Migraine is a neurological disorder involving recurrent unilateral headache attacks. During the attack, a cascade of events progresses over the course of hours to days. The four phases in a typical attack are the prodromal phase, aura, headache and postdromal phase. In the prodromal phase, patients may experience fatigue, decreased functioning or mood fluctuations. The aura is a reversible, focal neurological phenomenon including visual impairments (e.g. scotomas) or unilateral sensibility disturbance (e.g. in the face or a hand). It occurs in a quarter to a third of patients with migraine.
The headache phase generally follows within one hour after the onset of the aura and remains for four to up to 72 hours when untreated. The typical headache is unilateral with a throbbing or pulsatile quality and is moderate to severe in intensity, impeding daily functioning. The headache is usually accompanied by nausea, vomiting, or photoand phonophobia. In some migraine variants, the classical headache lacks. In the postdromal phase, fatigue and concentration problems may persist for up to two days.
The pathophysiologic mechanism of migraine is complex and not yet fully understood. The nervous system becomes disrupted, in part due to neurovascular mechanisms: the headache is caused by the activation of the vascular system around the trigeminal nerve, exciting nerve ends close to meningeal vessels. This process is mediated by a neurotransmitter (CGRP) which can be suppressed with selective serotonin (5HT1) agonists (triptans). In the migraine aura, the process of ‘cortical spreading depression’ causes a depolarisation wave spreading over the cerebral cortex, temporarily impeding brain activity. After a short hyperaemic phase, a longer phase with reduced speed of blood flow follows, probably causing the neurologic symptoms. In patients with migraine with aura persisting for more than an hour, this phase may, in rare cases, be complicated by migrainous infarction visible on neuroimaging.
Migraine is associated with an increased risk of cardiovascular disease, especially cerebrovascular accident. The risk is highest in migraine with aura, but migraine without aura also presents an increased risk of cardiovascular disease. Several factors are mentioned as potential triggers to a migraine attack, for example, fasting and sleep deprivation, but the literature is inconsistent. Most women with migraine notice an association between their menstruation and migraine, with attacks occurring more frequently, or solely, during menstruation.
The diagnosis is generally made by the GP after careful history taking. Diagnostic testing to confirm the diagnosis is not available. In secondary care, neuroimaging is sometimes performed to exclude other diagnoses, such as subarachnoid haemorrhage, cerebrovascular accident, intracranial aneurysm or brain tumour.
Migraine attacks are best managed by resting. It is advised to discuss the cardiovascular risk upon diagnosis and around the age of 40. Advice appropriate to the cardiovascular risk should be given, including ‘stop smoking’ advice if applicable. Migraine is a contra-indication for the contraceptive pill because of the increased cardiovascular risk.
Migraine attacks can be treated with paracetamol, NSAIDs, triptans, or combinations thereof, and with anti-emetics when needed. Betablockers, candesartan or amitripytiline can be used to prevent attacks.