A 79-year-old Asian male under regular follow-up for two years with non-neovascular AMD in both eyes complained of blurred vision in the left eye. He said the blurring symptom started two weeks ago. He had no documented medical history including hypertension, diabetes, and other cardiovascular diseases. In addition, intravitreal injection has not been performed previously. His best corrected visual acuity (BCVA) in the left eye decreased from 20/30 to 20/60, compared to the last visit. Fundus photograph in the left eye showed multiple drusen and newly developed choroidal neovascularization (CNV). Optical coherence tomography (OCT) scan image also revealed CNV with subretinal fluid (SRF) and drusenoid pigment epithelial detachment (PED). On fundus fluorescein angiography (FFA), there was hyperfluorescence by leakage due to CNV in the macular area of the left eye. Diagnosed as having progressed to nAMD, three times of intravitreal monthly injections of brolucizumab (6 mg, 0.05 mL of 120 mg/mL solution) were administered to the left eye as an initial loading dose therapy for nAMD. He responded to the first and second monthly injections with regression of CNV and resolution of SRF, and his BCVA was slightly improved to 20/50. In addition, no significant subjection symptoms of the patient were noticed until the second injection. The patient presented with acute painless visual loss in the left eye two days after the third intravitreal brolucizumab injection. His BCVA had deteriorated to counting fingers at 10 cm with a relative afferent pupillary defect in the left eye. There were no inflammatory signs in the anterior chamber. Fundus photographs showed retinal whitening on the posterior pole with a macular cherry-red spot sign. The cotton wool patches were also found along the superior major arcade area. The OCT scan image demonstrated generalized retinal swelling with hyperreflectivity in the inner retina. Furthermore, the wide-field FFA revealed markedly delayed arm-to-retina time and arteriovenous transit time in the left eye. There was no evidence suggesting IOI including anterior chamber inflammation, vitreous opacity, retinal vascular sheathing, and retinal infiltrations. Perivascular leakage or staining which suggests a retinal vasculitis was not identified in the FFA images, either. With the diagnosis of CRAO, anterior chamber paracentesis was conducted immediately, and topical intraocular pressure lowering agent, oral steroid, and oral anti-platelet agent were administered for 1 month. No further intravitreal anti-VEGF injection was performed. One month after his last injection, his BCVA was maintained as counting fingers. No evidence of posterior IOI was still observed, and the progression of atrophic inner retinal thinning induced by ischemia was also noticed on the OCT scan. Further evaluations about a possibility of cardiovascular embolism including cardiac or carotid neck ultrasounds could not be performed, because he refused additional workup for the eyes. There had been no improvement in visual acuity during the follow-up period of three months despite prolonged oral steroid and anti-platelet agent medication. There was no recurrence of nAMD for three months after the cease of intravitreal brolucizumab injection. A generalized atrophic retina with sclerotic vessels was found on the fundus photograph in the left eye, and inner retinal thinning caused by ischemia was more progressed on the OCT scan three months after the occurrence of CRAO.