1. Is migraine an important public health problem?

Migraine is a major public health problem by almost any standard. It is a highly prevalent disorder that affects 11% of the U.S. population and produces enormous suffering for individuals and their families. Recent estimates indicate that 28 million Americans suffer from migraine headaches; many experience severe pain and significant levels of headache-related disability. Economic estimates show that the cost of lost labor owing to migraine in the United States is $13 billion per year; these indirect costs resulting from missed work and disability at work greatly exceed direct medical expenditures on migraine treatment. In addition, headaches are the seventh leading reason for outpatient visits in the United States and account for 2% to 4% of all emergency room visits.

2. What are the phases of the migraine attack?

It is useful to divide the migraine attack into four phases: premonitory, aura, headache, and resolution. The premonitory phase typically occurs hours or days before the headache. The aura usually occurs within 1 hour of headache onset but may begin during the headache. The headache phase is characterized by pain and associated symptoms. In the resolution phase, spontaneous pain subsides, but other symptoms are present. It is important to recognize that no phase is obligatory for migraine and that most patients do not experience all four phases.

3. Describe the premonitory phase

Premonitory features include changes in mood or behavior that precede the headache by hours or days. This phase is sometimes referred to as the postdrome. Patients may feel depressed, euphoric, irritable, or restless, and occasionally report fatigue or hyperactivity. Constitutional symptoms may include changes in appetite, fluid balance, and bowel function. Some patients report food cravings; others describe a poorly characterized feeling that an attack is coming. Premonitory features vary from person to person and from attack to attack.

4. Describe the aura

The aura consists of focal neurologic symptoms that usually precede, but that may accompany, the attack. Only 20% to 30% of migraine sufferers ever experience auras, and most people who have attacks with aura also have attacks without aura. Aura symptoms typically develop slowly, over 5 to 20 minutes, and usually last 60 minutes. Auras most commonly involve changes in vision, although changes in motor and sensory function may also occur. The classic visual aura of migraine is characterized by both positive symptom features, such as flashes of light (scintillations) or zigzag lines (fortification spectra), and negative symptom features, such as visual loss (scotoma). The visual aura may begin in a small portion of the visual field and gradually expand to encompass an entire visual hemifield.

Sensory auras are also characterized by a mix of positive (tingling) and negative features (numbness), sometimes beginning on one side of the face or hand and slowly expanding to encompass an entire side of the body. Hemiparesis may occur, and if the dominant hemisphere is involved, dysphasia or aphasia may develop.

5. How do you differentiate migraine aura from other kinds of focal episodes of neurologic dysfunction?

Transient neurologic deficits may have several causes. These include migraine aura, epileptic seizure, stroke, metabolic derangements, and psychiatric disease. Seizure is most typically characterized by positive phenomena such as tonic or tonic/clonic movements. Stroke is most often characterized by negative phenomena, such as weakness. Both seizures and stroke tend to come on relatively suddenly. The gradual evolution of symptom features and the mix of positive and negative features, as well as the temporal association with headache help identify migraine aura. The patient’s age and risk-factor profile may also point the clinician in one diagnostic direction or another.

6. What are the characteristics of the headache phase?

The headache phase of migraine is characterized by a combination of pain and associated symptoms. Migraine pain has four characteristic features, and most migraine sufferers experience at least two of these. Migraine pain is typically:

By definition, the pain of migraine must be accompanied by other features. Nausea occurs in about 75% of patients and vomiting in up to one third. Many patients experience sensory sensitivity in the form of photophobia, phonophobia, and osmophobia. Other accompanying features include anorexia or food cravings, blurry vision, nasal stuffiness, abdominal cramps, polyuria, and pallor. Although impaired concentration is common, measurable memory impairment has rarely been documented.

7. What is the resolution phase?

The resolution phase of the migraine attack begins as the pain wanes. Following the headache, the patient may feel irritable, listless, tired, or washed-out. Many patients report residual scalp tenderness in the distribution of the remitted spontaneous pain. Some patients feel unusually refreshed or euphoric after a migraine attack.

8. What feature or features are absolutely required to diagnose migraine?

It is important to recognize that no single headache feature and no single associated symptom is pathognomonic for migraine. For example, 20% to 30% of migraineurs have auras; the physician who relies exclusively on aura will usually miss the diagnosis. If nausea occurs in 75% of patients, the clinician who relies exclusively on nausea will miss 25% of cases.

In 1988, the International Headache Society provided a classification system for headache disorders. That system defined seven different types of migraine. The two most important types are migraine without aura and migraine with aura (Boxes 10-1 and 10-2).

9. Describe considerations for diagnostic testing

Diagnostic testing in migraine serves primarily to exclude secondary causes of headache. The first step is to identify red flags that suggest the possibility of secondary headache (see Chapter 14, Brain Tumor Headaches). If the patient has no history of red flags, the general medical and neurologic exams sometimes raise the possibility of secondary headache. If there is a possibility of secondary headache, an appropriate diagnostic workup is required.

In the absence of alarms, the second step is to try to diagnose a specific primary headache disorder. If the patient has typical migraine or tension-type headache (TTH), it is appropriate to proceed with treatment. If there are atypical headache features, even in the absence of red flags, consider diagnostic testing to exclude secondary causes. If treatment is initiated and the expected response to therapy is not obtained, revisit the issue of secondary headache. However, because migraine and TTH are so common, it is neither appropriate nor cost-effective to obtain neuroimaging for every patient.

10. What diagnostic tests are required to establish the diagnosis of migraine?

There are no diagnostic texts required to diagnose migraine.

11. Why is migraine considered a neurologic disease?

Migraine is viewed as a disease of the brain. Changes in the brain give rise to inflammatory changes in cranial and meningeal blood vessels, which, in turn, produce pain. The premonitory phase, with its characteristic changes in mood, behavior, and autonomic function, is best understood on the basis of central nervous system dysfunction. Neuroimaging procedures, including positron emission tomography (PET), electroencephalogram, and magnetoencephalography, demonstrate abnormalities of the brain during or between attacks in patients with migraine. Finally, the drugs used to treat migraine often act on the brain, cranial nerves, or the cranial blood vessels.

12. Describe the mechanism of the aura

The phenomenon of “spreading cortical depression” may underlie the aura of migraine. Spreading depression was originally described as a wave of excitation (depolarization) followed by a wave of inhibition that spreads over the cortical surface of experimental animals after mechanical or chemical stimulation. Neuronal activity decreases during a wave of inhibition, producing decreased cerebral blood flow through the mechanism of cerebral autoregulation. As a consequence, inhibition is accompanied by a wave of spreading oligemia (decreased blood flow).

In migraine with aura, cerebral blood flow studies demonstrate a wave of oligemia that accompanies the aura, as predicted by the model of spreading depression. This wave of oligemia progresses at a rate of 2 to 3 mm per minute, the same rate reported for spreading depression in experimental animals. In addition, the rate of spreading oligemia and spreading depression corresponds with the evolution of the scintillating scotoma that marches across the visual field of the typical migraine aura. Spreading oligemia has been demonstrated using xenon inhalation and magnetic resonance imaging (MRI).

13. What is the substrate of migraine pain?

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