Headache (Undifferentiated)

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:

• 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]

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]

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]

• 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]

• 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]

• 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]

• 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]

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

• [2][7]

• 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]

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]

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]

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

• 0.2% yield[2]

• 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]

• 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

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]

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

• [1]

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

• [7]

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

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?

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.