Mechanism of ischemic infarct in spontaneous carotid dissection

• Published in: Stroke (1970) Vol. 35; no. 2; pp. 482 - 485
• Main Authors: BENNINGER, D. H, GEORGIADIS, D, KREMER, C, STUDER, A, NEDELTCHEV, K, BAUMGARTNER, R. W
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01-02-2004
• Subjects: Biological and medical sciences; Brain Ischemia - diagnosis; Brain Ischemia - etiology; carotid artery; Carotid Artery Thrombosis - complications; Carotid Artery Thrombosis - diagnosis; Carotid Artery, Internal - diagnostic imaging; Carotid Artery, Internal, Dissection - complications; Carotid Artery, Internal, Dissection - diagnostic imaging; Cerebral Infarction - classification; Cerebral Infarction - diagnosis; Cerebral Infarction - etiology; Clinical Medicine; diagnostic imaging; dissection; Female; Humans; internal; Klinisk medicin; Magnetic Resonance Imaging; Male; Medical and Health Sciences; Medical sciences; Medicin och hälsovetenskap; Middle Aged; Neurologi; Neurology; Retrospective Studies; Risk Factors; stroke; Tomography, X-Ray Computed; Ultrasonography; Vascular diseases and vascular malformations of the nervous system; Stroke; Internal carotid; Nervous system diseases; Infarct; ultrasonography; carotid artery, internal, dissection; Cardiovascular disease; diagnostic imaging; Cerebral disorder; Artery dissection; Arterial disease; Vascular disease; Dissecting aneurysm; Ischemia; Central nervous system disease; Echography; Diagnosis; Cerebrovascular disease
• ISSN: 0039-2499; 1524-4628; 1524-4628
• DOI: 10.1161/01.STR.0000109766.27393.52

It is unclear whether stroke in patients with spontaneous dissection of the cervical internal carotid artery (ICAD) is due to thromboembolism or impaired hemodynamics. This study investigated the mechanism of stroke in ICAD by examining brain imaging and cerebrovascular findings of such patients.
We retrospectively evaluated the prospectively collected brain CT, MR, and ultrasound findings of 141 consecutive patients with 143 ICADs causing ischemic stroke. Eleven patients were not included because they had an inappropriate temporal bone window (n=6) or were treated with thrombolysis (n=5). Thus, the data of 130 patients (76 men, 54 women) with 131 ICADs were analyzed.
All patients had territorial infarcts; 6 patients (5%) also had border-zone infarct patterns. Territorial infarcts affected the middle cerebral artery (MCA) in 130 of 131 cases (99%) and the anterior cerebral artery (ACA) in 1 case (1%). Additional vascular territories were affected in 8 patients with MCA infarcts (ACA, n=5 [4%]; posterior cerebral artery, n=3 [2%]). The pattern (hemodynamic versus thromboembolic) and extent of infarction were not influenced by vascular findings (MCA stenosis or occlusion, ACA occlusion, degree of obstruction in the dissected ICA, pattern of cross-flow in 115 patients with >80% ICA stenosis or occlusion).
This study suggests that thromboembolism, not hemodynamic infarction, is the essential stroke mechanism in ICAD.