Central Corneal Opacity Research Articles

Corneal Amyloidosis Associated with Keratoconus

Nodular, gray-white, central corneal opacities which extended from the subepithelial zone through the anterior four fifths of the stroma developed in a 50-year-old man with a longstanding history of hard contact lens wear for keratoconus. Results of histopathologic analysis of the corneal button obtained at the time of penetrating keratoplasty disclosed that the opacities were composed of amyloid. Corneal amyloidosis is rarely found in association with keratoconus. Although there were some similarities in the pattern of amyloid deposition to that seen in primary familial amyloidosis of the cornea, the authors believe that their patient is more likely to have had a secondary amyloidosis. Corneal amyloidosis should be considered in keratoconus patients with development of unusual forms of central corneal opacification.

Extended-wear Contact Lens Correction of Aphakia in Infant Primates: Corneal Studies

Extended-wear contact lenses (EWCL) are being used increasingly for the correction of aphakia in infants, but there is a lack of data documenting their effects on the corneas of young children. Therefore, corneal studies were performed on infant monkeys wearing EWCL for the correction of surgical aphakia. Nine newborn monkeys underwent unilateral lensectomy and anterior vitrectomy. Seven eyes were fitted with aphakic EWCL postoperatively and two wore no lenses. After at least six months, corneas were studied with slit-lamp and specular microscopy, and with light microscopy (LM) and electron microscopy (EM). Small central corneal opacities developed in two aphakic eyes corrected with EWCL after episodes of keratoconjunctivitis. One of these corneas was found to have a mildly increased coefficient of variation (CV) of endothelial cell size (polymegathism). Although EWCL are well tolerated by the corneas of aphakic infant primates, their association with endothelial polymegathism, which may indicate physiologic compromise, mandates careful long-term follow-up.

Ocular effects of treatment with various psoralen derivatives and ultraviolet-A (UVA) radiation in HRA/Skh hairless mice.

Hairless (HRA/Skh) mice were administered one of four dietary concentrations (50, 100, 625 or 1250 ppm) of 8-methoxypsoralen (8-MOP) or 5-methoxypsoralen (5-MOP), or molar equivalent concentrations of 5-methylisopsoralen (5-MIP) or 3-carbethoxypsoralen (3-CPS) by 'pulse feeding' technique, 3 days per week for 13 weeks. For the final 11 weeks psoralen derivative administration was followed by exposure to 0.2 or 48 J/cm2 of unfiltered ultraviolet-A (UVA) radiant energy from FR74T12PUVA lamps. At 0 and 13 weeks eyes were dilated with 0.2% atropine solution and were examined using a binocular indirect ophthalmoscope with a +20.0 D condensing lens. The lids, cornea, anterior chamber and the lens were evaluated for pathological changes. Ocular damage consisting of dense central corneal opacification was seen at significant levels in animals given 8-MOP or 5-MOP and exposed to UVA. In addition, opacities in the area of the posterior lens were seen in all experimental groups and appeared to be related to drug treatment, independent of light exposure, and therefore appeared not to be related to drug-light interaction. Some corneal and lenticular opacification was seen at non-significant levels in all experimental and control groups.

Leprosy in a trachomatous population.

In an Egyptian leprosy hospital, 17% of 133 patients had a visual acuity of less than 3/60. Corneal opacity, phthisis bulbi, and cataract accounted for 85% of blindness. Leprosy and trachoma together produce blinding corneal opacity by exposure, leprous keratitis, and trichiasis and entropion. Inturned lids, a late result of conjunctival scarring due to childhood trachoma, were less frequent in patients with lepromatous leprosy than in patients with tuberculoid leprosy; because conjunctival scarring from trachoma depends on cell-mediated immunity, patients with lepromatous leprosy may not have had severe trachomatous scarring develop due to their lifelong abnormality in cellular immunity. In patients with leprosy, even when complicated by trachoma, simple measures to prevent or restore vision include medical treatment of leprosy, surgical correction of lid deformities, sector iridectomy for constricted pupils or central corneal opacities, and cataract extraction.

