Headache disorders affect approximately 90% of people during their lifetime and are the fourth leading cause of ED visits in the US. [1] The primary goal in evaluating undifferentiated headache is to rapidly distinguish primary headaches (tension-type, migraine, cluster) from dangerous secondary causes requiring emergent intervention. [1-2]
The following figure from the AAFP provides a clinical decision algorithm for evaluating new headache presentations:
1. History
- Onset: Sudden/thunderclap (peak within seconds–minutes) vs. gradual; age at first onset (new headache after age 50 is a red flag) [1][3]
- Location: Unilateral (migraine, cluster, TACs) vs. bilateral (tension-type); orbital/temporal (cluster) [2]
- Character: Pulsating/throbbing (migraine) vs. pressing/tightening (tension-type) vs. boring/stabbing (cluster) [2]
- Duration: 30 min–7 days (tension-type), 4–72 hours (migraine), 15 min–3 hours (cluster) [2]
- Severity: Mild-moderate (tension-type), moderate-severe (migraine), severe (cluster) [2]
- Associated symptoms: Nausea/vomiting, photophobia, phonophobia, aura, autonomic features (lacrimation, rhinorrhea, ptosis), neck stiffness, fever [1-2]
- Aggravating/alleviating factors: Worsened by activity (migraine), positional (intracranial hypo/hypertension), cough/Valsalva (posterior fossa lesion) [2]
- Timing: Predictable pattern (menstrual migraine), nocturnal clusters, morning headache (raised ICP) [2]
- Important negatives: No fever, no neck stiffness, no visual changes, no weakness, no altered consciousness, no recent trauma [2-3]
2. Alarm Features (Red Flags — SNNOOP10)
Use the SNNOOP10 mnemonic to screen for secondary causes: [2-3]
- Thunderclap headache (peak intensity within seconds): SAH, RCVS — >40% pretest probability for serious pathology [2]
- Fever + meningismus: Meningitis/encephalitis [4]
- Papilledema ± focal neurologic signs or impaired consciousness: Intracranial mass, IIH [2]
- New neurologic deficit: Stroke, mass lesion, CNS infection [2]
- Onset after age 50: Giant cell arteritis, neoplasm [1]
- Pattern change or new headache type: Mass lesion, medication overuse [2]
- Positional headache: CSF leak, intracranial hypo/hypertension [2]
- Precipitated by cough/exertion/Valsalva: Posterior fossa lesion (Chiari), SAH [2]
- Progressive headache: Mass lesion [2]
- Pregnancy/postpartum: Preeclampsia, CVT, RCVS [2][5]
- Painful eye with autonomic features: Acute angle-closure glaucoma, cavernous sinus pathology [2]
- Immunosuppression: Opportunistic infection, abscess [2][6]
- Anticoagulant use: Intracranial hemorrhage [1]
3. Medications
Medications that contribute to headache
- Medication overuse headache (MOH): Analgesics ≥15 days/month, triptans/ergots/opioids/combination analgesics ≥10 days/month [1][7]
- Opioids and barbiturate combinations carry the highest MOH risk; triptans carry relatively lower risk [7]
- Nitrates, PDE5 inhibitors, oral contraceptives, and calcium channel blockers can cause headache [2]
Common acute treatments
- Tension-type: Acetaminophen 1000 mg, ibuprofen 400 mg, naproxen 550 mg [1]
- Migraine (outpatient): NSAIDs first-line → triptans (rizatriptan 10 mg, sumatriptan 50–100 mg PO or 6 mg SC) → gepants (ubrogepant, rimegepant) or lasmiditan if triptans fail/contraindicated [1][8-9]
- Migraine (ED parenteral): Prochlorperazine 10 mg IV (Level A — must offer), metoclopramide 10 mg IV (Level B), ketorolac 15–30 mg IV, dexamethasone 8–10 mg IV for recurrence prevention [10]
- Cluster: High-flow O₂ (12–15 L/min via non-rebreather × 15 min), sumatriptan 6 mg SC [2]
Contraindicated medications
- Triptans/ergots: Contraindicated in CAD, prior stroke, PAD, uncontrolled HTN, multiple cardiovascular risk factors [1][8]
- Opioids: Must NOT be offered for migraine in the ED (Level A — must not offer per AHS 2025) [10]
- NSAIDs: Caution with renal disease, GI bleeding, cardiac comorbidities [8]
4. Diet
- Common dietary triggers (evidence strongest for alcohol and caffeine): Alcohol (especially red wine), caffeine withdrawal or excess (≥3 servings/day), aged cheeses, processed meats (nitrites), chocolate, MSG, artificial sweeteners (aspartame) [11-13]
