Th1 cells contribute to retinal ganglion cell loss in glaucoma in a VCAM-1-dependent manner.

Glaucoma is a complex neurodegenerative disorder characterized by the progressive loss of retinal ganglion cells (RGC) and optic nerve axons, leading to irreversible visual impairment. Despite its clinical significance, the underlying mechanisms of glaucoma pathogenesis remain poorly understood. In this study, we aimed to unravel the multifaceted nature of glaucoma by investigating the interaction between T cells and retinas. By utilizing clinical samples, murine glaucoma models, and T cell transfer models, we made several key findings. Firstly, we observed that CD4+ T cells from glaucoma patients displayed enhanced activation and a bias towards T helper (Th) 1 responses, which correlated with visual impairment. Secondly, we identified the infiltration of Th1 cells into the retina, where they targeted RGC and integrated into the pro-inflammatory glial network, contributing to progressive RGC loss. Thirdly, we discovered that circulating Th1 cells upregulated vascular cell adhesion protein 1 (VCAM-1) on retinal microvessels, facilitating their entry into the neural retina. Lastly, we found that Th1 cells underwent functional reprogramming before reaching the retina, acquiring a phenotype associated with lymphocyte migration and neurodegenerative diseases. Our study provides novel insights into the role of peripheral CD4+ T cells in glaucoma pathogenesis, shedding light on the mechanisms underlying their infiltration into the retina and offering potential avenues for innovative therapeutic interventions in this sight-threatening disease.

Tuberculum meningioma with recovery of glaucoma-like visual field defects after chiasmal decompression: a case report.

BACKGROUND: To report a case of tuberculum meningioma with recovery of glaucoma-like visual field defects after chiasmal decompression. CASE PRESENTATION: A 39-year-old woman presenting with headache was found to have bilateral arcuate retinal nerve fiber layer (RNFL) thinning on optical coherence tomography (OCT) with a corresponding arcuate scotomas consistent with glaucomatous change. However a suprasellar tumor compressing the anterior chiasm from below was found on magnetic resonance imaging of the brain. After resection of the mass, which was diagnosed as meningothelial meningioma by the pathological examination, the glaucoma-like visual field defects resolved despite the RNFL thinning on the OCT showing no improvement. CONCLUSIONS: Chiasmal compression may mimic glaucoma and produce arcuate scotoma rather than temporal visual field loss. There is a possibility that the development of chiasmal compression somehow converted preperimetric glaucoma into a more advanced form accompanied by visual field defects and that the glaucoma reverted to the preperimetric state after chiasmal decompression.

Pathologic myopia in highly myopic patients with high axial anisomyopia.

PURPOSE: To determine prevalence of anisomyopia (axial length (AL) difference ≥2.5 mm) among high myopes ((HMs), defined by spherical equivalent of ≤6.0 diopters or AL ≥ 26.5 mm). To characterise the shorter anisomyopic eye (SAE) and evaluate if pathologic myopia (PM) in the longer anisomyopic eye (LAE) was associated with increased risk of PM in the SAE. METHODS: 1168 HMs were recruited from Singapore National Eye Centre clinic for this cross-sectional study. Biometry, fundus photography and swept-source optical coherence tomography were performed. Patients with high axial anisomyopia were identified. Structural characteristics and presence of PM were described. Stepwise multivariate regression explored associations between PM in the LAE and pathology in the SAE, controlling for confounding variables. RESULTS: Prevalence of anisomyopia was 15.8% (184 of 1168 patients). Anisomyopic patients (age 65.8±13.5 years) had mean AL of 30.6±2.0 mm and 26.2±2.3 mm in the LAE and SAE, respectively. 52.7% of SAEs had AL < 26.5 mm. Prevalence of myopic macular degeneration, macula-involving posterior staphyloma (PS), myopic traction maculopathy (MTM) and myopic choroidal neovascularisation (mCNV) in the SAE was 52.2%, 36.5%, 13.0% and 8.2%, respectively. Macular hole in the LAE was associated with increased risk of MTM in the SAE (OR=4.88, p=0.01). mCNV in the LAE was associated with mCNV in the SAE (OR=3.57, p=0.02). PS in the LAE was associated with PS in the SAE (OR=4.03, p<0.001). CONCLUSIONS: Even when controlled for AL, PM complications in the LAE predict similar PM complications in the SAE. Patients with high axial anisometropia with PM in the LAE should be monitored carefully for complications in the SAE.

