Vitreous Retina Macula Consultants of New York

We examined the choroid in both eyes from a donor with multifocal geographic atrophy (GA), enlarged choroidal vessels, and choroidal neovascularization (CNV) secondary to age-related macular degeneration, using histology and immunohistochemistry, and we correlated the findings with multimodal clinical imaging. A Caucasian woman with bilateral GA was followed clinically for 5 years, until 6 years prior to her death at age 93. To correlate clinical and histologic features, the right eyecup was photographed before dissecting the posterior pole. Choroidal blood vessels were labeled with Ulex europaeus agglutinin-1 (UEA-1) lectin following retinal pigment epithelium removal and imaged by confocal microscopy. Selected regions were embedded and sectioned for histologic staining. The left eye was used for ultrastructure analysis. The posterior pole exhibited areas of atrophy surrounded by mottled retinal pigment epithelium overlying calcified drusen. Confocal imaging of the UEA-1 lectin-labeled choroidal flatmounts showed limited visualization of the submacular vasculature, consistent with masking by basal laminar and lipid-rich deposits seen in histologic sections. In well-labeled regions of the posterior pole, the choriocapillaris was attenuated and widely separated by markedly thickened, hyalinized intercapillary pillars. Venules and veins appeared dilated, and arteries exhibited arteriosclerotic changes. A choroidal neovascular complex was observed superior to the optic nerve head near the atrophic border; the adjacent choriocapillaris was attenuated. In this single case of multifocal GA, choroidal thickening and large-caliber outer choroidal vessels coexisted with marked choriocapillaris degeneration and adjacent neovascularization. These observations suggest that structural choroidal enlargement does not preclude choriocapillaris failure and may be associated with ischemic and neovascular phenotypes.

To reassess the anatomical basis of optic disc pit maculopathy using swept source optical coherence tomography and to characterize the broader structural abnormalities comprising the optic pit complex. Sixteen patients with optic disc pit maculopathy were imaged using a high-resolution swept source optical coherence tomography system (DREAM optical coherence tomography). Cross-sectional and volume-rendered scans were analyzed for lamina cribrosa defects, intraneural cavitations, and pathways for fluid entry into or beneath the retina. All eyes demonstrated lamina cribrosa defects with associated cavitations extending a mean of 1855 ± 492 µ m posterior to a modified Bruch membrane opening. Four distinct patterns by which fluid entered the retina were observed: (1) direct channels from cavitations into the retina, (2) perivascular hyporeflective spaces, (3) intraneural channels extending toward cystoid spaces, and (4) isolated retinal cysts without a visible interconnection. Vitreous remnants, trabecular structures, or disorganized connective tissue were found within the optic nerve pit in several eyes. In 13% of cases, the pit was not visible by ophthalmoscopy due to overlying tissue. These structural variations frequently coexisted, and associated abnormalities extended beyond the optic disc margins. Optic disc pit maculopathy is associated with a spectrum of deep optic nerve abnormalities, collectively termed the optic pit complex. The combination of laminar disruption, cavitations, and multiple anatomical conduits for fluid ingress broadens the morphologic understanding of this condition. Swept source optical coherence tomography enables visualization of structures not accessible by ophthalmoscopy and may improve diagnostic precision, guide treatment decisions, and clarify the diverse mechanisms contributing to fluid accumulation in optic disc pit maculopathy.

PurposeTo develop and validate a novel method for quantifying blood flow velocity in ocular vessels using speckle pattern analysis in optical coherence tomography (OCT) images.MethodsWe developed an OCT-based methodology that quantifies flow velocity by analyzing speckle structures within OCT images to derive a relative flow value (RFV) based on the horizontal derivative of speckle patterns. A model eye with 150-µm capillary tubing was used to evaluate speckle pattern analysis at controlled flow rates of human and porcine blood. We assessed the correlation between RFV and actual flow velocities and examined measurement consistency across vessel sectioning angles varying ±20° from perpendicular.ResultsRFV exhibited a power-law relationship with actual flow velocities, RFV = 169.6 × (Actual Flow)0.264 (r2 = 0.983), and maintained accuracy without saturation up to 70 mm/s. Measurements remained consistent across vessel sectioning angles. Intraluminal speckle structures changed dynamically with flow velocity, and averaged images revealed characteristic hourglass profiles at higher velocities. In a patient with central retinal vein occlusion, RFV detected altered pulsatility and reduced venous flow, aligning with clinical expectations.ConclusionsThis speckle-based OCT method provides a non-invasive, depth-resolved approach for quantifying ocular blood velocity with minimal computational requirements. It holds potential for diagnosing and monitoring vascular abnormalities in ocular and systemic diseases. Further validation is necessary across diverse patient populations.Translational RelevanceThis method simplifies blood flow quantification, enhancing the role of OCT in hemodynamic assessment both ocularly and systemically.

