Clinical approach to headache

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Clinical Approach to Headache

Overview

Headache is one of the most common complaints in clinical practice. The vast majority of patients have a benign primary headache disorder, but a small proportion have an underlying medical or surgical condition requiring prompt diagnosis. The clinical challenge is identifying the "needle in the haystack" — life-threatening causes hidden among the overwhelming majority of benign presentations — while avoiding the widespread overuse of imaging.

The brain parenchyma itself is insensitive to pain. Pain-sensitive structures include the meninges, cerebral arteries and veins, and tissues lining the skull cavities. Much headache pain, especially vascular and migrainous, is mediated through cranial nerve V (trigeminal), which may refer pain to areas not directly involved. — ROSEN's Emergency Medicine, p. 196

Classification

Category	Examples
Primary	Migraine, tension-type, cluster headache, trigeminal autonomic cephalalgias
Secondary — benign	Post-traumatic, post-LP, cervicogenic, sinusitis, medication overuse
Secondary — emergent	SAH, ICH, meningitis/encephalitis, cerebral venous sinus thrombosis, cervical artery dissection
Secondary — critical/toxic	Carbon monoxide poisoning, temporal arteritis, acute angle-closure glaucoma, hypertensive emergency, preeclampsia, IIH

Step 1: History — The Most Important Tool

Physical findings may be minimal even in serious headache, making the history the cornerstone of evaluation.

Key historical elements:

Onset and pattern — Rapid ("thunderclap") onset reaching maximum intensity within seconds to a minute is highly associated with SAH and other vascular causes. Recurrent headaches similar to prior episodes favor a primary disorder; a marked change in pattern signals a new or serious problem.
Severity and quality — "Worst headache of life" is a red flag even when examination is normal.
Associated symptoms
- Fever → meningitis, encephalitis, abscess
- Nausea/vomiting — nonspecific; present in migraine, raised ICP, glaucoma, and systemic illness
- Visual changes → glaucoma, IIH, posterior circulation stroke, temporal arteritis
- Focal neurological symptoms → hemorrhage, stroke, mass lesion
- Neck stiffness → meningitis, SAH
Onset triggers — Exertion, sexual activity, or Valsalva → coital/exertional headache or SAH
Context — Multiple household members affected simultaneously → carbon monoxide poisoning

Step 2: "Red Flags" (SNOOP4 Mnemonic)

Feature	Possible Cause
Systemic signs (fever, weight loss, HIV, cancer)	Infection, malignancy, temporal arteritis
Neurological deficits (focal)	Mass lesion, hemorrhage, stroke
Onset sudden/thunderclap	SAH, RCVS, ICH
Older age (>50) new headache	Temporal arteritis, mass
Pattern change or progressive worsening	Mass, increasing ICP
Postural component	IIH, CSF leak, venous thrombosis
Precipitated by Valsalva/exertion/sex	SAH, coital/exertional headache
Papilledema	Raised ICP

Red-flag features requiring urgent evaluation, per Bradley & Daroff's Neurology:

New-onset severe headache with no significant headache history
Progression of headaches — increasing frequency or severity
Headache always localized to one area
Headaches in a cancer patient
Headache with fever, altered mental status, or focal neurological deficit — Bradley and Daroff's Neurology in Clinical Practice, p. 793

Step 3: Physical Examination

The examination focuses on:

Mental status (altered → emergency)
Fundoscopy — papilledema (raised ICP), subhyaloid hemorrhage (SAH)
Meningeal signs — Kernig's, Brudzinski's, nuchal rigidity
Cranial nerve examination — particularly CN II, III, IV, VI
Vital signs — fever, hypertension
Temporal artery — tenderness, thickening, or absent pulse (temporal arteritis)

Step 4: Differential Diagnosis by Urgency

Critical (life-threatening)

Subarachnoid hemorrhage (SAH)
Carotid/vertebral artery dissection
Cerebral venous sinus thrombosis
Carbon monoxide poisoning
Temporal arteritis (risk of permanent visual loss)

Emergent

Bacterial meningitis/encephalitis
ICH / subdural / epidural hematoma
Acute angle-closure glaucoma
IIH with impending vision loss
Mass lesion / traction headache
Hypertensive emergency / preeclampsia

Non-emergent (primary)

Tension-type headache
Migraine (with or without aura)
Cluster headache
Post-traumatic headache

Risk factors for emergent causes (selected)

Cause	Key Risk Factors
SAH	Sudden severe pain, exertion/sex trigger, "worst ever," family history, polycystic kidney disease, hypertension
Meningitis	Fever, immunocompromise, sinus/ear infection, age extremes, communal living
Temporal arteritis	Age >50, female sex (4:1), elevated ESR/CRP, jaw claudication
Carbon monoxide	Enclosed space, multiple household members, winter heating
Cerebral venous thrombosis	Female, pregnancy/OCP, prothrombotic state
Acute glaucoma	Age >30, pain in dark, prior history of glaucoma
IIH	Female, obesity, prior benign intracranial hypertension

Step 5: The Ottawa SAH Rule

Apply to patients ≥15 years with non-traumatic headache reaching peak intensity within 1 hour.

