Daniel L Adams1, John R Economides2, Jonathan C Horton3. 1. Department of Ophthalmology, University of California, San Francisco, San Francisco, California; Center for Mind/Brain Sciences, The University of Trento, Trento, Italy. 2. Department of Ophthalmology, University of California, San Francisco, San Francisco, California. 3. Department of Ophthalmology, University of California, San Francisco, San Francisco, California. Electronic address: hortonj@vision.ucsf.edu.
Abstract
PURPOSE: To determine how formation of an acquired myopic crescent adjacent to the optic disc affects metabolic activity in the primary visual cortex. DESIGN: Laboratory animal study. PARTICIPANTS: Three macaque monkeys. METHODS: The blind spot region in the primary visual cortex was labeled by cytochrome oxidase (CO) histochemistry analysis or [(3)H]proline autoradiography. MAIN OUTCOME MEASURES: Visualization of the representation of the blind spot and myopic peripapillary crescent in the visual cortex. RESULTS: In high myopia, a region resembling the myopic peripapillary crescent was visible in cortical sections processed for CO. In this region, metabolic activity was reduced in ocular dominance columns that normally would be driven by input from retina corresponding to the myopic peripapillary crescent. CONCLUSIONS: The formation of a myopic crescent is accompanied by loss of metabolic activity in the cortex supplied by the affected retina. This observation confirms that retinal tissue is damaged by the development of a myopic crescent, rather than simply translocated in a temporal direction. The cortical defect matches the myopic peripapillary crescent in size and shape, indicating that fill-in of the retinotopic map by healthy, surrounding retina does not occur.
PURPOSE: To determine how formation of an acquired myopic crescent adjacent to the optic disc affects metabolic activity in the primary visual cortex. DESIGN: Laboratory animal study. PARTICIPANTS: Three macaque monkeys. METHODS: The blind spot region in the primary visual cortex was labeled by cytochrome oxidase (CO) histochemistry analysis or [(3)H]proline autoradiography. MAIN OUTCOME MEASURES: Visualization of the representation of the blind spot and myopic peripapillary crescent in the visual cortex. RESULTS: In high myopia, a region resembling the myopic peripapillary crescent was visible in cortical sections processed for CO. In this region, metabolic activity was reduced in ocular dominance columns that normally would be driven by input from retina corresponding to the myopic peripapillary crescent. CONCLUSIONS: The formation of a myopic crescent is accompanied by loss of metabolic activity in the cortex supplied by the affected retina. This observation confirms that retinal tissue is damaged by the development of a myopic crescent, rather than simply translocated in a temporal direction. The cortical defect matches the myopic peripapillary crescent in size and shape, indicating that fill-in of the retinotopic map by healthy, surrounding retina does not occur.