Headache

Last updated: January 12, 2023

Summary

Headache is a symptom commonly encountered in everyday clinical practice, and, according to the WHO, one of the ten most common causes of functional disability. It may be primary (e.g., tension-type headaches, migraine) or secondary (e.g., following head trauma or infections) in nature. Although most episodes of headache are harmless, potentially life-threatening causes (e.g., subarachnoid hemorrhage, meningitis) should always be considered. Identifying the cause of headaches is often difficult and requires a detailed clinical history as well as a thorough physical examination. Additional diagnostics, e.g., imaging, are only indicated if headaches persist despite treatment or if specific clinical features are present that are signs of an underlying disease. This article gives an overview of the most common types of headache and serves as a guide to diagnosing different headache disorders.

Approach

Approach to management

Check vital signs.
Perform focused history and examination.
If red flags are present:
- Obtain brain imaging (either CT or MRI brain with and/or without contrast) based on the red flag symptoms. ^[1]
- Perform further targeted diagnostics (see below).
If no red flags are present and suspicion for life-threatening causes is low:
- Perform a detailed history and clinical exam.
- Consider whether further diagnostic testing is necessary.
Provide supportive care.
Identify and treat the underlying cause.

Approach to headache

Headache red flags (SNOOP10) ^[1]^[2]

The original mnemonic, SNOOP has more recently been expanded to cover the following total of 15 red flags:

Systemic symptoms (e.g., fever, signs of meningitis, myalgia, malaise)
Neoplasm in history
Neurological deficits/dysfunction (e.g., altered mental status, seizures) ^[3]
Onset of headache is sudden or abrupt
Older age at onset (> 50 years)
Pattern changes of headache or recent onset
Positional headache
Precipitated by sneezing, coughing, or exercise
Papilledema and other signs of increased ICP
Progressive headache and atypical features
Pregnancy or postpartum period
Pain of the eye with autonomic features and visual deficits
Posttraumatic onset
Pathology of the immune system (especially due to HIV)
Painkiller overuse or new drug at onset of headache

A new or progressive headache in a patient aged > 50 years may indicate tumor or hemorrhage and should always be treated as a high-risk headache.

Life-threatening conditions ^[1]

Intracranial hemorrhage: subarachnoid hemorrhage, epidural hemorrhage, intracerebral hemorrhage
CNS infection: meningitis, encephalitis, brain abscess, subdural empyema
Conditions causing increased ICP (e.g., intracranial neoplasm, brain abscess, ICH)
Hypertensive emergency
Internal carotid artery dissection
Vertebral artery dissection
Ischemic stroke
Pituitary apoplexy
Carbon monoxide poisoning
Cerebral venous sinus thrombosis
Hypoglycemia
Preeclampsia or eclampsia
Non-life-threatening conditions requiring urgent attention:
- Acute angle-closure glaucoma
- Giant cell arteritis

Definitions

Headache is a pain related to irritation and/or inflammation of intracranial or extracranial structures with pain receptors (e.g., meninges, cranial nerves, blood vessels).
Primary headache: a headache that is not caused by another underlying condition ^[4]
- Includes migraine headache, tension headache, trigeminal autonomic cephalalgias (e.g., cluster headache)
Secondary headache: a headache that is caused by another underlying condition (e.g., trauma, space-occupying lesion) ^[4]

Epidemiology

Lifetime prevalence: > 90%, with female predominance (except cluster headache) ^[5]
Most common forms of headache ^[5]
- Tension-type headache: 40–80% of cases
- Migraine: 10% of cases

Among patients presenting to the emergency department with headaches, primary headache (most frequently migraine) is the most common type, but up to 5% may have a secondary headache with a serious life-threatening cause. ^[6]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

See “Differential diagnoses” below.

