Migraine & Headache Disorders

Headaches come in two kinds. "Primary headache happens on its own, while" "secondary headache happens because of some other medical condition" (NINDS). "The brain itself doesn’t feel pain" — secondary headaches hurt because something presses on, pulls or pushes pain-sensitive structures. Most headaches are primary; the nurse’s first job is to find the secondary ones.

Three primary headaches to tell apart. Tension-type is the most common: mild-to-moderate, constant pressure, often on both sides, like a tightening band, lasting 30 minutes to 7 days, without aura, nausea or worsening on activity. Migraine is moderate-to-severe, often one-sided and throbbing, worse with activity, with nausea and light and sound sensitivity. Cluster is the most severe primary headache: one-sided pain around or behind one eye with a red, watering eye and runny nose on that side, peaking in 5–10 minutes and lasting up to 3 hours, often waking people from sleep — and, unlike migraine, the patient paces or rocks rather than lying still.

Migraine is common and disabling. It affects about 12% of people (up to 17% of women and 6% of men a year), peaks between ages 35 and 39, and ranks as the second leading cause of disability globally. It runs in families — about a 40% risk with one affected parent and 75% with two.

The old theory is gone. The idea that headache came from vasodilation and aura from vasoconstriction "is no longer considered viable." Migraine is now understood as a neuronal process that switches on the trigeminal pain system.

Aura = a wave across the cortex. Cortical spreading depression — "a propagating wave of neuronal and glial depolarization" — is the probable cause of the aura, and it can activate trigeminal nerve fibres. Because it spreads slowly, aura symptoms build gradually: each lasts 5 to 60 minutes, at least one spreads over 5 minutes or more, and headache follows within 60 minutes. Auras must be fully reversible.

Pain = neurogenic inflammation. Activated trigeminal nociceptors release substance P, neurokinin A and calcitonin gene–related peptide (CGRP). CGRP is a potent dilator of cerebral and dural vessels, drives neurogenic inflammation, and carries pain from the trigeminal system to the brain — which is why CGRP-blocking drugs work. Low serotonin between attacks may weaken the brain’s pain-inhibition system; triptans act like serotonin to switch the attack off.

Why attacks become chronic. Repeated neurogenic inflammation causes sensitization, in which neurons respond more readily — a likely route from episodic to chronic migraine, and, with central sensitization, the likely mechanism of medication-overuse headache.

Prodrome → aura → headache → postdrome. About 77% of patients have prodromal symptoms for up to 24 to 48 hours before the headache — yawning, mood changes, lethargy, neck stiffness, food cravings. Aura, when present, is usually visual — a shimmering zigzag-bordered blind spot, dots or sparks — and can affect speech; motor aura is rare. The headache is usually one-sided and throbbing, builds over the first hours, drives people to dark places and usually resolves with sleep. Afterwards people are often exhausted or confused, and the postdrome can last up to two days.

The numbers that define the types (own words, from the StatPearls restatement of the international criteria). Migraine without aura — about 75% of cases — means at least 5 attacks lasting 4 to 72 hours, typically one-sided, pulsating, moderate to severe and worsened by activity, with nausea or light and sound sensitivity. Migraine with aura needs at least 2 attacks with the aura timing above. Chronic migraine is headache on 15 or more days a month for more than 3 months, with migraine features on at least 8 of them. Status migrainosus is an attack lasting more than 72 hours — severe enough that some people need hospital care.

Variants to recognise. Hemiplegic migraine has motor weakness as its aura — temporary one-sided paralysis that may last days. Retinal migraine causes a one-eye visual loss. Menstrual migraine starts on the first day of the period in at least two of three cycles.

Thunderclap headache. What defines it is how fast it peaks, not how bad it is: abrupt, severe pain that reaches maximum intensity in less than one minute and lasts at least 5 minutes — what patients describe as the worst headache of their life. It is "often associated with a potentially fatal etiology, such as subarachnoid hemorrhage (SAH), and is considered a medical emergency." The work-up is a noncontrast head CT first; if it is negative and suspicion stays high, a lumbar puncture — and imaging must come before the LP because a mass lesion is possible. CT within 6 hours of onset, read with the Ottawa SAH rule, was 95% sensitive and 100% specific.

Red flags point to a secondary headache. The SNOOP checklist asks about Systemic illness (fever, cancer, pregnancy, HIV), Neurologic signs (confusion, focal deficits, seizures, papilledema), Onset that is new or sudden (especially after 50), Other features (head trauma, toxins, waking from sleep, worse with Valsalva or triggered by coughing or exertion), and Previous headache history that has progressed or changed.

Medication-overuse headache (MOH). Frequent use of acute headache drugs can itself cause daily headache: headache on 15 or more days a month in someone with a known headache disorder, with regular use of one or more acute medicines on 10 to 15 days a month for over three months. Opioids, butalbital combinations and acetaminophen-aspirin-caffeine combinations are the commonest culprits, then triptans, NSAIDs and CGRP antagonists. Patients typically wake with headache and neck pain from overnight withdrawal. Treatment is withdrawal of the overused drug, sometimes with a transitional bridge.