Secondary headache disorders

• A secondary headache is a headache that is a symptom of another disorder of the head, neck, or whole body. It is far less common than migraine or tension-type headache, but missing an urgent cause can be catastrophic.
• Every new or changed headache is screened with the SNNOOP list (systemic symptoms, neoplasm, neurologic deficit, sudden onset, older age, pattern change, positional headache, Valsalva or exercise headache, papilledema, pregnancy, eye pain with autonomic features, trauma, immunosuppression and medication overuse).
• The urgent causes to think of are subarachnoid haemorrhage and other vascular events, meningitis and encephalitis, brain tumour or metastasis, giant cell arteritis, intracranial hypertension (including idiopathic intracranial hypertension) and low cerebrospinal fluid pressure after a spinal tap.
• The history and examination look for red flags first; if none are present and the headache fits a primary pattern, imaging is usually unnecessary.
• Cluster headaches, tension-type headaches and migraines are primary disorders and are not the subject of this page; medication overuse is the commonest secondary headache and is curable with withdrawal of the overused drug.

By the end of this page you should be able to:

1. Define a secondary headache and list the major categories by aetiology, system, or urgency.
2. Screen a new or changed headache with the SNNOOP list and say which red flag points to which cause.
3. Recognise giant cell arteritis, idiopathic intracranial hypertension and post-dural-puncture headache from their clinical clues.
4. Plan investigations in a sensible order and state the imaging indications you should not miss.
5. Manage medication overuse headache, giant cell arteritis, idiopathic intracranial hypertension and post-lumbar-puncture headache through the immediate and definitive steps.
6. Avoid the common traps: treating a tumour headache with painkillers, delaying steroids in giant cell arteritis, and operating on a headache-only patient with intracranial hypertension.

A secondary headache is a headache that is attributed, by the International Classification of Headache Disorders 3 (ICHD-3), to another disorder. The 8 categories cover cranial or systemic disease: trauma to the head or neck; vascular disorders; non-vascular intracranial disease; substance use or withdrawal; infection; a disorder of homeostasis (for example hypoxia, hypertension, hypothyroidism); a disorder of the cranium, neck, eyes, ears, nose, sinuses, teeth or other facial or cervical structure; and a psychiatric disorder. ^[1]

Secondary headaches are less common overall than primary headaches, but they matter because they can kill. In most clinical series the proportion of people with headache who turn out to have a secondary cause ranges from about one in eight in tertiary centres to about one in five in some cohorts, and neurologists worldwide estimate that roughly 18% of people with headache have a secondary cause. ^[1] At the same time, headaches as a whole are usually benign: an emergency department review puts headaches at 3% of emergency department chief complaints and roughly 96% of headaches as benign. ^[2] The emergency clinician's task is not to scan every head but to spot the minority who harbour dangerous disease.

The causes below are those you must think of. They are grouped by a mechanism that you can reason from, not memorised; in practice the groups overlap.

A few population numbers are worth knowing. The worldwide annual incidence of brain tumours is about 3.4 new cases per 100,000 people, with a five-year prevalence of about 6.6 per 100,000; in a headache patient without a history of cancer the chance of finding a brain tumour is under 0.1%, most often after the age of 50 years. ^[1] Intracerebral haemorrhage and ischaemic stroke can also declare themselves with headache, which occurs in roughly a quarter of acute strokes; the annual incidence of stroke is about 300 to 500 per 100,000 people. ^[1] Traumatic brain injury has an annual incidence of 235 to 556 per 100,000 and accounts for 4.8% of emergency department visits in the United States. ^[1] Persistent or worsened headache after even mild injury can still be a secondary headache.

The most practical thing you will use. A red flag is anything that makes a secondary headache more likely than it would be on the prior odds. Do and colleagues proposed the SNNOOP10 list, an expansion of the older SNOOP mnemonic; both are taught, and this page uses SNNOOP10. ^[1] The absence of red flags in a person whose headache fits a primary pattern is the main argument for not imaging.

