Type 3 neovascularization is considered to originate within the retina with subsequent expansion of the neovascular network into the subretinal space. Choroidal circulatory disturbances seem to have a role in Type 3 neovascularization development, but the exact pathophysiology is still under debate. Although eyes with Type 3 neovascularization usually have thinner choroid compared to normal eyes, the increased choroidal thickness associated with Type 3 neovascularization may be a prognostic factor for its recurrence. This case report documents stage 1 Type 3 neovascularization with dilated choroid showing poor response to anti-vascular endothelial growth factor therapy, thus suggesting an active role of choroid in Type 3 lesions.
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