Carotid artery dissection
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| Carotid artery dissection Classification and external resources | |
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| DiseasesDB | 2145 |
| eMedicine | emerg/82 |
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Carotid artery dissection is an important cause of stroke in young patients.
Arterial dissection of the carotid arteries occurs when a small tear in the innermost lining of the arterial wall forms. Blood can enter into the space between the inner and outer layers of the vessel, causing narrowing (stenosis) or complete occlusion. The stenosis that occurs in the early stages of arterial dissection is a dynamic process and some occlusions can return to stenosis very quickly.1 When complete occlusion occurs, it may lead to ischemia. Often, even a complete occlusion is totally asymptomatic because collateral circulation in the head keeps the brain well perfused. However, when blood clots form and break off from the site of the tear, the clots travel through the blood to the brain and clog one or more of the arteries directly supplying the brain, resulting in an ischemic stroke, otherwise known as an infarct. Blood clots, or emboli, originating from the dissection are thought to be the cause of infarction in the majority of cases of stroke in the presence of carotid artery dissection.2 Cerebral infarction causes irreversible damage to the brain. In one study of patients with carotid artery dissection, 60% had infarcts documented on neuroimaging.3
The cause of internal carotid artery dissection can be broadly categorized into two classes: spontaneous or traumatic.
Spontaneous
Once considered uncommon, spontaneous carotid artery dissection is an increasingly recognized cause of stroke that preferentially affects the middle-aged.4 The incidence of spontaneous carotid artery dissection is low, and incidence rates for internal carotid artery dissection have been reported to be 2.6 to 2.9 per 100,000.5
Observational studies and case reports published since the early 1980s show that patients with spontaneous internal carotid artery dissection may also have hereditary connective tissue disorders. These include Marfan syndrome, vascular Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, pseudoxanthoma elasticum, fibromuscular dysplasia, and osteogenesis imperfecta type I.6 However, the reports on the prevalence of hereditary connective tissue diseases in people with spontaneous dissections is highly variable, ranging from 0% to 0.6% in one study to 5% to 18% in another study. Nevertheless, although an association exists with connective tissue disorders does exist, most people with spontaneous arterial dissections do not have associated connective tissue disorders.7
Traumatic
Carotid artery dissection is more commonly thought to be caused by trauma to the head and/or neck. An estimated 0.67% of patients admitted to the hospital after motor vehicle accidents were found to have blunt carotid injury, including intimal dissections, pseudoaneurysms, thromboses, or fistulas.8 Of these, 76% had intimal dissections, pseudoaneurysms, or a combination of the two.
The probable mechanism of injury for most internal carotid injuries is rapid deceleration, with resultant hyperextension and rotation of the neck, which stretches the internal carotid artery over the upper cervical vertebrae, producing an intimal tear.9 After such an injury, the patient may remain asymptomatic, have a hemispheric transient ischemic event, or suffer a stroke.10
Treatment
The goal of treatment is to prevent the development or continuation of neurologic deficits. Treatments include observation,anticoagulation, stent implantation and carotid artery ligation.
References
1. C Lucas, et al. Stroke patterns of internal carotid artery dissection in 40 patients. Stroke. 1998;29:2646-2648.
2. C Lucas, et al. Stroke patterns of internal carotid artery dissection in 40 patients. Stroke. 1998;29:2646-2648.
3. VH Lee, et al. Incidence and outcome of cervical dissection; a population-based study. Neurology 2006;67:1809-1812.
4. In: Neurology 2006;67:1809-1812. Mokri B. Spontaneous dissections of internal carotid arteries. Neurologist 1997;3:104–119.
5. VH Lee, et al. Incidence and outcome of cervical dissection; a population-based study. Neurology 2006;67:1809-1812.
6. JM de Bray, et al. History of spontaneous dissection of the cervical carotid artery. Arch Neurol. 2005;62:1168-1170.
7. JM de Bray, et al. History of spontaneous dissection of the cervical carotid artery. Arch Neurol. 2005;62:1168-1170.
8. TC Fabian, et al. Blunt Carotid Injury. Annals of Surgery. 1996; Vol. 223, No. 5: 513-52.
9. TC Fabian, et al. Blunt Carotid Injury. Annals of Surgery. 1996; Vol. 223, No. 5: 513-52.
10. JH Matsuura, et al. Traumatic Carotid Artery Dissection and Pseudoaneurysm Treated With Endovascular Coils and Stent Journal of Endovascular Surgery. 1997; Vol. 4, No. 4, pp. 339–343.
See also
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
