If things become serious, you have treatment options. If your eye doctor says you have VMA but your symptoms aren’t severe, they may want to wait and see if your vision gets better by itself. The test uses light to take pictures of your retina and map the layers of your eye. Part of that will be something called optical coherence tomography (OCT). Your doctor will give you special eye drops to dilate your pupils and a complete eye exam. If any of these are happening, see your eye doctor right away. You also could see things smaller than they actually are, which is called micropsia.You could have wavy vision, or things could look distorted.It rarely causes a permanent loss of sight. It can lead to distorted or blurry vision. It’s more likely to happen to women than men and to people who are nearsighted. VMA usually happens in folks older than 50. When that happens, it can affect vision - what doctors call symptomatic VMA. It can hold on so strongly, it pulls on the macula (your eye doctor may call this “traction”). Sometimes the jelly doesn’t completely separate. That’s the light-sensitive tissue on the back of your eye that includes the macula. It eventually pulls away from the retina. That’s mainly because of age and regular wear and tear. It’s considered the most sensitive part of the retina.Īs we grow older, the jelly in our eyes begins to shrink. The macula is important in seeing fine details, such as when you're reading. The other is the macula, a small area on the retina responsible for the central part of your field of vision. One is the vitreous, or the “jelly” part that fills the eyeball. Identifying NVCM on multimodal imaging, including fluorescein angiography if needed, allows guiding the diagnosis of the causative disease and choosing adequate treatment when available.Vitreomacular adhesion (VMA) can be serious, but it’s treatable. Lastly, drug toxicity may also induce cystoid maculopathy. Vitreomacular traction (VMT) syndrome is a potentially visually significant disorder of the vitreoretinal interface characterized by an incomplete posterior vitreous detachment with the persistently adherent vitreous exerting tractional pull on the macula and resulting in morphologic alterations and consequent decline of visual function. Various causes of optic atrophy, including open-angle glaucoma, result in microcystoid spaces in the inner nuclear layer due to a retrograde transsynaptic degeneration. In these diseases, cystoid spaces occur in a context of retinal cell loss. Non-exudative age macular degeneration may also be complicated by intraretinal cystoid spaces in the absence of fluorescein leakage. Various causes affecting RPE function may result in NVCM such as chronic central serous chorioretinopathy and paraneoplastic syndromes. In macular telangiectasia type 2, cystoid spaces and cavitations do not depend on the fluid leakage from telangiectasia.

In inherited retinal dystrophies, cystoid spaces may be part of the disease as in X-linked retinoschisis or enhanced S-cone syndrome, or occur occasionally as in bestrophinopathies, retinitis pigmentosa and allied diseases, congenital microphthalmia, choroideremia, gyrate atrophy and Bietti crystalline dystrophy. Surgical treatment does not always allow cystoid space resorption. Vitreomacular traction syndrome (VMT) is a retinal disorder that is commonly associated with posterior vitreous detachment (PVD). Tractional causes include vitreomacular traction, epiretinal membranes and myopic foveoschisis. Various causes may disrupt retinal cell cohesion or impair retinal pigment epithelium (RPE) and Müller cell functions in the maintenance of retinal dehydration, resulting in cystoid spaces formation. Besides cystoid macular edema due to a blood-retinal barrier breakdown, another type of macular cystoid spaces referred to as non-vasogenic cystoid maculopathies (NVCM) may be detected on optical coherence tomography but not on fluorescein angiography.

Vmt retina