Jonathan C. Horton, USA

Vascular Supply of Human Striate Cortex Explains Visual Field Defects from Embolic Stroke

Jonathan C. Horton MD PhD

What accounts for the patterns of visual field loss present in patients after occipital stroke?  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.

 

Brief Biography

Jonathan C. Horton is the William F. Hoyt Professor at the University of California, San Francisco, where he is a member of the Departments of Ophthalmology, Neurology, and Physiology.  He received his undergraduate degree at Stanford University, majoring in medieval history.  In 1984 he received an MD and PhD from Harvard University, where he was a graduate student in the laboratory of Dr. David H. Hubel and Dr. Torsten N. Wiesel.  The title of his dissertation was “Cytochrome Oxidase Patches: A New Cytoarchitectonic Feature of Primate Visual Cortex”.  He completed a medical internship and one year of neurology residency at Massachusetts General Hospital, followed by an ophthalmology residency at Georgetown University and a fellowship in neuro-ophthalmology and pediatric ophthalmology at UCSF.  His research interests fall into three broad categories: 1) clinical neuro-ophthalmology and pediatric ophthalmology, inquiring into the features, causes, and treatment of disorders that impair vision; 2) physiology and anatomy of the primate visual system, using knowledge acquired from laboratory experiments  in monkeys to understanding how the brain mediates perception; 3) strabismus, elucidating the neural mechanisms of visual suppression, amblyopia, and eye movement control in subjects with ocular misalignment.