Membrane lipid composition is central to the highly specialized functions of neurological tissues. In the retina, abnormal lipid metabolism causes severe forms of blindness, often through poorly understood neuronal cell death. Here, we demonstrate that deleting the de novo lipogenic enzyme fatty acid synthase (FAS) from the neural retina, but not the vascular retina, results in progressive neurodegeneration and blindness with a temporal pattern resembling rodent models of retinitis pigmentosa. Blindness was not rescued by protection from light-evoked activity; by eating a diet enriched in palmitate, the product of the FAS reaction; or by treatment with the PPARα agonist fenofibrate. Vision loss was due to aberrant synaptic structure, blunted responsiveness to glial-derived neurotrophic factor and ciliary neurotrophic factor, and eventual apoptotic cell loss. This progressive neurodegeneration was associated with decreased membrane cholesterol content, as well as loss of discrete n-3 polyunsaturated fatty acid– and saturated fatty acid–containing phospholipid species within specialized membrane microdomains. Neurotrophic signaling was restored by exogenous cholesterol delivery. These findings implicate de novo lipogenesis in neurotrophin-dependent cell survival by maintaining retinal membrane configuration and lipid composition, and they suggest that ongoing lipogenesis may be required to prevent cell death in many forms of retinopathy.

Purpose: This study examines treatment-based outcomes of endophthalmitis due to antivascular endothelial growth factor (anti-VEGF) intravitreal injection and its effect on subsequent management of neovascular disease. Methods: A retrospective multicenter study was conducted of 157 patients with a diagnosis of endophthalmitis following anti-VEGF intravitreal injection at 10 major ophthalmic centers. Results: The median number of injections before endophthalmitis was 10 (range, 1 to 84 injections). Initial treatment with tap and inject with or without subsequent vitrectomy trended toward smaller visual acuity changes from baseline (4 ETDRS [Early Treatment Diabetic Retinopathy Study] letter difference vs 19 ETDRS letter difference) compared with initial vitrectomy, but the difference was not statistically significant. There was no significant change in medication choice among injections after endophthalmitis. There was a statistically significant shift away from regular interval (1- to 2-month) injections and a shift toward treat-and-extend and as-needed injection algorithms. Conclusions: The visual outcomes were not significantly different between patients who initially underwent tap and injection of antibiotics and those who underwent vitrectomy. There was no significant change in medication choice before and after endophthalmitis but there was a shift toward lower-frequency injection algorithms after postintravitreal injection endophthalmitis compared with prior.

A very uncommon instance of facial nerve palsy involving isolated temporal bone with associated uncontrolled diabetes mellitus has been noticed. A 53-year-old diabetic male presented himself with facial asymmetry, ear pain, and discharge in the right ear of one-month duration. Clinical examination revealed grade IV [House-Brackmann] right sided facial palsy, and otoscopy of small central perforation. Clinically acute otitis media with facial palsy diagnosis was made. There was minimal response to medical treatment. As per CT scan and audiometry findings, patient was subjected for exploratory mastoidectomy showing pale granulation tissue involving geniculate ganglion of facial nerve. The histopathology was suggestive of mucormycosis, an unusual presentation in middle ear. The patient was treated with injectable Amphotericin B. This case highlights a rare cause of isolated facial palsy and physicians should be aware of such atypical clinical presentation.

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