Risk factors associated with progression from papilloedema to optic atrophy: results from a cohort of 113 patients.

BACKGROUND: The aim of this study was to assess the risk factors for atrophic progression of patients with papilloedema secondary to intracranial hypertension, using optical coherence tomography parameters. METHODS: A retrospective study was conducted at Marseille University Hospitals' Ophthalmology departments between December 2015 and December 2021. All patients with papilloedema resulting from elevated intracranial hypertension at the initial presentation were included. Ophthalmological evaluations included analysing retinal nerve fibre layer (RNFL), ganglion cell layer (GCL) and total peripapillary retinal thickness (RT). RESULTS: The study included 222 eyes from 113 patients. The main aetiologies of intracranial hypertension were idiopathic intracranial hypertension (49/113), intracranial tumours (33/113) and cerebral venous thrombosis (15/113). The initial RNFL and RT showed significant correlations with optic atrophy. The mean RNFL was 199.63 µm in the 'no atrophy' group and 365.28 µm in the 'atrophy' group (p<0.001). Similarly, the mean RT was 483.72 µm in the 'non-atrophy' group and 796.69 µm in the 'atrophy' group (p<0.001). The presence of peripapillary haemorrhages showed a strong correlated with optic atrophy with an OR=19.12 (p<0.001). Impaired initial visual acuity was also associated with final optic atrophy with an OR=7.76 (p=0.020). Furthermore, impaired initial GCL was a major predictor of optic atrophy (OR=18.25 (p=0.021)). CONCLUSION: Our study highlights the risk factors for optic atrophy in papilloedema, aiming to facilitate the early detection of patients at a high risk of vision loss and enable more aggressive medical or surgical management.

Objective Assessment of Visual Field Defects Caused by Optic Chiasm and Its Posterior Visual Pathway Injury.

OBJECTIVES: To investigate the characteristics and objective assessment method of visual field defects caused by optic chiasm and its posterior visual pathway injury. METHODS: Typical cases of visual field defects caused by injuries to the optic chiasm, optic tracts, optic radiations, and visual cortex were selected. Visual field examinations, visual evoked potential (VEP) and multifocal visual evolved potential (mfVEP) measurements, craniocerebral CT/MRI, and retinal optical coherence tomography (OCT) were performed, respectively, and the aforementioned visual electrophysiological and neuroimaging indicators were analyzed comprehensively. RESULTS: The electrophysiological manifestations of visual field defects caused by optic chiasm injuries were bitemporal hemianopsia mfVEP abnormalities. The visual field defects caused by optic tract, optic radiation, and visual cortex injuries were all manifested homonymous hemianopsia mfVEP abnormalities contralateral to the lesion. Mild relative afferent pupil disorder (RAPD) and characteristic optic nerve atrophy were observed in hemianopsia patients with optic tract injuries, but not in patients with optic radiation or visual cortex injuries. Neuroimaging could provide morphological evidence of damages to the optic chiasm and its posterior visual pathway. CONCLUSIONS: Visual field defects caused by optic chiasm, optic tract, optic radiation, and visual cortex injuries have their respective characteristics. The combined application of mfVEP and static visual field measurements, in combination with neuroimaging, can maximize the assessment of the location and degree of visual pathway damage, providing an effective scheme for the identification of such injuries.

Losing, preserving, and restoring vision from neurodegeneration in the eye.

