Headache

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.

• Lifetime prevalence: > 90%, with female predominance ^[3]
• Most common forms of headache ^[3]
  • Tension-type headache: 40–80% of cases
  • Migraine: 10% of cases

Epidemiological data refers to the US, unless otherwise specified.

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
• Associated symptoms
  • Nausea/vomiting
  • Horner syndrome
  • Aura
  • Photopsia, photophobia
  • Neck stiffness
  • Seizures
  • Change in vision
  • Lacrimation, rhinorrhea
  • New skin lesions
  • Allodynia of the head region

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
  • Examination of the teeth and oral cavity
  • Examination of the eye and extraocular movements
  • Assessment of cervical spine mobility
  • Palpation of the sinuses
  • Direct fundoscopy
• Neurological
  • Neurological examination for neurologic deficits
  • Signs of meningism
• 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!

Approach ^[4]

• Diagnostic evaluation should be performed 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.
• Primary headache is a clinical diagnosis and typically does not require laboratory or imaging evaluation.

Risk stratification of headache ^[4][5]

	Clinical features
Low-risk headache	Age < 30 years Features of primary headache Prior experience of similar headache Absence of neurologic 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 Tenderness over the temporal artery History of cancer, HIV, Lyme disease

Laboratory studies

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

Imaging ^[6]

• Indications
  • For emergency neuroimaging
    • Abnormal neurologic examination
    • New, sudden-onset severe headache (e.g., thunderclap headache)
    • Patients with HIV with a new type of headache
  • For urgent (arranged prior to discharge) neuroimaging in the emergency department:
    • Patients > 50 years old with a new type of headache but normal neurologic 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.

Recommended initial imaging modality for headache [7]
		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

Additional diagnostics to consider ^[6]

• 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

The diagnostic modality should be determined by the patient history and clinical presentation. Neuroimaging is usually not indicated for primary or low-risk headaches.

	Tension headache	Migraine headache	Cluster headache
Sex	♂ < ♀	♂ < ♀	♂ > ♀ (3:1)
Duration	30 minutes to a couple of days	4–72 hours	30–180 minutes Short, recurring attacks
Frequency	Occasionally to daily Episodic or chronic	Occasionally to several times a month	1–3 episodes every 24 hours Usually occur in a cyclical pattern (clusters)
Localization	Holocephalic or bifrontal	60% are unilateral.	Mostly unilateral Localized to the periorbital and/or temporal region
Character	Dull, nonpulsating, band-like or vise-like pain Constant	Pulsating, boring/hammering pain	Often burning or piercing pain Attacks develop within several minutes Often wakes patients up from sleep
Intensity	Mild to moderate	Moderate to severe	Severe, agonizing pain Because of the severity of pain, some patients report experiencing suicidal thoughts (hence the name “suicidal headache”).
Additional symptoms	No autonomic symptoms (vomiting, nausea, phonophobia, or photophobia) Tightness in the posterior neck muscles Pericranial tenderness	Nausea, vomiting Hyperacusis Photophobia Phonophobia Preceding aura Prodrome	Ipsilateral autonomic symptoms: conjunctival injection and/or lacrimation, rhinorrhea and nasal congestion Partial Horner syndrome: ptosis and miosis, but no anhidrosis
Triggers/exacerbating factors	Stress Lack of sleep, fatigue Routine activities (e.g., climbing stairs) do not exacerbate symptoms.	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
Diagnostic findings	Clinical diagnosis	Clinical diagnosis [8] Neuroimaging: typically normal findings [9][10]	Clinical diagnosis [11]
Acute management	See the acute management checklist for tension headache.	See the acute management checklist for migraine headache.	See the acute management checklist for cluster headache.

The typical migraine headache can be remembered by “POUND”: pulsatile, one-day duration, unilateral, nausea, disabling intensity.

Diagnosis	Clinical features	Diagnostic findings	Acute management
Meningitis [12][13][14]	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 [15][16]	Acute, severe, nonspecific headache Focal neurologic 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 [17]	Acute onset of a thunderclap headache Focal neurologic 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 neurologic 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 [18]	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 [19]	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) [20] Cerebral venography: filling defect [19]	See the acute management checklist for cerebral venous sinus thrombosis.
Giant cell arteritis [21][22][23][24]	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 [25][26]	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 [27][28]	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) [29][30][31]	A dull headache that is usually bifrontal and worsens over weeks/months Signs of increased intracranial pressure (e.g., papilledema) Focal neurologic 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) [32][33][34]	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.
Trigeminal neuralgia [35][36]	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 neurologic deficits	Clinical diagnosis [36] 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.

Primary headache

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

Secondary headache

• Bleeding
  • Epidural hemorrhage
  • Subdural hemorrhage
  • Subarachnoid hemorrhage
  • Intracerebral hemorrhage

• Vascular
  • Cerebral venous thrombosis
  • Pituitary apoplexy
  • Stroke, TIA
  • Aneurysms
  • Carotid artery dissection
  • Vertebral artery dissection
• Autoimmune
  • Temporal arteritis
• Drug/toxin-related
  • Alcohol use
  • Alcohol withdrawal
  • Sympathomimetics (e.g., nicotine)
  • Medication overuse headache
  • Caffeine withdrawal
  • Opioid withdrawal
  • Nitroglycerin
  • Carbon monoxide poisoning
• Infectious
  • Intracranial infections
    • Meningitis
    • Encephalitis
    • Brain abscess
    • Subdural empyema
    • Aseptic meningitis
    • Toxoplasmosis
  • Systemic infections (e.g., influenza)
• Other
  • Increased intracranial pressure
  • Decreased intracranial pressure (e.g., post-lumbar puncture headache)
  • Glaucoma
  • Brain tumors
  • Trigeminal neuralgia
  • Hypoxia and/or hypercapnia (e.g., high-altitude headache)
  • Hypertension
  • Hypoglycemia
  • Hypothyroidism
  • Iridocyclitis
  • Refractive errors
  • Rhinosinusitis
  • Post-ictal headache
  • Cervicogenic headache (e.g., cervical disc disease)
  • Temporomandibular joint disorders
  • Post-herpetic neuralgia
  • Optic neuritis
• Psychiatric
  • Somatization disorder
  • Psychotic disorder

The differential diagnoses listed here are not exhaustive.