Vertebral and carotid artery dissection

Background

  • Primarily categorized as spontaneous vs traumatic/mechanical
  • Most frequent cause of CVA in young and middle-aged patients (median age ~40 years)
  • Incidence: ~2.6 per 100,000/year for carotid; ~1-1.5 per 100,000/year for vertebral[1]
  • Pathophysiology: tear in arterial wall → false lumen formation → luminal stenosis + exposure of subendothelial collagen → local thrombus formation → thromboembolism to intracranial vessels
    • Less commonly, dissection of thinner intracranial arteries may lead to SAH through vessel rupture
CTA brain showing filling defect in the right carotid artery (circled)

Key EM Pearls

  • Headache/neck pain may precede stroke by up to 14 days — this is the diagnostic window
  • Consider in any trauma patient with neurologic deficits despite normal head CT
  • Consider in any patient with CVA + neck pain, especially age <50
  • Consider in any young patient with Horner syndrome + head/neck pain
  • Stroke risk is highest in the first 24 hours after dissection; early diagnosis and treatment are critical
  • In the trauma setting, falls under Blunt cerebrovascular injury (BCVI) screening — see Denver screening criteria

Anatomy

  • Carotid: internal carotid artery (ICA) is most commonly affected ~2 cm distal to the bifurcation; divided into cervical, petrous, cavernous, and cerebral segments
  • Vertebral: arises from the subclavian, runs through the transverse foramina of C6-C2; most vulnerable at C1-C2 (V3 segment) where it is mobile during neck rotation; joins contralateral vertebral to form the basilar artery

Risk Factors

Clinical Features

Internal Carotid Dissection

  • Unilateral headache, face pain, anterior neck pain
    • Pain can precede other symptoms by hours-days (median 4 days)
    • Headache most commonly is frontotemporal; severity may mimic SAH or preexisting migraine
  • Partial Horner syndrome (miosis and ptosis without anhidrosis) in ~50% — sympathetic fibers run along the ICA
  • Cranial nerve palsies — especially CN XII (hypoglossal); also CN IX, X, XI (lower cranial nerves compressed by expanding vessel wall)
  • Vision loss (amaurosis fugax, retinal artery occlusion)
  • Symptoms of anterior circulation stroke or TIA

Vertebral Artery Dissection

Differential Diagnosis

Neck Trauma

Other considerations:

Evaluation

Workup

  • CT head (non-contrast): obtain first to assess for concomitant SAH, intracranial hemorrhage, or established infarct
    • A normal head CT does NOT exclude dissection
  • CTA head and neck (aortic arch through circle of Willis): imaging modality of choice
    • Sensitivity/specificity ~95-98% with modern ≥16-slice CT[5]
    • CTA has been shown to be equivalent to MRA
    • Look for: luminal narrowing ("string sign"), intimal flap, intramural hematoma (crescent sign), pseudoaneurysm, occlusion, "flame-shaped" tapering
  • MRI/MRA with fat-suppressed T1: shows intramural hematoma as hyperintense crescent; preferred if already obtaining MRI for stroke workup; better for follow-up imaging
  • MRI brain (DWI): most sensitive for acute posterior fossa ischemia (CT misses many small cerebellar/brainstem strokes)
  • Labs: CBC, BMP, coags, troponin, glucose, type and screen
  • ECG: baseline; stroke can cause ECG changes (deep TWI, prolonged QT)
  • Doppler ultrasound: insufficient — misses skull base segments; a negative ultrasound does NOT exclude dissection

Screening in Trauma

Denver screening criteria for blunt cerebrovascular injury

The Denver Screening Criteria are divided into risk factors and signs and symptoms

Signs and Symptoms

  • Arterial hemorrhage
  • Cervical bruit
  • Expanding neck hematoma
  • Focal neurologic deficit
  • Neuro exam inconsistent with head CT
  • Stroke on head CT