The retina is a part of the brain that sits at the back of the eye, looking out onto the world. The first neurons of the retina are the rod and cone photoreceptors, which convert changes in photon flux into electrical signals that are the basis of vision. Rods and cones are frequent targets of heritable neurodegenerative diseases that cause visual impairment, including blindness, in millions of people worldwide. This review summarizes the diverse genetic causes of inherited retinal degenerations (IRDs) and their convergence onto common pathogenic mechanisms of vision loss. Currently, there are few effective treatments for IRDs, but recent advances in disparate areas of biology and technology (e.g., genome editing, viral engineering, 3D organoids, optogenetics, semiconductor arrays) discussed here enable promising efforts to preserve and restore vision in IRD patients with implications for neurodegeneration in less approachable brain areas.

Insights into mustard gas keratopathy- characterizing corneal layer-specific changes in mice exposed to nitrogen mustard.

Exposure to mustard agents, such as sulfur mustard (SM) and nitrogen mustard (NM), often results in ocular surface damage. This can lead to the emergence of various corneal disorders that are collectively referred to as mustard gas keratopathy (MGK). In this study, we aimed to develop a mouse model of MGK by using ocular NM exposure, and describe the subsequent structural changes analyzed across the different layers of the cornea. A 3 µL solution of 0.25 mg/mL or 5 mg/mL NM was applied to the center of the cornea via a 2-mm filter paper for 5 min. Mice were evaluated prior to and after exposure on days 1, 3, 7, 14, and 28 for 4 weeks using slit lamp examination with fluorescein staining. Anterior segment optical coherence tomography (AS-OCT) and in vivo confocal microscopy (IVCM) tracked changes in the epithelium, stroma, and endothelium of the cornea. Histologic evaluation was used to examine corneal cross-sections collected at the completion of follow-up. Following exposure, mice experienced central corneal epithelial erosion and thinning, accompanied by a decreased number of nerve branches in the subbasal plexus and increased activated keratocytes in the stroma in both dosages. The epithelium was recovered by day 3 in the low dose group, followed by exacerbated punctuate erosions alongside persistent corneal edema that arose and continued onward to four weeks post-exposure. The high dose group showed persistent epitheliopathy throughout the study. The endothelial cell density was reduced, more prominent in the high dose group, early after NM exposure, which persisted until the end of follow-up, along with increased polymegethism and pleomorphism. Microstructural changes in the central cornea at 4 weeks post-exposure included dysmorphic basal epithelial cells and reduced epithelial thickness, and in the limbal cornea included decreased cellular layers. We present a mouse model of MGK using NM that successfully replicates ocular injury caused by SM in humans who have been exposed to mustard gas.

Transitions in vascular ultrasonography findings of temporal arteritis in a GCA case with progressive temporal headache and visual impairment.

The European League Against Rheumatism and the American College of Rheumatology have stated that the halo sign on vascular ultrasonography (v-US) is relevant in diagnosing giant cell arteritis (GCA) and is equivalent to temporal artery biopsy. However, there are only a few reports about transitions in v-US findings after glucocorticoid (GC) therapy. We report the transitions in the v-US findings in a case of GCA after GC therapy. The patient had rapidly progressive symptoms, and there were concerns about blindness. After GC therapy, we first observed improvement in headache and visual impairment symptoms within 1 week, followed by rapid improvement in laboratory findings within 2 weeks. Subsequently, there were improvements in v-US findings after more than 2 months. In conclusion, these findings showed a dissociation between improvements in clinical symptoms and v-US findings of the temporal artery. Additionally, this case suggests that regular examination of v-US findings is useful in evaluating GCA with evident vascular wall thickness before GC therapy.

How Myopia and Glaucoma Influence the Biomechanical Susceptibility of the Optic Nerve Head.

