Neuroprotection for Nonarteritic Central Retinal Artery Occlusion: Lessons from Acute Ischemic Stroke

Ogugua Ndubuisi Okonkwo,1 Chineze Thelma Agweye,2 Toyin Akanbi1 1Department of Ophthalmology, Eye Foundation Hospital and Eye Foundation Retina Institute, Ikeja, Lagos, Nigeria; 2Department of Ophthalmology, University of Calabar and University of Calabar Teaching Hospital, Cross River, NigeriaCorrespondence: Ogugua Ndubuisi Okonkwo, Eye Foundation Retina Institute, 27, Isaac John Street, GRA, Ikeja, Lagos, Nigeria, Tel +234 803 502 7308, Email o_okonkwo@yahoo.comAbstract: Nonarteritic central retinal artery occlusion (NA-CRAO) is a variant of acute ischemic stroke (AIS) and is a cause of sudden severe loss of vision. There are guidelines by the American Heart Association and the American Stroke Association for the care of CRAO patients. This review explores the basis of retinal neuroprotection for CRAO and its potential for improving the outcome of NA-CRAO. Recently, there have been significant advances in research into the use of neuroprotection to treat retinal diseases, including retinal detachment, age-related macular degeneration, and inherited retinal diseases. Also, neuroprotective research in AIS has been extensive, and newer drugs tested, including Uric acid, Nerinetide, and Otaplimastat, with promising results. Progress in cerebral neuroprotection after AIS offers hope for retinal neuroprotection after CRAO; and a possibility of extrapolating research findings from AIS into CRAO. Combining neuroprotection and thrombolysis can extend the therapeutic window for NA-CRAO treatment and potentially improve outcomes. Experimented neuroprotection for CRAO includes Angiopoietin (Comp Ang1), KUS 121, Gene therapy (XIAP), and hypothermia. Efforts in the field of neuroprotection for NA-CRAO should focus on better imaging to delineate the penumbra after an acute episode of NA-CRAO (using a combination of high-definition optical coherence angiography and electrophysiology). Also, research should explore details of pathophysiologic mechanisms involved in NA-CRAO, allowing for further neuroprotective intervention, ...