The aim of this study was to describe novel findings seen on optical coherence tomography angiography (OCTA) and indocyanine green angiography in a young male patient presenting with bilateral topiramate-induced choroidal effusion. This is a retrospective case report. A comprehensive ophthalmic examination was conducted and multimodal imaging techniques, including B-scan ultrasound, OCT, OCTA, and indocyanine green angiography were analyzed. A male patient in his 30s presented with a myopic shift due to bilateral choroidal effusion induced by a medication containing topiramate prescribed for weight loss. Indocyanine green angiography showed multiple hypofluorescent spots within the choroid corresponding to areas of reduced OCTA flow signal in both the inner and deeper en face choroidal slabs. Symptoms and abnormal imaging findings resolved within 5 days of discontinuing the medication. Findings observed with OCTA and indocyanine green angiography together suggest multifocal reversible areas of reduced choroidal vascular flow occurring in a topiramate-induced choroidal effusion. The authors propose that this transient hypoperfusion is due to compression from deeper choroidal vessels with a congested choroid.

To report a case of combined cilioretinal artery and central retinal vein occlusion in a patient with extremely large, asymptomatic optic disk drusen. A patient with sudden vision loss underwent a comprehensive examination, including multimodal imaging. A 45-year-old man with no previous visual symptoms presented with a combined cilioretinal artery and central retinal vein occlusion in the right eye. The optic nerve in the right eye was slightly hyperemic and the nerve appeared normal in the left eye. His optic nerves did not have a nodular appearance but showed subtle hyperautofluorescence. A hematologic and clotting work-up was unrevealing. Optical coherence tomography revealed an exceptionally large, deeply embedded optic disk druse (1,604 × 1,390 µ m) that almost spanned the width of the optic canal, starting from 464 µ m beneath the optic disk surface extending to below any visible lamina cribrosa. The right eye demonstrated a paracentral scotoma, while a minimal visual field defect was observed in the left eye despite the presence of a large-sized (1,125 × 803 µ m) druse. While optic disk drusen are typically small nodular aggregates in the prelaminar optic nerve head, this patient had an enormous buried solitary druse of the optic nerve in each eye. The unexpected size and location of the drusen, along with the lack of preceding symptoms, suggest that they may not be detected in routine evaluations, thus necessitating multimodal imaging. The redundancy of nerve fibers in the optic nerve may allow significant asymptomatic damage before vascular occlusion.

To describe a patient with progressive visual symptoms and reduced retinal sensitivity corresponding to dark without pressure (DWP). Retrospective chart review of a single patient. Comprehensive ophthalmic examinations and multimodal imaging techniques, including optical coherence tomography (OCT), OCT-angiography, and microperimetry, were analyzed. A 23-year-old man presented with progressive peripheral areas of blurred vision superiorly in his right eye and temporally in his left eye. These disturbances corresponded with dark areas of retina inferiorly in his right eye and nasally in his left eye having characteristic features of DWP on multimodal imaging. Although Humphrey visual field 24-2 testing was normal, microperimetry showed decreased retinal sensitivity in areas of DWP relative to adjacent areas without DWP. Previous descriptions of DWP have described it as a benign retinal finding showing no functional deficits. We demonstrate that DWP can be associated with progressive visual complaints showing decreased retinal sensitivity on microperimetry and undetected with Humphrey visual field 24-2 testing.

Type 3 macular neovascularization (MNV) is a unique form of neovascular age-related macular degeneration (AMD) that presents distinct pathogenetic features, clinical manifestations, and prognostic considerations when compared to types 1 and 2 MNV. Insights gained from clinicopathological correlations, bridging in vivo examination techniques with ex vivo histological analysis, have significantly enhanced our comprehension of this MNV phenotype, shaped current management strategies and influenced future directions for therapeutics. The particularities of type 3 MNV, which may largely stem from its origin from the retinal vasculature, are critically important for predicting the disease course. Our current understanding suggests that type 3 MNV occurs in response to retinal pigment epithelium (RPE) disruption and photoreceptor loss when neovessels originating from the deep capillary plexus are accompanied by activated Müller glia as they infiltrate sub-retinal pigment epithelium basal laminar deposits. Dysregulation of angiogenic and angiostatic factors are thought to play a key role in its pathogenesis. The prognosis for type 3 MNV is likely bilateral involvement and progression towards macular atrophy. It may be imperative for practitioners to distinguish type 3 MNV from other mimicking pathologies such as intraretinal microvascular anomalies, which are also part of the type 3 disease spectrum. For instance, deep retinal age-related microvascular anomalies (DRAMA) may present with similar features on multimodal imaging yet may necessitate distinct management protocols. Distinguishing between these conditions may be vital for implementing tailored treatment regimens and improving patient outcomes in the diverse landscape of AMD phenotypes in the future.