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Emergency And Acute Medicine – Head Pain Syndromes
Overview And Pathophysiology
Headache is pain perceived in the cranium, orbits, or upper cervical region. Pain originating from intracranial structures is often projected to the surface. Intracranial pain-sensitive structures include arteries, veins, dura, and meninges. Extracranial sources include the skin, scalp, fascia, muscles, mucosal linings of the sinuses, arteries, temporomandibular joints, and teeth. Pain transmission occurs primarily via the trigeminal (V) cranial nerve. Mechanisms include nerve irritation, traction on pain-sensitive vessels, vasodilation, hypoxia, hypercapnia, fever, histamine exposure, or nitroglycerin ingestion. Headache accounts for 2–4% of ED visits; approximately 95% are benign, though serious etiologies are more common in patients older than 50 years.
Causes And Risk Factors
Migraine results from intra- and extracranial vasodilation and constriction of pain-sensitive vessels and may involve cortical spreading depression. Pain is typically throbbing. Tension-type headache requires at least ten similar episodes and has an unclear etiology, possibly involving serotonin imbalance, reduced endorphins, or muscle spasm. It is the most common recurrent headache, often triggered by poor posture, stress, anxiety, depression, or cervical osteoarthritis. Pain is usually bilateral, nonpulsatile, band-like, mild to moderate, and lasts 4–13 hours.
Cluster headache may be triggered by alcohol, certain foods, sleep disruption, or strong emotions and may involve vasospasm near cranial nerves.
Intracranial pressure or traction causes include mass lesions and idiopathic intracranial hypertension. Extracranial compression headaches arise from peripheral nerve pathology of the head and neck. Inflammatory causes include temporal arteritis and cerebral vasculitis. Thrombotic causes include cerebral venous sinus thrombosis. Disorders of vascular autoregulation include posterior reversible leukoencephalopathy syndrome and reversible cerebral vasoconstriction syndrome.
Children rarely have serious headache causes but require follow-up. Older adults with new-onset headache have higher risk for serious disease and warrant low thresholds for imaging. Pregnancy and the postpartum period increase risk for CVST, eclampsia, PRES, and RCVS.
Clinical Assessment
History should characterize pain using PQRST. Provoking factors include head position, coughing, or straining; worsening with these suggests elevated intracranial pressure. Quality may be throbbing or continuous, deep or superficial. Assess region, severity, “worst headache of life,” timing (sudden vs. gradual), and associated symptoms such as visual changes, dizziness, nausea, or vomiting.
Red flags include new onset, age >50 years, immunosuppression, malignancy, trauma or falls, persistent vomiting, focal neurologic or visual deficits, and risk factors for CVST (pregnancy/postpartum, malignancy, oral contraceptives, protein C/S deficiency, ulcerative colitis, Behçet syndrome).
Physical Examination
Perform a complete neurologic exam including cranial nerves, motor and sensory testing, reflexes, and gait. Examine fundi for papilledema. Inspect skin for rashes (e.g., zoster, purpura). Palpate temporal arteries for tenderness or thickening.
Initial Evaluation Strategy
A thorough history and focused CNS, HEENT, and neck examination are essential. Additional testing is indicated with severe hypertension, fever, altered mental status, papilledema, abnormal neurologic findings, or meningismus.
Diagnostic Studies
Laboratory testing includes cerebrospinal fluid analysis when meningitis or subarachnoid hemorrhage is suspected and ESR when temporal arteritis or inflammatory disease is considered.
Noncontrast head CT is indicated for uncertain diagnosis, signs of increased ICP, first or worst headache, abrupt onset, new focal deficits, papilledema, recurrent morning headaches, persistent vomiting, headache with fever or rash, trauma with LOC, altered mental status, or meningismus. CT within 6 hours of onset is highly sensitive for SAH; sensitivity declines after 24 hours.
MRI evaluates posterior fossa lesions, pituitary apoplexy, CVST, and causes missed by CT and LP. MRA is indicated when SAH is suspected with negative CT and LP cannot be performed, or when arterial dissection or nonmigrainous vascular causes are suspected.
Lumbar puncture is required after CT when focal deficits, papilledema, abnormal mental status, or immunosuppression are present. It detects infection, occult SAH, opening pressure abnormalities, and distinguishes traumatic tap from hemorrhage. Xanthochromia is typically present by 12 hours after SAH onset.
Differential Diagnosis
Acute single headache includes SAH, meningitis, intracerebral hemorrhage, hypertensive encephalopathy, arterial dissection, CVST, cerebellar stroke, acute angle-closure glaucoma, pituitary apoplexy, temporal neuritis, trauma, acute sinusitis, toxic or metabolic states, withdrawal syndromes, and post–lumbar puncture headache.
