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Mechanism of ischemic infarct in spontaneous cervical artery dissection
Audrey Morel1, Olivier Naggara, Emmanuel Touzé
1Neuroradiology, Hôpital Sainte-Anne, Paris, France.
Insights
Stroke in cervical artery dissection (CAD) is most often caused by artery-to-artery embolization. This finding, supported by imaging, can inform future treatment strategies for CAD-related strokes.
Area of Science:
- Neurology
- Radiology
- Vascular Medicine
Background:
- Spontaneous cervical artery dissection (CAD) can lead to stroke, but the underlying mechanism (thromboembolism vs. hemodynamic compromise) remains unclear.
- Distinguishing stroke mechanisms in CAD is crucial for effective treatment and trial design.
Purpose of the Study:
- To determine the primary mechanism of stroke in patients diagnosed with cervical artery dissection (CAD).
- To utilize advanced imaging parameters to differentiate between embolic and hemodynamic causes of stroke in CAD patients.
Main Methods:
- Retrospective analysis of cerebrovascular ultrasound, cervical MR angiography, and brain MRI in 172 consecutive CAD patients.
- Defined embolic mechanism by direct embolism visualization or pial artery territory infarction.
- Defined hemodynamic mechanism by watershed infarction, severe stenosis/occlusion, reduced flow velocity, or hyperintense vessel sign.
Main Results:
- Of 172 CAD patients, 100 (58%) experienced acute stroke.
- Stroke was attributed to a thromboembolic mechanism in 85% of stroke patients.
- Hemodynamic and mixed mechanisms accounted for 12% and 3% of strokes, respectively.
Conclusions:
- Stroke in cervical artery dissection (CAD) is predominantly caused by artery-to-artery embolization.
- Imaging findings strongly suggest an embolic origin for most CAD-related strokes.
- These results provide critical insights for developing targeted therapeutic interventions in future clinical trials.
Background And Purpose:
It is unclear whether strokes in patients with spontaneous cervical artery dissection (CAD) are due to secondary thromboembolism or to a reduction in cerebral blood flow from the primary cervical lesion. The aim of this study was to identify the most likely mechanism of stroke using cervical and cerebral imaging parameters in patients with CAD.
Methods:
The study was approved by the local Ethics Committee. Informed consent was waived. We retrospectively evaluated the cerebrovascular ultrasound, cervical MR angiography, and stroke brain MRI in consecutive patients with CAD. An embolic mechanism was considered in the case of direct visualization of an intracranial embolism as a susceptibility vessel sign on T2* or in the case of pial artery territory infarction on diffusion-weighted imaging. A hemodynamic mechanism was considered in the case of watershed infarction and in the case of an association of watershed infarction and pial artery territory infarction when ≥ 2 of the following were present: severe stenotic or occlusive CAD, reduced intracranial velocity on cerebrovascular ultrasound or signal on MR angiography, or hyperintense vessel sign on fluid-attenuated inversion recovery. The remaining patients were considered to have a mixed mechanism.
Results:
Of 172 consecutive patients with CAD, 100 (58%) had acute stroke on diffusion-weighted imaging. Stroke was attributed to a thromboembolic mechanism in 85 of 100 patients, a hemodynamic mechanism in 12 of 100 patients, and a mixed mechanism in 3 of 100 patients.
Conclusions:
Stroke in patients with CAD is most frequently associated with both direct and indirect signs of artery-to-artery embolization on imaging, a finding that should help design future therapeutic trials.
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