Malformations of the vitreous: causes, symptoms, diagnosis, treatment

Development of the vitreous humor

The primary vitreous body occurs approximately at the 6th week of intrauterine development and consists of mesodermal cells, collagen fibers, hyaloid vessels and macrophages. The secondary vitreous humor is formed in the second month and contains a compact fibrillar network, hyalocytes, monocytes and some hyaluronic acid. At the end of the third month of intrauterine development, a tertiary vitreous body is formed, which is a condensed accumulation of collagen fibers between the lens equator and the optic nerve disc. It is the precursor of the main vitreous body and the polar ligament of the lens. Near the end of the fourth month of intrauterine development, the primary vitreous humor and the hyaloid vascular network atrophy, turning into a transparent narrow central zone related to the cloquet channel. Persistence of the primary vitreous humor is an important factor in certain vitreous developmental malformations.

[1], [2], [3]

Persistent Hyaloid Artery

Persistence of the hyaloid artery is observed in more than 3% of healthy full-term infants. It is almost always found at the 30th week of intrauterine development and in preterm infants in screening for the detection of retinopathy of prematurity. The remnants of the posterior part of this hyaloid net can manifest as an elevated mass of hyaloid tissue on the optic nerve disk and are called the nipple of Bergmeister. The anterior remains, appear adherent to the posterior capsule of the lens, and are called the spot of Mittendorf (Mittendorf).

Persistent hyperplasia of the primary vitreous humor

Persistent hyperplasia of the primary vitreous humor is a congenital pathology of the eye, associated with a violation of the regression of the primary vitreous humor. It is rare and unilateral. In most reports of bilateral and familial persistent hyperplasia of the primary vitreous humor, it appears that there are various syndromes involving vitreoretinal dysplasia. Classical signs of persistent hyperplasia of the primary vitreous humor:

• fibrous membrane, fused with the posterior surface of the lens;
• microphthalmos;
• small front camera;
• vasodilation of the iris;
• vascularized retrolental membrane, causing traction of ciliary processes.

Other eye symptoms accompanying persistent hyperplasia of the primary vitreous humor are rare and include:

• megalocornea;
• the Rieger anomaly;
• the anomaly of the disk "morning glow".

Although the so-called posterior form of persistent hyperplasia of the primary vitreous has been described, it remains unclear how these cases differ from crescent folds or vitreous retinal dysplasia.

Treatment of persistent hyperplasia of the primary vitreous humor is usually aimed at the prevention of glaucoma and phthisis of the eyeball. The removal of the lens and the posterior membrane can prevent the development of glaucoma even on the eye with a low functional prognosis. However, it should be noted that there are reports of the occurrence of glaucoma after lenvitretomy. Some authors note the possibility of a significant increase in visual acuity in early surgery and active pleoptical treatment.