Headache: Diagnostic Approach

The ICHD-3 (International Classification of Headache Disorders, 3rd edition) splits headache into three groups:

1. Primary headaches — migraine, tension-type headache, trigeminal autonomic cephalalgias (TACs), other primary headache disorders.
2. Secondary headaches — due to a structural cause (space-occupying lesion, subarachnoid haemorrhage, venous sinus thrombosis) or a disease process (giant cell arteritis, meningitis, systemic infection).
3. Painful cranial neuropathies and other facial pain — e.g. trigeminal neuralgia, glossopharyngeal neuralgia. See facial pain for the full differential.

Less than 10% of headache presentations in general practice are secondary, and only about 1% reflect serious underlying disease.

Clinical evaluation — the “5 Ps”

A thorough headache history determines both the diagnosis and the need for imaging. Australian Prescriber frames this as five domains worth covering systematically: patient (age, general health — new headache late in life, or with malignancy/immunosuppression, always needs further evaluation), pattern (unchanged since childhood or tied to menstruation is reassuring; new/changed pattern is not), phenotype (the headache’s own characteristics — but a phenotype resembling a primary headache should not provide false reassurance if red flags are present: in one study, 77% of patients with a primary or metastatic brain tumour presented with a tension-type-headache phenotype), precipitants (alcohol/food triggers suggest a primary cause; Valsalva/cough/posture-related triggers raise concern for posterior fossa pathology or raised intracranial pressure; task-specific headaches — exertion, intercourse, sleep — need specific consideration), and pharmacology (new drugs, and overuse of acute analgesia — see medication overuse headache).

Warning features in new-onset headache

The mnemonic SNOOP4 covers the same ground as the table below: Systemic symptoms/secondary risk factor, Neurological deficit, Onset (thunderclap), Older age (>50), and the P4 group — Positional, Pattern change, Precipitated by Valsalva, Papilloedema.

Feature	Possible diagnosis
Sudden (“thunderclap”) onset	Subarachnoid haemorrhage, pituitary apoplexy, haemorrhage into a mass lesion, arterial dissection, reversible cerebral vasoconstriction syndrome
First-ever headache with focal signs, confusion or drowsiness	Stroke, venous sinus thrombosis, reversible cerebral vasoconstriction syndrome, meningitis/encephalitis
Age >50 years	Giant cell arteritis, mass lesion, stroke
Onset after head trauma	Subdural/epidural haemorrhage
Worsening frequency/severity over weeks–months	Mass lesion, subdural haemorrhage, analgesic rebound
New onset with HIV, cancer or immunosuppression	Meningitis, abscess, metastasis
Systemic illness signs (fever, rash, neck stiffness)	Systemic infection, meningitis, encephalitis, vasculitis
Papilloedema	Mass lesion, idiopathic intracranial hypertension, venous sinus thrombosis
Positional (worse lying down) or prolonged cough headache	Space-occupying/posterior fossa lesion, Chiari malformation
Severe headache on anticoagulants	Intracranial haemorrhage

”Green flags” — features that favour a primary headache

Reassuring, though not validated in a prospective study: the current headache has been present since childhood; it is temporally related to the menstrual cycle; the patient has headache-free days between episodes (secondary causes, aside from brain tumours, are less often intermittent); and close family members have the same headache type (migraine and cluster headache are both heritable).

Primary headache classification

Tension-type headache — see dedicated page.

Migraine — see dedicated page.

Trigeminal autonomic cephalalgias (TACs) — unilateral headaches with prominent cranial parasympathetic autonomic features ipsilateral to the pain, distinguished by attack frequency/duration and indomethacin responsiveness:

• Cluster headache — attacks 15–180 min, up to 8/day.
• Paroxysmal hemicrania — attacks 2–30 min, several to many times daily; remits completely with indomethacin.
• SUNCT/SUNA (short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing/cranial autonomic symptoms) — attacks seconds to minutes, ≥1/day; does not respond to indomethacin.
• Hemicrania continua — persistent headache ≥3 months; remits completely with indomethacin.

All patients with a suspected TAC require MRI, primarily to exclude a pituitary-region lesion — though dedicated pituitary sequences are only needed for atypical features (older age, prolonged/frequent/bilateral attacks, absence of autonomic symptoms), pituitary-related symptoms, an abnormal exam or poor treatment response; among 376 patients with cluster headache the rate of incidental pituitary adenoma was no higher than the general population.

Indomethacin regimen (paroxysmal hemicrania/hemicrania continua): 25 mg TDS for 3 days → 50 mg TDS if incomplete response → 75 mg TDS if still incomplete. Reconsider the diagnosis if no improvement after 10 days at the highest dose. Add a PPI for gastroprotection. Continue the lowest effective dose for up to 6 months before cautious tapering. SUNCT/SUNA doesn’t respond to indomethacin — seek neurology advice for anticonvulsants (lamotrigine, topiramate — not PBS-listed for this indication).

Secondary headache red flags

• Progressive non-episodic worsening; headache severe enough to wake the patient or present on waking.
• Vomiting without other migraine features; fixed focal neurology; personality/cognitive change.
• Aggravated by coughing/sneezing/bending/exertion; thunderclap onset.
• History of malignancy or immunodeficiency; new onset age >50 (giant cell arteritis, space-occupying lesion).
• Eye symptoms (monocular pain, red eye, visual disturbance — angle-closure glaucoma).
• Severe headache on anticoagulants.
• Possible drug-induced headache (review CCBs, nitrates, COCP).

