What is the treatment for vitreomacular traction?

What is the treatment for vitreomacular traction?

In most cases, vitrectomy surgery is the most effective treatment to release the vitreomacular traction. During vitrectomy surgery, the vitreous is removed from the eye and the vitreous is separated from the back of the eye.

Is vitreomacular traction an emergency?

Vitreomacular adhesion (VMA) can be serious, but it’s treatable. It involves two parts of your eye. One is the vitreous, or the “jelly” part that fills the eyeball.

Is vitreomacular traction serious?

Vitreomacular traction (VMT) syndrome is an eye condition involving the vitreous, the clear gel that fills the inside of the eyeball. It is a vision-threatening condition and can cause symptoms ranging from blurry vision to distorted and blacked-out central vision.

What causes vitreomacular traction?

What causes vitreomacular traction? VMT is usually caused by part of the vitreous remaining stuck to the macula during a posterior vitreous detachment. In healthy eyes, VMT is not common.

What does vitreomacular traction look like?

The most common symptoms of patients with VMT include: Distorted vision (metamorphopsia) that makes a grid of straight lines appear wavy or blank. Flashes of light in the eye. Decreased sharpness of vision.

What is vitreomacular traction syndrome?

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 …

Can VMT correct itself?

Some cases of VMT may spontaneously resolve. For patients whose symptoms are severe enough to require intervention, pars plana vitrectomy surgery is one treatment option. The procedure involves the manual release of vitreous attachment and alleviation of traction, but it is invasive and inconvenient to most patients.

What is traction Ophthalmology?

In some people with PVD, the vitreous doesn’t detach completely. Part of the vitreous remains stuck to the macula, at the center of the retina. The vitreous pulls and tugs on the macula, causing vitreomacular traction (VMT). This can damage the macula and cause vision loss if left untreated.

What does VMT look like?

VMT: Symptomatic with blurred or reduced vision, metamorphopsia, micropsia, scotoma, and difficulties with daily vision-related tasks such as reading. Onset and progression of symptoms are usually gradual, except in a few cases of sudden onset of vision loss/scotoma due to severe traction causing foveal detachment.

What is vitreomacular adhesion?

Vitreomacular adhesion or traction refers to an attachment between the vitreous gel which fills the eyeball and the central part of the retina which lines the back of the eye.

What is a vitreomacular traction?

Is ocriplasmin an effective nonsurgical treatment for vitreomacular traction?

Pharmacologic vitreolysis with ocriplasmin, a 27 kilodalton serine protease, is an effective nonsurgical treatment option for vitreomacular traction (VMT).

What is the medical treatment for vitreomacular traction syndrome (VMT)?

The medical therapy of VMT consists of pharmacologic vitreolysis. Pictorial representation of vitreoretinal interface and tractional forces active in vitreomacular traction: Solid black arrows represent posterior to anterior forces generated by the vitreous due to liquefaction and condensation.

What is the prevalence of vitreomacular interface abnormality (VMT) on Oct?

Interstingly, about 70% of fellow eyes in patients with VMT have some evidence of vitreomacular interface abnormality noted on OCT, including ERM (40%), VMA (15%), VMT (10%), and lamellar macular hole (5%). This may denote a more widespread abnormality in the components that make up the vitreous.

Does ocriplasmin cause vitreolysis?

More importantly, ocriplasmin lacks activity against type IV collagen, an important component of ILM, which allows targeted action at the vitreoretinal interface without significant retinal toxicity. It also causes vitreolysis by its activity on native collagens in the vitreous.