Wound Healing of Grafts in Congenitally Opaque Infant Corneas

Wound healing, determined by uneventful suture removal, was evaluated in 28 corneal transplants (20 eyes) with congenital corneal opacities. Seven transplants in seven eyes with the typical central corneal opacities of Peters' anomaly had suture removal between 17 and 90 days postoperatively. All seven transplants remained transparent. Corneal grafts for sclerocornea or regrafts in sclerocornea healed much more quickly than those in eyes with Peters' anomaly (as early as four days postoperatively in the 13 most recent cases). In these corneas suture microabscesses and superficial neovascularization of the wound were signs indicating wound healing and also a host inflammatory response that led to graft rejection if the sutures were not removed.

Central Cornea Involvement in Terrien's Degeneration

A 15-year-old female showed classical signs of Terrien's corneal degeneration including peripheral corneal thinning, vascularization, lipid deposition, and ectasia. She also showed episodes of conjunctival inflammation and perforation following minor trauma, all in the presence of an intact epithelium. She also showed progressive central corneal thinning and opacification, features not reported in the literature in the last 30 years.

Clinical aspects of corneal trachoma.

Classification of trachoma by site rather than density of opacities is better related to visual prognosis and helps in selection for graft surgery. The cases are divided into 3 groups: peripheral corneal opacities, central corneal opacities, and diffuse corneal opacities (ground-glass cornea). A central lesion has the poorest prognosis, especially in children.

Peters-Rieger's Syndrome

The joint occurrence of Peter's anomaly, congenital central deep corneal opacity with an enterior cone-shaped polar cataract, and Rieger's anomaly, hypoplasia of iris stroma, dyscoria, and iridocorneal adhesions in the angle of the anterior chamber, is described. The term Peters-Riger's syndrome is proposed for this clinical association. Associated ocular anomalies which apparently have not been previously mentioned in the literature were dysversion of the optic disc, ganglionic neuroretinal hypoplasia (hypoplasia of the optic nerve), and downward ectopia of the macula. Other associated ocular and systemic anomalies of Peters-Rieger's syndrome are also mentioned.

The Histopathology and Ultrastructure of Congenital, Central Corneal Opacity (Peters' Anomaly)

The Histopathology and Ultrastructure of Congenital, Central Corneal Opacity (Peters' Anomaly)

Severe Silver Nitrate Injury to the Eye

A 35-year-old housewife had a chalazion re­ moved from the left upper eyelid, and at the com­ pletion of the procedure the base of the surgical bed was cauterized with a silver nitrate applicator stick. The eye was then patched. The patient was referred to one of us (M.G.) four days following the injury and at that time the eyelids and conjunctiva were markedly inflamed. The cornea was completely opaque except for a nar­ row limbal ring of clear cornea (Fig. 1). The opac­ ity appeared to extend the full thickness of the cor­ nea and the visual acuity at this time was faulty light perception. After six months, considerable clearing had taken place (Fig. 2), but a central brown corneal opacity remained which contributed to the marked impairment of her central vision. It was also noted that the lens was grayish-brown and densely opaque. A single large blood vessel traversed the

EXPERIMENTAL INDUCTION OF DISCIFORM KERATITIS.

Disciform keratitis is a term introduced by Fuchs in 1901 to describe a central corneal opacification that is seen most often as a late complication of herpes simplex keratitis. 1 Clinically, two kinds of stromal disease may occur after herpes simplex infection. In one type, dense, white, cheesy opacities which are generally eccentric occur. The pathogenesis of these lesions appears to be different from those of the typical disciform lesion. The disciform lesion is characterized by a round patch of corneal edema which is generally central and is typically surrounded by normal cornea. In the involved area of cornea, there are folds in Descemet's membrane, swelling of the stroma, and often epithelial bullae. In the early stages the disciform lesion is reversible, but as the edema persists, corneal scarring and permanent opacities often develop. Although the exact incidence of disciform keratitis following corneal herpes simplex is not known, in 1956,