Clinical features

History of present illness

Timing
- Duration of a single episode
- Frequency
- Clinical course (e.g., chronic, acute)
Nature of the headache
- Localization
- Character
- Intensity
- Radiation of pain
- Severity (e.g., impact on patient's life)
Triggers and exacerbating factors
- Altered sleep-wake cycle
- Physical exertion
- Stress
- Certain types of food or alcohol
- Fluctuations in hormone levels: oral contraceptives; , menstruation
- Lying down or standing up
- Recent trauma
- Environmental exposures
Associated symptoms
- Nausea/vomiting
- Horner syndrome
- Aura
- Photopsia, photophobia
- Neck stiffness
- Neck pain
- Seizures
- Change in vision
- Lacrimation, rhinorrhea
- New skin lesions
- Allodynia of the head region

Maintain a high index of suspicion for secondary headache in patients with a new, sudden-onset severe headache.

Past medical history, social history, and family history

Past medical history (e.g., hypertension, hypothyroidism, seizures, migraine, infections)
Medications (e.g., anticoagulants , analgesics, OCPs)
Allergies
Caffeine intake
Substance use
- Alcohol consumption
- Smoking
Family history

Physical examination

Vital signs
- Blood pressure
- Presence of fever
HEENT
- Signs of trauma
- Auscultation for bruits
- Palpation of pericranial muscles
- Palpation of the temporal artery; and assessment of jaw movement
- Palpation along the course of the trigeminal nerve branches
- Examination of the teeth and oral cavity
- Examination of the eye
- Examination of ocular movements
- Assessment of cervical spine mobility
- Palpation of the sinuses
- Direct fundoscopy
Neurological
- Neurological examination for neurological deficits
- Meningeal signs
- Signs of Horner syndrome
Abdomen: inspection and palpation of the abdomen
Skin: : Evaluate for rash or signs of drug use.

Consider secondary life-threatening causes if red flags for headache are present!

Diagnosis

Approach ^[7]

Check vital signs, obtain a history, and perform a physical and neurological examination.
Determine the need for further testing based on risk stratification and the suspected diagnosis.
- Low-risk headache: No routine laboratory tests or imaging are recommended.
- High-risk headache: Consider diagnostic workup based on the suspected diagnosis.

In patients who are unstable or have signs of increased ICP, diagnostics should not delay stabilization (e.g., ABCDE approach) and neuroprotective measures.

The diagnostic modality should be determined by the patient history and clinical presentation. Primary headache is a clinical diagnosis and typically does not require laboratory or imaging evaluation.

Risk stratification of headache ^[7]^[8]

	Clinical features
Low-risk headache	Age < 30 years Features of primary headache Prior experience of similar headache Absence of neurological deficits Typical headache pattern No recent history of cancer, HIV, or Lyme disease No red flags for headache
High-risk headache	Any red flags for headache Any features of secondary headache Horner syndrome Accompanying systemic illness (e.g., fever, myalgias) Triggered by cough , exertion, or sexual intercourse ^[9] Tenderness over the temporal artery History of cancer, HIV, Lyme disease

Response to analgesics should not be used for risk stratification! Pursue a diagnostic workup for high-risk features even if headache improves with initial treatment. ^[10]^[11]

In the emergency department, use the Ottawa subarachnoid hemorrhage (SAH) clinical decision rule to rule out SAH in patients presenting with rapid onset headache and a normal neurological examination. ^[12]

Laboratory studies

There are no routine recommended laboratory studies for headaches. Consider the following based on clinical suspicion:
- CBC
- TSH
- ESR, CRP

Imaging ^[12]^[13]

Indications
- For emergency neuroimaging
  - Abnormal neurological examination
  - New, sudden-onset severe headache if Ottawa SAH rule criteria are met
  - Patients with HIV with a new type of headache
- For urgent (arranged prior to discharge) neuroimaging in the emergency department:
  - Patients > 50 years of age with a new type of headache but normal neurological examination
- In all other situations, imaging should be considered based on the suspected diagnosis and risk stratification.
Test of choice
- The initial test of choice is usually a head CT without contrast.
- See the table below for other imaging modalities to consider.

