18A. Migraine and other primary headaches
Migraine
Migraine is an episodic primary headache disorder with disabling attacks lasting 4-72 hours with moderate or severe headache, usually accompanied by nausea, vomiting and/or photophobia and phonophobia, and sometimes preceded by a short-lasting aura of unilateral fully-reversible visual, sensory or other central nervous system symptoms.
It affects 12% of the population and affects women more often than men.
The etiology is unknown, but there is likely an underlying genetic predispisition which makes some more susceptible to certain internal and external triggers.
Pathomechanism
Cortical spreading depression, a wave of electrophysiological hyperactivity across the brain followed by inhibition is implicated in migraine.
Trigeminovascular system, a system of trigeminal sensory neurons that innervate large cerebral vessels, vessels of the meninges, large venous sinuses, and the dura mater, is also involved. Cortical spreading depression may activate meningeal nociceptors in the trigeminovascular system, leading to pain and sensitisation of these neurons.
Clinical features
Migraine can occur with or without aura. Approximately 1/3 of patients have migraine with aura. Some have chronic migraine with daily mild-moderate headaches with exacerbations with migranious features.
Aura refers to sudden onset reversible neurological symptoms. In migraine, the auras are usually visual and cause vision loss or bright spots, but they may affect any neurological modality. Aura symptoms can be visual, sensory, related to speech, motor, or affect the brainstem or cerebellum. The aura can occur with or before the headache.
The headache itself is usually unilateral, throbbing or pulsatile, and accompanied by nausea, photophobia, and phonophobia. It can last for hours and is usually severe.
Patients sometimes have prodromal symptoms in the days before the attack, symptoms like depression and irritability.
Migraine attacks can be triggered by factors like stress, menstruation, nitrates, fasting, wine, sleep disturbances, smoking, certain foods, etc.
Treatment
Acute episodes of migraine are treated with triptans or ergots, other analgesics like paracetamol/NSAIDs, and antiemetics like metoclopramide. Because of prevalent nausea/vomiting, administration other than p.o. is often preferred to administer these drugs, often as a nasal spray. Triptans are more efficacious than other analgesics.
Many drugs can be used for migraine prophylaxis, including:
- Tricyclic antidepressants – amitriptylin
- Antihypertensives – metoprolol, propranolol, candesartan
- Antiepileptics – topiramate, valproate
- Anti-CGRP antibodies – erenumab, framanezumab, galcanezumab
Anti-CGRP antibodies are recent drugs, expensive, and only administered by injection. They’re often the last choice.
It’s also important to learn to avoid possible triggers.
Cluster headache
Cluster headache is a type of trigeminal-autonomic cephalgia. It’s sometimes called “the worst pain a human can experience”. 80% of patients are smokers, and 80% of patients are men.
Clinical features
The patients have very severe headache usually lasting from 15 minutes – 3 hours. They are always unilateral and can occur multiple times a day. Patients often have ipsilateral autonomic symptoms like rhinorrhoea, ptosis, or miosis. Patients may sometimes go months or years without attacks.
Treatment
Acute episodes of cluster headache are treated with triptans and other analgesics, as well as 100% oxygen inhalation.
Many drugs can be used for cluster headache prophylaxis, including verapamil, lithium, and antiepileptics. However, the prophylactic effect comes only after a few weeks. In patients not currently taking prophylactic treatment, bridging therapy with glucocorticoids following an acute attack gives a rapid suppression of headache attacks while waiting for the prophylactic treatment to become effective.
Patients should identify and avoid triggers, like alcohol.
Tension headache
Tension headache is the most common type of primary headache. It may be due to tenderness of the neck muscles. Stress is a potential trigger.
Clinical features
Tension headache is dull, non-pulsating, and bilateral, often described as a tight cap or hat on the patient’s head. The severity is light to moderate. There is no aura or autonomic symptoms.
Treatment
Acute episodes of tension headache are treated with NSAIDs, but it’s important to prevent chronic treatment with analgesics to prevent medication overuse headache. Tricyclic antidepressants and antiepileptics can be used for prophylaxis. Non-pharmacological interventions like physiotherapy and psychotherapy are also important.