• S -- Systemic symptoms or disease. Fever, weight loss, night sweats, cancer, pregnancy, HIV, immunosuppression. Fever with headache should make you think of meningitis, encephalitis, brain abscess and systemic vasculitis, but it is usually a respiratory or urinary infection that has nothing to do with the head. ^[1] In advanced HIV the risk of an opportunistic central nervous system infection or malignancy rises markedly when the CD4 count is 200 cells per microlitre or lower. ^[1] Headache is the most common pain problem in HIV, affecting up to 34 to 61% of patients. ^[1]
• N -- Neurological deficit. Confusion, weakness, dysphasia, visual field or eye movement deficit, ataxia, seizure. Headache accompanies about 16 to 65% of transient ischaemic attacks and non-disabling strokes. ^[1] A reversible deficit with a headache may still be migraine with aura, familiar to the patient, and not a red flag on its own; new, persistent or atypical deficits are.
• O -- Onset sudden. Thunderclap headache reaches maximum intensity within one minute and is a red flag for subarachnoid haemorrhage and other vascular or catastrophic causes. In large emergency cohorts of acute severe headache peaking within one hour, subarachnoid haemorrhage was found in 6.2% of patients, a serious neurological condition in roughly one in eight. ^[1] Maximum intensity within five minutes is the cut-off NICE uses to flag urgent assessment. ^[3]
• O -- Older age. New headache after age 50, and especially after 65, carries a higher chance of a secondary cause: in a tertiary headache clinic the rate was 11.2% in patients over 65 years against 8.0% in younger patients. ^[1]
• P -- Pattern change or recent onset of new headache. A change in a previously stable headache, a new daily headache, or a headache lasting under 3 months can be the only sign of an intracranial tumour or cerebral venous thrombosis. ^[1]
• P -- Positional headache. Pain that starts within seconds on standing and settles quickly when the patient lies down is the hallmark of low cerebrospinal fluid (CSF) pressure, most familiar after a lumbar puncture. It can be masked by migraine or other primary headache. ^[1]
• P -- Provoked by sneezing, coughing, straining or exercise. This Valsalva pattern occurs with primary cough headache but is also seen with Chiari malformation, posterior fossa lesions and other structural causes. ^[1]
• P -- Papilledema. Papilledema predicted intracranial abnormalities on MRI and always warrants imaging and ophthalmological assessment. ^[1] Pseudo-papilledema (for example optic nerve head drusen) is common, so document the disc carefully and get an ophthalmologist involved.
• P -- Pregnancy or puerperium. De novo headache during pregnancy carries about a one in three chance of a secondary cause in acute care, most often hypertensive disorders of pregnancy, then pituitary disease; vascular and thrombotic causes dominate. ^[1]
• P -- Painful eye with autonomic features. Red, watery eye with ptosis, miosis or nasal symptoms can be cluster headache, but trigeminal autonomic cephalalgia must be imaged because even typical cases can be secondary to a pituitary or cavernous sinus lesion. ^[1]
• P -- Post-traumatic onset. Headache directly related to trauma is a red flag; chronic post-traumatic headache is an orange flag. The headache usually has the phenotype of migraine or tension-type headache and is treated by phenotype. ^[1]
• P -- Pharmacologic or drug-related headache. Medication overuse is the commonest secondary headache (below), and any new drug can cause headache. ^[1]

The NICE guideline on headaches in people over 12 takes a similar but slightly different approach. It also directs assessment and referral for worsening headache with fever; sudden-onset headache reaching maximum intensity within five minutes; new neurological deficit, cognitive dysfunction, or personality change, or an impaired level of consciousness; recent head trauma, typically within the past three months; cough, Valsalva or sneeze-triggered headache; exercise-triggered headache; orthostatic headache; suspected giant cell arteritis; acute narrow-angle glaucoma; or a substantial change in the characteristics of the headache. ^[3]

S -- Systemic symptoms, signs and disease; N -- Neurologic symptoms and signs; O -- Onset (sudden, abrupt, thunderclap, or after age 40/50); O -- Older (patient over 50, or new onset or changed headache); P -- Pattern change or progressive. ^[1] The longer SNNOOP10 list above is simply a more granular version of the same idea. In practice, either mnemonic is fine; what matters is asking the questions.

