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Shah Q, Messé SR. Cervicocranial arterial dissection. Curr Treat Options Neurol. 2007;9(1):55-62doi: 10.1007/s11940-007-0031-4.
Shah, Q., & Messé, S. R. (2007). Cervicocranial arterial dissection. Current treatment options in neurology, 9(1), 55-62. https://doi.org/10.1007/s11940-007-0031-4
Shah, Qaisar, and Messé, Steven R. "Cervicocranial arterial dissection." Current treatment options in neurology vol. 9,1 (2007): 55-62. doi: https://doi.org/10.1007/s11940-007-0031-4
Shah Q, Messé SR. Cervicocranial arterial dissection. Curr Treat Options Neurol. 2007 Jan;9(1):55-62. doi: 10.1007/s11940-007-0031-4. PMID: 17288890.
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Curr Treat Options Neurol. 2007 Jan;9(1):55-62. doi: 10.1007/s11940-007-0031-4.

Cervicocranial arterial dissection.

Current treatment options in neurology

Qaisar Shah, Steven R Messé

Affiliations

  1. Steven R. Messé, MD Hospital of the University of Pennsylvania, Department of Neurology, 3400 Spruce Street, 3 West Gates Building, Philadelphia, PA 19104, USA. [email protected].

PMID: 17288890 DOI: 10.1007/s11940-007-0031-4

Abstract

Cervicocranial arterial dissection (CCAD) occurs when there is a tear in the intimal layer of the carotid or vertebral arteries with subsequent extravasation of blood into the subintimal layers. The dissection may be extradural, intradural, or extend over both segments. The contents of the subintimal layers are highly thrombogenic, and thus, embolism, vessel stenosis, or occlusion may follow. Symptoms of dissection may be caused by local injury to the blood vessel or by ischemia to the retina or brain. Thus, dissection should always be considered in patients who present with Horner syndrome associated with ipsilateral headache, carotidynia, ocular pain, or amaurosis fugax. Rare neuro-ophthalmologic presentations of dissection include anterior and posterior ischemic optic neuropathy; central retinal artery occlusion; ophthalmic artery occlusion; transient ophthalmoparesis; and third, fourth, or sixth cranial nerve palsy. The most common serious complication of dissection is ischemic stroke. No randomized controlled trials have evaluated therapies for patients presenting with CCAD. Thus, treatment is essentially empiric and often varies by region. Medical management is first line in most patients. Given the propensity for thrombus formation and early embolization or occlusion, acute anticoagulation using intravenous heparin or low-molecular-weight heparinoids followed by short-term, dose-adjusted warfarin is the treatment of choice for most patients with extradural CCAD who present early after symptom onset. The risk of cerebral ischemia is greatest in the first few weeks after dissection; thus, it is reasonable to recommend antiplatelet agents for patients who present late and have not had evidence of ischemia. Intradural dissection is rare but is associated with a meaningful risk of subarachnoid hemorrhage (SAH). As a result, anticoagulants and antiplatelet agents should not be used if SAH is suspected or confirmed. Endovascular intervention may be necessary in a small minority of cases with recurrent events despite anticoagulation or SAH due to intradural dissection. Of special note, CCAD is not considered a contraindication for tissue plasminogen activator use in acute stroke patients who are otherwise eligible for treatment.

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