The cerebral cortex is supplied by vascular microlobules, each comprised of a half dozen penetrating arterioles that surround a central draining venule. The surface arterioles that feed the penetrating arterioles are interconnected via an extensively anastomotic plexus. Embolic occlusion of a small surface arteriole rarely produces a local infarct, because collateral blood flow is available through the vascular reticulum. Collateral flow also protects against infarct after occlusion of a single penetrating arteriole. Cortical infarction requires blockage of a major arterial trunk, with arrest of blood flow to a relatively large vascular territory. For striate cortex, the major vessels compromised by emboli are the inferior calcarine and superior calcarine arteries, as well as the distal branches of the middle cerebral artery. Their vascular territories have a fairly consistent relationship with the retinotopic map. Consequently, occlusion by emboli results in stereotypical visual field defects. The organization of the arterial supply to the occipital lobe provides an anatomical explanation for a phenomenon that has long puzzled neuro-ophthalmologists, namely, that of the myriad potential patterns of cortical visual field loss, only a few are encountered commonly from embolic cortical stroke.
Department of Ophthalmology (JCH, DLA), Program in Neuroscience, University of California San Francisco, San Francisco, California; and Center for Mind/Brain Sciences (DLA), The University of Trento, Trento, Italy.
Address correspondence to Jonathan C. Horton, MD, PhD, Beckman Vision Center, 10 Koret Way, University of California San Francisco, San Francisco, CA 94143-0730; E-mail: Jonathan.Horton@ucsf.edu
Supported by grants EY10217 (J.C.H.) and EY02162 (Beckman Vision Center) from the National Eye Institute and by an unrestricted grant and a Physician Scientist Award from Research to Prevent Blindness.
The authors report no conflicts of interest.