Purpose: The purpose of this study was to assess optic nerve head (ONH) deformations following acute intraocular pressure (IOP) elevations and horizontal eye movements in control eyes, highly myopic (HM) eyes, HM eyes with glaucoma (HMG), and eyes with pathologic myopia (PM) alone or PM with staphyloma (PM + S). Methods: We studied 282 eyes, comprising of 99 controls (between +2.75 and -2.75 diopters), 51 HM (< -5 diopters), 35 HMG, 21 PM, and 75 PM + S eyes. For each eye, we imaged the ONH using spectral-domain optical coherence tomography (OCT) under the following conditions: (1) primary gaze, (2) 20 degrees adduction, (3) 20 degrees abduction, and (4) primary gaze with acute IOP elevation (to ∼35 mm Hg) achieved through ophthalmodynamometry. We then computed IOP- and gaze-induced ONH displacements and effective strains. Effective strains were compared across groups. Results: Under IOP elevation, we found that HM eyes exhibited significantly lower strains (3.9 ± 2.4%) than PM eyes (6.9 ± 5.0%, P < 0.001), HMG eyes (4.7 ± 1.8%, P = 0.04), and PM + S eyes (7.0 ± 5.2%, P < 0.001). Under adduction, we found that HM eyes exhibited significantly lower strains (4.8% ± 2.7%) than PM + S eyes (6.0 ± 3.1%, P = 0.02). We also found that eyes with higher axial length were associated with higher strains. Conclusions: Our study revealed that eyes with HMG experienced significantly greater strains under IOP compared to eyes with HM. Furthermore, eyes with PM + S had the highest strains on the ONH of all groups.

Inhibition of complement C3 signaling ameliorates locomotor and visual dysfunction in autoimmune inflammatory diseases.

Neuromyelitis optica (NMO) is an autoimmune inflammatory disease of the central nervous system (CNS) characterized by transverse myelitis and optic neuritis. The pathogenic serum IgG antibody against the aquaporin-4 (AQP4) on astrocytes triggers the activation of the complement cascade, causing astrocyte injury, followed by oligodendrocyte injury, demyelination, and neuronal loss. Complement C3 is positioned as a central player that relays upstream initiation signals to activate downstream effectors, potentially stimulating and amplifying host immune and inflammatory responses. However, whether targeting the inhibition of C3 signaling could ameliorate tissue injury, locomotor defects, and visual impairments in NMO remains to be investigated. In this study, using the targeted C3 inhibitor CR2-Crry led to a significant decrease in complement deposition and demyelination in both slice cultures and focal intracerebral injection models. Moreover, the treatment downregulated the expression of inflammatory cytokines and improved motor dysfunction in a systemic NMO mouse model. Similarly, employing serotype 2/9 adeno-associated virus (AAV2/9) to induce permanent expression of CR2-Crry resulted in a reduction in visual dysfunction by attenuating NMO-like lesions. Our findings reveal the therapeutic value of inhibiting the complement C3 signaling pathway in NMO.

A Hybrid System for Automatic Identification of Corneal Layers on In Vivo Confocal Microscopy Images.

Purpose: Accurate identification of corneal layers with in vivo confocal microscopy (IVCM) is essential for the correct assessment of corneal lesions. This project aims to obtain a reliable automated identification of corneal layers from IVCM images. Methods: A total of 7957 IVCM images were included for model training and testing. Scanning depth information and pixel information of IVCM images were used to build the classification system. Firstly, two base classifiers based on convolutional neural networks and K-nearest neighbors were constructed. Second, two hybrid strategies, namely weighted voting method and light gradient boosting machine (LightGBM) algorithm were used to fuse the results from the two base classifiers and obtain the final classification. Finally, the confidence of prediction results was stratified to help find out model errors. Results: Both two hybrid systems outperformed the two base classifiers. The weighted area under the curve, weighted precision, weighted recall, and weighted F1 score were 0.9841, 0.9096, 0.9145, and 0.9111 for weighted voting hybrid system, and were 0.9794, 0.9039, 0.9055, and 0.9034 for the light gradient boosting machine stacking hybrid system, respectively. More than one-half of the misclassified samples were found using the confidence stratification method. Conclusions: The proposed hybrid approach could effectively integrate the scanning depth and pixel information of IVCM images, allowing for the accurate identification of corneal layers for grossly normal IVCM images. The confidence stratification approach was useful to find out misclassification of the system. Translational Relevance: The proposed hybrid approach lays important groundwork for the automatic identification of the corneal layer for IVCM images.

