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Migraine is a periodic headache often accompanied by nausea and sensitivity to light and noise (photophobia and phonophobia).

A typical attack consists of a prodromal phase of warning (premonitory) symptoms, followed by an aura, the actual headache phase, and a resolution phase.

Attack characteristics often change over time. Attacks often tend to occur in the morning or evening but may occur at any time. They typically last 4–72 hours.

Symptoms and Signs

Prodromal phase

• The migraine attack may be preceded by a period of variable prodromal phenomena lasting a few hours to two days.
• Most patients complain of sensitivity to smells and noise, irritability, restlessness, drowsiness, fatigue, lack of concentration, depression, and polyuria.
• In children, the chief complaints are abdominal pain and dizziness.
  

Aura

• This is the period preceding the focal cerebral symptoms of the actual migraine headache.
• Some patients experience attacks without an aura (common migraine), while others have attacks with an aura (classic migraine) that develops over 5–20 minutes and usually lasts less than one hour, but may persist as long as one week (prolonged aura).

Auras typically involve :

• Visual disturbances, which can range from undulating lines (resembling hot air rising), lightning flashes, circles, sparks or flashing lights (photopsia), or zig-zag lines (fortification figures, teichopsia, scintillating scotoma). The visual images, which may be white or colored, cause gaps in the visual field and usually have scintillating margins.
• Unilateral paresthesiae (tingling or cold sensations) may occur.
• Emotional changes (anxiety, restlessness, panic, euphoria, grief, aversion) of variable intensity are relatively common.

Headache phase

• Most patients (ca. 60%) complain of pulsating, throbbing, or continuous pain on one side of the head (hemicrania).
• Others have pain in the entire head, particularly behind the eyes (“as if the eye were being pushed out”), in the nuchal region, or in the temples.
• Migraine headache worsens on physical exertion and is often accompanied by anorexia, malaise, nausea, and vomiting.

Resolution phase

• This phase is characterized by listlessness, lack of concentration, and increased pain sensitivity in the head.

Pathogenesis

During the interval between attacks, various disturbances (genetically determined) may be observed, e. g., cerebral hypomagnesemia, elevated concentration of excitatory amino acids (glutamate, aspartate), and increased reactivity of cranial blood vessels. The cumulative effect of

these disturbances is a heightened sensitivity to nociceptive stimuli (migraine pain threshold).

Impulses from the cortex, thalamus, and hypothalamus activate the so-called migraine center responsible for the generation of migraine attacks, putatively located in the brain stem.

The migraine center triggers cortical spreading depression (suppression of brain activity across the cortex) accompanied by oligemia, resulting in an aura. Trigeminovascular input from meningeal vessels is relayed to the brain stem, via projecting fibers to the thalamus and then, by the parasympathetic efferent pathway, back to the meningeal vessels (trigeminal autonomic reflex circuit). Perivascular trigeminal C-fiber endings (trigeminovascular system) are stimulated

to release vasoactive neuropeptides such as substrate P, neurokinin A, and calcitonin gene-regulated polypeptide (CGRP), causing a (sterile) neurogenic inflammatory response. Vasoconstriction and vascular hyperesthesia with subsequent vasodilatation spread via trigeminal axon reflexes. The perception of pain is mediated by the pathway from the trigeminal nerve to the nucleus caudalis, thalamus (p. 94) and cortex. Trigeminal impulses also reach autonomic centers.

Treatment

Good patient–physician communication is essential for the diagnosis and treatment of headache. The most important clues to differential diagnosis are derived from the case history. The medication history must be obtained, and psychological factors must also be considered headache is often associated with anxiety, e. g., fear of a brain tumor, of a mental illness, or of not having one’s complaints taken seriously.

Acute Migraine

General measures

• Rest, ice packs

Pharmacotherapy

• Antiemetic (metoclopramide or domperidone)
• Aspirin or acetaminophen
• Triptans (if ineffective)

Prophylaxis

General measures

• Behavioral therapy

Pharmacotherapy

• 1st line: Beta-blockers (e. g., metoprolol, propranolol);
• 2nd line: flunarizine or valproate;
• 3rd line: methysergide or pizotifen