Use onset, duration, associated symptoms, and examination to distinguish primary headaches from vascular, inflammatory, infectious, and pressure emergencies.
Two patients describe the worst headache they have experienced. One has a familiar attack that grew over an hour; the other reached maximum pain while lifting a box. Severity matters, but the time to peak changes the immediate decision. Establish the onset before assigning a headache name.
A normal neurologic examination does not make every headache benign. Conversely, a stable recurrent migraine pattern with a normal examination does not require imaging solely for reassurance. The task is to identify the pattern and the features that fall outside it. [1]
First determine which clock you are reading
Ask separately about time to maximum pain, duration of an untreated attack, and frequency over months. Thunderclap describes abrupt peak intensity, usually within one minute; it is an onset pattern, not a final diagnosis. New focal deficits, altered consciousness, fever with meningismus, papilledema, a major pattern change, cancer or immunosuppression, pregnancy or the postpartum period, and a new headache after age 50 require attention to secondary causes. New cough-, exertion-, or sex-triggered pain also warrants evaluation before a primary diagnosis. [1][2]
Time to peak
Seconds to a minute: investigate hemorrhage and other vascular causes. The later duration does not cancel this onset.
Duration of one attack
Seconds: consider neuralgia. Fifteen to 180 minutes: consider cluster. Four to 72 hours: consider migraine. Thirty minutes to seven days: tension-type remains possible.
Calendar pattern
Count headache days, migraine-feature days, and acute medicine days separately. Daily pain is not automatically chronic migraine.
Three clocks answer different questions. Duration ranges overlap and must be combined with symptoms and examination; they are not diagnostic by themselves. [2][3][4]
A headache diary can record disability, menstruation, associated symptoms, and treatment response without turning an emergency into a home observation exercise. A familiar migraine history does not protect someone from a new secondary headache.
Migraine and tension-type pain differ by the whole attack
Migraine without aura typically lasts four to 72 hours untreated. The diagnostic pattern combines at least two of unilateral pain, pulsating quality, moderate or severe intensity, and aggravation by routine activity, plus nausea/vomiting or both photophobia and phonophobia. Thus migraine can be bilateral, can occur without nausea, and need not include an aura. Established diagnosis generally requires at least five qualifying attacks and exclusion of a better explanation. [3]
Typical aura consists of fully reversible visual, sensory, or language symptoms that often spread gradually or occur in succession. Each typical nonmotor symptom commonly lasts five to 60 minutes. A spreading scintillating pattern followed by headache differs from a sudden fixed field defect, but these descriptions are not perfectly specific. A first, abrupt, persistent, or otherwise atypical neurologic deficit needs evaluation for stroke or another cause. Aura can occur without headache. [5]
Migraine involves trigeminovascular signaling, not simply a large artery dilating. Trigeminal afferents convey pain from cranial structures, and CGRP participates in the signaling network. A human provocation trial showed that administered CGRP can trigger migraine-like attacks in susceptible participants. This supports a therapeutic target without reducing a complex brain disorder to a single peptide. [6]
Episodic tension-type headache is usually bilateral, pressing or tightening, mild to moderate, and not worsened by ordinary activity. Nausea and vomiting are absent; no more than one of photophobia or phonophobia is present. Stress or pericranial tenderness may coexist but does not prove the diagnosis. Marked activity avoidance with both light and sound sensitivity should prompt reconsideration of migraine. [2]
For an established migraine attack, an appropriate triptan with an NSAID or paracetamol is one guideline-supported approach; an antiemetic and a nonoral route may help when vomiting limits absorption. Contraindications, pregnancy, vascular disease, and prior response affect selection. For tension-type attacks, simple analgesics may help. Avoid opioids as routine treatment for either pattern. Oxygen is a standard acute treatment for cluster headache, not routine migraine therapy. [1]
Cluster pain recruits a same-sided autonomic response
Cluster headache produces very severe unilateral orbital, supraorbital, or temporal pain lasting 15 to 180 minutes untreated, with ipsilateral autonomic findings and/or restlessness. Attacks may recur from every other day to eight times daily during an active period. Tearing, conjunctival injection, nasal congestion, rhinorrhea, eyelid edema, ptosis, or miosis can accompany the pain. The patient may pace rather than seek the stillness often preferred during migraine. Migraine can also cause cranial autonomic symptoms, so tearing alone does not establish cluster. [4][3]
Sensory limb: trigeminal input from the painful cranial region reaches brainstem pain circuits.