Giant cell arteritis (temporal arteritis) is the vasculitis you must not miss in a person over 50 with new headache. It is a chronic inflammatory vasculitis of large and medium-sized arteries, particularly the cranial branches of the carotid artery; the branches involved mean that the most feared complication is anterior ischaemic optic neuropathy and permanent blindness. ^[8] It is closely linked to polymyalgia rheumatica. ^[8]

Who gets it: predominantly people older than 50 (commonly in their seventh and eighth decades), with a female majority. ^[8] The 2025 EULAR recommendations for polymyalgia rheumatica and large-vessel vasculitis direct that all patients with suspected giant cell arteritis be referred to a specialist and assessed within 24 hours. ^[7]

Symptoms. New or changed unilateral temporal or frontal headache that is persistent and often severe; scalp tenderness so that a hair-brush or a pillow hurts; jaw claudication (pain or fatigue of the jaw muscles on chewing) and sometimes tongue claudication; visual symptoms ranging from transient monocular visual loss (amaurosis fugax) to diplopia; and constitutional symptoms (fever, weight loss, night sweats, polymyalgia) with very high inflammatory markers (erythrocyte sedimentation rate or CRP). ^[3] A normal inflammatory marker does not exclude giant cell arteritis, and in a clinically suspicious patient you should treat first.

Examination. Temporal artery tenderness or thickening, an absent or diminished pulse, focal tenderness over the artery, and visual acuity or field loss. Auscultate for bruits if large-vessel disease is suspected. The American College of Rheumatology 1990 criteria (age 50 or above, new headache, temporal artery abnormality on examination, raised erythrocyte sedimentation rate, and an abnormal temporal artery biopsy) give a framework; a new set of ACR/EULAR classification criteria was introduced in 2022. ^[8]

Diagnosis is usually confirmed by temporal artery biopsy (showing granulomatous arteritis with mononuclear infiltrates and giant cells, which is pathognomonic) or by imaging (ultrasound showing a halo sign, PET or MRI of the large vessels), combined with the clinical picture. ^[8] Do not delay treatment for the biopsy; biopsy can still be positive after up to two weeks of steroids, although earlier is better.

Treatment. Start high-dose glucocorticoids immediately in any patient in whom you strongly suspect giant cell arteritis, particularly if there are visual symptoms, while arranging confirmatory investigations. ^[7] The 2025 EULAR recommendations give an induction dose of 40 to 60 mg per day prednisone-equivalent for giant cell arteritis. ^[7] Adjunctive therapy with an interleukin-6 receptor inhibitor (tocilizumab) or upadacitinib is recommended for selected patients, with methotrexate as an alternative, to allow glucocorticoid tapering. ^[7] Antiplatelet therapy is added for selected patients with large-vessel or ocular involvement. ^[8] Plan for a slowly reducing steroid course over many months, with bone protection, and monitor the erythrocyte sedimentation rate and CRP.

Trap: Do not wait for the temporal artery biopsy result before starting steroids when vision is at risk; the biopsy can still be taken within one to two weeks and should not delay treatment by a day.

Idiopathic intracranial hypertension (IIH, pseudotumour cerebri) is raised intracranial pressure without hydrocephalus or a mass lesion, with normal cerebrospinal fluid composition and no identified secondary cause. ^[6] It classically affects younger women of childbearing age with obesity, but men and non-obese patients occur and require deeper investigation for a secondary cause. The age-adjusted and sex-adjusted annual incidence is about 2.4 per 100,000, and the incidence has been rising. ^[6]

A patient typically presents with a progressive, severe, frequent daily headache, often worse on waking or with Valsalva, plus transient visual obscurations, pulsatile tinnitus, diplopia from a sixth nerve palsy, and sometimes transient radicular or back pain. Brain imaging shows nothing, which is the point.