Exclusions: New neurological deficit, prior aneurysm, prior SAH, known intracranial mass, chronic recurrent headaches.

If none of the following are present, SAH can be reasonably excluded:

Age >40 years
Neck pain or stiffness
Witnessed loss of consciousness
Onset during exertion
Thunderclap onset (immediate peak pain)
Limited neck flexion

High sensitivity, low specificity — use to reduce unnecessary testing, not as a standalone rule-out tool. — ROSEN's Emergency Medicine, p. 199

Step 6: Diagnostic Algorithm

Fig. 16.1 — Evaluation Algorithm for Headache (ROSEN's Emergency Medicine)

When NO red flags are present: Symptomatic treatment without imaging is appropriate for clinically suspected primary headache (gradual onset, minor severity, no meningeal signs, normal neurology, normal fundoscopy).

When a specific etiology is suspected: Directed testing is indicated (e.g., intraocular pressure for glaucoma, LP for meningitis).

For suspected SAH:

Apply Ottawa SAH Rule
CT within 6 hours of onset: high sensitivity (~99%) for SAH with a 3rd-generation scanner
CT normal + >6 hours from onset: LP and/or CT angiography (CTA)
LP findings in SAH: xanthochromia (CSF yellow discoloration), elevated RBCs that do not clear between tubes

Step 7: Investigations

Test	Indication	Expected Finding
Non-contrast CT head	Suspected SAH, ICH, mass	Blood in subarachnoid/epidural/subdural space, mass, hydrocephalus
CT venogram / MR venogram	Suspected cerebral venous thrombosis	Filling defect in dural sinus
MRI brain (±gadolinium)	Posterior circulation stroke, mass, infection, IIH	Better than CT for posterior fossa
LP	SAH (>6 h), meningitis, IIH	Xanthochromia / RBCs; ↑WBC, ↓glucose, ↑protein; ↑opening pressure
ESR / CRP	Temporal arteritis	ESR >50 mm/h; elevated CRP
Intraocular pressure	Acute angle-closure glaucoma	Elevated IOP
CO-oximetry / carboxyhemoglobin	Carbon monoxide poisoning	Elevated COHb
ECG	SAH	Non-specific ST/T wave changes
CBC	Anemia-related headache	Severe anemia

Most patients with headache do not require neuroimaging. Advanced imaging should be tailored to specific elements of the differential diagnosis, not used as a default. — ROSEN's Emergency Medicine, p. 199

Step 8: Management

Benign primary / non-specific headache

Mild–moderate: NSAIDs (ibuprofen, naproxen), acetaminophen
Moderate–severe migraine: Dopamine antagonists (metoclopramide, prochlorperazine IV/IM); triptans; ketorolac (IV/IM)
Opioids: Not indicated for primary headaches
Non-pharmacological: Rest, moist heat, massage, cognitive behavioral therapy, trigger avoidance

Specific emergent causes

Cause	Initial Management
SAH	Neurosurgical consult, nimodipine, BP control, supportive care
Bacterial meningitis	Empirical antibiotics before LP if meningitis strongly suspected
Temporal arteritis	High-dose corticosteroids (prednisolone) immediately to prevent visual loss
CO poisoning	Remove from source, 100% high-flow O₂
Acute glaucoma	Ophthalmology consult, IOP-lowering agents
ICH	BP control, neurosurgical consult, reversal of anticoagulation

Summary: The Clinical Mindset

Most headaches are benign — avoid reflexive CT scanning for every headache.
A change in pattern is always suspicious — even in a known migraineur.
Thunderclap = SAH until proven otherwise.
Physical examination cannot exclude SAH — a normal neuro exam does not rule it out.
Nausea/vomiting is nonspecific — present in migraine, raised ICP, glaucoma, and systemic illness alike.
"CT before LP" for suspected mass — primarily because CT may give the diagnosis and render LP unnecessary, not because LP definitively causes herniation.

Sources:

ROSEN's Emergency Medicine: Concepts and Clinical Practice — Headache chapter (Walker LE)
Bradley and Daroff's Neurology in Clinical Practice — Imaging in headache
Creasy & Resnik's Maternal-Fetal Medicine — Headache in pregnancy

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