Significant cause of strokes in young/middle aged patients (5-22% of strokes in this age group)
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)
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
Patient with severe head/face/neck trauma that develops neurologic deficits
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
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
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
Patel RR, Adam R, et al. Cervical carotid artery dissection: current review of diagnosis and treatment Cardiology in Review. 2012 May-Jun; 20(3):145-52.
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.
Debette S, Leys D. Cervical-artery dissections: predisposing factors, diagnosis, and outcomes. Lancet Neurol 2009; 8:668.
Engelter, ST, Brandt, T, et al. Antiplatelets versus anticoagulation in cervical artery dissection. Stroke. 2007;38:2605-2611.
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