Carotid artery dissection

Carotid artery dissection (CAD) can be classified based on various criteria including etiology, location, extent, and imaging characteristics.

  • Spontaneous Carotid Dissection (sCAD):
    • Occurs without a known traumatic cause.
    • Associated with connective tissue disorders (e.g., Ehlers-Danlos, Marfan) or fibromuscular dysplasia.
  • Traumatic Carotid Dissection (tCAD):
    • Caused by direct or indirect trauma (e.g., cervical hyperextension, blunt trauma, penetrating injury).

see External carotid artery dissection.

  • Involves the cervical portion of the internal carotid artery (ICA).
  • Most common (~80% of cases).
  • Intracranial CAD (ICAD):
  • Affects the petrous, cavernous, or supraclinoid segments of the ICA.
  • Higher risk of subarachnoid hemorrhage (SAH).
  • Localized Dissection: Confined to a short segment.
  • Extensive Dissection: Involves a long segment, possibly extending extracranially to intracranially.
  • Stenotic vs. Aneurysmal Dissection:
    • Stenotic Type: False lumen compresses the true lumen, causing vessel narrowing and ischemia.
    • Aneurysmal Type: Pseudoaneurysm formation due to vessel wall weakening.
Type Description
I Narrowing of the lumen with an intimal flap or double lumen.
II Irregular lumen narrowing without an apparent intimal flap.
III Pseudoaneurysm formation due to vessel wall weakening.
IV Complete occlusion due to thrombosis in the false lumen.
V Dissection extending into distal branches.
  • Mild: No neurological deficits, incidental finding.
  • Moderate: Transient ischemic attack (TIA) or minor stroke.
  • Severe: Major ischemic stroke, SAH (if intracranial dissection), or significant mass effect.

—-

see Internal carotid artery dissection.

The incidence rate of Spontaneous Cervical Artery Dissection increased nearly 4-fold over 19 years from 2002 to 2020. The incidence rate in women rose over 12-fold. The increase in incidence rates likely reflects the increased use of noninvasive vascular imaging 1)

Luminal stenosis (65%), occlusion (28%), pseudoaneurysm (28%), luminal irregularity (13%), embolic distal branch occlusion (13 %), intimal flap (12 %) and slow ICA - MCA flow (11 %) 3).

Endovascular technique of acute ischemic stroke (AIS) in the setting of carotid artery dissection (CAD) is a feasible, safe, and promising strategy 4).

Endovascular therapy was associated with better outcomes and higher cost-recovery than IV thrombolysis in patients with large vessel strokes 5).


The initial management in the absence of ICH is intravenous heparin for 7 days followed by warfarin 6).

The goal aPTTwith heparin is 1.5 – 2.0 times the control value (50–80 sec). Warfarin is continued for 3–6 months with target INR range of 2.0 – 3.0. If anticoagulation is contraindicated, antiplatelet therapy is a consideration. In pregnant individuals, obtain obstetric consultation prior to initiating anticoagulation or anti-platelet therapy.

● Persistent ischemic symptoms despite anticoagulation therapy.

● Flow-limiting lesion with hemodynamic compromise

● Impending risk of stroke

● Expanding pseudoaneurysm formation

● Iatrogenic dissection during endovascular procedure where flow compromise is apparent

The endovascular treatment for carotid dissection is stenting. In case of intimal flap, the stent will appose the flap back to the arterial wall. Pseudoaneurysms have also been successfully occluded with stenting. Both uncovered and covered stents have been used successfully 7)

JoStent is a PTFE covered stent that is available in US. A vein covered stent has also been used 8). In case of a pseudoaneurysm that continues to show significant residual filling after stenting, coiling of the pseudoaneurysm will cause occlusion 9)

After stenting, the patient remains on dual antiplatelet therapy (ASA+Plavix) for at least a month and ASAalone indefinitely.

Follow-up should be arranged for patients on warfarin (e.g., “Coumadin clinic”).

Follow-up study in 3–6 months, which could be CTA, Doppler ultrasonography or catheter angiogram.


1)
Griffin KJ, Harmsen WS, Mandrekar J, Brown RD Jr, Keser Z. Epidemiology of Spontaneous Cervical Artery Dissection: Population-Based Study. Stroke. 2024 Jan 30. doi: 10.1161/STROKEAHA.123.043647. Epub ahead of print. PMID: 38288608.
2)
Keser Z, Diehn FE, Lanzino G. Photon-Counting Detector CT Angiography in Cervical Artery Dissection. Stroke. 2024 Jan 31. doi: 10.1161/STROKEAHA.123.046174. Epub ahead of print. PMID: 38293798.
3)
Anson J, Crowell RM. Cervicocranial Arterial Dissection. Neurosurgery. 1991; 29:89–96
4)
Haussen DC, Jadhav A, Jovin T, Grossberg J, Grigoryan M, Nahab F, Obideen M, Lima A, Aghaebrahim A, Gulati D, Nogueira RG. Endovascular Management vs Intravenous Thrombolysis for Acute Stroke Secondary to Carotid Artery Dissection: Local Experience and Systematic Review. Neurosurgery. 2015 Oct 21. [Epub ahead of print] PubMed PMID: 26492430.
5)
Rai AT, Evans K. Hospital-based financial analysis of endovascular therapy and intravenous thrombolysis for large vessel acute ischemic strokes: the 'bottom line'. J Neurointerv Surg. 2014 Jan 29. doi: 10.1136/neurintsurg-2013-011085. [Epub ahead of print] PubMed PMID: 24476964.
6)
Hart RG, Easton JD. Dissections of Cervical and Cerebral Arteries. Neurol Clin North Am. 1983; 1:255– 282
7) , 9)
Liu AY, Paulsen RD, Marcellus ML, Steinberg GK, Marks MP. Long-term outcomes after carotid stent placement treatment of carotid artery dissection. Neurosurgery. 1999; 45:1368–73; discussion 1373- 4
8)
Marotta TR, Buller C, Taylor D, Morris C, Zwimpfer T. Autologous vein-covered stent repair of a cervical internal carotid artery pseudoaneurysm: technical case report. Neurosurgery. 1998; 42:408–12; dis- cussion 412-3
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