Proposing a Neurotropic Etiology for Acute Posterior Multifocal Placoid Pigment Epitheliopathy and Relentless Placoid Chorioretinitis

Purpose To reassess the underlying pathophysiology of acute posterior multifocal placoid pigment epitheliopathy (APMPPE) and relentless chorioretinitis (RPC) through comparison with non-inoculated eye von Szily animal model neurotropic viral retinal infection. Methods Narrative review. Results Literature reports isolated entities rising serological titers in APMPPE after presentation support a potential direct infective etiology. In general, transport along axons results mitochondrial stasis disruption axoplasmic flow. Clinical manifestations flow APMPPE/RPC may signify passage virus neuronal pathway. From case series 11 patients, we demonstrate timely, spatial, proportional association optic disc swelling lesion occurrence. Signs within inner retina appear to precede outer lesions; areas nuclear layer (ONL) hyperreflectivity be result coalescence multiple hyperreflective foci resembling axonal spheroids (which occur as consequence disruption) follow Henle fiber neurons. Underlying epithelium (RPE) hyper-autofluorescence ONL localized Areas apparent choriocapillaris hypoperfusion mirror RPE/Bruch’s membrane separation secondary tractional forces above. Increases choroidal thickness occurrence focal are observed both model. Conclusions The neurotrophic infection provides significant advantages over existing primary ischemia hypothesis account for range imaging signs RPC.