Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Differentiate cluster headache, paroxysmal hemicrania, SUNCT or SUNA and hemicrania continua by temporal pattern and indometacin response, while excluding structural mimics.
TACs reflect activation of trigeminal pain pathways and cranial parasympathetic outflow, producing unilateral orbital, supraorbital or temporal pain with a red watering eye, rhinorrhoea, nasal blockage, eyelid oedema, facial sweating, ear fullness, miosis or ptosis. The autonomic sign must be interpreted with attack timing: unilateral tearing can accompany migraine, and persistent eye redness can be ocular disease. Record exact untreated duration with a stopwatch where possible, daily frequency, pain-free intervals, background pain, triggers and restlessness. Examine pupils, ocular movements, acuity, fields and cranial nerves during and between attacks. A fixed deficit or autonomic sign outside attacks weakens a straightforward primary diagnosis.
The syndromes occupy different temporal scales. Cluster headache attacks last 15–180 minutes and occur from every other day to eight times daily in bouts. Paroxysmal hemicrania lasts 2–30 minutes, often more than five times daily, and remits completely with therapeutic indometacin. SUNCT and SUNA attacks are brief unilateral neuralgiform pains lasting 1–600 seconds and occurring at least daily during active periods; attacks may be single stabs, series or saw-tooth patterns. SUNCT specifies both conjunctival injection and lacrimation, while SUNA does not meet that combination. Hemicrania continua produces persistent side-locked pain beyond 3 months with exacerbations, autonomic symptoms or agitation, and an absolute indometacin response. These criteria prevent 'cluster variant' from becoming a catch-all.
Cluster headache, paroxysmal hemicrania, SUNCT, SUNA and hemicrania continua are primary disorders of cranial pain and autonomic networks.
Disordered central timing is especially relevant to cluster headache and helps explain predictable daily attacks and bouts.
Pituitary, posterior-fossa, orbital and vascular lesions can generate a TAC-like phenotype, particularly at new or atypical presentation.
First-division trigeminal pain pathways generate severe strictly unilateral orbital, temporal or facial pain during each attack.
Trigeminal input activates parasympathetic outflow, producing tearing, conjunctival injection, nasal symptoms and eyelid change on the pain side.
Hypothalamic and brainstem networks determine distinctive attack duration, frequency, continuous background and restlessness across TAC subtypes.
Marked indometacin responsiveness in selected TACs reflects a distinct biological treatment response that also assists specialist classification.
Strictly unilateral 2–30-minute attacks occurring many times daily with autonomic signs and complete indometacin response define the characteristic pattern.
Unilateral neuralgiform attacks lasting seconds to minutes with both conjunctival injection and tearing suggest short-lasting unilateral neuralgiform headache with conjunctival injection and tearing.
Very brief unilateral neuralgiform attacks with cranial autonomic activation but without the required combination of both red eye and tearing fit SUNA after mimics are excluded.
Continuous side-locked headache for more than 3 months with superimposed exacerbations and an absolute indometacin response is distinct from recurrent pain-free attacks.
Stimulus-triggered electric-shock pain lasting fractions of a second to 2 minutes suggests trigeminal neuralgia, although short TACs can also be triggered and need expert separation.
Abnormal ocular movements, field loss, endocrine symptoms, persistent Horner syndrome, bilateral or changing signs, late atypical onset or incomplete syndrome raises concern for structural disease.
Longer attacks with nausea, sensory sensitivity and preference for stillness favour migraine, though cranial autonomic symptoms can occur.
Electric shocks triggered by touch or chewing with a refractory interval favour neuralgia; prominent autonomic signs and longer attacks support a TAC.
Persistent eye signs, fever, proptosis or local structural abnormality indicates ocular, orbital or sinus pathology rather than a primary TAC.
New headache with neurological, endocrine or visual-field findings requires specialist imaging for dissection, aneurysm or sellar disease.
Frequent excruciating attacks can cause panic, depressed mood and profound distress, especially when diagnosis and effective rescue are delayed.
Repeated daily or nocturnal attacks impair sleep, concentration, driving and ability to work during active bouts.
Grouping all TACs as cluster headache exposes patients to unsuitable treatment while withholding therapy appropriate for the correct subtype.
Indometacin, triptans, preventives and invasive procedures carry gastrointestinal, renal, cardiovascular, conduction and neurological risks during treatment.
Untreated attack duration functions almost like a bedside investigation: seconds, tens of minutes, hours and continuous pain lead to different TAC diagnoses.
The classical syndromes require complete prevention at adequate exposure. Merely feeling somewhat better after an NSAID is not the defining response.
Nasal blockage, discharge and eye watering during unilateral pain reflect cranial autonomic activation and commonly lead to unnecessary antibiotics or sinus procedures.
Touch can provoke both SUNCT or SUNA and trigeminal neuralgia, so duration, autonomic combination, refractory period and imaging remain important.
Pituitary or posterior-fossa lesions may produce convincing TAC phenotypes; new presentations deserve specialist structural assessment even when criteria appear tidy.
Calling every unilateral headache with tearing cluster headache without measuring attack duration, frequency and continuous background pain.
Diagnosing paroxysmal hemicrania after partial benefit from a small over-the-counter NSAID dose rather than an adequate supervised indometacin trial.
Prescribing indometacin without checking renal, gastrointestinal, cardiovascular, anticoagulant and pregnancy risk or arranging gastroprotection.
Treating SUNCT or SUNA with repeated ordinary analgesics that cannot act within a seconds-long attack and may create medication overuse.
Escalating lamotrigine rapidly or ignoring a rash, particularly when an interacting drug has altered the safe titration schedule.
Omitting imaging and interval neurological examination because the attack satisfies a primary TAC checklist.
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A patient has 12 strictly unilateral orbital attacks each day, each lasting 10 minutes with tearing and nasal blockage. Which finding is required to confirm the most likely primary headache syndrome?
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.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Specialist confirmation matters because treatment and secondary mimics differ. MRI brain with attention to the pituitary and posterior fossa, and vascular or orbital imaging when indicated, may reveal a lesion capable of reproducing the syndrome. Paroxysmal hemicrania and hemicrania continua require a supervised adequate indometacin trial; rapid complete response supports diagnosis, while partial relief at an inadequate dose does not. Gastroprotection and renal, gastrointestinal and cardiovascular risk must be managed. SUNCT or SUNA is difficult to treat acutely because attacks are so short; lamotrigine is a commonly used specialist preventive, titrated slowly because of rash risk, with intravenous lidocaine reserved for selected severe transitional care in monitored specialist settings. Cluster-specific oxygen, triptans and verapamil should not be automatically transferred to every TAC.
High gastrointestinal, renal, cardiovascular and bleeding toxicity requires risk assessment, gastroprotection and monitoring; avoid casual unsupervised trials or combination with other NSAIDs.
Stop and seek urgent assessment for rash or systemic hypersensitivity; valproate greatly changes titration, and abrupt escalation increases severe cutaneous-reaction risk.
Requires continuous cardiac and neurological monitoring because arrhythmia, hypotension, seizures and systemic toxicity can occur; it is not community rescue treatment.