Parasympathetic limb: superior salivatory nucleus output travels with facial-nerve pathways through the greater petrosal pathway to the pterygopalatine, also called sphenopalatine, ganglion.
Same-sided target tissues: postganglionic output to lacrimal and nasal tissues helps explain tearing and rhinorrhea.
Separate sympathetic finding: reduced oculosympathetic function explains ptosis and miosis; these are not direct lacrimal parasympathetic effects.
The pain and autonomic components share a reflex circuit, but the signs arise from different efferent functions. This schematic separates those functions without implying that all cluster biology is peripheral. [7][18]
Treat an acute cluster attack with 100% oxygen at a flow of at least 12 L/min through a non-rebreather mask with reservoir and/or a subcutaneous or nasal triptan when appropriate. Oral agents are generally too slow for this brief severe attack. Verapamil is a preventive option with specialist advice and ECG monitoring during dose adjustment. Discuss neuroimaging for a first cluster bout; a persistent Horner syndrome, atypical examination, or changed pattern should not be dismissed as another cluster feature. [1]
Hemorrhage and arteritis demand different urgent decisions
Thunderclap and subarachnoid hemorrhage
Obtain urgent noncontrast CT when subarachnoid hemorrhage (SAH) is suspected. AHA/ASA guidance distinguishes selected patients presenting within six hours without a new neurologic deficit, when a high-quality scan interpreted by a neuroradiologist can be sufficient, from those presenting later or with a new deficit. In the latter group, a negative CT should be followed by lumbar puncture when appropriate to diagnose or exclude SAH. A negative scan is not a universal stopping rule. [8]
Once aneurysmal SAH is identified, specialist care includes securing the aneurysm and managing complications. Enteral nimodipine reduces delayed cerebral ischemia and improves functional outcomes; it does not repair the aneurysm. A first sex- or exercise-associated thunderclap requires the same initial seriousness. Recurrent thunderclaps over days can indicate reversible cerebral vasoconstriction syndrome (RCVS), and vascular imaging can be normal early. Persistent clinical concern may require reassessment and repeat vascular imaging rather than a premature primary-thunderclap label. [8][2]
Giant cell arteritis and threatened vision
In an adult over 50, new headache with jaw claudication, scalp tenderness, constitutional symptoms, polymyalgia symptoms, or visual disturbance should raise concern for giant cell arteritis (GCA). It is a large- and medium-vessel inflammatory disorder; the temporal artery is a diagnostic target, not the only vessel involved. Ocular ischemia can cause irreversible visual loss. ESR and CRP support assessment but neither establishes nor absolutely excludes the diagnosis. [9][10][22]
When suspicion is high, begin glucocorticoids promptly while arranging confirmation and urgent specialist assessment. ACR/Vasculitis Foundation guidance conditionally favors IV pulse glucocorticoids over high-dose oral treatment for newly diagnosed GCA with threatened vision loss; without cranial ischemia, it conditionally favors high-dose oral treatment over IV pulses. These recommendations have low or very low certainty, so the patient's ischemic risk and treatment risks matter. Do not prescribe IV pulses for every older patient with a headache. Obtain a temporal artery biopsy promptly, preferably within two weeks after starting glucocorticoids when biopsy is the chosen test; later biopsy can still be informative. Local expertise affects the role of vascular ultrasound. [9]
Long-term care includes an individualized glucocorticoid taper, monitoring for relapse and treatment toxicity, and consideration of steroid-sparing treatment such as tocilizumab. ACR/VF conditionally recommends baseline noninvasive vascular imaging in newly diagnosed GCA to assess large-vessel involvement. When that involvement is present, follow-up imaging can monitor aneurysms and stenoses; repeated imaging is not automatically required on one fixed schedule for every patient. [9]
Look beyond the five familiar headache labels
Fever, neck stiffness, headache, and altered cognition raise concern for bacterial meningitis. All features need not be present, and absence of a rash does not identify or exclude an organism. Obtain cultures and CSF when safe, but do not delay needed antibiotics for imaging or an unsafe lumbar puncture. A neutrophilic CSF pattern with low glucose supports bacterial disease; viral disease more often has lymphocytes and preserved glucose, with exceptions and organism-specific testing required. [11][19]
