Migraine is not simply a widened blood vessel

Migraine is a recurring neurologic disorder. Attacks may involve throbbing pain, nausea, or sensitivity to light and sound, but no single symptom proves that a headache is migraine. Current models include interactions among sensory processing, pain-control networks, and peripheral nerves around the meninges. The older idea that an attack is explained by blood vessels widening is too simple. Vascular changes can accompany an attack without being its sole cause.

How does trigeminovascular signaling carry pain?

Sensory branches of the trigeminal nerve supply the meninges and structures around cranial blood vessels. Signals from these endings pass through the trigeminal ganglion to brainstem relays, including the trigeminal nucleus, and then into wider networks involving the thalamus and cortex. As an attack develops, sensitization can make ordinary movement, touch, or sensory input feel painful or unusually intense. The pathway is not a one-way wire: brainstem and higher brain circuits modulate the incoming signals, and the balance varies among people and attacks.

CGRP is an important participant, not a complete explanation

Calcitonin gene-related peptide (CGRP) is a neuropeptide active in trigeminal sensory pathways and an important focus of migraine research. In a small double-blind crossover experiment, intravenous CGRP was followed by delayed headache more often than placebo in participants with migraine. Such provocation studies, together with the effects of treatments that target the CGRP pathway, support a contributory role. They do not show that CGRP alone starts every spontaneous attack or that all people share one sequence of events. Whether a preventive treatment is appropriate depends on a person’s history, safety considerations, and local guidance. The American Headache Society’s 2024 statement includes CGRP-targeted prevention among first-line options in U.S. practice; it does not prescribe a treatment for an individual or define policy in every country.

Aura and cortical spreading depolarization are related, not interchangeable

Some people experience temporary neurologic symptoms such as flashing or zigzag visual patterns, tingling, or language difficulty around an attack; these are called aura. Cortical spreading depolarization (CSD), a propagating change in neuronal and glial activity across the cortex, is studied as a possible physiologic basis for aura. Many people with migraine do not have aura, and symptom timing varies. The International Headache Society’s classification describes features such as reversibility, gradual spread, and duration for typical aura. Those criteria help clinicians classify a pattern; they are not a home test that can rule out stroke or another cause. New weakness, loss of vision, difficulty speaking, or sudden neurologic symptoms need prompt medical assessment rather than an assumption that they are migraine.

A diary can turn a vague pattern into useful history

Imagine a person whose headaches have changed over the past month. A calendar can capture when each headache begins and ends, how intense it feels, whether it interrupts usual activity, and whether nausea or light and sound sensitivity occur. If aura occurs, note the symptom and when it starts and resolves. Record the dates an acute medicine is used and its name or ingredient; this helps a clinician assess the pattern and is not a prompt to increase the dose. Sleep disruption, missed meals, menstrual timing, or stress can be noted as observations, without assuming each is a proven trigger. At a visit, the person might ask: “Has the pattern changed enough to evaluate differently?”, “Could the number of medicine-use days matter?”, and “Does this new symptom need a separate assessment?” Sudden severe headache, fever with neck stiffness, altered awareness, or a new neurologic deficit can require urgent care. This is general education, not a diagnosis or medication plan.

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