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Spontaneous cerebral and cervical artery dissection: Clinical features and diagnosis

David S Liebeskind, MD
Section Editor
Scott E Kasner, MD
Deputy Editor
John F Dashe, MD, PhD


Arterial dissections are a common cause of stroke in the young, but may occur at any age. Dissection occurs when structural integrity of the arterial wall is compromised, allowing blood to collect between layers as an intramural hematoma.

This topic will review the pathophysiology, etiology, clinical features, and diagnosis of spontaneous cerebral and cervical artery dissection. The treatment and prognosis of cervicocephalic dissection is reviewed in detail separately. (See "Spontaneous cerebral and cervical artery dissection: Treatment and prognosis".)

Other mechanisms of ischemic stroke and subarachnoid hemorrhage are discussed elsewhere. (See "Ischemic stroke in children and young adults: Etiology and clinical features" and "Etiology, classification, and epidemiology of stroke" and "Clinical manifestations and diagnosis of aneurysmal subarachnoid hemorrhage" and "Nonaneurysmal subarachnoid hemorrhage".)


Separation of the arterial wall layers results in dissection. A false lumen arises in the space where blood seeps into the vessel wall (figure 1). Hemorrhage may be due to an intimal tear or result from rupture or other pathology in the vasa vasorum [1,2]. Subintimal dissections cause luminal stenosis or occlusion whereas subadventitial dissections largely result in dissecting aneurysm formation (figure 2). False lumen extension back into the true lumen can form a double channel for blood flow in the artery.

Neurologic sequelae of extracranial and intracranial dissection may result from cerebral ischemia due to thromboembolism, hypoperfusion, or a combination of both. However, thromboembolism rather than hypoperfusion is considered the major cause of ischemic symptoms [3,4]. In addition, dissection and aneurysmal dilatation may cause local symptoms from compression of adjacent nerves and their feeding vessels, resulting in pain, partial oculosympathetic paresis (Horner syndrome), lower cranial neuropathies [5], or cervical nerve root involvement. Pain is thought to be caused by activation of nociceptors from distension of the vessel wall due to the hematoma [6].

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Literature review current through: Nov 2017. | This topic last updated: Aug 25, 2017.
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