Headache with papilledema, transient visual obscurations, or pulsatile tinnitus warrants evaluation for raised intracranial pressure. MRI and venous imaging help exclude a mass and cerebral venous thrombosis before lumbar puncture. Idiopathic intracranial hypertension (IIH) requires the appropriate clinical, imaging, and CSF findings, not obesity alone. Tetracyclines and other implicated medicines can produce secondary intracranial hypertension. Assess visual fields and protect vision; weight management in typical IIH and acetazolamide may be useful. Serial lumbar punctures are not routine long-term headache treatment. Declining vision needs urgent specialist escalation. [12]
Fever, painful ophthalmoplegia, proptosis, and chemosis after facial or sinus infection raise concern for orbital infection or cavernous sinus thrombosis. Contrast imaging with appropriate venous assessment distinguishes extension and thrombosis; symptoms alone cannot settle the anatomy. Progressive headache with a new seizure or focal deficit also needs structural imaging. Ring enhancement describes an imaging pattern, not a histologic diagnosis: specialist assessment may need advanced MRI and tissue diagnosis. [13][21][14]
Seconds-long electric pain triggered by touching the cheek or chewing suggests trigeminal neuralgia, especially when localized to a trigeminal division. It is not simply a short migraine. A painful red eye with blurred vision, a poorly reactive pupil, or corneal haze requires urgent assessment for angle closure; orbital pain alone should not be labeled cluster. [17] New cough headache can reflect a posterior fossa or craniocervical lesion; a primary cough diagnosis follows adequate exclusion of secondary disease. [2]
Count days before changing long-term treatment
Chronic migraine requires headache on at least 15 days per month for more than three months, with migraine features on at least eight days per month in a person with the requisite migraine history. Status migrainosus is a debilitating migraine attack lasting more than 72 hours, with specified allowances for brief remissions. These describe different dimensions: a prolonged attack does not by itself establish chronic migraine. [2]
Medication-overuse headache requires headache on at least 15 days per month in a person with a pre-existing headache disorder, together with regular excessive acute medication use for more than three months. Thresholds depend on the drug: triptans, opioids, and combination analgesics generally use at least 10 days per month; simple nonopioid analgesics generally use at least 15. Count medication days rather than tablets. Chronic migraine and medication overuse can coexist. Withdrawal planning, support, and effective prevention should address both. [2][1]
Frequent tension-type headache also deserves review of sleep, stress, analgesic exposure, and prevention. Amitriptyline is a preventive option for chronic tension-type headache in appropriate patients, with attention to anticholinergic effects, cardiac risk, and local prescribing guidance. It is not an immediate attack treatment. [20]
Discuss prevention when attacks cause substantial disability, are frequent, or acute therapy is ineffective or overused. Options include propranolol, topiramate, amitriptyline, and CGRP-targeting therapies, chosen around patient goals and contraindications. The 2024 American Headache Society position allows CGRP-targeting therapies as a first-line preventive option without requiring prior failures; access rules may differ. Topiramate has important pregnancy restrictions. Migraine with aura also changes contraceptive counseling: combined hormonal contraception is US MEC category 4, while other methods may be suitable after full assessment. [1][15][16]
Practice choosing the next headache decision
Case 1
Show answer and explanations for case 1
A. Cluster headache (Why this does not fit)
Cluster attacks are usually shorter and prominently orbital with autonomic signs or restlessness.
B. Episodic tension-type headache (Why this does not fit)
Nausea and activity-aggravated pulsating pain argue against this pattern.
C. Trigeminal neuralgia (Why this does not fit)
Neuralgia causes brief triggered electric pains rather than these prolonged attacks.
D. Migraine without aura (Best answer)
Duration, activity aggravation, pulsation, and nausea form the migraine pattern; aura is not required.
Takeaway: Migraine is a combination of features, not a requirement for aura.
Visual seizures are often briefer and have a different temporal pattern. Gradual spreading positive symptoms lasting 25 minutes followed by the usual headache favor visual aura here.
B. Typical visual aura (Best answer)
Gradual spread, positive visual symptoms, reversibility, and this duration fit the aura pattern.