Acute recurrent headache over days to weeks includes migraine, cluster, tension, CVST, pseudotumor cerebri, temporal arteritis, SAH rebleed, hypoxia-related headache, trigeminal neuralgia, postherpetic neuralgia, exertional and coital headaches.
Subacute headache over weeks to months suggests chronic subdural hematoma, brain tumor, brain abscess, chronic sinusitis, temporomandibular joint disorders, chronic post-traumatic headache, pseudotumor cerebri, or temporal arteritis.
Chronic headache over months to years includes chronic tension headache, medication overuse headache, depression-related headache, trigeminal neuralgia, severe anemia, acute glaucoma, and cervical spine disease.
Management Principles
Initial stabilization focuses on airway, breathing, and circulation in patients with altered mental status. Start empiric antibiotics promptly for suspected bacterial meningitis and add acyclovir in immunocompromised patients.
ED management is etiology-specific. Migraine, cluster, and tension headaches receive symptomatic therapy. Temporal arteritis, intracranial infection, and intracranial hemorrhage require targeted treatment.
Disposition And Follow-Up
Admit patients with suspected organic disease, intractable vomiting with dehydration, or pain refractory to outpatient therapy. Consider ICU admission for suspected aneurysm, acute subdural hematoma, SAH, stroke, increased ICP, or intracranial infection.
Discharge is appropriate for resolved migraine, cluster, or tension headaches and minor infections with adequate follow-up. Patients with recurrent headaches should follow up with a primary care physician or neurologist.
Medications Commonly Used
Common agents include chlorpromazine, dexamethasone, dihydroergotamine, ergotamine, ketorolac, intranasal lidocaine, metoclopramide, morphine, prochlorperazine, and sumatriptan, selected based on headache type and patient factors.
Clinical Warnings And Pitfalls
Do not use treatment response to determine benign etiology. CT sensitivity for SAH decreases rapidly after 24 hours; lumbar puncture remains essential after delayed presentation. Neurology consultation should not delay urgent imaging in high-risk cases. Use dopamine antagonists cautiously in QT prolongation or electrolyte abnormalities. Use triptans and ergotamines cautiously in coronary artery disease. Chronic headache patients benefit from consistent plans, but new or changing features require reassessment. Never delay empiric treatment of suspected meningitis while awaiting lumbar puncture results.
Overview And Pathophysiology
Headache is pain perceived in the cranium, orbits, or upper cervical region. Pain originating from intracranial structures is often projected to the surface. Intracranial pain-sensitive structures include arteries, veins, dura, and meninges. Extracranial sources include the skin, scalp, fascia, muscles, mucosal linings of the sinuses, arteries, temporomandibular joints, and teeth. Pain transmission occurs primarily via the trigeminal (V) cranial nerve. Mechanisms include nerve irritation, traction on pain-sensitive vessels, vasodilation, hypoxia, hypercapnia, fever, histamine exposure, or nitroglycerin ingestion. Headache accounts for 2–4% of ED visits; approximately 95% are benign, though serious etiologies are more common in patients older than 50 years.
Causes And Risk Factors
Migraine results from intra- and extracranial vasodilation and constriction of pain-sensitive vessels and may involve cortical spreading depression. Pain is typically throbbing. Tension-type headache requires at least ten similar episodes and has an unclear etiology, possibly involving serotonin imbalance, reduced endorphins, or muscle spasm. It is the most common recurrent headache, often triggered by poor posture, stress, anxiety, depression, or cervical osteoarthritis. Pain is usually bilateral, nonpulsatile, band-like, mild to moderate, and lasts 4–13 hours.
Cluster headache may be triggered by alcohol, certain foods, sleep disruption, or strong emotions and may involve vasospasm near cranial nerves.
Intracranial pressure or traction causes include mass lesions and idiopathic intracranial hypertension. Extracranial compression headaches arise from peripheral nerve pathology of the head and neck. Inflammatory causes include temporal arteritis and cerebral vasculitis. Thrombotic causes include cerebral venous sinus thrombosis. Disorders of vascular autoregulation include posterior reversible leukoencephalopathy syndrome and reversible cerebral vasoconstriction syndrome.
Children rarely have serious headache causes but require follow-up. Older adults with new-onset headache have higher risk for serious disease and warrant low thresholds for imaging. Pregnancy and the postpartum period increase risk for CVST, eclampsia, PRES, and RCVS.
Clinical Assessment
History should characterize pain using PQRST. Provoking factors include head position, coughing, or straining; worsening with these suggests elevated intracranial pressure. Quality may be throbbing or continuous, deep or superficial. Assess region, severity, “worst headache of life,” timing (sudden vs. gradual), and associated symptoms such as visual changes, dizziness, nausea, or vomiting.