- Caffeine: Withdrawal triggers headache; moderate intake (1–2 servings/day) may be protective; ≥3 servings/day associated with migraine onset [12]
- Hydration: Dehydration is an underrecognized trigger; increased water intake associated with reduced headache frequency [12]
- Dietary approaches: Ketogenic diet and DASH diet have average-quality evidence for reducing migraine frequency, duration, and severity [14]
- Patient beliefs about food triggers have low positive predictive value — food cravings may be premonitory symptoms misattributed as triggers [12]
5. Review of Systems
- Neurologic: Visual changes (aura, diplopia, field cuts), weakness, numbness, speech difficulty, altered consciousness, seizures
- Ophthalmologic: Eye pain, redness, blurred vision, halos (acute glaucoma)
- ENT: Nasal congestion, rhinorrhea, facial pressure (sinusitis vs. migraine autonomic features)
- Systemic: Fever, weight loss, night sweats (infection, malignancy, GCA)
- Vascular: Jaw claudication, scalp tenderness, visual loss (GCA in age >50) [1]
- Psychiatric: Depression, anxiety (comorbid with chronic migraine; risk factor for chronification) [1]
- Musculoskeletal: Neck pain, limited cervical ROM (cervicogenic headache) [7]
6. Collateral History and Family History
- Collateral: Witnessed LOC, seizure activity, behavioral changes, confusion — critical for SAH, meningitis, and encephalitis workup [15]
- Family history: Migraine has strong genetic predisposition; family history of aneurysmal SAH increases suspicion [1][16]
- Social context: Occupation, stress, sleep habits, substance use (alcohol, caffeine, illicit drugs), recent travel (infectious etiologies)
- Pregnancy/postpartum status — critical for CVT, preeclampsia, RCVS risk stratification [5][17]
7. Risk Factors
- Migraine: Female sex, age 20–50, family history, obesity, depression/anxiety, sleep disorders, excessive caffeine, medication overuse [1]
- Tension-type: Stress, poor posture, sleep deprivation, anxiety/depression [1]
- Cluster: Male sex (3:1), tobacco use, alcohol during cluster periods [2]
- SAH: Hypertension, smoking, heavy alcohol use, family history of aneurysm, polycystic kidney disease, connective tissue disorders [16]
- CVT: Oral contraceptives/estrogen (8-fold increased odds), pregnancy/puerperium, thrombophilia (factor V Leiden, protein C/S deficiency), malignancy, autoimmune disease, recent infection, dehydration [17-18]
- GCA: Age >50, polymyalgia rheumatica [1]
8. Differential Diagnosis
Most likely (primary headaches)
- Tension-type headache — most common overall; bilateral, pressing, mild-moderate, not worsened by activity [2]
- Migraine — most common disabling headache presenting to care; unilateral, pulsating, moderate-severe, with nausea/photo/phonophobia [1-2]
- Medication overuse headache — ≥15 headache days/month with regular overuse of acute medications [7]
- Cervicogenic headache — associated with neck pain and limited cervical ROM [7]
Cannot-miss (secondary headaches)
- Subarachnoid hemorrhage — thunderclap headache, "worst headache of life"; ~5% of acute-onset headaches in ED [16][19]
- Bacterial meningitis/encephalitis — headache + fever + neck stiffness + altered mental status (classic triad present in only 40–50%) [4]
- Intracranial mass (tumor, abscess) — progressive headache, focal deficits, papilledema [2]
- Cerebral venous sinus thrombosis — subacute progressive headache (90%), often in young women on OCP; may present with seizures, focal deficits [17-18]
- Acute angle-closure glaucoma — eye pain, injection, blurred vision, halos, mid-dilated fixed pupil [2]
- Giant cell arteritis — new headache in age >50, jaw claudication, scalp tenderness, visual symptoms; ESR/CRP elevated [1]
Other mimics
9. Past Medical History
- Prior headache type and pattern (established migraine vs. new headache — pattern change is a red flag) [2]
- Previous episodes of similar headache (strongly associated with primary headache; OR 2.7) [6]
- History of cancer (brain metastases), HIV/immunosuppression (opportunistic CNS infections) [1-2]
- Coagulopathy or anticoagulant use (intracranial hemorrhage risk) [1]
- Prior neurosurgery, LP, or head trauma (post-traumatic headache, CSF leak) [2]