Ottawa SAH rule for headache evaluation

Recommended initial imaging modality for headache ^[14]
	Initial test of choice	Alternatives
Sudden-onset severe headache (i.e., thunderclap headache)	CT head without IV contrast	CTA with IV contrast
New headache with papilledema	MRI head Without contrast Without and with IV contrast CT head without IV contrast	CTV head with IV contrast MRV head Without IV contrast Without and with IV contrast CT head with IV contrast
New or worsening headache related to head trauma or accompanied by red flags	CT head without IV contrast MRI head Without IV contrast Without and with IV contrast	N/A
New primary headache suspected to be of trigeminal autonomic origin (e.g., cluster headache)	MRI head without and with IV contrast	MRI head without IV contrast
Chronic headache with new features or change in character, severity, or frequency	MRI head Without IV contrast Without and with IV contrast	CT head Without and with IV contrast Without IV contrast

In patients presenting to the emergency department with acute headache and a normal neurological examination, a negative head CT without contrast indicates that the diagnosis of SAH is unlikely, even when performed < 6 hours from the onset of headache (see “Diagnostics” in “Subarachnoid hemorrhage.”) ^[12]

Avoid imaging in patients presenting with a recurrent known migraine unless new concerning features are present, e.g., seizures, focal neurological deficits, or recent change in headache pattern.

Additional diagnostics to consider ^[13]

Lumbar puncture (LP) with CSF analysis: for suspected meningitis, suspected inflammatory process or malignancy, or if there is a high suspicion of SAH without proof on CT scan
Tonometry: if increased intraocular pressure is suspected
EEG: for any form of suspected seizures or complex migraine
Temporal artery biopsy: if GCA is suspected

In the emergency department, if SAH is still suspected despite a normal head CT without contrast, either LP or CTA can be used as a second-line test to safely rule out the diagnosis (see “Diagnostics” in “Subarachnoid hemorrhage”). ^[12]

In patients with suspected meningitis or encephalitis, do not delay lumbar puncture unless the patient meets the criteria for imaging prior to LP.

Primary headaches

Types of primary headaches ^[15]
Characteristics		Tension-type headache	Migraine headache	Cluster headache	Mixed type headache ^[4]
Epidemiology		♀ > ♂	♀ > ♂	♂ > ♀ (3:1)	♀ > ♂
Triggers/exacerbating factors		Stress, anxiety, depression Lack of sleep, fatigue Poor posture	Stress Fluctuation in hormone levels: oral contraceptives, menstruation Certain types of food (e.g., those containing tyramines or nitrates such as processed meat, chocolate, cheese) Exacerbated by exertion	Alcohol	Stress Lack of sleep, fatigue Poor posture Fluctuation in hormone levels: oral contraceptives, menstruation Certain types of food (e.g., those containing tyramines or nitrates such as processed meat, chocolate, cheese) Exacerbated by exertion
Clinical features	Attack duration	30 minutes to 7 days	4–72 hours	15–180 minutes Short, recurring attacks	Hours to days
	Frequency	Occasionally to daily (usually at the end of the day) Episodic or chronic	Occasionally to several times a month Episodic or chronic	1–3 episodes every 24 hours Usually occur in a cyclical pattern (cluster periods) with remissions lasting ≥ 3 months (i.e., episodic CH), but may also occur with remissions lasting < 3 months or no remission (i.e., chronic CH)	Episodic or chronic
	Localization	Holocephalic or bifrontal	60% of cases are unilateral.	Exclusively unilateral Localized to the periorbital and/or temporal region	Holocephalic, bifrontal, or unilateral
	Character	Dull, nonpulsating, band-like or vise-like pain Constant	Pulsating, boring/hammering pain	Often burning or piercing pain Attacks develop within minutes Often wakes patients up from sleep	Features of migraine and tension-type headache Either pulsating or nonpulsating
	Intensity	Mild to moderate	Moderate to severe	Severe, agonizing pain	Mild to severe
	Additional symptoms	Either phonophobia or photophobia (but not both) No nausea, vomiting, or aura Tightness in the posterior neck muscles Pericranial tenderness	Nausea, vomiting Hyperacusis Photophobia Phonophobia Preceding aura Prodrome (e.g., excessive yawning, difficulty writing or reading, sudden hunger or lack of appetite, mood changes)	Ipsilateral autonomic symptoms: conjunctival injection and/or lacrimation, rhinorrhea, and nasal congestion Partial Horner syndrome: ptosis and miosis, but no anhidrosis	Nausea, vomiting Hyperacusis Photophobia Phonophobia Tightness in the posterior neck muscles Pericranial tenderness
Diagnostics		Clinical diagnosis
Diagnostics		For further information see “Diagnostic criteria for tension-type headaches.”	For further information see “Diagnostic criteria for migraine.” Neuroimaging: CT or MRI to rule out differential diagnoses (see below) ^[16]^[17]	For further information see “Diagnostic criteria for cluster headache.”	For further information see “Diagnostic criteria for tension-type headaches” and “Diagnostic criteria for migraine.”
Management		Episodic tension-type headache: NSAIDs (e.g., ibuprofen, aspirin) or acetaminophen Chronic tension-type headache and frequent episodic type: consider prophylactic therapy (e.g., with amitriptyline) For further information see “Tension-type headache treatment” and “Acute management checklist for tension headache.”	Reduce stimuli (e.g., light, loud noises) and activity Treat nausea/vomiting Mild to moderate headache: NSAIDs, acetaminophen, acetylsalicylic acid, or combinations including caffeine Moderate to severe headache: triptans For further information see “Migraine: Management” and “Acute management checklist for migraine headache.”	Oxygen therapy with FiO₂ 100% Triptans (e.g., sumatriptan or zolmitriptan) For further information see “Treatment of cluster headache” and “Acute management checklist for cluster headache.”	Combination of management of “Tension-type headache treatment” and “Migraine: management.”