Diagnosis. Confirm the raised intracranial pressure and exclude secondary causes. The consensus from Mollan and colleagues is that urgent MRI of the brain should be done within 24 hours, with CT and CT or MR venography within 24 hours if MRI is unavailable, because cerebral venous sinus thrombosis must be excluded; the MRI then shows empty sella and other signs of raised pressure. ^[6] Magnetic resonance venography is mandatory within 24 hours. ^[6] A diagnostic lumbar puncture in the lateral decubitus position records the opening pressure and normal CSF; the diagnostic cut-off is an opening pressure above 25 cm of CSF, although one measurement in a single position should not be interpreted in isolation. ^[6] Blood pressure must be checked (to exclude malignant hypertension) and the ophthalmic examination documented (visual acuity, pupils, formal visual fields, dilated fundus) for every patient with papilloedema. ^[6] Serum studies and other blood tests exclude anaemia and other secondary causes, particularly in atypical patients (men, children, older adults or those with a normal body mass index).

Management has three principles: treat the underlying disease (obesity), protect vision, and minimise headache morbidity. ^[6]

Weight and underlying cause. Weight loss is the only disease-modifying therapy in typical IIH. ^[6] Weight gain of 5 to 15% in the year before diagnosis is commonly seen, and up to 15% weight loss may be required to induce remission. ^[6] Counsel every patient with a body mass index above 30 kg per square metre about weight management as early and as sensitively as possible; refer to a community or hospital weight-management programme. ^[6] Bariatric surgery has an increasing role for sustained loss, but the evidence in IIH is still observational. ^[6]

Protecting vision. For rapidly deteriorating vision, the acute treatment is surgical: optic nerve sheath fenestration or urgent cerebrospinal fluid diversion, with a temporary lumbar drain as a bridge. ^[6] Ventriculoperitoneal shunting is preferred in the UK on the basis of lower revision rates; programmable valves with antigravity or antisiphon devices reduce low-pressure headaches. ^[6] Neurovascular stenting has an unestablished role. ^[6] Serial lumbar punctures are not recommended. ^[6] Corticosteroids are not recommended for fulminant IIH. ^[6]

Drug treatment for IIH. Acetazolamide (a carbonic anhydrase inhibitor) is the standard medical treatment, although the 2015 Cochrane review found the evidence modest. ^[6] A popular starting dose is 250 to 500 mg twice daily, titrated upwards; the IIH Treatment Trial used up to 4 g daily, of which 44% of participants reached that dose. ^[6] Topiramate is an alternative that also suppresses appetite, starting at 25 mg weekly and building to 50 mg twice daily, with cautions about contraception, mood and cognitive effects. ^[6] Furosemide, amiloride and coamilofruse are used by some clinicians but with uncertain evidence. ^[6]

Headache in IIH. The migrainous phenotype occurs in 68% of IIH patients with headache; non-steroidal anti-inflammatory drugs or paracetamol are used short term, indomethacin has a possible advantage because it lowers intracranial pressure, opioids are not prescribed, greater occipital nerve blocks help some, and lumbar puncture should not be used as headache treatment. ^[6] Acetazolamide has not been shown to be effective for headache alone. ^[6] Early introduction of migraine preventatives is sensible because they take three to four months to work; caution is needed with drugs that increase weight (beta blockers, tricyclics, sodium valproate, pizotifen, flunarizine) or worsen depression. ^[6] Patients must be warned about medication overuse: simple analgesics on more than 15 days per month, or opioids, combined preparations or triptan medication on more than 10 days per month, for more than three months. ^[6]

Cerebrospinal fluid diversion for headache alone is generally not recommended; in follow-up, 68% of patients still had headache at six months and 79% by two years after shunting, and 28% develop low-pressure headaches. ^[6]

Pregnancy. Seek specialist advice before medical, surgical or interventional management of IIH in pregnancy; women of childbearing age must be counselled about teratogenic risks when starting new therapy. ^[6] IIH can be managed in pregnancy, usually with acetazolamide used cautiously and surgical treatment where vision is threatened; lumbar puncture as a treatment is discouraged.

