Posterior Cerebral Artery Infarction: Diffusion-Weighted MRI Analysis of 205 Patients

Abstract

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.