Glaucomatous optic nerve damage in the contralateral eye of a patient with peripapillary retinoschisis: a case report.

BACKGROUND: Peripapillary retinoschisis (PPRS) is often associated with glaucomatous eyes. It usually occurs in eyes with a more advanced stage of glaucoma with obvious optic nerve damage. We report a patient who was found to have PPRS in one eye during a routine physical examination without obvious glaucoma symptoms. Further examination revealed glaucomatous visual field loss and retinal nerve fiber layer defects in the contralateral eye. CASE PRESENTATION: A 55-year-old man presented for a routine physical examination. The anterior segment was normal in both eyes. Fundus examination revealed an elevated and red optic disc in the right eye. In addition, scattered patchy red lesions were seen on the retina on the temporal side of the optic disc. The color and boundary of the left optic disc were normal, and the cup-to-disc ratio was 0.6. Optical coherence tomography showed retinoschisis on the optic nerve head of the right eye throughout the entire circumference, extending to the retina on the temporal side of the optic disc. The intraocular pressure was 18 mmHg OD and 19 mmHg OS. The patient was diagnosed with PPRS (OD). However, no optic disc pit or optic disc coloboma was found. Further examination showed that the visual field of the patient's right eye was generally normal, while a glaucomatous visual field defect was found in the left eye, which manifested as a nasal step visual field defect. Moreover, stereophotography and a red-free fundus image revealed two retinal nerve fiber layer defects in the supratemporal and infratemporal regions of the retina of the left eye. Continuous intraocular pressure measurement found that the intraocular pressure fluctuated between 18 and 22 mmHg OD and 19-26 mmHg OS during the daytime. Primary open-angle glaucoma was then diagnosed. CONCLUSIONS: In this case, we found that PPRS was associated with glaucomatous optic nerve changes and visual field defects in the fellow eye.

Diagnostic accuracy of retinal optical coherence tomography in children with a newly diagnosed brain tumour.

PURPOSE: To estimate the diagnostic accuracy of circumpapillary retinal nerve fibre layer (RNFL) thickness and macular ganglion cell layer-inner plexiform layer (GCL-IPL) thickness measurements to discriminate an abnormal visual function (i.e. abnormal age-based visual acuity and/or visual field defect) in children with a newly diagnosed brain tumour. METHODS: This cross-sectional analysis of a prospective longitudinal nationwide cohort study was conducted at four hospitals in the Netherlands, including the national referral centre for paediatric oncology. Patients aged 0-18 years with a newly diagnosed brain tumour and reliable visual acuity and/or visual field examination and optical coherence tomography were included. Diagnostic accuracy was evaluated with sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV). RESULTS: Of 115 patients included in the study (67 [58.3%] male; median age 10.6 years [range, 0.2-17.8 years]), reliable RNFL thickness and GCL-IPL thickness measurements were available in 92 patients (80.0%) and 84 patients (73.0%), respectively. The sensitivity for detecting an abnormal visual function was 74.5% for average RNFL thickness and 41.7% for average GCL-IPL thickness at a specificity of 44.5% and 82.9%, respectively. The PPV and NPV were 33.0% and 82.6% for the average RNFL thickness and 57.1% and 82.2% for the average GCL-IPL thickness. CONCLUSION: An abnormal visual function was discriminated correctly by using the average RNFL thickness in seven out of ten patients and by using the average GCL-IPL thickness in four out of ten patients. The relatively high NPVs signified that patients with normal average RNFL thickness and average GCL-IPL thickness measurements had a relative high certainty of a normal visual function.

Analysis of Immediate Early Gene Expression Levels to Interrogate Changes in Cortical Neuronal Activity Patterns upon Vision Loss.