C. Persistent homonymous hemianopia from completed infarction (Why this does not fit)
The visual symptom fully resolves and evolves gradually rather than remaining fixed.
D. Papilledema-related transient visual obscuration (Why this does not fit)
Those episodes are often brief dimming rather than a spreading scintillating pattern lasting 25 minutes.
Takeaway: Describe the evolution and reversibility of a neurologic symptom before calling it aura.
A. Sympathetic fibers traveling with the internal carotid artery (Why this does not fit)
This pathway is relevant to ocular sympathetic function and Horner findings. Facial parasympathetic output through the pterygopalatine ganglion more directly accounts for tearing and nasal secretion.
B. Oculomotor parasympathetic fibers through the ciliary ganglion (Why this does not fit)
This pathway controls pupillary constriction and accommodation. It does not provide the principal secretomotor supply to lacrimal and nasal glands.
C. Facial-nerve parasympathetic output through the pterygopalatine ganglion (Best answer)
This outflow supplies lacrimal and nasal secretory tissues.
D. Glossopharyngeal parasympathetic fibers through the otic ganglion (Why this does not fit)
That pathway supplies the parotid gland. The lacrimal and nasal secretory response uses the facial-nerve pterygopalatine pathway.
Takeaway: Cluster secretory signs reflect a cranial parasympathetic response.
A. No; the tearing instead favors paroxysmal hemicrania over migraine (Why this does not fit)
Paroxysmal hemicrania produces frequent, much shorter attacks. The 16-hour pulsating nauseating attack with preference for rest still favors migraine.
B. No; cranial autonomic symptoms can accompany migraine, and the whole attack still favors migraine (Best answer)
Long duration, nausea, and activity avoidance remain informative.
C. Yes; tearing never occurs in migraine (Why this does not fit)
That absolute distinction is false.
D. Yes; the autonomic finding should outweigh the attack duration (Why this does not fit)
Tearing is not exclusive to cluster. Duration, associated symptoms and behavior must be interpreted together, and this prolonged attack favors migraine.
Takeaway: Autonomic symptoms are useful but not exclusive to cluster headache.
A. Normal CT excludes RCVS, venous thrombosis, and meningitis as well (Why this does not fit)
The SAH pathway does not automatically exclude all secondary causes.
B. CT angiography is mandatory after every adequate early negative CT in this selected population (Why this does not fit)
The AHA/ASA pathway allows an adequate early CT to exclude aneurysmal SAH in the specified neurologically intact population. Further testing depends on the clinical concern and other possible causes.
C. This can be sufficient to exclude aneurysmal SAH in the specified setting, while other causes still require clinical consideration (Best answer)
The recommendation depends on timing, scan quality, interpretation, and no new deficit.
D. The same conclusion applies to every negative CT obtained several days later (Why this does not fit)
The early timing is central to the evidence.
Takeaway: Know the conditions and limits of the early-CT approach.
A. Prevent early rebleeding by reducing systemic blood pressure (Why this does not fit)
Nimodipine's established role is reducing delayed cerebral ischemia and improving outcome. Preventing rebleeding requires aneurysm-directed management and appropriate hemodynamic care.
B. Reduce delayed cerebral ischemia and improve functional outcome (Best answer)
It addresses a secondary complication of SAH alongside definitive aneurysm care.
C. Replace clipping or coiling as definitive aneurysm treatment (Why this does not fit)
Nimodipine does not secure the aneurysm. Aneurysm treatment and delayed-ischemia prevention address different risks.
D. Treat acute obstructive hydrocephalus (Why this does not fit)
Hydrocephalus requires separate evaluation and, when indicated, CSF diversion. Nimodipine's principal role is prevention of delayed cerebral ischemia.
Takeaway: Nimodipine complements, rather than substitutes for, aneurysm treatment.
A. RCVS remains possible and warrants specialist reassessment, including repeat vascular imaging when indicated (Best answer)
Early angiography may be normal before vasoconstriction becomes demonstrable.
B. The initial angiogram permanently excludes RCVS (Why this does not fit)
The vascular abnormalities may appear later.
C. Treat as primary sexual or exertional headache without further vascular assessment (Why this does not fit)
Recurrent thunderclaps, especially postpartum, warrant evaluation for RCVS and other vascular disease. A benign primary trigger diagnosis cannot replace that assessment.
