Diagnose migraine positively from its episodic phenotype, distinguish typical aura from vascular or epileptic mimics, and recognise when a changing pattern needs secondary-headache investigation.
Migraine is a recurrent neurological disorder with a broader attack than head pain alone. Premonitory symptoms can include yawning, mood change, neck discomfort, thirst and food craving; headache is followed by a postdrome of fatigue or cognitive slowing. In adults, untreated headache commonly lasts 4–72 hours and has at least two of unilateral location, pulsating quality, moderate or severe intensity, or aggravation by routine activity, together with nausea or vomiting or both photophobia and phonophobia. Children may have shorter and more bilateral attacks. Ask about disability, work and caring impact, frequency of all headache days, acute medicine use, sleep, menstruation and family history. Normal examination between typical attacks supports a primary syndrome but does not replace deliberate red-flag screening.
Aura reflects transient cortical dysfunction and is diagnosed from evolution, duration and reversibility. Common visual aura includes a gradually enlarging scintillating scotoma; sensory aura may spread from hand to face; dysphasic aura affects language. Different symptoms may occur in succession and each typically lasts 5–60 minutes. Urgent or specialist assessment is appropriate for motor weakness, double vision, visual symptoms affecting one eye only, poor balance or
Migraine is a complex polygenic brain disorder in which inherited differences in sensory, pain and excitability networks lower the threshold for attacks.
Menstrual change, sleep disruption, stress, missed meals and illness can alter attack probability without acting as one universal underlying cause.
Light, odour, alcohol and other reported exposures may precipitate attacks in some people, while apparent triggers can also represent early premonitory symptoms.
Hypothalamic, brainstem and cortical networks alter before pain, producing fatigue, yawning, mood, appetite and sensory symptoms in some attacks.
Trigeminal afferents and meningeal pain pathways release neuropeptides and activate central nociceptive circuits, generating headache and activity-related worsening.
Brainstem and thalamic processing amplifies light, sound, smell, touch and nausea signals as the attack evolves.
In aura, a slowly propagating wave of cortical electrical change produces sequential, fully reversible visual, sensory or language symptoms.
Recurrent disabling attacks lasting hours, with activity aggravation and nausea or light-and-sound sensitivity, support migraine even when pain is bilateral or not described as pulsating.
A fully reversible positive or negative visual phenomenon that spreads gradually across the field and resolves within about an hour is more characteristic than abrupt monocular darkness.
Pins and needles that march over minutes, sometimes followed by numbness, or gradually evolving reversible language disturbance can precede or accompany migraine headache.
Motor weakness, diplopia, monocular visual symptoms, reduced consciousness or impaired balance requires further assessment because it falls outside straightforward typical-aura diagnosis.
At least 15 headache days monthly for over 3 months, including at least 8 days with migraine features, defines chronic migraine after alternative causes and overuse are assessed.
Abrupt maximal negative loss occurring simultaneously favours TIA, while gradually spreading positive symptoms followed by headache support typical aura.
Very brief stereotyped positive symptoms, impaired awareness or motor automatisms favour seizure; postictal deficit can further complicate distinction.
Short restless unilateral attacks with autonomic signs suggest cluster headache, while bilateral non-disabling pressure without nausea favours tension-type headache.
Thunderclap onset, persistent focal deficit, papilloedema, fever or a substantially changed pattern requires investigation beyond a previous migraine diagnosis.
Sudden fixed deficit, first or worst abrupt pain, seizure features, fever, papilloedema or progressive personality change should move the clinician away from uncomplicated migraine.
Increasing attack and headache frequency can produce near-continuous disability, especially when sleep, mood and acute-treatment use become maladaptive.
Frequent rescue treatment can sensitise pain networks and make headache more frequent, obscuring the original episodic pattern.
Pain, nausea, sensory intolerance and aura impair work, education, driving, caring roles and participation despite normal function between attacks.
Migraine with aura influences combined hormonal contraception safety and vascular-risk counselling without making stroke inevitable for an individual.
Premonitory symptoms and postdrome form part of the attack biology; recognising them can improve planning and prevents every associated symptom being labelled a drug adverse effect.
Gradual spread across cortex produces evolving visual or sensory phenomena, whereas a sudden fixed negative deficit deserves vascular assessment until a safer explanation is established.
Unilateral pulsation is classic but not universal. Bilateral pain can still be migraine when duration, activity aggravation and associated symptoms form a coherent pattern.
Prospective recording is particularly valuable for chronic migraine, menstrual association and medication overuse, where recall over several months is often inaccurate.
Migraine is diagnosed clinically, and a scan does not prove the disorder. Unnecessary imaging can uncover incidental findings that worsen anxiety without improving care.
Excluding migraine because headache is bilateral, non-pulsatile or not preceded by aura despite a strongly characteristic overall attack.
Calling sudden monocular darkness or persistent unilateral weakness typical aura without urgent vascular or ophthalmic assessment.
Using a previous migraine diagnosis to explain a first thunderclap episode or a substantial new pattern during pregnancy.
Counting only severe migraine days and missing the additional milder headache days that meet chronic-migraine or medication-overuse thresholds.
Ordering brain imaging to confirm migraine rather than because a specific secondary diagnosis is clinically suspected.
Providing a diagnosis without acute-treatment, prevention, contraception and safety-net discussions, leaving the patient dependent on repeated urgent consultations.
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A woman has a shimmering zig-zag in both visual fields that enlarges gradually over 15 minutes, resolves after 35 minutes and is followed by her usual migraine headache. Which feature most strongly supports typical aura?
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Migraine frequency exists on a spectrum. Episodic migraine has fewer than 15 headache days monthly; chronic migraine crosses the 15-day threshold for over 3 months with migraine features on at least 8 days. Medication overuse, depression, anxiety, sleep disorders and other pain can amplify disability and should be assessed without implying that symptoms are psychological. Menstrual-related migraine is suspected when attacks cluster from 2 days before to 3 days after menstruation in at least two of three cycles, confirmed with a diary. Pregnancy often changes pattern, so a new severe pregnancy headache needs its own secondary assessment. The diagnosis should be revisited if attacks become continuously progressive, awaken the patient in a new way, change after age 50, or acquire systemic or persistent neurological features.