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A.K. Junk, P.S. Rosenbaum, H.M. Engel, D.M. Rosenbaum; Visual Recovery after Central Retinal Artery Occlusion (CRAO) - A New Pathophysiologic Approach to the Clinical Entity of Partial CRAO . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4055.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Ischemic tolerance has been studied extensively in experimental models of heart and brain ischemia. We have recently demonstrated that this phenomenon occurs in the retina as well and it may, in part, be related to anti-apoptotic mechanisms (IOVS 2002, 43, 3059-66). While there is some clinical evidence of ischemic tolerance in the heart and brain, it is not known whether the same is true in the human retina. The purpose of this study was to determine if prior brief episodes of ischemia protect the retina from subsequent ischemic insults. Methods: Retrospective review of four cases of partial CRAO: all patients experienced typical prodromal visual symptoms consistent with retinal ischemia. Complete eye examination included retinal photography, fluorescein angiography, and visual field testing. Echocardiogram and carotid doppler studies were part of the medical work up. Ophthalmological and medical treatment followed the concurrent recommendations of the AAO and AMA. Results: All four patients demonstrated a sudden decrease in visual acuity, relative afferent pupillary defect, and retinal edema with extensive cotton wool spots subsequent to prodromal ophthalmological symptoms. Fluorescein angiogram revealed a severe delay of the arterial filling phase (34 to 61 sec) consistent with CRAO. Visual field tests showed generalized defects. Carotid doppler studies were normal in all four patients. Echocardiograms revealed a patent foramen ovale in one subject. Three patients partially recovered vision after four to six weeks, the fourth had complete visual recovery. Conclusions: Our experimental data suggest that endogenous intraretinal, neuroprotective agents are released by a brief ischemic episode and may protect the retina from extensive damage by a subsequent insult. The distinct clinical appearance and remarkable visual recovery despite angiographic evidence of CRAO distinguish patients with partial CRAO from the classical presentation. We believe that the visual prodromal symptoms our patients experienced represent a brief preconditioning event that induced up-regulation of protective and anti-apoptotic factors. This in turn moderates the overall ischemic insult of a complete CRAO and results in reduced anatomical and functional damage. The experimental data support our hypothesis of effective retinal preconditioning by brief ischemic episodes.
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