Aetiology
Pathophysiology
There is no absolute consensus regarding the mechanisms underlying migraine with and without aura. Migraine with aura is initially characterised by pathognomonic spreading oligaemia in the cerebral cortex corresponding to the clinically affected area and often beyond. Blood flow reduction usually above the ischaemic threshold starts posteriorly and spreads anteriorly, and a gradual transition into hyperaemia occurs in the same region after a time period of one to several hours.[1]
Published studies on migraine without aura are discordant on whether changes in cerebral blood flow precipitate cortical spreading depression during attacks. Blood flow changes in the brainstem may occur, as may cortical changes secondary to pain activation. Glial waves or other cortical phenomena may be involved in migraine without aura, and nitric oxide, 5-hydroxytryptamine (5-HT), and calcitonin gene-related peptide (CGRP) have been implicated as messenger molecules. Once regarded as a primarily vascular entity, attacks may originate in the central nervous system with sensitisation of pain pathways in part contributory. The circuitry of migraine pain is steadily gaining definition, and the treatment efficacy of triptans (5-HT1B/D receptor agonists, 5-HT1F receptor agonists, and CGRP receptor antagonists) provides further insight into migraine disease mechanisms.[1]
Classification
International Classification of Headache Disorders, 3rd edition (beta version)[1]
The 2013 update of the International Classification of Headache Disorders (ICHD) restructures how migraine subtypes are defined, the principal consideration now being whether migraine occurs without or with aura. Many patients may have both subtypes, which can be summarised as follows.
Migraine without aura
A recurrent headache disorder with specific features and associated symptoms. At least five attacks are required to substantiate the diagnosis. Episodes typically last 2 to 72 hours and the headache in children and adolescents is usually frontotemporal and more commonly bilateral than in adults. Occipital headache in children is not common and should prompt diagnostic caution.
Unilateral pain usually emerges in late adolescence or early adult life. Pain is typically pulsating in character, of moderate or severe intensity, aggravated by routine physical activity, and associated with nausea/vomiting and/or phonophobia and photophobia. Photophobia in young children can reasonably be inferred from their behaviour. A menstrual relationship to attacks may become evident in older adolescents.
Migraine with aura
A syndrome characterised by recurrent attacks (lasting minutes) of unilateral fully reversible visual, sensory, or other central nervous system symptoms that typically develop gradually and are then usually followed by headache and associated migraine symptoms. Diagnostic difficulty may arise in assessing younger children, who may naturally struggle to articulate their symptomatology and be more difficult to examine with complete precision. Aura may be visual (most commonly), sensory, speech and/or language, motor, brainstem, or retinal, each typically spreading gradually over ≥5 minutes, with sometimes two or more auras occurring in succession, each lasting 5 to 60 minutes. At least one aura symptom is typically unilateral, and is accompanied, or followed within 60 minutes, by headache. There may also be premonitory symptoms that may begin hours or a day or two before the other symptoms of a migraine attack (with or without aura), and they include combinations of fatigue, difficulty in concentrating, neck stiffness, sensitivity to light and/or sound, nausea, blurred vision, yawning, and pallor.
A full description of clinical phenotypes (previously described as stand-alone entities) that now fall within this subtype can be found within the ICHD description, and include presentations previously described as classical, ophthalmic, basilar, hemiparaesthetic, hemiplegic, or aphasic migraine.
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