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Retinal artery occlusion (RAO), often caused by a microembolus and resulting in inner retinal ischemia, could be considered as the retinal analog to cerebral stroke. Although several therapeutic targets have been suggested in animal models of retinal ischemia and several potential treatments have been evaluated on small series of patients, central retinal artery occlusion (CRAO) is still rarely treatable in clinical practice. Here, we review several animal models of RAO, including increased intraocular pressure, laser, vasoconstriction, embolization and clamp. We also review the pathogenic mechanisms that contribute to cell death cascades during ischemia, and the therapeutic strategies targeting these events. These strategies aim to restore blood flow by fibrinolysis, increase the oxygen or glucose supply, decrease the energy demands, restrict ionic leak fluxes or reduce the detrimental effects of glutamate, calcium and free radicals. The current literature suggests that tPA treatment could be effective for CRAO. Eye care professionals must make a rapid and accurate diagnosis and immediately refer patients with acute retinal stroke to specialized centers. CRAO management should also be facilitated by developing local networks to encourage collaboration among ophthalmologists, retina specialists and stroke neurologists.

Retinal stroke: research models, targets and experimental drugs