Post-dural-puncture headache (post-lumbar-puncture headache) is low cerebrospinal fluid pressure from a leak at the dural puncture site. It should be suspected with any headache or neurological symptom occurring within five days of a neuraxial procedure; symptoms include neck stiffness, thoracic or lumbar back pain, subjective hearing change, visual disturbance and vertigo, and are characteristically worse upright and better lying flat. ^[9] It is more common in younger patients, particularly women, and in people with a history of headache; smoking appears to reduce its likelihood and body weight does not matter. ^[9]

Prevention at the time of the tap: use non-cutting (pencil-point) spinal needles where possible; if cutting needles are used, insert the bevel parallel to the long axis of the spine; use the smallest needle that is practicable. ^[9] After an inadvertent dural puncture during attempted epidural placement, prophylactic epidural blood patches do not prevent post-dural-puncture headache and are not recommended; the value of routine bed rest is uncertain. ^[9]

Treatment. For all patients, regular analgesia with paracetamol (acetaminophen) and non-steroidal anti-inflammatory drugs is the primary treatment; short-term opioids may be considered if these are ineffective, but not long term. For symptoms within the first 24 hours, up to 900 mg of caffeine per day may be used, reduced to no more than 300 mg per day if the patient is breastfeeding. Oral hydration is usually sufficient. ^[9] Then an epidural blood patch is recommended when the headache impairs daily living or is associated with neurological symptoms despite conservative therapy. ^[9]

Imaging note: brain imaging is considered for a non-orthostatic headache starting more than five days after the suspected puncture, for focal neurological deficits, visual change or altered consciousness, particularly in the postpartum period, to exclude an alternative diagnosis such as cerebral venous sinus thrombosis. ^[9]

Space-occupying lesions. Primary brain tumours have an annual incidence of about 3.4 per 100,000 worldwide, and the five-year prevalence is about 6.6 per 100,000. ^[1] The risk of finding a brain tumour in a headache patient with no history of cancer is under 0.1%; those that are found are usually in patients over 50. ^[1] With a known cancer that metastasises to the brain (lung, breast, malignant melanoma), a new headache is highly suspect for metastasis; in cohorts of cancer patients with new headache, intracranial metastases were found in about one third. ^[1] Oncological patients with new headache should therefore be imaged, and in a new headache with a neurologic deficit, cognitive dysfunction, a change in personality, or impaired consciousness, image at once. ^[3]

Infection. Bacterial meningitis occurs at an annual incidence of 0.7 to 1.38 per 100,000, viral meningitis at 4.7 to 7.6 per 100,000 in adults (27.8 per 100,000 in children under 14 and 219 per 100,000 in infants under one year), acute encephalitis at 6.4 to 7.4 per 100,000, and brain abscesses at 1.3 per 100,000 in developed countries. ^[1] The combination of headache with fever should make you exclude neuroinfection, but fever accounted for only 4.8% of emergency department consultations in the United States and most febrile patients have pneumonia or urinary infection. ^[1] In bacterial meningitis, headache occurs in 52 to 87% of cases, fever in 77 to 97% and neck stiffness in 50 to 88%; the classic triad of fever, neck stiffness and altered consciousness is present in only 21 to 67% of confirmed cases, and in viral meningitis the triad never occurred in a ten-year cohort. ^[1] In herpes simplex encephalitis, headache is present in 79% and fever in 87%; in brain abscess the frequency of headache is 49 to 81% and of fever 29 to 57%. ^[1] Consequently, a lack of fever or neck stiffness never excludes meningitis when the clinical picture argues for it. Brain abscesses are rare but must not be missed after cyanotic heart disease, endocarditis, immunosuppression, chronic ear disease or trauma.

