Carotid Artery Dissection

Introduction

• Incidence 2.5-3 per 100,000
• Peak incidence in 5^th decade of life
• Significant cause of strokes in young/middle aged patients (5-22% of strokes in this age group)

Etiology/Predisposing Factors

• Spontaneous, minor trauma (e.g. sneezing, chiropractor manipulation, nose blowing, yoga), connective tissue disorders (e.g. Marfan’s, Ehlers-Danlos syndrome), genetic
• Underlying arteriopathy likely exists in patients with spontaneous dissection or due to minor trauma
• Major trauma: Elevated risk of carotid dissection with blunt or penetrating injuries involving the head, face, neck or thorax (and particularly in patients with skull base fractures, facial fractures, or TBI)

Pathophysiology

• Intimal tear or direct bleeding in arterial wall -> intramural hematoma -> stenosis of arterial lumen or aneurysm formation -> formation of associated thrombi which may embolize distally to cause ischemia
• If intracranial extension, may lead to subarachnoid hemorrhage
• Most commonly occurs in ICA, 2cm cephalad from bifurcation of common carotid to skull base

Signs and Symptoms

• Pain: Unilateral headache, neck pain, facial pain
• Partial horner’s syndrome (ptosis and miosis without anhidrosis); sympathetic fibers associated with facial sweating are associated closely with external carotid artery and NOT the ICA
• Cranial nerve palsies (CN XII most common), abnormal taste, pulsatile tinnitus
• Ischemia: TIA/stroke with associated anterior circulation deficits (hemiparesis, hemisensory loss, aphasia, neglect, amaurosis fugax)
• Patient with severe head/face/neck trauma that develops neurologic deficits

Diagnosis

• First line: CTA neck or MR angiography depending on local availability/practice pattern
  • CTA generally used in patients with significant trauma
• Doppler ultrasound: Highly operator dependent, relatively poor sensitivity if low grade stenosis. Should NOT be used as first line test
• Angiography is traditional gold standard for diagnosis, but invasive and associated with complications
  • Only if initial screening study is negative but high suspicion for carotid dissection

Management

• Spontaneous carotid dissection with evidence of acute ischemic stroke
  • Recent meta-analysis shows similar safety in giving thrombolysis in dissection vs non-dissection related strokes (retrospective data, no RCTs)
  • Thrombolysis CONTRAINDICATED if dissection is intracranial (risk of ICH) or involves the aorta (risk of aortic rupture)
• Antiplatelet vs anticoagulation
  • Controversial; no published RCTs comparing either strategy (ongoing CADISS trial)
  • Currently, no evidence of superiority in antiplatelet vs anticoagulation strategy.  2011 AHA/ASA guidelines state relative efficacy of either strategy is unknown
  • Anticoagulation generally preferred if thrombus present in arterial lumen or severe stenosis
  • Antiplatelet preferred if contraindication to anticoagulation, NIHSS >15, large infarct, intracranial extension of dissection
• No clear criteria for endovascular therapy (stent)
  • Considered when new ischemic symptoms develop despite being on antiplatelet or anticoagulation — “failure of medical therapy”
• Continue antiplatelet or anticoagulation for 3 to 6 months and re-imaging is generally done within the time frame prior to discontinuing therapy

Pearls

• Should always consider carotid/cervical dissection as cause of ischemic symptoms in patients that are young, lack risk factors for thrombotic/embolic stroke, or complaining of neck pain
• Trauma patients with significant head/neck trauma and neurologic deficits, should evaluate for carotid or vertebral artery dissection
• Consider carotid dissection in patients presenting with neck pain or headache that started in the context of activities that cause torsion or blunt trauma to neck

References/Further Reading