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An In Vivo Assessment of Blood-Brain Barrier Disruption in a Rat Model of Ischemic Stroke
Published on: March 11, 2018
Mechanism of ischemic infarct in spontaneous carotid dissection
D H Benninger1, D Georgiadis, C Kremer
1Department of Neurology, University Hospitals of Zürich, Switzerland.
Insights
Stroke in spontaneous cervical internal carotid artery dissection (ICAD) is primarily caused by thromboembolism, not hemodynamic changes. This finding clarifies the essential stroke mechanism in ICAD patients.
Area of Science:
- Neurology
- Vascular Medicine
- Radiology
Background:
- Spontaneous dissection of the cervical internal carotid artery (ICAD) is a significant cause of stroke in younger adults.
- The underlying mechanism of stroke in ICAD, whether thromboembolic or hemodynamic, remains debated.
Purpose of the Study:
- To investigate the primary mechanism of ischemic stroke in patients with spontaneous cervical internal carotid artery dissection (ICAD).
- To differentiate between thromboembolic and hemodynamic causes of stroke in the context of ICAD.
Main Methods:
- Retrospective analysis of prospectively collected brain CT, MR, and ultrasound data from 130 patients with 131 ICADs.
- Exclusion of patients with inappropriate temporal bone windows or those treated with thrombolysis.
- Evaluation of infarct patterns and vascular findings, including stenosis and occlusion.
Main Results:
- All analyzed patients presented with territorial infarcts, predominantly affecting the middle cerebral artery (MCA) territory (99%).
- The pattern and extent of infarction were not significantly influenced by vascular findings such as MCA stenosis, occlusion, or degree of internal carotid artery (ICA) obstruction.
- No correlation was found between hemodynamic factors and the observed infarct patterns.
Conclusions:
- Thromboembolism is identified as the essential stroke mechanism in spontaneous cervical internal carotid artery dissection (ICAD).
- Hemodynamic compromise is not the primary driver of infarction in this patient cohort.
Background And Purpose:
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.
Methods:
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.
Results:
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).
Conclusions:
This study suggests that thromboembolism, not hemodynamic infarction, is the essential stroke mechanism in ICAD.
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