Initial management of suspected infection or tumour is empirical where appropriate (antibiotics and aciclovir while awaiting results, corticosteroids where indicated by oncology or neurosurgical advice) and then the definitive disease-specific management, with neuroimaging before any lumbar puncture in the absence of a normal CT. See also the chapter on stroke if focal deficits dominate.

Medication overuse headache is the commonest secondary headache. It is a chronic headache disorder that develops in a patient with a pre-existing primary headache (usually migraine or tension-type), driven by too-frequent use of acute treatment; it is defined as headache on 15 or more days per month for at least three months in such a person. ^[10] The threshold for overuse is medication-specific: simple analgesics or non-steroidal anti-inflammatory drugs taken on 15 or more days per month, or triptans, combination analgesics, ergots, opioids or barbiturate-containing preparations taken on 10 or more days per month, for three months or more. ^{[3] [10]}

The prevalence of medication overuse headache in the adult population is 0.5 to 7.2%, and it is more common in women aged 40 to 50 years. ^[1] Withdrawal of the overused medication can turn chronic headache back to episodic headache in up to 70% of patients. ^[1]

The 2020 European Academy of Neurology guideline on medication overuse headache puts education and counselling first in a multidisciplinary team of a neurologist or pain specialist with a behavioural psychologist. ^[5] If education alone fails, the overused drug is withdrawn and effective migraine prevention is started; if prevention alone does not work, drug withdrawal follows. ^[5] Simple analgesics, ergots and triptans can usually be stopped abruptly or restricted to two days per week (no more than ten days per month); opioids, barbiturates and tranquilisers are tapered slowly over at least a month; withdrawal can be done in the outpatient, day-case or inpatient setting. ^{[5] [6]} NICE recommends that all overused acute medication is stopped for at least one month, abruptly rather than gradually, with close follow-up and support, a review at four to eight weeks, and prophylactic treatment for the underlying headache. ^[3] Inpatient withdrawal is not routine and is reserved for strong opioids, significant comorbidity or failed outpatient attempts. ^[3]

The trap here is to add ever more acute analgesia (or opioids) to a chronic headache without addressing the overuse; the only cure is withdrawal.

The flowchart below sets out the approach. The two decisions that matter are whether any red flag is present, and, if so, which cause it points to.

Imaging indications. Do not scan everyone; too many scans only create incidental findings. At the same time, do not miss a real indication. The following should make you image (or refer) a person with headache:

• From the Do (red-flag) review: an abnormal neurological examination, focal deficit, thunderclap headache, headache after age 50 that is new or changed, headache radiating to the neck, trigeminal (periorbital) pain, persistent or positional headache, temporal headache over the age of 55, and new headache in preschool children or in children with disability. ^[1]
• From NICE: new-onset neurological deficit, cognitive dysfunction or change in personality; impaired consciousness; new headache in someone with compromised immunity (HIV, immunosuppressants), or under 20 with a history of cancer, or with a cancer that metastasises to the brain; vomiting without obvious cause; sudden-onset headache within five minutes; recent head trauma; cough, Valsalva or exercise trigger; orthostatic headache; suspected giant cell arteritis; acute glaucoma; or a substantial change in the headache. ^[3]
• From the American Academy of Neurology quality measure on neuroimaging in primary headache: head trauma, new or changed headache over 50 years, abnormal neurological examination, thunderclap headache, headache radiating to the neck, trigeminal pain, persistent and positional headaches, temporal headaches over 55 years, new onset headache in preschool children (under 6 years) or in paediatric patients with disabilities, and occipital headache in children. ^[4]
• In practice the two short lists above are very similar; in doubt, or where the clinical picture does not fit a primary headache, image or refer.