Stroke Syndromes

Anterior Circulation

  • Blood supply via internal carotid system
  • Includes ACA and MCA

Internal Carotid Artery

  • Tonic gaze deviation towards lesion
  • Global aphasia, dysgraphia, dyslexia, dyscalculia, disorientation (dominant lesion)
  • Spatial or visual neglect (non-dominant lesion)

Anterior Cerebral Artery (ACA)

Signs and Symptoms:

  • Contralateral sensory and motor symptoms in the lower extremity (sparing hands/face)
  • Urinary and bowel incontinence
  • Left sided lesion: akinetic mutism, transcortical motor aphasia
  • Right sided lesion: Confusion, motor hemineglect
  • Presence of primitive grasp and suck reflexes
  • May manifest gait apraxia

Middle Cerebral Artery (MCA)

Patient with stroke (forehead sparing).

Signs and Symptoms:

  • Hemiparesis, facial plegia, sensory loss contralateral to affected cortex
  • Motor deficits found more commonly in face and upper extremity than lower extremity
  • Dominant hemisphere involved: aphasia
    • Wernicke's aphasia (receptive aphasia) -> patient unable to process sensory input and does not understand verbal communication
    • Broca's aphasia (expressive aphasia) -> patient unable to communicate verbally, even though understanding may be intact
  • Nondominant hemisphere involved: dysarthria (motor deficit of the mouth and speech muscles; understanding intact) w/o aphasia, inattention and neglect side opposite to infarct
  • Contralateral homonymous hemianopsia
  • Gaze preference toward side of infarct
  • Agnosia (inability to recognize previously known subjects)

Posterior circulation

Signs and Symptoms:

Basilar artery

Signs and Symptoms:

  • Quadriplegia, coma, locked-in syndrome
  • "Crossed signs" in which a patient has unilateral cranial nerve deficits but contralateral hemiparesis and hemisensory loss suggest brainstem infarction
    • Millard-Gubler syndrome (ventral pontine syndrome) -- ipsilateral CN VI and VII palsy with contralateral hemiplegia of extremities
  • Sparing of vertical eye movements (CN III exits brainstem just above lesion)
    • Thus, may also have miosis b/l
  • One and a half syndrome (seen in a variety of brainstem infarctions)
    • "Half" - INO (internuclear ophthalmoplegia) in one direction
    • "One" - inability for conjugate gaze in other direction
    • Convergence and vertical EOM intact
  • Medial inferior pontine syndrome (paramedian basilar artery branch)
    • Ipsilateral conjugate gaze towards lesion (PPRF), nystagmus (CN VIII), ataxia, diplopia on lateral gaze (CN VI)
    • Contralateral face/arm/leg paralysis and decreased proprioception
  • Medial midpontine syndrome (paramedian midbasilar artery branch)
    • Ipsilateral ataxia
    • Contralateral face/arm/leg paralysis and decreased proprioception
  • Medial superior pontine syndrome (paramedian upper basilar artery branches)
    • Ipsilateral ataxia, INO, myoclonus of pharynx/vocal cords/face
    • Contralateral face/arm/leg paralysis and decreased proprioception

Superior Cerebellar Artery (SCA)

Posterior Cerebral Artery (PCA)

Signs and Symptoms:

  • Common after CPR, as occipital cortex is a watershed area
  • Unilateral headache (most common presenting complaint)
  • Visual field defects (contralateral homonymous hemianopsia, unilateral blindness)
  • Visual agnosia - can't recognize objects
  • Possible macular sparing if MCA unaffected
  • Motor function is typically minimally affected
  • Lateral midbrain syndrome (penetrating arteries from PCA)
    • Ipsilateral CN III - eye down and out, pupil dilated
    • Contralateral hemiataxia, tremor, hyperkinesis (red nucleus)
  • Medial midbrain syndrome (upper basilar and proximal PCA)
    • Ipsilateral CN III - eye down and out, pupil dilated
    • Contralateral paralysis of face, arm, leg (corticospinal)

