Triage headache by onset, context and neurological findings, identify time-critical secondary causes, and choose imaging or lumbar puncture for a defined diagnostic question.
Secondary-headache assessment is a risk-stratification exercise rather than a memorised acronym. Characterise onset to maximum intensity, first versus recurrent occurrence, progression, posture, Valsalva or exertional provocation, sleep interruption, trauma and relation to pregnancy. Ask about fever, rash, weight loss, cancer, immune compromise, anticoagulants, recent procedures, carbon monoxide exposure and vasoactive substances. Define eye pain, visual obscurations, diplopia, jaw claudication, neck pain and focal or cognitive symptoms. Medication history should include nitrates, phosphodiesterase inhibitors, hormonal treatments and analgesic frequency. Examination needs observations, mental state, neck stiffness, pupils, eye and temporal-artery assessment when relevant, fundoscopy and a reproducible neurological record. Red flags change urgency and the diagnostic question; they do not all mandate the same scan.
Subarachnoid or intracerebral haemorrhage, cervical dissection, cerebral venous thrombosis, ischaemic stroke and reversible vasoconstriction can present with new severe or thunderclap headache.
Meningitis, encephalitis, giant-cell arteritis and systemic inflammatory disease cause headache with fever, meningism, visual, cognitive or constitutional features.
Tumour, hydrocephalus, abscess, idiopathic intracranial hypertension and cerebrospinal-fluid leak alter pressure or distort pain-sensitive structures, usually with contextual neurological clues.
Hypertensive pregnancy disorders, acute glaucoma, severe hypertension, hypoxia, carbon-monoxide exposure and metabolic illness require targeted physiological and specialty assessment.
Disease irritates meninges, cerebral vessels, cranial nerves, venous sinuses or extracranial tissues, as brain parenchyma itself is relatively insensitive to pain.
Pressure change, vessel-wall stretch, blood, infection or cytokines activate trigeminovascular and upper-cervical nociceptive pathways and produce secondary headache.
When the causal process also impairs perfusion, raises intracranial pressure or inflames brain tissue, focal deficits, seizures, visual loss or altered consciousness accompany pain.
Pain reaching maximal severity instantly or within a few minutes, particularly during exertion or sexual activity, needs urgent vascular assessment even when examination later normalises.
Papilloedema, transient visual obscurations, pulsatile tinnitus, diplopia, progressive morning headache or vomiting suggests pressure pathology; a sixth-nerve palsy can be a false localising sign.
Fever, meningism, rash, photophobia, seizure, behavioural change or reduced consciousness should trigger immediate sepsis and meningitis or encephalitis pathways, recognising that the complete cluster may be absent.
New headache with scalp tenderness, jaw or tongue claudication, visual disturbance, constitutional features or polymyalgia in an older person threatens irreversible sight and requires immediate action.
New unilateral head or neck pain with partial Horner syndrome, pulsatile tinnitus, cranial-nerve symptoms or delayed cerebral ischaemia warrants urgent arterial imaging and stroke expertise.
Severe new or changing headache during pregnancy or after birth, especially with hypertension, proteinuria, seizure, focal signs or thrombosis risk, must not be dismissed as ordinary migraine.
Recurrent episodic headache with nausea, light or sound sensitivity and a stable pattern favours migraine, but a changed phenotype or focal deficit requires reassessment.
Bilateral mild-to-moderate pressure without vomiting or activity aggravation supports tension-type headache when examination and context show no secondary concern.
Strictly unilateral short attacks with ipsilateral autonomic signs and restlessness suggest a trigeminal autonomic cephalalgia rather than a diffuse secondary process.
Frequent headache with regular acute-medicine exposure supports overuse, but this diagnosis should not suppress investigation of a new red-flag feature.
Failure to recognise haemorrhage, infection, arteritis, venous thrombosis or mass effect can lead to stroke, blindness, herniation or death.
Puncture in the presence of mass effect, severe instability or bleeding risk can precipitate neurological deterioration or serious haemorrhagic complications.
Indiscriminate scanning of secure primary headache can reveal unrelated abnormalities, generating anxiety, invasive follow-up and diagnostic distraction.
Delayed diagnosis or poorly explained uncertainty can drive medication overuse, sleep loss, work absence and repeated emergency attendance.
Patients use 'sudden' variably. Asking how many seconds or minutes elapsed before maximal pain is more discriminating for a thunderclap mechanism.
Unenhanced CT, venography, angiography and pituitary MRI answer different questions; a normal study cannot exclude a disease it was not designed to show.
Suspected raised intracranial pressure generally requires urgent imaging before lumbar puncture, followed by a properly measured opening pressure only when the procedure is safe.
Secondary headaches may improve with analgesia or antiemetics. Response to treatment should never replace assessment of onset, context and objective neurological signs.
Someone with migraine can still develop haemorrhage, meningitis or venous thrombosis; the useful question is whether this episode matches the established pattern exactly.
Writing 'no red flags' without documenting onset to peak, systemic context, fundoscopy or the key neurological findings that justify that conclusion.
Performing lumbar puncture reflexively after every negative early CT rather than applying the NICE subarachnoid-haemorrhage timing pathway.
Allowing CT or lumbar puncture to delay time-critical antibiotics, antivirals or corticosteroids when the clinical emergency already requires treatment.
Requesting routine brain imaging for a secure primary-headache phenotype solely to reassure, without discussing incidental findings and downstream harm.
Treating normal inflammatory markers as definitive exclusion of giant cell arteritis when cranial ischaemic symptoms are compelling.
Assuming papilloedema is absent after an unskilled or technically limited examination instead of arranging urgent competent assessment.
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A patient presents 10 hours after a thunderclap headache. Non-contrast CT is reported by a radiologist as showing no subarachnoid haemorrhage, but clinical suspicion remains. What does the NICE pathway support next?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
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Subacute secondary patterns demand different pathways. Fever, neck stiffness, altered cognition or a non-blanching rash raises meningitis or encephalitis; obtain cultures and give time-critical antimicrobials under the local protocol without allowing imaging to create avoidable delay. Papilloedema suggests raised intracranial pressure and requires urgent neuroimaging, usually including venous imaging when cerebral venous sinus thrombosis is plausible, before a properly measured lumbar puncture when safe. New headache over 50 with visual or ischaemic symptoms suggests giant cell arteritis and needs immediate steroids plus same-working-day specialist coordination. Painful red eye with halos and vomiting suggests angle-closure glaucoma. In pregnancy and the puerperium, pre-eclampsia, venous thrombosis, dissection and pituitary disease lower the imaging threshold. Choose CT, MRI, angiography, venography, eye review or cerebrospinal-fluid analysis to answer the suspected mechanism.
Do not delay treatment for blood tests or imaging when suspicion is strong; visual symptoms require same-day ophthalmic or rheumatology advice and may need intravenous therapy.