A primary-headache-like phenotype does not rule out a secondary cause — some presentations always need imaging regardless of how “typical” they look: thunderclap headache, and any trigeminal autonomic cephalalgia. Headache attributed to sexual activity should be treated as reversible cerebral vasoconstriction syndrome until an angiographic study proves otherwise, and primary exertional headache is a diagnosis of exclusion for the same reason.

Other primary headache patterns

• Medication overuse headache — overuse thresholds are >10 days/month for opioid or triptan analgesia, or >15 days/month for simple analgesia (paracetamol/NSAIDs); may affect over 70% of patients with chronic daily headache.
• Caffeine withdrawal headache — within 24h of stopping >200mg/day caffeine (≈4 instant coffees, 2 espressos, 4 colas, 2 energy drinks, 6–7 teas) after >2 weeks’ regular use; may take 7 days to remit.
• Headache attributed to fasting — diffuse, non-pulsating, mild–moderate, after ≥8h fasting, relieved by eating. Inadequate/infrequent nutritional intake can also contribute to headache in patients with a primary headache disorder even without meeting strict fasting-headache criteria.

Examination

• Vital signs (especially BP, temperature, HR).
• Head/mouth/neck inspection (skin malignancy, dentition); temporal artery palpation; neck exam (tenderness, stiffness).
• Visual acuity and fields; eye movements; fundoscopy for papilloedema (ideally confirmed by ophthalmology/optometry).
• Full neurological exam including cranial nerves, limbs and gait.

Investigations

A thorough history and examination is diagnostic in most patients — order tests to confirm a specific concern, not routinely. Evidence-based guidelines consistently recommend against routine imaging of headache — the decision should be guided by the clinical evaluation above, weighed against the risk of an incidental finding (roughly 2% of MRI brains show one: neoplasia 0.7%, aneurysm 0.35%, arachnoid cyst 0.5%, Chiari I 0.24%, demyelination 0.06%).

• Bloods: FBC, biochemistry; ESR/CRP if age >50 with new headache (consider giant cell arteritis). For giant cell arteritis, use an age-adjusted ESR upper limit — (age in years + 10) ÷ 2 — since a “normal” unadjusted ESR can be falsely reassuring in an older patient.
• Imaging (CT/MRI brain): for signs/symptoms of secondary headache — focal neurology, recent change in frequency/severity, past malignancy (especially lung, breast, melanoma). MRI (± MRA/MRV) is preferred unless acute haemorrhage is suspected, in which case CT is more readily available. Thunderclap headache needs urgent brain + cerebral vessel imaging (e.g. CT angiography). A non-contrast CT within 6 hours of thunderclap onset has ~99% sensitivity for subarachnoid haemorrhage, but this falls considerably after 6 hours — a negative scan beyond that window needs a lumbar puncture before SAH can be excluded, and CT alone can miss other causes (cerebral venous sinus thrombosis, reversible cerebral vasoconstriction syndrome, pituitary apoplexy, arterial dissection). Medicare rebates GP-requested MRI head (age >16) for chronic headache with suspected intracranial pathology — not for primary headache disorders.

Management principles

• Address the patient’s concerns about serious pathology; provide reassurance and education.
• Assess and manage sleep disturbance/insomnia/OSA — significantly exacerbates primary headaches.
• Encourage the patient to identify/avoid triggers, try non-drug measures (heat packs, physiotherapy), consider relaxation/stress management/acupuncture, and address lifestyle factors (smoking, alcohol, caffeine, activity, diet, avoiding fasting).
• A headache diary aids self-management and diagnosis (Headache Australia templates; headache diary apps).
• See the dedicated pages for acute and preventive management of tension-type headache, migraine, MOH and cluster headache.

Referral

• Red flags/suspected serious secondary headache: emergency department; or specialist assessment if less urgent.
  • Neurosurgery — space-occupying lesion, aneurysm or other vascular lesion on imaging.
  • Ophthalmology — eye symptoms (angle-closure glaucoma, papilloedema).
  • Neurology/general physician — new headache with raised-ICP features (worse on coughing/straining/bending, morning waking, papilloedema, blurred vision), or any severe headache not covered by the red flags above.
• Non-acute neurology referral if: troublesome headache not meeting urgent/emergency criteria; abnormal neuroimaging without urgent criteria; severe frequent headaches despite ≥3 migraine preventers and/or ≥4 days/month lost from work/study; chronic or complicated headache unresponsive to treatment.
• Consider ED transfer for IV fluids/parenteral therapy if no improvement or worsening migraine despite standard management.

Age-specific notes

• Children: respiratory/febrile illness is a common cause. Migraine (usually without aura) is common pre-adolescence, girls > boys, strong family history. Tension headache becomes common post-adolescence. Overlooked causes: eye strain, hair traction, hypoglycaemia. Space-occupying lesions classically cause early-morning headache with ataxia, dizziness, personality change, diplopia, vomiting, night waking, unilateral/progressive symptoms — see headaches in children.
• Elderly: treat new-onset headache with caution — consider giant cell arteritis (median age 70, uncommon <50), space-occupying lesion, TIA, trigeminal neuralgia, vertebrobasilar insufficiency, cervical spondylosis. Age itself is a red flag: serious secondary headaches are more common in older adults and must be excluded before attributing a new headache to a primary disorder, even though tension-type headache (followed by migraine) remains the most common cause of headache at any age.