- Psychiatric history (depression, anxiety — comorbid with chronic migraine) [1]
10. Physical Exam
Vital signs
Focused neurologic exam
- Mental status, cranial nerves (especially pupil reactivity, visual fields, extraocular movements, facial symmetry), motor/sensory, cerebellar testing, gait
- Fundoscopy: Papilledema (raised ICP), subhyaloid hemorrhage (SAH) [2]
- Neck: Stiffness/meningismus (meningitis, SAH); Kernig and Brudzinski signs have poor sensitivity (5–30%) but high specificity [4]
- Temporal arteries: Tenderness, reduced pulsation, nodularity (GCA) [1]
Focused exam maneuvers
- Jolt accentuation: Worsening of headache with rapid horizontal head rotation — sensitive but not specific for meningitis
- Cervical ROM: Limited ROM with provocation reproducing headache (cervicogenic) [7]
- Eye exam: Conjunctival injection, corneal haziness, mid-dilated fixed pupil (acute glaucoma) [2]
Expected vs. concerning findings
- Normal neurologic exam with recurrent stereotyped headache → likely primary headache [2]
- Any focal neurologic deficit, papilledema, or altered consciousness → warrants urgent imaging [1-2]
11. Lab Studies
Recommended labs (when secondary cause suspected)
- CBC, CMP: Baseline; infection, metabolic derangement
- ESR and CRP: Mandatory if GCA suspected (age >50 with new headache); ESR typically >50 mm/hr [1-2]
- Blood cultures: Before antibiotics if meningitis suspected [20]
- Coagulation studies: If LP planned or anticoagulant use
- Pregnancy test: All women of reproductive age (preeclampsia, CVT risk) [2]
- D-dimer: May have a role in CVT screening but not definitive [17]
CSF analysis (when LP indicated)
- Cell count, protein, glucose, Gram stain, culture, PCR panel (sensitivity ~90%, specificity ~97%) [20]
- Opening pressure (elevated in meningitis, IIH, CVT) [4]
- Xanthochromia (SAH — develops 6–12 hours post-hemorrhage; best detected by spectrophotometry) [21]
- RBC count that does not decline tube 1 to tube 4 (SAH vs. traumatic tap) [21]
12. Imaging
First-line
- Non-contrast CT head98.7% sensitivity for SAH within 6 hours[16][21-22]
When CT is insufficient
- CT + LP: Standard pathway if SAH suspected and CT negative, especially >6 hours from onset [19][23]
- CT angiography (CTA): If SAH confirmed → identify culprit aneurysm; ACEP allows CT-CTA as alternative to CT-LP (weak recommendation), but AHA/ASA 2023 strongly favors CT-LP [19][23]
Gold standard / advanced imaging
- MRI brain with/without contrast: Preferred for non-emergent concerning features — mass lesions, posterior fossa pathology, CVT, encephalitis, cervicomedullary lesions [2]
- MR venography (MRV) or CT venography (CTV): Diagnostic for CVT [17]
- Digital subtraction angiography (DSA): Gold standard for aneurysm characterization [24]
When imaging is unnecessary
13. Special Tests
- Ottawa SAH Rule: Age ≥40, neck pain/stiffness, witnessed LOC, onset during exertion, thunderclap headache, limited neck flexion — 100% sensitive, 15% specific; rules out need for further testing if ALL criteria absent in alert patients ≥15 years with sudden severe headache [15][23]
- ID Migraine screening: Light sensitivity + nausea/vomiting + activity-limiting headache (≥2 of 3 positive = likely migraine) [2]
- Greater occipital nerve block (GONB): Level A — must offer in ED for migraine requiring parenteral therapy [10]
- Temporal artery biopsy: Gold standard for GCA diagnosis
- Lumbar puncture: Diagnostic for meningitis, SAH (post-CT), IIH; obtain CT first if focal deficits, seizures, immunocompromise, or altered consciousness [4]
14. ECG
- Indications: Before administering triptans in patients with cardiovascular risk factors; before IV prochlorperazine/haloperidol/droperidol (QTc prolongation risk) [10]
- Dangerous patterns: ST changes (if considering triptan use in borderline cardiovascular patients), prolonged QTc (dopamine antagonist use)
- Not routinely indicated for primary headache evaluation
15. Assessment
Clinical summary framework
- The vast majority (~60%) of ED headache presentations are primary headaches; ~32% are secondary [6]
- The key clinical task is risk stratification: Does this headache have features suggesting a life-threatening secondary cause?