D. Exclude a vascular cause because several episodes resolved between attacks (Why this does not fit)
Resolution between thunderclaps does not exclude RCVS. Vascular narrowing may evolve and initial imaging can be normal.
Takeaway: Recurrent thunderclap pain can require reassessment after an initially normal vascular study.
A. Moderate-dose oral glucocorticoids as the default for all newly diagnosed patients (Why this does not fit)
ACR/VF conditionally favors high-dose over moderate-dose initial oral treatment in general. Lower dosing may be considered for selected toxicity-risk circumstances, which are not given here.
B. High-dose oral glucocorticoids (Best answer)
Without cranial ischemia, guidance generally favors oral treatment rather than routine IV pulses.
C. IV pulse glucocorticoids for every GCA patient regardless of phenotype (Why this does not fit)
IV pulses are conditionally favored particularly for threatened vision, not universally.
D. Tocilizumab alone without initial glucocorticoids (Why this does not fit)
Guidance supports considering tocilizumab with glucocorticoids, rather than replacing initial glucocorticoid treatment with tocilizumab alone.
Takeaway: GCA steroid route depends on ischemic risk, especially threatened vision.
A. Normal bacterial culture would instantly exclude infection after prior antibiotics (Why this does not fit)
Prior treatment can reduce culture yield; other tests and the clinical picture remain relevant.
B. The pattern strongly supports bacterial meningitis, with microbiologic testing needed to identify the cause (Best answer)
The CSF combination directs urgent treatment but does not specify an organism by itself.
C. Pneumococcus is proved because there is no rash (Why this does not fit)
Rash absence does not identify a bacterial species.
D. Tuberculous meningitis is more likely solely because CSF glucose is low (Why this does not fit)
Low glucose occurs in several infections, but marked neutrophilic pleocytosis in this acute febrile presentation strongly supports bacterial meningitis. Microbiology establishes the cause.
Takeaway: Use the CSF pattern to guide urgency without inventing organism certainty.
A. Idiopathic disease solely because imaging is normal (Why this does not fit)
An identified medication association must be considered before using an idiopathic label.
B. Cerebral venous sinus thrombosis (Why this does not fit)
Venous thrombosis can produce this syndrome, but the stem states that venous imaging excludes it. The newly introduced implicated medicine supports secondary medication-associated intracranial hypertension.
C. Chronic migraine with incidental optic disc swelling (Why this does not fit)
Papilledema and elevated opening pressure require an intracranial-hypertension diagnosis and protection of vision. They cannot be dismissed as incidental migraine findings.
D. Secondary intracranial hypertension associated with an implicated medication (Best answer)
The exposure provides a potential cause that should be reviewed and addressed.
Takeaway: Normal imaging does not make a drug-associated pressure syndrome idiopathic.
A. CGRP-targeting therapies may be considered a first-line preventive option without mandatory prior failures (Best answer)
Treatment choice still depends on the patient and access, but the position no longer requires sequential failure of older classes.
B. Every patient must fail three older classes before CGRP therapy is clinically appropriate (Why this does not fit)
That is not the position statement's requirement.
C. CGRP-targeting prevention is reserved for chronic migraine only (Why this does not fit)
The AHS statement permits these therapies as first-line migraine prevention without that blanket restriction. Suitability still depends on the individual patient and product.
D. Prevention is unnecessary whenever one acute dose sometimes works (Why this does not fit)
Substantial disability can justify prevention despite acute treatment benefit.
Takeaway: Preventive selection should reflect current evidence and individual goals.
Tuberculosis can cause lymphocytic CSF, but often lowers glucose and has a different course. The compatible syndrome and positive enterovirus PCR directly support enteroviral meningitis.
B. Enteroviral meningitis (Best answer)
The organism-specific result and compatible CSF support a viral meningeal infection.
C. Pneumococcal meningitis despite the positive viral PCR (Why this does not fit)
The absent rash does not identify an organism. The microbiologic and CSF findings supplied here favor enterovirus; a clinically suspected bacterial coinfection would require its own evidence.
D. Migraine with aura (Why this does not fit)
An inflammatory CSF profile and pathogen detection are not explained by migraine.
Takeaway: Identify the cause with microbiology rather than assuming every photophobic headache is migraine.
