisms.
Premonitory or prodromal phenomena occur in approximately 60% of migraineurs, often hours to days before the onset of headache.13–15 Types of phenomena experienced include:
Some patients report a poorly characterized feeling that a migraine attack is coming. Although prodromal features vary widely among individuals, they are often consistent within an individual. Premonitory symptoms have also been reported in patients before the onset of the seizure.16
The migraine aura consists of focal neurologic symptoms that precede or accompany an attack. About 20–30% of migraineurs experience auras. Most aura symptoms develop slowly over 5 to 20 minutes and usually last for less than 60 minutes. The aura almost always includes visual phenomena, but may involve somatosensory or motor phenomena, as well as language or brain stem disturbances.
The most common aura is the visual aura. A visual aura often has a hemianoptic distribution and includes both positive (e.g., scintillations, fortification spectra, photopsia) and negative (e.g., scotoma) features.
Elementary visual disturbances include colorless scotoma, photopsia, or phosphenes. Simple flashes, specks, or hallucinations of geometric forms (e.g., points, stars, lines, curves, circles, sparks, flashes, or flames) may occur and may be single or number in the hundreds.
More complicated hallucinations include teichopsia (also called fortification spectrum, a luminous wall-like outline), which is the most characteristic visual aura and is almost always diagnostic of migraine. An arc of scintillating lights classically begins near the point of fixation and may form a herringbone-like pattern that expands to encompass an increasing portion of a visual hemifield. It migrates across the visual field with a scintillating edge of zigzag or flashing lights that are often black and white. On occasion, colored dots appear at the end of the white stripe.
A scotoma is a negative phenomenon consisting of a blanking or graying out of vision. Scotomas are usually accompanied by a positive visual display but may occur independently.
The most common somatosensory phenomenon is numbness or tingling (paresthesia) over one side of the face and in the ipsilateral hand or arm. Olfactory hallucinations are rare, unpleasant, and short lived (5 minutes to 24 hours).
Symptoms involving other brain areas also occur: These include complex difficulties in the perception and use of the body (e.g., apraxia, agnosia, hemiparesis); speech and language disturbances; states of double or multiple consciousness, associated with déjà vu or jamais vu; and elaborate, dreamy, nightmarish, trancelike, or delirious states.18–22 Anxiety, déjà vu, and jamais vu are presumably of temporal lobe origin.18
One type of aura may follow another: Sensory phenomena may occur as visual phenomena fade, or motor phenomena may develop as sensory phenomena dissipate. Although auras are relatively specific for migraine, related phenomena may occur in cerebrovascular disease, including carotid dissection, and in epilepsy, especially of the occipital lobes.
In epilepsy, the aura is brief and rapid in development. At times, it is associated with unusual symptoms, such as a rising abdominal sensation followed by a déjà vu illusion, or a visual hallucination associated with nausea and fear.23
Cortical spreading depression (CSD) is believed to underlie the migraine aura. CSD consists of a wave of cortical excitation followed by a wave of inhibition. In an experimental animal, it is induced by stimulating the cortex with a needle or with potassium chloride. This wave marches over the cortical mantle at a rate of 3 mm per minute, crossing vascular territories.
In humans with migraine, cerebral blood flow studies demonstrate a wave of oligemia that spreads forward from the occipital area; it precedes the aura and may persist into the headache phase.24 The rate of progression of the oligemia is comparable to the rate of CSD.25
Magnetoencephalographic (MEG) studies have suggested the existence of spreading depression in humans with migraine,26 implying that spreading depression may be the mechanism that produces the aura.27–31 Subjects who had spontaneous migraine visual auras have been studied with functional magnetic resonance imaging (fMRI).32 Interictally (using perfusion-weighted imaging), cerebral blood flow, cerebral blood volume, and mean transit time were normal and symmetric. During visual auras, however, blood flow decreased 15–53%, blood volume decreased 6–33%, and mean transit time increased 10–54% in the occipital cortex gray matter contralateral to the affected visual hemifield. When multiple perfusion images were obtained during the same aura, the margin of the perfusion defect moved anteriorly. The absence of diffusion abnormalities in these patients suggests that ischemia does not occur during the migraine aura.33
In epilepsy, the aura is that portion of the seizure experienced before loss of consciousness and for which memory is retained. The aura is the entire seizure for simple partial seizures. When consciousness is lost, the aura is the simple symptom of a complex partial seizure. The aura is associated with the electroencephalographic (EEG) correlate of the seizure type in which it occurs.34
The typical migraine headache is unilateral and described as throbbing in 85% of patients. Headache severity ranges from moderate to marked and is aggravated by head movement or physical activity. The onset is usually gradual, and the attack usually lasts 4 to 72 hours in adults and 2 to 48 hours in children.2
To make a diagnosis of migraine, the pain must be accompanied by other features. Anorexia is common, although food cravings can occur. Nausea occurs in up to 90% of patients, and vomiting occurs in approximately one-third of migraineurs.12 Many patients experience sensory hyperexcitability, manifested by photophobia, phonophobia, and osmophobia, and seek a dark, quiet room.22,35 Particular associated features are required for diagnosis Table: Migraine Without Aura.36
In the postdromal phase of migraine, the patient may feel tired, washed out, irritable, and listless and may have impaired concentration. Many patients report scalp tenderness. Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise.
In epilepsy, the postictal phase may include a depressed level of awareness or focal neurologic deficits that sometimes provide clues to the site of onset of the seizure.
Reviewed and revised April 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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