Mapping immediate early gene (IEG) expression levels to characterize changes in neuronal activity patterns has become a golden standard in neuroscience research. Due to straightforward detection methods such as in situ hybridization and immunohistochemistry, changes in IEG expression can be easily visualized across brain regions and in response to physiological and pathological stimulation. Based on in-house experience and existing literature, zif268 represents itself as the IEG of choice to investigate the neuronal activity dynamics induced by sensory deprivation. In the monocular enucleation mouse model of partial vision loss, zif268 in situ hybridization can be implemented to study cross-modal plasticity by charting the initial decline and subsequent rise in neuronal activity in visual cortical territory deprived of direct retinal visual input. Here, we describe a protocol for high-throughput radioactive zif268 in situ hybridization as a readout for cortical neuronal activity dynamics in response to partial vision loss in mice.

FULL-THICKNESS MACULAR HOLE WITH PERSISTENT BROAD VITREOMACULAR ATTACHMENT: Clinical Characteristics and Surgical Outcomes.

PURPOSE: To describe the characteristics and surgical outcomes of full-thickness macular holes (FTMHs) with persistent broad vitreomacular attachment. METHODS: This was a retrospective, observational case series. Consecutive patients undergoing pars plana vitrectomy for FTMHs with persistent broad vitreomacular attachment (study group) were reviewed. Clinical charts, optical coherence tomography (OCT) features of macular holes, and surgical outcomes were reviewed and compared with those with typical FTMH with focal vitreomacular traction (control group). RESULTS: A total of 15 eyes of 14 consecutive patients (eight males and six females with a mean age of 60.6 years) were included in the study group. OCT showed a zone of at least 1,500 µm all around the circumference of the fovea where the vitreous was attached. On OCT, epiretinal membrane and epiretinal proliferation were observed in 73% and 87% of cases, respectively. Compared with the control group, the study group was younger (P = 0.027) and had better preoperative visual acuity (P = 0.007). All FTMHs closed after one surgery in both groups, and the postoperative visual acuity of the study group was better than that of the control group (P = 0.002). CONCLUSION: Full-thickness macular holes may have developed under the condition that the vitreous cortex was broadly attached around the hole. These FTMHs were associated with younger age, better baseline visual acuity, and a higher incidence of epiretinal membranes and epiretinal proliferations compared with macular hole with focal vitreomacular traction. The surgical outcome was favorable, but the pathogenesis of FTMH development remains unclear.

Evaluation of blood vessel network formation and visual field defect in optic disc melanocytoma.

AIM: To investigate the association between visual field defects and blood vessel network (BVN) formation in optic disc melanocytomas (ODMs) using optical coherence tomography angiography (OCTA). METHODS: Single-centre, retrospective case series of 32 eyes of 32 patients with ODM, in which eyes were divided into two groups based on complete and incomplete BVN formations. RESULTS: OCTA revealed incomplete BVN formation in 16 of 32 ODMs. The location of BVN absence corresponded to the location of hypofluorescence from fluorescein angiography (FA) in 12 (75%) and to the location of visual field defect in 13 (81%) ODMs in the incomplete BVN group. Perimetric indices were significantly worse in the incomplete BVN group than in the complete BVN group. Linear regression of mean deviation (MD) and Visual Field Index (VFI) on the area of BVN absence were statistically significant (p=0.01 and p=0.003, respectively), whereas linear regressions of MD and VFI on the tumour area were not statistically significant (both p=0.09) in the incomplete BVN group. CONCLUSION: The location of BVN absence within ODMs corresponded to the location of visual field defect and the location of FA hypofluorescence. Visual field defect was more severe in the incomplete BVN group than in the complete BVN group. Visual field defect was more significantly associated with the area of BVN absence than the tumour area.

Abnormal foveal morphology in carriers of oculocutaneous albinism.