Anterior Inferior Cerebellar Artery (AICA)

Posterior Inferior Cerebellar Artery (PICA)

Signs and Symptoms:

  • Lateral medullary/Wallenberg syndrome
  • Ipsilateral cerebellar signs, ipsilateral loss of pain/temperature of face, ipsilateral Horner syndrome, ipsilateral dysphagia and hoarseness, dysarthria, vertigo/nystagmus
  • Contralateral loss of pain/temp over body
  • Also caused by vertebral artery occlusion (most cases)

Internal Capsule and Lacunar Infarcts

  • May present with either lacunar c/l pure motor or c/l pure sensory (of face and body)[8]
    • Pure c/l motor - posterior limb of internal capsule infarct
    • Pure c/l sensory - thalamic infarct (Dejerine and Roussy syndrome)
  • C/l motor plus sensory if large enough
  • Clinically to cortical large ACA + MCA stroke - the following signs suggest cortical rather than internal capsule[9]:
    • Gaze preference
    • Visual field defects
    • Aphasia (dominant lesion, MCA)
    • Spatial neglect (non-dominant lesion)
  • Others
    • Ipsilateral ataxic hemiparesis, with legs worse than arms - posterior limb of internal capsule infarct
    • Dysarthria/Clumsy Hand Syndrome - basilar pons or anterior limb of internal capsule infarct

Anterior Spinal Artery (ASA)

Superior ASA

  • Medial medullary syndrome - displays alternating pattern of sidedness of symptoms below
  • Contralateral arm/leg weakness and proprioception/vibration
  • Tongue deviation towards lesion

Inferior ASA

  • ASA syndrome
  • Watershed area of hypoperfusion in T4-T8
  • Bilateral pain/temp loss in trunk and extremities (spinothalamic)
  • Bilateral weakness in trunk and extremities (corticospinal)
  • Preservation of dorsal columns

Risk Factors

  • Midface Fractures (Le Fort II or III)
  • Basilar Skull Fracture with carotid canal involvement
  • Diffuse axonal injury with GCS<6
  • Cervical spine fracture
  • Hanging with anoxic brain injury
  • Seat belt abrasion or other soft tissue injury of the anterior neck resulting in significant swelling or altered mental status
    • Isolated seatbelt sign without other neurologic symptoms has not been identified as a risk factor[10][11][12]
Algorithm for evaluation of BCVI with high risk criteria based on Memphis and Denver Screening Criteria

Diagnosis

  • Confirmed by CTA or MRA showing vessel wall abnormality (intimal flap, intramural hematoma, stenosis, pseudoaneurysm, occlusion)
  • Biffl Grading Scale (for traumatic BCVI; determines management):
Grade Injury Management
I Intimal irregularity or dissection with <25% luminal narrowing Antithrombotic therapy (ATT)
II Dissection/intramural hematoma with ≥25% luminal narrowing, intraluminal thrombus, or raised intimal flap ATT; follow-up imaging at 7-10 days; endovascular if progresses
III Pseudoaneurysm ATT ± endovascular repair
IV Complete occlusion ATT ± endovascular repair
V Transection with active extravasation Emergent hemorrhage control (surgery/endovascular)
  • Many grade I-II injuries heal spontaneously within 7-10 days with antithrombotic therapy
  • Intracranial extension changes management — higher SAH risk; anticoagulation may be contraindicated

Management

Acute Stroke Management

  • Activate stroke team — do not delay
  • IV alteplase (tPA): dissection-related stroke is NOT a contraindication to thrombolysis within standard time windows per AHA/ESO guidelines[13]
    • Do NOT give if dissection is intracranial — risk of SAH or ICH
    • Do NOT give if aortic dissection involved — may worsen dissection
    • Otherwise, give per same guidelines as ischemic CVA
    • In meta-analysis, thrombolytics appear equally efficacious in dissection-related stroke vs stroke from other causes[14]
  • Mechanical thrombectomy: consider for large vessel occlusion (basilar artery, proximal MCA) per standard stroke protocols
  • Obtain emergent vascular surgery or neurointerventional consult for possible endovascular intervention

