Abstract:
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.
journal_name
Neurologyjournal_title
Neurologyauthors
Belden JR,Caplan LR,Pessin MS,Kwan Edoi
10.1212/wnl.53.6.1312subject
Has Abstractpub_date
1999-10-12 00:00:00pages
1312-8issue
6eissn
0028-3878issn
1526-632Xjournal_volume
53pub_type
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