BACKGROUND/AIMS: To investigate the foveal morphology in carriers of oculocutaneous albinism (OCA) using spectral domain optical coherence tomography (SD-OCT). A cross-sectional, observational study. METHODS: Handheld SD-OCT (Envisu C2300) was used to acquire horizontal scans through the centre of the fovea in biological parents of patients with OCA (n=28; mean age±SD=40.43±8.07 years) and age-matched and ethnicity-matched controls (n=28; mean age±SD=38.04±10.27 years). Sequence analysis was performed for variants in known genes associated with OCA. Best-corrected visual acuity (BCVA), presence of foveal hypoplasia and grade, foveal, parafoveal and perifoveal thickness measurements of total retinal layers (TRL), inner retinal layers (IRL) and outer retinal layers (ORL) thickness were measured. RESULTS: Foveal hypoplasia was identified in 32.14% of OCA carriers; grade 1 in all cases. OCA carriers demonstrated significant thicker TRL thickness (median difference: 13.46 µm, p=0.009) and IRL thickness (mean difference: 8.98 µm, p<0.001) at the central fovea compared with controls. BCVA of carriers was between -0.16 and 0.18 logMAR (mean: 0.0 logMAR). No significant differences in BCVA was noted between OCA carriers or controls (p=0.83). In the OCA carriers, we identified previously reported pathogenic variants in TYR, OCA2 and SLC45A2, novel OCA2 variants (n=3) and heterozygosity of the pathogenic TYR haplotype. CONCLUSION: We have, for the first time, identified foveal abnormalities in OCA carriers. This provides clinical value, particularly in cases where limited phenotype data are available. Our findings raise the possibility that previously reported mild cases of foveal hypoplasia or isolated foveal hypoplasia could correspond to OCA carrier status.

Isolated bilateral lateral geniculate body necrosis following acute pancreatitis: A rare cause of bilateral loss of vision in a young female.

Sudden bilateral visual loss because of bilateral lateral geniculate body (LGB) necrosis is a very rare entity. The mechanisms causing these isolated lesions have still not been fully understood. We report a case of sudden loss of vision in a 22-year-old female following an attack of acute pancreatitis, just after starting the paleo diet. Neuroimaging revealed bilateral LGB necrosis. Multidisciplinary approach was sought and she was subsequently managed successfully. On follow-up, her visual acuity showed improvement, and neuroimaging revealed resolution of hyperintensities in bilateral LGB with residual blooming suggestive of old hemorrhagic gliosis. The possible reasons for isolated lesions of the LGB are hemorrhagic infarction and osmotic demyelination. In the present case, we postulate a vascular pathology, possibly hypo-perfusion because of shock following acute pancreatitis.

Case Report: Complete tomographic resolution of focal choroidal excavation complicated with choroidal neovascularization after anti-VEGF treatment.

Purpose We report a case of focal choroidal excavation (FCE) that resolved after intravitreal injection of anti-vascular endothelial growth factor (VEGF) for choroidal neovascularization (CNV) and we describe its tomographic features. Case report A 43-year-old female presented with blurred vision and metamorphopsia in her left eye (LE) evolving for 10 years. The best corrected visual acuity (BCVA) was 20/20 in the right eye and 20/32 in the LE. Fundus examination revealed the presence of a yellowish foveal lesion which corresponded to a conforming FCE associated to a pachychoroid on swept-source optical coherence tomography (OCT). The OCT-Angiography showed a foveal flow void in the choriocapillaris layer corresponding to the FCE area. Three years later, the patient complained of visual impairment, more metamorphopsia with a BCVA of 20/80 on her LE. The OCT showed intraretinal fluid with a foveal retinal pigment epithelium (RPE) detachment. The OCT-angiography confirmed the presence of CNV. Two months after one intravitreal bevacizumab injection, the OCT documented the complete resolution of macular edema, the regression of the CNV tissue and the restoration of a normal aspect of the fovea without any FCE. Her BCVA improved to 20/32 with resolution of the metamorphopsia. The OCT aspect remained stable during 3 years of follow-up. Conclusion CNV can develop in FCE and anti-VEGF therapy is a good option treatment. After treatment, FCE pattern can change et may completely resolve.