Antiplatelet vs Anticoagulation Therapy

  • CADISS trial (2015) and TREAT-CAD trial (2021): no significant difference between antiplatelets vs anticoagulation in preventing stroke/death after cervical artery dissection[15][16]
  • Choice is guided by location and clinical scenario:
    • Heparin → warfarin (anticoagulation): if dissection is extracranial AND causes neurologic deficit[17]
      • Also consider if: free-floating thrombus, high-grade stenosis, recurrent TIAs despite aspirin
    • Aspirin: if dissection is intracranial — anticoagulants avoided due to weaker medial walls and higher SAH risk[18]
    • Aspirin: if dissection is extracranial with no neurologic deficit (stroke prevention)
    • Aspirin: if large completed infarct (risk of hemorrhagic transformation with anticoagulation)
    • Aspirin: preferred in polytrauma or other active bleeding concerns
  • Practical summary: when in doubt, aspirin is the safer choice — the evidence shows no superiority of anticoagulation, and aspirin carries less bleeding risk
  • If tPA was given, wait 24 hours before starting antithrombotic therapy
  • Do not anticoagulate if NIHSS ≥15 (high risk of hemorrhagic transformation)
  • Duration: typically 3-6 months; follow-up imaging (CTA or MRA) guides discontinuation; ~90% of dissections heal in this period

Endovascular/Surgical Intervention

  • Emergent for Grade V (transection with hemorrhage)
  • Consider for Grade II-IV injuries that progress despite antithrombotic therapy
  • Consider if antithrombotic therapy is contraindicated (e.g., concurrent intracranial hemorrhage, solid organ injury)
  • Stenting is increasingly used but data on superiority over ATT alone remains limited

Complications

  • CVA: risk of stroke is highest in the first 24 hours after dissection; remains elevated for first 2 weeks
  • SAH: if dissection extends intracranially (especially vertebral V4 segment)
  • Recurrent dissection: ~1% annual risk; higher in those with connective tissue disorders or family history
  • Pseudoaneurysm formation: may require long-term follow-up and possible intervention

Disposition

  • Admit all confirmed or strongly suspected cervical artery dissections
    • ICU/stroke unit if acute stroke, SAH, or neurologic deterioration
    • Telemetry/monitored bed if stable with pain only (no stroke)
  • Symptomatic patients (headache/neck pain only, no stroke): still admit — stroke risk is highest in first 2 weeks; serial neurologic examinations
  • Start antithrombotic therapy in the ED — do not defer to the floor
  • Follow-up imaging: CTA or MRA at 7-10 days (traumatic/BCVI) or 3-6 months (spontaneous) to assess healing
  • Counsel:
    • Avoid cervical manipulation (chiropractic, aggressive physiotherapy) — indefinitely
    • Seek immediate care if new neurologic symptoms develop
    • Medication compliance with antithrombotic therapy
    • Annual recurrence risk ~1% after initial episode; higher with connective tissue disorders
  • Return precautions: any new weakness, numbness, speech difficulty, dizziness, imbalance, visual changes, severe worsening headache