- Fulfilling ICHD-3 criteria for a primary headache strongly predicts a primary etiology (OR 18.7) [6]
- History of similar prior episodes and known migraine diagnosis are strong "green flags" [6]
Severity stratification
- Emergent: Thunderclap headache, fever + meningismus, papilledema + focal deficits, impaired consciousness, acute glaucoma [2]
- Urgent: New headache age >50 (GCA), progressive/atypical pattern, positional, immunocompromised [2]
- Non-urgent: Recurrent stereotyped headache meeting primary headache criteria with normal exam [2]
Complications to consider
- Status migrainosus (migraine >72 hours)
- Migrainous infarction (rare)
- MOH from escalating analgesic use
- Rebleeding in missed SAH (4% within 24 hours, up to 50% within 6 months) [16]
16. Treatment Plan
Initial stabilization (ED)
- ABCs, IV access if ill-appearing
- Treat pain and nausea promptly — delays worsen outcomes
ED migraine treatment (per AHS 2025 guidelines): [10]
- Prochlorperazine 10 mg IV + diphenhydramine 25 mg IV (to prevent akathisia/EPS) — Level A
- Greater occipital nerve block — Level A
- Ketorolac 15–30 mg IV — Level B
- Metoclopramide 10 mg IV — Level B (if prochlorperazine unavailable)
- Sumatriptan 6 mg SC — Level B
- Dexamethasone 8–10 mg IV — Level C (for recurrence prevention, not acute pain)
- Avoid opioids (hydromorphone IV — Level A must NOT offer) [10]
Tension-type headache
Cluster headache
- High-flow O₂ 12–15 L/min × 15 min via non-rebreather
- Sumatriptan 6 mg SC or zolmitriptan 5 mg nasal spray [2]
Outpatient migraine
- Stepped care: NSAIDs → triptans → gepants/lasmiditan [1][9]
- Consider preventive therapy if ≥4 headache days/month, significant disability, or medication overuse [1]
MOH management
17. Disposition
Admission criteria
- Confirmed or suspected SAH, meningitis, encephalitis, CVT, intracranial mass with mass effect
- Status migrainosus refractory to ED treatment
- Altered mental status, new focal neurologic deficits
- Inability to tolerate oral intake (intractable vomiting)
- Need for serial neurologic exams or ongoing IV therapy
Observation indications
- Awaiting LP results or advanced imaging
- Partial response to ED treatment with need for repeat dosing
- Diagnostic uncertainty with concerning features
Discharge criteria
- Pain adequately controlled
- Able to tolerate PO
- Normal neurologic exam
- No red flags identified
- Reliable follow-up arranged
- Clear return precautions given
Specialist consultation triggers
- Neurosurgery: SAH, intracranial hemorrhage, mass with mass effect
- Neurology: New focal deficits, suspected CVT, refractory/atypical headache, status migrainosus, TACs
- Ophthalmology: Papilledema, suspected acute glaucoma [2]
- Infectious disease: CNS infection in immunocompromised patient
18. Follow Up / Return Precautions
Follow-up timing
- Primary headache with good ED response: PCP or headache specialist within 1–2 weeks
- New headache requiring outpatient MRI: Neurology follow-up within 1–4 weeks
- Post-LP headache evaluation: 48–72 hours [25]
Symptoms requiring immediate return
- Sudden severe "worst headache of life"
- New weakness, numbness, vision loss, speech difficulty, or confusion
- Fever with worsening headache or neck stiffness
- Seizure
- Worsening or persistent vomiting preventing oral intake
- Headache progressively worsening despite prescribed treatment
Patient counseling points
- Avoid overuse of OTC analgesics (≤2 days/week to prevent MOH) [7]
- Maintain regular sleep, hydration, meals, and exercise
- Identify and avoid personal triggers (headache diary recommended) [12]
- Migraine is a neurologic disease, not "just a headache" — effective preventive treatments exist [1]
Expected recovery course
- Tension-type and migraine attacks typically resolve within hours to days with appropriate treatment
- Referral to headache specialist if ≥4 headache days/month or escalating frequency [1][25]
Would you like me to expand on any specific section — for example, the ED treatment algorithm in more detail, preventive migraine therapies, or the workup for a specific secondary cause like SAH or CVT?
