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Stroke patterns of internal carotid artery dissection in 40 patients
C Lucas1, T Moulin, D Deplanque
1Departments of Neurology and Neuroradiology, Lille, France. clucas@chru-lille.fr
Insights
Internal carotid artery dissection (ICAD) often causes stroke in young adults. Most ICAD-related infarcts are large and cortical, suggesting an embolic origin, supporting early anticoagulation therapy.
Area of Science:
- Neurology
- Vascular Neurology
- Neuroimaging
Background:
- Internal carotid artery dissection (ICAD) is a common cause of ischemic stroke in young individuals.
- The origin of cerebral ischemia in ICAD (embolic vs. hemodynamic) is not fully understood.
- Therapeutic strategies for ICAD are often based on presumed stroke mechanisms due to low recurrence rates making drug trials difficult.
Purpose of the Study:
- To investigate the stroke patterns in patients with internal carotid artery dissection (ICAD).
- To determine if infarct size and location correlate with embolic or hemodynamic origins.
- To inform therapeutic approaches for ICAD based on identified stroke patterns.
Main Methods:
- Retrospective analysis of 40 consecutive patients diagnosed with ICAD.
- Review of CT scans, MRI scans, and angiographic features by blinded observers.
- Categorization of infarcts into cortical, large subcortical (>=15 mm), small subcortical (<15 mm), and junctional types.
Main Results:
- A total of 65 ICADs were analyzed in 40 patients.
- The majority of infarcts were cortical (34) and large subcortical (25).
- Small subcortical (1) and junctional (5) infarcts were infrequent.
Conclusions:
- Infarcts associated with ICAD are predominantly cortical or large subcortical.
- The observed stroke patterns suggest that embolic events are the likely cause of most infarcts in ICAD.
- Anticoagulation is proposed as a logical early treatment strategy for carotid artery dissection (CAD) based on the presumed embolic mechanism.
Background And Purpose:
Internal carotid artery dissection (ICAD) is a frequent cause of ischemic stroke in young patients. Whether cerebral ischemia is of embolic or hemodynamic origin remains to be determined. Heparin is often administered in ICAD; however, a drug trial can hardly be conducted because of the low recurrence rate after the acute stage. Therefore, the best therapeutic approach should be determined on the basis of the presumed mechanism of cerebral ischemia. One way to approach the mechanism of stroke in ICAD is to determine stroke patterns. We postulated that most cortical and large subcortical infarcts (>/=15 mm) are of embolic origin and that small subcortical infarcts (<15 mm) and junctional infarcts are not. The aim of our study was to determine the stroke patterns in 40 consecutive patients with ICAD.
Methods:
The patients (26 women and 14 men; mean age, 42.8 years) had a total of 65 ICADs. Seventeen patients were free of any vascular risk factor. CT scans, MRI scans, and angiographic features were analyzed by observers who were blinded to the clinical findings.
Results:
We found 34 cortical infarcts, 25 large subcortical infarcts, 1 small subcortical infarct, and 5 junctional infarcts.
Conclusions:
Most infarcts related to ICAD are cortical infarcts or large subcortical infarcts; small subcortical infarcts and junctional infarcts are infrequent. Therefore, these findings suggest that most infarcts occurring in carotid artery dissection (CAD) are probably embolic rather than hemodynamic in origin. According to this presumed mechanism, anticoagulation seems a logical treatment at the early stage of CAD.