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Published on: September 25, 2019
Posterior cerebral artery infarction: diffusion-weighted MRI analysis of 205 patients
Eugene Lee1, Dong-Wha Kang, Sun U Kwon
1Stroke Center and Department of Neurology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea.
Insights
In Korean patients, large artery atherosclerosis, particularly intrinsic posterior cerebral artery (PCA) disease, is a key cause of PCA territory infarction, leading to varied stroke patterns. This contrasts with the typical cardiac embolism cause.
Area of Science:
- Neurology
- Vascular Neurology
- Neuroimaging
Background:
- Cardiac embolism is a common cause of posterior cerebral artery (PCA) infarction.
- Intrinsic PCA atherosclerotic disease may be more prevalent in certain populations.
Purpose of the Study:
- To investigate the etiologies and stroke patterns of PCA territory infarction.
- To assess the role of intrinsic PCA atherosclerotic disease in Korean patients.
Main Methods:
- Retrospective review of 205 patients with acute PCA territory infarction.
- Diffusion-weighted MRI (DWI) and magnetic resonance angiography (MRA) performed within 7 days of onset.
Main Results:
- Large artery atherosclerosis (LAA) was the most frequent etiology (42.4%), with intrinsic PCA disease noted in 38 of 87 LAA patients.
- Stroke mechanisms in intrinsic PCA disease included atheromatous branch occlusion, in situ thrombotic occlusion, and artery-to-artery embolism.
- Infarct patterns varied, with ventrolateral thalamic involvement more common in intrinsic PCA atherosclerotic disease compared to occipital involvement.
Conclusions:
- PCA territory infarction patterns differ based on etiology.
- Intrinsic atherosclerotic disease is a significant cause of PCA infarction in this Korean population, involving diverse mechanisms.
Background And Purpose:
Although cardiac embolism has been shown to be the leading stroke mechanism of posterior cerebral artery (PCA) territory infarction, intrinsic PCA atherosclerotic disease may play a more important role in regions where intracranial diseases are prevalent. We aimed to assess the etiologies and stroke pattern of PCA territory infarction in a Korean population.
Method:
We reviewed consecutive patients with acute PCA territory infarction who underwent diffusion-weighted MRI (DWI) and magnetic resonance angiography (MRA) within 7 days after onset.
Results:
A total of 205 patients (male 56%, mean age 65.4 +/- 12.4 years) were recruited. 'Superficial', 'deep' and 'superficial plus deep' infarcts accounted for 26.3, 47.8 and 25.9% of infarcts, respectively. There were 126 patients who had infarcts limited to the PCA territory, whereas 79 patients had concomitant infarcts in other territories. Large artery atherosclerosis (LAA, 42.4%) was the most frequent etiology, followed by cardiogenic embolism (20%), small-vessel occlusion (20%), undetermined (18%) and other determined (3%) etiology. Among the 87 patients with LAA, 38 had intrinsic PCA disease without atherosclerosis in the proximal vessels. In these patients, stroke mechanisms included atheromatous branch occlusion (n = 19), in situ thrombotic occlusion (n = 11) and artery-to-artery embolism (n = 8). While the occipital area was the most frequently involved in general, the ventrolateral thalamic area was more frequently involved than the occipital area in patients with intrinsic PCA atherosclerotic disease.
Conclusion:
The patterns of PCA territory infarction are different according to underlying etiologies. In our population, intrinsic atherosclerotic disease is a relatively important cause of PCA territory infarction that produces strokes through a variety of mechanisms.