See Also


External Links

References

  1. ↑ Vertebral Artery Dissection. StatPearls. NCBI. 2025.
  2. ↑ De Giuli V et al. Association Between Migraine and Cervical Artery Dissection: The Italian Project on Stroke in Young Adults. JAMA Neurol. Published online March 6, 2017. doi:10.1001/jamaneurol.2016.5704
  3. ↑ Lee MJ, Park YG, Kim SJ, Lee JJ, Bang OY, Kim JS. Characteristics of stroke mechanisms in patients with medullary infarction. Eur J Neurol. 2012;19(11):1433-1439.
  4. ↑ Kim JS. Pure lateral medullary infarction: clinical-radiological correlation of 130 acute, consecutive patients. Brain. 2003;126(Pt 8):1864-1872.
  5. ↑ Provenzale JM, Sarikaya B. Comparison of test performance characteristics of MRI, MR angiography, and CT angiography in the diagnosis of carotid and vertebral artery dissection: a review of the medical literature. AJR Am J Roentgenol. 2009 Oct;193(4):1167-74. doi: 10.2214/AJR.08.1688. PMID: 19770343.
  6. ↑ Macdonell RA, Kalnins RM, Donnan GA. Cerebellar infarction: natural history, prognosis, and pathology. Stroke. 18 (5): 849-55.
  7. ↑ Lee H, Kim HA. Nystagmus in SCA territory cerebellar infarction: pattern and a possible mechanism. J Neurol Neurosurg Psychiatry. 2013 Apr;84(4):446-51.
  8. ↑ Rezaee A and Jones J et al. Lacunar stroke syndrome. Radiopaedia. http://radiopaedia.org/articles/lacunar-stroke-syndrome.
  9. ↑ Internal Capsule Stroke. Stanford Medicine Guide. http://stanfordmedicine25.stanford.edu/the25/ics.html
  10. ↑ DiPerna CA, Rowe VL, Terramani TT, et al. Clinical importance of the “seat belt sign” in blunt trauma to the neck. Am Surg. 2002;68:441–445
  11. ↑ Rozycki GS, Tremblay L, Feliciano DV, et al. A prospective study for the detection of vascular injury in adult and pediatric patients with cervicothoracic seat belt signs. J Trauma. 2002;52:618–623; discussion 623–624
  12. ↑ Sherbaf FG, Chen B, Pomeranz T, et al. Value of emergent neurovascular imaging for “Seat belt injury”: A multi-institutional study. American Journal of Neuroradiology. 2021;42(4):743-748
  13. ↑ Zinkstok SM, Vergouwen MD, Engelter ST, et al. Safety and functional outcome of thrombolysis in dissection-related ischemic stroke: a meta-analysis of individual patient data. Stroke. 2011;42:2515–2520.
  14. ↑ Zinkstok SM, Vergouwen MD, Engelter ST, Lyrer PA, Bonati LH, Arnold M, Mattle HP, Fischer U, Sarikaya H, Baumgartner RW, Georgiadis D, Odier C, Michel P, Putaala J, Griebe M, Wahlgren N, Ahmed N, van Geloven N, de Haan RJ, Nederkoorn PJ. Safety and functional outcome of thrombolysis in dissection-related ischemic stroke: a meta-analysis of individual patient data. Stroke. 2011 Sep;42(9):2515-20. doi: 10.1161/STROKEAHA.111.617282. Epub 2011 Jul 28. PMID: 21799165.
  15. ↑ CADISS trial investigators; Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015 Apr;14(4):361-7. doi: 10.1016/S1474-4422(15)70018-9. Epub 2015 Feb 12. Erratum in: Lancet Neurol. 2015 Jun;14(6):566. PMID: 25684164.
  16. ↑ Engelter ST, Traenka C, Gensicke H, et al. Aspirin versus anticoagulation in cervical artery dissection (TREAT-CAD): an open-label, randomised, non-inferiority trial. Lancet Neurol. 2021;20(5):341-350.
  17. ↑ Vasc Med. 2011 Feb;16(1):35-77. doi: 10.1177/1358863X11399328. Erratum in: Vasc Med. 2011 Aug;16(4):317. PMID: 21471149.
  18. ↑ Debette S, Mazighi M, Bijlenga P, et al. ESO guideline for the management of extracranial and intracranial artery dissection. Eur Stroke J. 2021 Sep;6(3):XXXIX-LXXXVIII. doi: 10.1177/23969873211046475. PMID: 34746432; PMCID: PMC8564160.
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