Vertebral artery dissection

Vertebral artery dissection (VAD) is a tear in the wall of the vertebral artery allowing blood to enter and separate the vessel layers, causing stenosis, thromboembolism, or occlusion that can lead to posterior circulation stroke. VAD accounts for ~2% of all ischemic strokes but up to 20% of strokes in patients under 45. The EM diagnostic challenge is that patients often present with nonspecific headache and neck pain days before stroke onset, are misdiagnosed as migraine or musculoskeletal pain, and return with completed stroke. Any new-onset posterior headache or neck pain in a young patient — especially after minor trauma or neck manipulation — must be evaluated for VAD.

Background

• Incidence ~1-1.5 per 100,000/year; most common in ages 30-50; slight female predominance
• Causes: trauma (MVCs, sports, falls), cervical manipulation (chiropractic, physiotherapy), trivial mechanisms (coughing, sneezing, yoga, vomiting, roller coasters), or spontaneous
• Predisposing conditions: fibromuscular dysplasia, Ehlers-Danlos syndrome type IV, Marfan syndrome, osteogenesis imperfecta
• Vertebral artery is most vulnerable at C1-C2 (the V3 segment) where it is mobile and exposed during neck rotation
• Headache/neck pain may precede stroke by up to 14 days — this is the window for diagnosis and prevention
• ~90% of dissections heal spontaneously within 3-6 months with antithrombotic therapy; mortality ~5%

Clinical Features

• Headache: posterior/occipital; often sudden onset, severe, unlike patient's usual headache — the most common presenting symptom
• Neck pain: ipsilateral posterior neck pain; may be the only initial complaint
• Posterior circulation stroke symptoms (may be delayed hours to days after pain onset):
  • Vertigo, dizziness, ataxia (cerebellar ischemia)
  • Dysarthria, dysphagia (brainstem)
  • Diplopia, nystagmus, visual field deficits (brainstem, occipital)
  • Lateral medullary syndrome (Wallenberg) — ipsilateral facial pain/numbness, Horner syndrome, ataxia, contralateral body pain/temperature loss, hoarseness, dysphagia, hiccups
  • Hemiparesis or quadriparesis — may progress rapidly to locked-in syndrome
  • Decreased consciousness — basilar artery occlusion
• Subarachnoid hemorrhage: if intracranial V4 segment is involved (subadventitial dissection → SAH); carries worse prognosis

When to suspect VAD

• Young patient (<50) with new severe posterior headache/neck pain + ANY posterior circulation symptom
• Headache/neck pain after cervical manipulation, minor trauma, sports injury, or trivial neck movement
• Posterior circulation TIA or stroke in a young patient without traditional vascular risk factors
• Unexplained SAH with negative aneurysm workup — consider intracranial VAD

Differential Diagnosis

• Carotid artery dissection — anterior circulation stroke; may coexist with VAD
• Migraine — most common misdiagnosis; but new headache type in a patient without migraine history should not be attributed to migraine
• Musculoskeletal neck pain/cervical strain — the other common misdiagnosis; absence of neurologic symptoms does NOT exclude early VAD
• Subarachnoid hemorrhage — thunderclap headache; intracranial VAD can cause SAH
• Cerebellar hemorrhage or infarct from other causes
• Posterior fossa mass
• Vestibular disorders (BPPV, vestibular neuritis) — true vertigo without other neurologic findings; but always examine for cerebellar signs
• Blunt cerebrovascular injury — VAD in the trauma setting; see BCVI screening criteria

Evaluation

Workup

• CTA of head and neck (aortic arch through circle of Willis): imaging modality of choice in the ED; rapid, widely available, sensitivity/specificity ~95-98%
  • Look for: luminal irregularity/narrowing, intimal flap, intramural hematoma (crescent sign), pseudoaneurysm, occlusion
• MRI/MRA with fat-suppressed T1: equivalent sensitivity; shows intramural hematoma as hyperintense crescent on axial fat-sat T1; preferred if already getting MRI for stroke workup
• CT head (non-contrast): obtain first to evaluate for intracranial hemorrhage or stroke; a normal CT head does NOT exclude VAD
• MRI brain (DWI): most sensitive for acute posterior fossa ischemia (CT often misses small cerebellar/brainstem strokes)
• Doppler ultrasound: insufficient — misses V3/V4 segments near skull base; a negative ultrasound does NOT exclude VAD

Diagnosis

• VAD is confirmed by CTA or MRA showing vessel wall abnormality (intimal flap, intramural hematoma, stenosis, pseudoaneurysm, or occlusion)
• Grade using the Biffl scale (see Blunt cerebrovascular injury) if traumatic
• Intracranial extension (V4 segment) changes management — higher SAH risk, anticoagulation may be contraindicated

Management

• If presenting with acute ischemic stroke:
  • IV thrombolysis (alteplase) is reasonable if within standard time window (≤4.5 hours) and meets inclusion criteria — dissection-related stroke is NOT a contraindication to tPA per AHA/ESO guidelines
  • Mechanical thrombectomy: consider for large vessel occlusion (basilar artery) per standard stroke protocols
  • Stroke team activation — do not delay
• Antithrombotic therapy (the mainstay for all VAD):
  • Antiplatelet (aspirin 325 mg) OR anticoagulation (heparin → warfarin) — CADISS and TREAT-CAD trials showed no significant difference between the two in stroke prevention
  • Choice depends on: bleeding risk, stroke size, presence of intracranial extension, other injuries
  • Aspirin is simpler, safer, and preferred when: large infarct (hemorrhagic transformation risk), intracranial extension (SAH risk), or polytrauma
  • Anticoagulation may be preferred when: free-floating thrombus, high-grade stenosis, recurrent TIAs despite antiplatelet
  • Duration: typically 3-6 months (most dissections heal within this period); follow-up imaging guides discontinuation
• Intracranial VAD with SAH: do NOT anticoagulate — neurosurgery/neurointerventional consultation for possible endovascular treatment
• Consult: neurology (all cases); neurosurgery/neurointerventional if intracranial, SAH, or failing medical therapy

Disposition

• Admit all patients with confirmed VAD — for neurologic monitoring, initiation of antithrombotic therapy, and stroke prevention
  • ICU if acute stroke, SAH, or neurologic deterioration
  • Telemetry/stroke unit if stable
• Symptomatic patients (headache/neck pain only, no stroke): still admit — stroke risk is highest in the first 2 weeks; close neurologic monitoring is critical
• Follow-up imaging (CTA or MRA) at 3-6 months to assess healing; guides duration of antithrombotic therapy
• Counsel patients:
  • Avoid cervical manipulation (chiropractic, aggressive physiotherapy)
  • Seek immediate care if new neurologic symptoms develop
  • Medication compliance with antithrombotic therapy
  • Annual recurrence risk is ~1% after the initial episode

See Also

• Carotid artery dissection
• Blunt cerebrovascular injury
• Stroke
• Subarachnoid hemorrhage
• Posterior circulation stroke
• Wallenberg syndrome

External Links

• StatPearls — Vertebral Artery Dissection
• StatPearls — Vertebral Artery Injury
• Medscape — Vertebral Artery Dissection Treatment & Management
• AJNR — Blunt Cerebrovascular Injuries: Advances in Screening, Imaging, and Management (2021)