The vitreous is firmly attached before the equator, just posterior to the ora serrata, at the vitreous base. 13-15 Condensed collagen fibrils that form the vitreous cortex superficially insert into the ILM of the retina or basal lamina of the Müller cells. Collagen fibers and hyaluronate particles bind the water, creating a support structure for the vitreous body. The vitreous is a clear, gelatinous matrix that is largely composed of water. This includes refractive error corneal disease anterior chamber phenomena, such as cells and protein from uveitis blood from hyphema lenticular opacity or vitreous abnormality, such as vitreous cells, hemorrhage or retinal traction. 2,6-10Īny disruption that causes the retina to inefficiently receive light, or any discontinuity in the pathway from the neurosensory retina to the brain, can cause visual disability. Supporting glial cells and Müller cells interdigitate with this neuronal pathway, enabling the necessary structural architecture. With the assistance of horizontal, bipolar, amacrine and retinal ganglion cells, light reaches the occipital lobe of brain via the visual pathway. The photons then reflect off the retinal pigment epithelium (RPE) to depolarize the photoreceptors (rods and cones). Light is comprised of photons that enter the eye through the pupil and penetrate the ocular media (cornea, aqueous, lens, vitreous) and neurosensory retina. Horizontal and vertical SD-OCT scans of our patient’s right eye revealed tractional elevation of the retina at the macula. We scheduled our patient for a four-month follow-up with the general ophthalmic service as well as a six-month follow-up with the retina service. The retinal specialist informed our patient of the surgical procedures necessary to potentially improve her vision however, she declined to proceed. We referred her to a retinal specialist to confirm the diagnosis and rule out a surgical solution. The diagnosis in this case was VMT syndrome in the patient’s right eye. Dilated fundus examination exhibited premacular fibrosis with macular traction O.D., which was confirmed on spectral domain optical coherence tomography (SD-OCT).
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Retinoscopy demonstrated a clear reflex without distortion, and refraction found negligible changes to the current spectacle prescription (which measured +0.50D O.U.).īiomicroscopy revealed normal and healthy anterior segment structures mild, but symmetrical, nuclear lenticular opacities open angles and normal intraocular pressure, which measured 16mm Hg O.U. Confrontational visual fields uncovered a blurry, distorted, central field, which was confirmed with formal Amsler grid testing. We detected no afferent defect, change in color vision or alteration in comparative brightness sense. and 20/30 O.S., with no improvement upon pinhole testing. Her best-corrected entering visual acuity measured 20/200 O.D. She took no medications and denied having allergies of any kind. She denied any new trauma and described the central vision in her right eye as “smudged.” Her systemic history was unremarkable. She also had a long-standing history of stable 20/30 visual acuity O.U. Her ocular history was significant for ERM, advanced optic nerve cupping and an optic pit in her right eye. A 78-year-old black female presented with a chief complaint of visual acuity loss in her right eye that had persisted for the past 10 days. In addition, we review the condition’s pathophysiology as well as discuss several established and novel treatment options. Here, we examine a patient who presented with VMT syndrome. 1-5 It is important to note, however, that ERM is the most common precursor to vitreomacular traction (VMT) syndrome. This unique pathophysiological phenomenon develops secondary to cellular changes, which co-mingle between the posterior vitreous and internal limiting membrane (ILM) of the neurosensory retina. 1,2 When ERM evolves in the macular region, it can cause a host of ocular sequellae, ranging from an asymptomatic presence to reduced visual acuity and metamorphopsia. 1-5 In most instances ERM development is idiopathic and age-related. Potential causes of ERM include trauma, retinal detachment, inflammatory disease and vascular disease. Epiretinal membrane (ERM)––also known as macular pucker, vitreoretinal interface maculopathy and cellophane maculopathy––results when a thin formation of fibrous tissue develops on the surface of the retina.
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