“POUND:“ pulsatile, one-day duration, unilateral, nausea, and disabling intensity are the typical features of migraine headache.

In the emergency department, nonopioid pain medications are preferred for the treatment of acute primary headaches. ^[12]

Tension headache fact sheet Migraine fact sheet Cluster headache fact sheet Differential diagnoses of primary headaches fact sheet

Secondary headaches

Diagnosis	Clinical features	Diagnostic findings	Acute management
Meningitis ^[18]^[19]^[20]	Classic triad: fever, headache, and neck stiffness (nuchal rigidity) Meningism (e.g., photophobia) Dull, diffuse (holocephalic) headache that worsens over hours/days Altered mental status Nausea, vomiting Seizures	↑ WBC, ↑ procalcitonin (if bacterial) CSF analysis Bacterial: WBC ≥ 1000 cells/μL (predominantly neutrophils), elevated protein, low glucose, positive gram stain Viral: WBC 10-500 cells/μL (predominantly lymphocytes), normal-elevated protein, normal glucose	See the acute management checklist for meningitis.
Intracerebral hemorrhage ^[21]^[22]	Acute, severe, nonspecific headache Focal neurological signs and symptoms Nausea and vomiting Confusion and loss of consciousness Seizures	CT head without contrast: hyperdense lesion with hypodense perifocal edema	See the acute management checklist for intracerebral hemorrhage.
Subarachnoid hemorrhage ^[23]	Acute onset of a thunderclap headache Focal neurological deficits Meningism Impaired consciousness, rapidly worsening neurological status Seizures	CT head without contrast: blood in subarachnoid space (hyperdense) Lumbar puncture : ↑ RBC count	See the acute management checklist for subarachnoid hemorrhage.
Subdural hematoma (SDH)	Diffuse headache that is worst on the side of the hematoma Impaired consciousness and confusion Focal neurological deficits (e.g., hemiparesis , gait, speech, visual impairment, personality changes, dilated pupil , or nonreactive pupil ) Signs of increased intracranial pressure Chronic subdural hemorrhage : psychomotor impairment, memory loss	CT head without contrast: crescent-shaped, concave, hyperdense hemorrhage that crosses suture lines but not the midline	See the acute management checklist for subdural hematoma.
Epidural hematoma ^[24]	Headache localized to the side of the hematoma Contralateral focal symptoms/hemiplegia Impaired mental status, loss of consciousness, seizures, nausea, and vomiting Nearly half of patients who lose consciousness will have a lucid interval followed by clinical deterioration due to further expansion.	CT head without contrast: biconvex, hyperdense lesion	See the acute management checklist for epidural hematoma.
Cerebral venous sinus thrombosis ^[25]	Nonspecific headache (acute, subacute, or chronic) Cranial nerve symptoms (e.g., diplopia, tinnitus, unilateral deafness, facial palsy) Cavernous sinus syndrome Focal neurological deficits Seizures Impairment in consciousness and awareness Signs of increased intracranial pressure (e.g., nausea, vomiting) Risk factors: pregnancy, prothrombotic states, vasculitis, smoking, use of oral contraceptives	Labs: ↑ WBC , ↑ D-dimer Fundoscopy: papilledema MRI/MRV or CT/CTV: direct or indirect signs of thrombus (see also “Diagnostics” in cerebral venous thrombosis) ^[26] Cerebral venography: filling defect ^[25]	See the acute management checklist for cerebral venous sinus thrombosis.
