Vitreous body malformations: causes, symptoms, diagnosis, treatment

Development of the vitreous body

The primary vitreous body appears at approximately the sixth week of fetal development and consists of mesodermal cells, collagen fibers, hyaloid vessels, and macrophages. The secondary vitreous body forms in the second month and contains a compact fibrillar network, hyalocytes, monocytes, and some hyaluronic acid. At the end of the third month of fetal development, the tertiary vitreous body forms, which is a condensed accumulation of collagen fibers between the equator of the lens and the optic disc. It is the precursor of the main vitreous body and the zonular ligaments of the lens. Toward the end of the fourth month of fetal development, the primary vitreous body and hyaloid vascular network atrophy, turning into a transparent narrow central zone related to the Cloquet's canal. Persistence of the primary vitreous body is an important factor in some vitreous malformations.

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Persistent hyaloid artery

Persistence of the hyaloid artery occurs in more than 3% of healthy full-term infants. It is almost always detected by the 30th week of gestation and in premature infants during screening for retinopathy of prematurity. Remnants of the posterior portion of this hyaloid network may appear as a raised mass of hyaloid tissue on the optic disc and are called a Bergmeister spot. Anterior remnants appear adherent to the posterior lens capsule and are called a Mittendorf spot.

Persistent hyperplasia of the primary vitreous body

Persistent hyperplasia of the primary vitreous body is a congenital pathology of the eye associated with impaired regression of the primary vitreous body. It is rare and unilateral. Most reports of bilateral and familial persistent hyperplasia of the primary vitreous body apparently refer to various syndromes, including vitreoretinal dysplasia. Classic signs of persistent hyperplasia of the primary vitreous body:

• fibrous membrane fused with the posterior surface of the lens;
• microphthalmos;
• small anterior chamber;
• dilation of the iris vessels;
• vascularized retrolental membrane causing traction of the ciliary processes.

Other ocular symptoms associated with persistent primary vitreous hyperplasia are rare and include:

• megalocornea;
• Rieger's anomaly;
• "morning glory" disk anomaly.

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

Treatment of persistent hyperplasia of the primary vitreous body is usually aimed at preventing glaucoma and phthisis of the eyeball. Removal of the lens and posterior membrane can prevent the development of glaucoma even in an eye with a low functional prognosis. However, it should be noted that there are reports of glaucoma occurring after lensvitrectomy. Some authors note the possibility of a significant increase in visual acuity with early surgery and active pleoptic treatment.