Low-resource settings: a funded MRI or CT is often unavailable. The most useful screening is still the history and examination using SNNOOP, fundoscopy where possible, and blood pressure; basic CT is adequate for most emergencies (haemorrhage, hydrocephalus, large mass or abscess); MRI is reserved for suspected low-grade tumour, posterior fossa or cryptogenic stroke; and if nothing can be imaged, look again at the red flags and refer. If giant cell arteritis is suspected and steroids cannot be continued long term, refer.

Management splits into the immediate measures that keep the patient safe (in the first minutes to hours) and the definitive measures that change the course of the disease.

Immediate. Airway and intravenous access when indicated; analgesia that does not mask a new deficit in a suspicious patient (keep reassessment); high-flow oxygen and a non-rebreathing mask for cluster headache (not this page's subject but part of the emergency headache picture); start empiric antibiotics and aciclovir when bacterial meningitis or herpes encephalitis is plausible without waiting for the tap; start high-dose glucocorticoids immediately for suspected giant cell arteritis, particularly with visual symptoms; control blood pressure for malignant hypertension; analgesia and antiemetics and refer for imaging when red flags persist without a diagnosis.

Definitive. Withdraw the overused drug and start prevention for medication overuse; high-dose steroids then a taper over months, plus tocilizumab or methotrexate where indicated, for giant cell arteritis; weight loss, acetazolamide or topiramate and protection of vision (fenestration or shunt where threatened) for idiopathic intracranial hypertension; conservation and (if needed) an epidural blood patch for post-lumbar-puncture headache; urgent neurosurgical or oncological management for tumour or abscess; targeted infection treatment guided by culture.

Pregnancy and puerperium. Headache in pregnancy has a secondary cause in roughly one third of patients presenting to acute care, most often hypertensive disorders of pregnancy (including pre-eclampsia), then pituitary disease, and vascular and thrombotic causes. ^[1] Visual change, abdominal pain, oedema or hypertension make this an emergency. For idiopathic intracranial hypertension in pregnancy, specialist advice is needed before medical or surgical treatment. ^[6]

Children. Children can present with papilledema, vomiting and a sixth nerve palsy rather than a description of headache; imaging before explanation is the rule, and IIH in children is usually idiopathic but secondary causes (medications, endocrine disease, venous thrombosis, obesity in teenagers) need excluding. Papilledema in children is often pseudo-papilledema.

Older adults. New headache after the age of 65 has a higher rate of secondary causes, particularly giant cell arteritis, cardiovascular and cerebrovascular disease, infection, polymyalgia and malignancy. ^[1] Temporal headache after 55 is a red flag. ^{[1] [4]}

Immunocompromised patients. Headache with fever in a person with HIV, on chemotherapy or immunosuppressants prompts imaging and lumbar puncture, empiric antibiotics and aciclovir, and consideration of opportunistic infection; cryptococcal, toxoplasma, tuberculous and other infections dominate, and in advanced immunosuppression (CD4 count 200 or under) the risk of opportunistic central nervous system infection is high. ^[1]