Giant cell arteritis ^[27]^[28]^[29]^[30]	Unilateral headache over the temporal/occipital area Prominent, tender temporal artery Jaw claudication, scalp tenderness Constitutional symptoms: fever, malaise, fatigue If temporal arteritis is associated with polymyalgia rheumatica: shoulder/pelvic pain, depression, tiredness, fever, weight loss Partial or complete vision loss (unilateral or bilateral), amaurosis fugax, diplopia	Anemia, ↑ ESR ≥ 40–50 mm/hour , ↑ CRP, ↑ IL–6 Temporal artery biopsy (gold standard): segmental vasculitis with predominant mononuclear cells or granulomatous inflammation MRI with contrast: enhancement of the temporal artery	See the acute management checklist for giant cell arteritis.
Hypertensive crises ^[31]^[32]	Diffuse (sometimes bifrontal), pulsating headache that is exacerbated by physical activity Hypertension > 180/120 mm Hg Signs of end-organ damage (e.g., chest pain, dyspnea, oliguria, altered mental status)	Clinical diagnosis: elevated BP with or without signs of end-organ damage Labs: anemia, ↑ creatinine, ↑ BNP, proteinuria, hematuria ECG: left ventricular hypertrophy, signs of cardiac ischemia (e.g., ST depressions or elevations) Chest x-ray: cardiomegaly, pulmonary edema	See the acute management checklist for hypertensive crises.
Ischemic stroke ^[33]^[34]	Tension-type headache Focal neurological deficits Altered mental status	CT head without contrast: hyperdense occluded vessels, hypodense parenchyma, effacement of the sulci and loss of corticomedullary differentiation CTA head and neck: vessel occlusion DW-MRI: T1 hypointense signal, T2 hyperintense signal in the area of the infarction	See the acute management checklist for ischemic stroke.
Intracranial space-occupying lesions (e.g., brain tumors) ^[35]^[36]^[37]	A dull headache that is usually bifrontal and worsens over weeks/months Signs of increased intracranial pressure (e.g., papilledema) Focal neurological deficits, altered mental status, seizures, nausea and vomiting	T1-weighted MRI brain with gadolinium: hypo-, hyper-, or isointense mass lesion with peritumoral edema CT brain with IV contrast: mass lesion, commonly with contrast enhancement	See the acute management checklist for brain tumor.
Concussion (e.g., mild traumatic brain injury) ^[38]^[39]^[40]	Headache of variable intensity Confusion Retrograde amnesia and/or anterograde amnesia Nausea, vomiting, dizziness Ageusia , anosmia, tinnitus, photophobia, blurring of vision Loss of consciousness (rare) History of trauma	Clinical diagnosis CT head without contrast: usually normal	See the acute management checklist for concussion.
Acute angle-closure glaucoma ^[41]^[42]	Sudden onset of unilateral, severe ocular pain or headache Impaired, blurry vision with halos around lights Palpation of the eye: hard ^[43] Fixed mid-dilated pupil Conjunctival hyperemia, hazy cornea Nausea, vomiting	Increased IOP (> 21 mm Hg) Gonioscopy: visualization of angle closure Slit-lamp examination: shallow anterior chamber Visual field losses	See the acute management checklist for acute angle-closure glaucoma.
Trigeminal neuralgia ^[44]^[45]	Paroxysmal (seconds to 2 minutes) and stabbing pain Unilateral facial pain, strictly localized to the distribution of the branches of the trigeminal nerve Frequency and intensity of episodes usually increase over time Tender trigger points Triggered by chewing, talking, cold, and touching specific areas of the face No neurological deficits	Clinical diagnosis ^[45] MRI brain: vascular compression of the trigeminal root	See the acute management checklist for trigeminal neuralgia.
Medication overuse headache	Headache with variable characteristics History of analgesic overuse Autonomic symptoms (e.g., nausea) Cognitive or behavioral symptoms (e.g., comorbid depression)	Clinical diagnosis	See medication overuse headache.