Red flags include new onset, age >50 years, immunosuppression, malignancy, trauma or falls, persistent vomiting, focal neurologic or visual deficits, and risk factors for CVST (pregnancy/postpartum, malignancy, oral contraceptives, protein C/S deficiency, ulcerative colitis, Behçet syndrome).
Physical Examination
Perform a complete neurologic exam including cranial nerves, motor and sensory testing, reflexes, and gait. Examine fundi for papilledema. Inspect skin for rashes (e.g., zoster, purpura). Palpate temporal arteries for tenderness or thickening.
Initial Evaluation Strategy
A thorough history and focused CNS, HEENT, and neck examination are essential. Additional testing is indicated with severe hypertension, fever, altered mental status, papilledema, abnormal neurologic findings, or meningismus.
Diagnostic Studies
Laboratory testing includes cerebrospinal fluid analysis when meningitis or subarachnoid hemorrhage is suspected and ESR when temporal arteritis or inflammatory disease is considered.
Noncontrast head CT is indicated for uncertain diagnosis, signs of increased ICP, first or worst headache, abrupt onset, new focal deficits, papilledema, recurrent morning headaches, persistent vomiting, headache with fever or rash, trauma with LOC, altered mental status, or meningismus. CT within 6 hours of onset is highly sensitive for SAH; sensitivity declines after 24 hours.
MRI evaluates posterior fossa lesions, pituitary apoplexy, CVST, and causes missed by CT and LP. MRA is indicated when SAH is suspected with negative CT and LP cannot be performed, or when arterial dissection or nonmigrainous vascular causes are suspected.
Lumbar puncture is required after CT when focal deficits, papilledema, abnormal mental status, or immunosuppression are present. It detects infection, occult SAH, opening pressure abnormalities, and distinguishes traumatic tap from hemorrhage. Xanthochromia is typically present by 12 hours after SAH onset.
Differential Diagnosis
Acute single headache includes SAH, meningitis, intracerebral hemorrhage, hypertensive encephalopathy, arterial dissection, CVST, cerebellar stroke, acute angle-closure glaucoma, pituitary apoplexy, temporal neuritis, trauma, acute sinusitis, toxic or metabolic states, withdrawal syndromes, and post–lumbar puncture headache.
Acute recurrent headache over days to weeks includes migraine, cluster, tension, CVST, pseudotumor cerebri, temporal arteritis, SAH rebleed, hypoxia-related headache, trigeminal neuralgia, postherpetic neuralgia, exertional and coital headaches.
Subacute headache over weeks to months suggests chronic subdural hematoma, brain tumor, brain abscess, chronic sinusitis, temporomandibular joint disorders, chronic post-traumatic headache, pseudotumor cerebri, or temporal arteritis.
Chronic headache over months to years includes chronic tension headache, medication overuse headache, depression-related headache, trigeminal neuralgia, severe anemia, acute glaucoma, and cervical spine disease.
Management Principles
Initial stabilization focuses on airway, breathing, and circulation in patients with altered mental status. Start empiric antibiotics promptly for suspected bacterial meningitis and add acyclovir in immunocompromised patients.
ED management is etiology-specific. Migraine, cluster, and tension headaches receive symptomatic therapy. Temporal arteritis, intracranial infection, and intracranial hemorrhage require targeted treatment.
Disposition And Follow-Up
Admit patients with suspected organic disease, intractable vomiting with dehydration, or pain refractory to outpatient therapy. Consider ICU admission for suspected aneurysm, acute subdural hematoma, SAH, stroke, increased ICP, or intracranial infection.
Discharge is appropriate for resolved migraine, cluster, or tension headaches and minor infections with adequate follow-up. Patients with recurrent headaches should follow up with a primary care physician or neurologist.
Medications Commonly Used
Common agents include chlorpromazine, dexamethasone, dihydroergotamine, ergotamine, ketorolac, intranasal lidocaine, metoclopramide, morphine, prochlorperazine, and sumatriptan, selected based on headache type and patient factors.
Clinical Warnings And Pitfalls
Do not use treatment response to determine benign etiology. CT sensitivity for SAH decreases rapidly after 24 hours; lumbar puncture remains essential after delayed presentation. Neurology consultation should not delay urgent imaging in high-risk cases. Use dopamine antagonists cautiously in QT prolongation or electrolyte abnormalities. Use triptans and ergotamines cautiously in coronary artery disease. Chronic headache patients benefit from consistent plans, but new or changing features require reassessment. Never delay empiric treatment of suspected meningitis while awaiting lumbar puncture results.
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