References
1. Diagnosis and Management of Headache: A Review. — Robbins MS. The Journal of the American Medical Association. 2021.
2. Acute Headache in Adults: A Diagnostic Approach. — Viera AJ, Antono B. American Family Physician. 2022.
3. Red and Orange Flags for Secondary Headaches in Clinical Practice: SNNOOP10 List. — Do TP, Remmers A, Schytz HW, et al. Neurology. 2019.
4. Community-Acquired Bacterial Meningitis. — van de Beek D, Brouwer MC, Koedel U, Wall EC. Lancet. 2021.
5. Diagnosis of Acute Neurological Emergencies in Pregnant and Post-Partum Women. — Edlow JA, Caplan LR, O'Brien K, Tibbles CD. The Lancet. Neurology. 2013.
6. Headache at the Emergency Room: Etiologies, Diagnostic Usefulness of the ICHD 3 Criteria, Red and Green Flags. — Munoz-Ceron J, Marin-Careaga V, Peña L, Mutis J, Ortiz G. PloS One. 2019.
7. Management of Headache (2023). — Jane Abanes PhD DNP MSN/Ed PMHCNS PMHNP-BC RN, Natasha M. Antonovich PharmD BCPS, Andrew C. Buelt DO, et al Department of Veterans Affairs. 2023.
8. Acute Treatments for Episodic Migraine in Adults: A Systematic Review and Meta-analysis. — VanderPluym JH, Halker Singh RB, Urtecho M, et al. The Journal of the American Medical Association. 2021.
9. Migraine. — Ashina M. The New England Journal of Medicine. 2020.
10. 2025 Guideline Update to Acute Treatment of Migraine for Adults in the Emergency Department: The American Headache Society Evidence Assessment of Parenteral Pharmacotherapies. — Robblee J, Minen MT, Friedman BW, et al. Headache. 2025.
11. Diet and Headache: Part 1. — Martin VT, Vij B. Headache. 2016.
12. Lifestyle Factors and Migraine. — Seng EK, Martin PR, Houle TT. The Lancet. Neurology. 2022.
13. The Role of Diet and Nutrition in Migraine Triggers and Treatment: A Systematic Literature Review. — Hindiyeh NA, Zhang N, Farrar M, et al. Headache. 2020.
14. Diet and Migraine: What Is Proven?. — Gazerani P. Current Opinion in Neurology. 2023.
15. Management of Patients With Aneurysmal Subarachnoid Hemorrhage: Guidelines From the AHA and ASA. — Arnold MJ. American Family Physician. 2024.
16. Spontaneous Subarachnoid Haemorrhage. — Claassen J, Park S. Lancet. 2022.
17. Diagnosis and Management of Cerebral Venous Thrombosis: A Scientific Statement From the American Heart Association. — Saposnik G, Bushnell C, Coutinho JM, et al. Stroke. 2024.
18. Cerebral Venous Thrombosis. — Ropper AH, Klein JP. The New England Journal of Medicine. 2021.
19. Shifts in Diagnostic Testing for Headache in the Emergency Department, 2015 to 2021. — Mark DG, Horton BH, Reed ME, Kaiser Permanente CREST Network Investigators. JAMA Network Open. 2024.
20. Aseptic and Bacterial Meningitis: Diagnosis, Treatment, and Prevention. — Krebs L, Durden B, Saguil A. American Family Physician. 2026.
21. Nontraumatic Subarachnoid Hemorrhage and Ruptured Intracranial Aneurysm: Recognition and Evaluation. — Kane SF, Butler E, Sindelar BD. American Family Physician. 2023.
22. Management of Patients Presenting to the Emergency Department With Sudden Onset Severe Headache: Systematic Review of Diagnostic Accuracy Studies. — Walton M, Hodgson R, Eastwood A, et al. Emergency Medicine Journal : EMJ. 2022.
23. 2023 Guideline for the Management of Patients With Aneurysmal Subarachnoid Hemorrhage: A Guideline From the American Heart Association/American Stroke Association. — Hoh BL, Ko NU, Amin-Hanjani S, et al. Stroke. 2023.
24. Subarachnoid Hemorrhage. — Lawton MT, Vates GE. The New England Journal of Medicine. 2017.
25. Acute Headache Management in Emergency Department. A Narrative Review. — Giamberardino MA, Affaitati G, Costantini R, Guglielmetti M, Martelletti P. Internal and Emergency Medicine. 2020.