Consider eye examination in patients with unexplained acute-onset severe headache with nausea and vomiting to evaluate for signs of acute angle-closure glaucoma.

Differential diagnoses

Primary headache

Migraine
Tension-type headache
Trigeminal autonomic cephalalgias: cluster headaches, paroxysmal hemicrania, hemicrania continua
Other primary headaches: cough headaches, headaches due to physical exertion, postcoital headache, primary stabbing headache

Secondary headache

Bleeding
Vascular
Autoimmune
- Temporal arteritis; (giant cell arteritis)
Drug/toxin-related
- Alcohol use
- Alcohol withdrawal
- Food additives (e.g., MSG)
- Sympathomimetics (e.g., nicotine)
- Medication overuse headache
- Caffeine withdrawal headache
- Opioid withdrawal
- Nitroglycerin
- Carbon monoxide poisoning
Infectious
- Intracranial infections
  - Meningitis
  - Encephalitis
  - Brain abscess
  - Subdural empyema
  - Aseptic meningitis
  - Toxoplasmosis
- Systemic infections (e.g., influenza)
ICP-related
- Increased intracranial pressure (e.g., due to pseudotumor cerebri)
- Decreased intracranial pressure (e.g., post-lumbar puncture headache)
- Hydrocephalus
Metabolic
- Hypoxia and/or hypercapnia (e.g., high-altitude headache)
- Hypoglycemia
- Hypothyroidism
Extracranial
- Glaucoma
- Iridocyclitis
- Refractive errors
- Optic neuritis
- Rhinosinusitis
- Cervicogenic headache (e.g., cervical disk disease)
- Temporomandibular joint disorders
Other
- Hypertension
- Brain tumors
- Trigeminal neuralgia
- Postherpetic neuralgia
- Postictal headache
Psychiatric
- Somatization disorder
- Psychotic disorder

The differential diagnoses listed here are not exhaustive.

Disposition

Most patients with primary headaches and benign secondary headaches can be managed as outpatients. ^[6]

Indications for hospitalization

Life-threatening secondary headache requiring inpatient management
Suspected nonbenign secondary cause of headache that requires further investigation
Intractable pain or inability to tolerate oral nutrition or hydration
Medication overuse headache requiring supervised withdrawal (see “Disposition and referrals” in “Medication overuse headache”)

Discharge from the emergency department

Discharge home is appropriate once life-threatening causes of headache have been ruled out and the patient's symptoms improve with initial treatment (even if the headache is not completely resolved). ^[6]

Consider appropriate prescription of analgesics and preventive medication based on the underlying diagnosis.
Provide patient counseling and education.
Ensure outpatient primary care follow-up, especially for patients at high risk of early recurrence. ^[10]
Consider referral to neurology or a specialized headache clinic.

Appropriate discharge planning is important to ensure ongoing care and reduce unnecessary return visits to the emergency department e.g., due to recurrent headaches or incomplete treatment.

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