We describe the clinical course of a patient with therapy refractory polypoidal choroidal vasculopathy (PCV) who was treated with intravitreal bevacizumab (IVB). Prior treatments included photodynamic therapy and intravitreal pegaptanib with poor therapeutic response. Within four weeks of follow-up after a single IVB, the visual acuity improved from count fingers to 20/400 coincident to resolution of subretinal fluid. The visual acuity demonstrated sustained improvement and the macula remained without exudation for 12 months post treatment. Intravitreal injection of bevacizumab should be studied as an effective and relatively inexpensive option for patients with active polypoidal choroidal vasculopathy.

It is important for clinicians to consider exposure to toxic substances and nutritional deficiencies when diagnosing and managing cases of vision loss. In these cases, physiologic damage can alter the function of key components of the visual pathway before morphologic changes can be detected by traditional imaging methods. Electrophysiologic tests can aid in the early detection of such functional changes to visual pathway components, including the retina or optic nerve. This review provides an overview of various electrophysiologic techniques, including multifocal electroretinogram (mfERG), full-field ERG (ffERG), electrooculogram (EOG), pattern electroretinogram (PERG), and visual evoked potential (VEP) in monitoring the retinal and optic nerve toxicities of alcohol, amiodarone, cefuroxime, cisplatin, deferoxamine, digoxin, ethambutol, hydroxychloroquine, isotretinoin, ocular siderosis, pentosane, PDE5 inhibitors, phenothiazines (chlorpromazine and thioridazine), quinine, tamoxifen, topiramate, vigabatrin, and vitamin A deficiency.

Purpose: To examine an underreported and underdiagnosed phenomenon with implications for the pathophysiological mechanisms of tattoo-induced uveitis. Methods: Two cases highlighting the clinical presentation of tattoo-related uveitis were evaluated. Results: A 28-year-old man with biopsy-proven sarcoidosis and ocular manifestations presented with worsening retinal vasculitis after acquiring a red-ink tattoo. Each subsequent flare followed acquisition of a new tattoo. A 31-year-old woman without systemic sarcoidosis presented with multiple episodes of bilateral intermediate uveitis and macular edema concurrent with inflammatory granulomas to recently acquired black-ink tattoos. A skin biopsy in both patients showed cutaneous noncaseating granulomas. Conclusions: These cases add to those reported in the literature and emphasize the importance of understanding the modifiable factors of inflammatory ocular disease. Future study is necessary to understand the mechanisms of tattoo-related uveitis.

This review covers the utility of electrophysiological studies relevant to inflammatory diseases of the retina in conditions such as acute posterior multifocal placoid pigment epitheliopathy, acute zonal occult outer retinopathy, Adamantiades–Behçet disease, autoimmune retinopathy and neuro-retinopathy, birdshot chorioretinopathy, multiple evanescent white dot syndrome, and Vogt–Koyanagi–Harada disease. Electrophysiological studies can help with the diagnosis, prognostication, evaluation of treatment effects, and follow-up for these conditions.

BAX plays an essential role in retinal ganglion cell (RGC) death induced by optic nerve injury. Recently, we developed M109S, an orally bioactive and cytoprotective small compound (CPSC) that inhibits BAX-mediated cell death. We examined whether M109S can protect RGC from optic nerve crush (ONC)-induced apoptosis. M109S was administered starting 5 h after ONC for 7 days. M109S was orally administered in two groups (5 mg/kg twice a day or 7.5 mg/kg once a day). The retina was stained with anti-BRN3A and cleaved Caspase-3 (active Caspase-3) that are the markers of RGC and apoptotic cells, respectively. ONC decreased the number of BRN3A-positive RGC and increased the number of active Caspase-3-expressing apoptotic cells. In ONC-treated retina, there were cells that were double stained with anti-BRN3A and ant-cleaved Caspase-3, indicating that apoptosis in BRN3A-positive RGCs occurred. M109S inhibited the decrease of BRN3A-positive cells whereas it inhibited the increase of active Caspase-3-positive cells in the retina of ONC-treated mice, suggesting that M109S inhibited apoptosis in RGCs. M109S did not induce detectable histological damage to the lungs or kidneys in mice, suggesting that M109S did not show toxicities in the lung or kidneys when the therapeutic dose was used. The present study suggests that M109S is effective in rescuing damaged RGCs. Since M109S is an orally bioactive small compound, M109S may become the basis for a portable patient-friendly medicine that can be used to prevent blindness by rescuing damaged optic nerve cells from death.