Acute Macular Neuroretinopathy Following COVID-19 mRNA Vaccination.

A 21-year-old female developed bilateral acute-onset paracentral scotomas three days after receiving the second dose of her Moderna COVID-19 vaccination. A clinical diagnosis of acute macular neuroretinopathy (AMN) was confirmed after classic findings were demonstrated on near-infrared reflectance imaging, spectral-domain optical coherence tomography, and colored fundus photography. The patient presented with visual acuity of 20/100-1 OD and 20/20 OS. After treatment with brimonidine and difluprednate, at a two-week follow-up, her visual acuity was 20/100-2 OD and 20/25-2 OS. There have been reported cases of AMN following flu-like illnesses as well as after receiving vaccines. However, this is the first report of AMN following vaccination with a Moderna COVID-19 vaccine.

Unusual Presentation of Presumed Arteritic Ischemic Optic Neuropathy in Waxy Pale Disc of Retinitis Pigmentosa.

This case report describes an unusual presentation of arteritic anterior ischemic optic neuropathy (AAION) in a 68-year-old patient with retinitis pigmentosa (RP) secondary to Usher syndrome. The authors report a patient with RP who presented with rapid unilateral vision loss. A diagnosis of AAION was made by fluorescein angiography and temporal artery biopsy despite the lack of typical optic nerve features of anterior ischemic neuropathy, which were likely masked due to the waxy pale disc associated with RP. [Ophthalmic Surg Lasers Imaging Retina. 2021;52:350-352.].

Mitochondrial oxidative stress in the retinal pigment epithelium (RPE) led to metabolic dysfunction in both the RPE and retinal photoreceptors.

Age-related macular degeneration (AMD) is the leading cause of vision loss in the western world. Recent evidence suggests that RPE and photoreceptors have an interconnected metabolism and that mitochondrial damage in RPE is a trigger for degeneration in both RPE and photoreceptors in AMD. To test this hypothesis, this study was designed to induce mitochondrial damage in RPE in mice to determine whether this is sufficient to cause RPE and photoreceptor damage characteristic of AMD. In this study, we conditionally deleted the gene encoding the mitochondrial antioxidant enzyme, manganese superoxide dismutase (MnSOD encoded by Sod2) in the retinal pigment epithelium (RPE) of albino BALB/cJ mice. VMD2-Cre;Sod2flox/flox BALB/cJ mice were housed in either 12-h dark, 12-h 200 lux white lighting (normal light), or 12-h dark, 12-h <10 lux red lighting (dim light). Electroretinography (ERG) and spectral-domain optical coherence tomography (SD-OCT) were performed to assess retinal function and morphology. Immunofluorescence was used to examine protein expression; quantitative RT-PCR was used to measure gene expression. Sod2 knockout (KO) mice had reduced RPE function with age and increased oxidative stress compared to wild type (WT) controls as expected by the cell-specific deletion of Sod2. This was associated with alterations in RPE morphology and the structure and function of RPE mitochondria. In addition, data show a compensatory increase in RPE glycolytic metabolism. The metabolic shift in RPE correlated with severe disruption of photoreceptor mitochondria including a reduction in TOMM20 expression, mitochondrial fragmentation, and reduced COXIII/ß-actin levels. These findings demonstrate that mitochondrial oxidative stress can lead to RPE dysfunction and metabolic reprogramming of RPE. Secondary to these changes, photoreceptors also undergo metabolic stress with increased mitochondrial damage. These data are consistent with the hypothesis of a linked metabolism between RPE and photoreceptors and suggest a mechanism of retinal degeneration in dry AMD.