Figure 2-12. OCT images comparing an idiopathic full-thickness macular hole (A), a macular pseudohole due to an epiretinal membrane (B), and a lamellar or partial-thickness hole (C), The full-thickness hole displays a complete loss of retinal tissue in the fovea and surrounding retinal edema. The pseudohole and lamellar hole, however, exhibit an intact photoreceptor layer in the fovea. The pseudohole is characterized by a steepened fovea 1 pit contour due to traction by the epi retinal membrane. The membrane is sometimes visible when it is separated from the sensory retina (B, arrow). The foveal contour of the lamellar hole is indicative of the rupture of a central cyst.
owing occurs with soft drusen and mild reflectivity, often indistinguishable from the choroidal reflectivity, extends from the elevated RPE down the choroid.
Changes in the morphology of the fovea are often indicative of disease on the OCT image. Loss of fovea 1 photoreceptors can be assessed with OCX as occurs with full-thickness macular holes (Figure 2-12), central scarring or fibrosis, and other macular lesions. Steepening of the foveal contour is commonly associated with epiretinal membranes and macular pseudoholes or lamellar holes (Figure 2-12). Loss or flattening of the foveal contour may occur with impending macular holes, foveal edema, or foveal neurosensory detachments. Vitreomacular traction may result in flattening or protrusion of the fovea ,
While the RPE and choriocapi I laris are difficult to distinguish on the OCT tomogram, their combined reflection, which defines the posterior boundary of the neurosensory retina on the OCT image, provides useful information on chorioretinal pathologies such as age-related macular degeneration and choroidal neovascularization.
Uyperpigmentation of the RPE leads to increased reflectivity, mild thickening of the posterior reflective boundary, and concomitant shadowing of the back-scattering from the choroid. Detachments of the RPE also lead to choroidal shadowing, as discussed above. Disciform scars and other fibrosis appear as a severely thickened posterior reflection due to the high reflectivity and extension of fibrotic structures into the retina.
Hypopig mentation or pigment epithelial atrophv results in decreased reflection and an associated window defect, enabling increased penetration of the probe beam to l he choroid, and higher reflectivity from the deeper layers.
Disruption of the reflection corresponding to the RPE and choriocapillaris is a good indicator of choroidal neovascularization (Figure 2-13). The ingrowth of new blood vessels through breaks in Bruchs membrane results in fragmentation and thickening of the posterior reflection due to the architecture of the neovascular membrane, This fragmentation and thickening may sometimes be difficult to discern, but may be associated with a thickening of the overlying neurosensory retina due to intra re tina! or subretinal fluid leakage from the new vessels.
Manv diseases of the vitreous and retina affect the vitreoretinal interface. The normal vitreous gel is optically transparent, providing a high contrast bound-
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