• Writing off a new headache in an older patient as "migraine" or "sinus headache", and so missing giant cell arteritis or temporal arteritis; jaw claudication, visual symptoms or a palpable temporal artery in a patient over 50 should make you start steroids the same day.
• Delaying steroids in giant cell arteritis while awaiting the biopsy or inflammatory markers; vision can be lost permanently over days, and treatment can be started without waiting. ^[7]
• Giving anticoagulation or antiplatelet agents instead of starting steroids, or doing neither, for a headache with raised erythrocyte sedimentation rate; neither anticoagulation nor discharging the patient is acceptable when giant cell arteritis is likely.
• For idiopathic intracranial hypertension, starting acetazolamide without a proper investigation, performing a lumbar puncture without papilledema and without analysis, or trying serial "therapeutic" lumbar punctures, which are short lived, can cause chronic back pain and do not induce remission. ^[6]
• Shunting or stenting a patient whose only problem is headache; cerebrospinal fluid diversion is generally not recommended for headache alone in idiopathic intracranial hypertension, and post-shunt headaches are common. ^[6]
• Treating a metastatic headache with ever stronger analgesia while missing the cancer; new headache in a person with a cancer that seeds the brain needs imaging, and imaging the head first. ^[1]
• Forgetting medication overuse in a patient with daily headache who is taking triptans or paracetamol on most days; the headache will not respond to escalation of preventive treatment until the overused drug is withdrawn. ^{[3] [5]}
• Performing a lumbar puncture for a post-dural-puncture headache when the headache is non-orthostatic, starts more than five days later, or is associated with focal neurological signs; in that setting image first to exclude thrombosis. ^[9]
• Using cutting spinal needles, or not aligning the bevel with the fibres, or routinely ordering "prophylactic" epidural blood patches after an inadvertent dural puncture, which the guidelines do not support. ^[9]
• Reassuring a patient with red flags by a negative CT; CT misses many things, and a normal scan never rules out early giant cell arteritis or intracranial hypertension.

• A secondary headache is a symptom of another disorder. Most headaches are benign, but the dangerous minority is recognised by red flags, not by how bad the pain is.
• Screen every new or changed headache with SNNOOP10: systemic symptoms or disease; neurological deficit; sudden or thunderclap onset; older age or new onset over 50; pattern change; positional; provoked by Valsalva or exercise; papilledema; pregnancy or puerperium; painful eye with autonomic features; post-traumatic; immunosuppression; medication overuse.
• Thunderclap headache that peaks within one minute (NICE within five minutes) carries a high risk of vascular catastrophe, especially subarachnoid haemorrhage, which was found in about 6.2% of severe acute headache in emergency cohorts.
• Infection is usually viral meningitis (annual incidence 4.7 to 7.6 per 100,000 adults) rather than a brain abscess; the triad of fever, neck stiffness and altered consciousness is absent in many bacterial and in all studied viral cases.
• Brain tumour is under 0.1% in an unselected headache patient without cancer, and about 3.4 per 100,000 annually in total; with cancer that seeds the brain, new headache is metastasis until proven otherwise.
• Medication overuse headache (prevalence 0.5 to 7.2%) is the commonest secondary headache; it is defined by overuse thresholds of 15 days per month for simple analgesics and NSAIDs, and 10 days per month for triptans, opioids, ergots and combination preparations, each for three or more months. Withdrawal cures most cases.
• Giant cell arteritis affects people over 50; start glucocorticoids 40 to 60 mg prednisone-equivalent per day immediately when suspicion is high, refer within 24 hours, and arrange biopsy or imaging.
• Idiopathic intracranial hypertension: protective vision is the priority; MRI and MR venography within 24 hours, opening pressure above 25 cm of CSF, acetazolamide starting at 250 to 500 mg twice daily up to 4 g daily, and weight loss as the only disease-modifying therapy. Avoid lumbar puncture or shunting as headache treatment.
• Post-dural-puncture headache arises within five days of a puncture, is orthostatic, and is treated first with paracetamol and NSAIDs plus caffeine up to 900 mg per day in the first 24 hours, then with an epidural blood patch if daily life is impaired. Non-cutting needles and small gauge reduce risk.
• Image when red flags are present, and do not image solely to reassure; when a red flag is present, image or refer with urgency proportionate to the suspected cause.

Primary headache disorders, including migraine, tension-type headache and cluster headache. Meningitis and encephalitis. Subarachnoid haemorrhage and intracerebral haemorrhage. Stroke: overview and management. Brain tumours. Polymyalgia rheumatica. Idiopathic intracranial hypertension is also a common topic in its own right. Emergency headache pathways and analgesia. Ophthalmology and papilledema. Rheumatology of giant cell arteritis.