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
• 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

• Any mechanical event involving the neck; symptoms typically occur 2-3 days after event
  • Neck trauma (often minor), MVC, falls
  • Cervical manipulation (chiropractic, physiotherapy)
  • Coughing/sneezing, vigorous exercise, weightlifting, intercourse, roller coasters, yoga
• Connective tissue disease: Ehlers-Danlos syndrome type IV, Marfan syndrome, osteogenesis imperfecta
• History of migraine
• Recent infection (proposed inflammatory vessel wall weakening)
• Hypertension

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

• Posterior neck pain, occipital headache
  • May be unilateral or bilateral
• Unilateral facial paresthesia
• Dizziness or Vertigo
• Nausea/vomiting
• Diplopia, nystagmus, and other visual disturbances
• Ataxia
• Dysarthria, dysphagia
• Lateral medullary syndrome (Wallenberg) seen in up to 20% of VAD
  • 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 (basilar involvement)

Differential Diagnosis

Neck Trauma

• Penetrating neck trauma
• Blunt neck trauma
  • Vertebral and carotid artery dissection
  • Strangulation
  • Whiplash injury
• Cervical injury
  • Cervical fractures and dislocations
  • Cervical injury (peds)
  • Cervical spine clearance
• Neurogenic shock
• Spinal cord injury

Other considerations:

• Migraine — most common misdiagnosis; but new-type headache in a patient without migraine history warrants imaging
• Cervical strain / musculoskeletal neck pain — absence of neurologic symptoms does NOT exclude early dissection
• Subarachnoid hemorrhage — thunderclap headache; intracranial dissection can cause SAH
• Cerebellar stroke from other embolic sources
• Vertebrobasilar insufficiency
• Meningitis — neck pain + headache; check for fever, meningismus
• Giant cell arteritis (patients >50 with new headache)
• Cavernous sinus thrombosis — if cranial nerve palsies with proptosis

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
  • 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

• Apply the Denver screening criteria for BCVI screening in blunt trauma patients
  • If positive findings on screening → obtain CTA

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

• Blood supply via the vertebral artery
• Branches include, AICA, Basilar artery, PCA and PICA

Signs and Symptoms:

• Crossed neuro deficits (i.e., ipsilateral CN deficits w/ contralateral motor weakness)
• Multiple, simultaneous complaints are the rule (including loss of consciousness, nausea/vomiting, alexia, visual agnosia)
• 5 Ds: Dizziness (Vertigo), Dysarthria, Dystaxia, Diplopia, Dysphagia
• Isolated events are not attributable to vertebral occlusive disease (e.g. isolated lightheadedness, vertigo, transient ALOC, drop attacks)
• Approximately 25% associated with aortic dissection

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)

• ~2% of all cerebral infarctions
• May present with nonspecific symptoms - nausea/vomiting, dizziness, ataxia, nystagmus (more commonly horizontal)
• Lateral superior pontine syndrome
  • Ipsilateral ataxia, nausea/vomiting, nystagmus, Horner syndrome, conjugate gaze paresis
  • Contralateral loss of pain/temperature in face/extremities/trunk, and loss of proprioception/vibration in LE > UE

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)

• Lateral inferior pontine syndrome
• Ipsilateral facial paralysis, loss of corneal reflex (CN VII)
• Ipsilateral loss of pain/temperature (CN V)
• Nystagmus, nausea/vomiting, vertigo, ipsilateral hearing loss (CN VIII)
• Ipsilateral limb and gait ataxia
• Ipsilateral Horner syndrome
• Contralateral loss of pain/temperature in trunk and extremities (lateral spinothalamic)

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)
  • 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:
  • 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

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
  • 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
• 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
• Choice is guided by location and clinical scenario:
  • Heparin → warfarin (anticoagulation): if dissection is extracranial AND causes neurologic deficit
    • 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
  • 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

• Blunt cerebrovascular injury
• Denver screening criteria
• Blunt neck trauma
• Penetrating neck trauma
• Ischemic stroke
• Stroke (main)
• CVA (tPA)
• Thrombolytics for acute ischemic stroke
• Cerebellar stroke
• Vertebrobasilar insufficiency
• Subarachnoid hemorrhage
• Horner syndrome
• Lateral medullary syndrome
• Alteplase
• Anticoagulation
• Antiplatelet
• Heparin
• Aspirin
• TIA
• Vertigo
• Neck pain
• Cervical fractures and dislocations
• Strangulation

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)
• Scand J Trauma — Best practice guidelines for BCVI (2018)
• EAST — BCVI Practice Management Guideline (2020)