Mechanisms and clinical features of posterior border-zone infarcts

Background: Previous studies link posterior border-zone cerebral infarcts between the middle cerebral artery (MCA) and the posterior cerebral artery (PCA) to hemodynamic causes, not embolism. Objective: To study the cause of these infarcts. Methods: We studied 21 patients (unilateral = 18, bilateral = 3) with acute, symptomatic posterior border-zone infarcts shown on CT or MRI to clarify stroke mechanisms. Patients were identified by review of CT and MRI logs and medical records during a 35-month period. An embolic mechanism was assigned when a source of embolism from either the heart, aorta, or parent large artery was present in the absence of intrinsic MCA or PCA disease. A hemodynamic mechanism was assigned when systemic hypotension was present. Results: Among patients with unilateral lesions, 10 were embolic (7 cardiac, 3 carotid). 7 were unknown, and one patient had vasospasm from a ruptured aneurysm. Visual field abnormalities predominated over motor, sensory, and language abnormalities. All patients with bilateral posterior border-zone lesions had perioperative hypotension. Prolonged lethargy, bilateral limb weakness, and cortical blindness were common. Conclusions: Embolism, either cardiac or from the parent carotid artery, is the predominant stroke mechanism in unilateral posterior border-zone infarcts, not distal field perfusion failure. Bilateral posterior border-zone infarcts have a distinctive clinical presentation and are caused by systemic hypotension. Variability of irrigation of the major arteries, passage of emboli to border-zone areas, and decreased clearance of emboli in these areas explain the findings in the patients with unilateral lesions.