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G W Cibis

Publications and source records attributed to G W Cibis.

At least 55 records · Page 3Linked to original sources
PubMed1984

Paravenous pigmentary retinochoroidal atrophy.

Three cases with ophthalmoscopic findings of paravenous pigmentary retinochoroidal atrophy are described. One case had markedly abnormal electrophysiologic studies suggestive of a hereditary chorioretinal degeneration. The other two cases did not. Similarly conflicting results are found in the literature. Because of the great similarity in clinical appearance we none the less feel that all of these cases represent a distinct hereditary disease entity and are not acquired.

Adult↗
PubMed1984

Noncycloplegic vs cycloplegic retinoscopy in pre-school children.

Refractive errors in 311 children between the ages of 18 and 48 months were assessed utilizing standard cycloplegic retinoscopy and a noncycloplegic near retinoscopy technique as promulgated by Mohindra. Results from this study indicate little agreement between the two objective refraction methods.

Child, Preschool↗
PubMed1983

Mucolipidosis I.

A case of mucolipidosis I had clinical and histopathologic features that were a combination of changes found in both mucopolysaccharidoses and sphingolipidoses. Corneal clouding, spokelike cataracts, tortuous conjunctival and retinal vessels, and strabismus were clinical findings. Histopathologically, there were inclusion vacuoles similar to those seen in mucopolysaccharidoses; lamellar bodies typical of sphingolipidoses were rare. These vacuoles were seen in conjunctival and corneal epithelium and fibrocytes, conjunctival and retinal vessel endothelium, and all retinal cell layers.

Conjunctiva↗
PubMed1982

Corneal keloid in Lowe's syndrome.

Bilateral corneal keloids in a boy wih Lowe's syndrome were examined by conventional light and electron microscopy. There were no signs of perforating corneal trauma or iridocorneal incarceration in either eye. The corneal keloids consisted of haphazardly arranged bundles of collagen fibers, fibroblasts, and fenestrated blood vessels. The anterior region of the keloids showed signs of active progression and epithelial epidermalization. The etiology of keloids in Lowe's syndrome remains obscure. Considerations include excessive local delivery of amino acids and unknown noxious substances through the leak corneal vessels, seepage of similar substances across the defective blood-aqueous barrier and the decompensated endothelium, repeated external trauma with associated inflammation, phenytoin (Dilantin) therapy, and congenital predisposition. No data are available on the management of the progressive course of corneal keloids. Possible empirical regimens include local excision, pressure therapy, topical corticosteroids, and cromolyn sodium.

Child↗
PubMed1982

The differential diagnosis of Descemet's tears (Haab's striae) and posterior polymorpous dystrophy bands. A clinicopathologic study.

Band-like structures, clinically similar to Haab's striae, occur in posterior polymorphous dystrophy (PPMD) and are often confused with them. The difference in clinical appearance based on difference in histopathology allows a clear differentiation. The edge of Haab's striae are thickened, curled, and secondarily proliferate Descemet's membrane, while the area between the edge is thin and smooth. Posterior polymorphous dystrophy bands are the exact opposite. The band is a thickening of Descemet's membrane between the edges with thinner, more normal Descemet's membrane outside of them. PPMD bands may be associated with typical vesicles or appear as the only sign of dystrophy, even in the eyes of patients with a known family history.

Adolescent↗
PubMed1982

Lowe's syndrome.

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Child↗
PubMed1982

Mucolipidosis I.

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Cataract↗
PubMed1981

Brückner test.

Brückner, in 1962, published a paper in German describing a "trans-illumination" test extremely useful in the diagnosis of small angle deviations and amblyopia in young uncooperative children. A bright coaxial light source, such as a direct ophthalmoscope, is used. Both eyes of the patient are simultaneously illuminated from approximately one meter distance. First, the position of the corneal light reflex, (Hirschberg test), along with brightness difference of the fundus reflex as seen in the pupil through the ophthalmoscope, is evaluated. When strabismus is present. the fixing eye has a darker reflex than the deviated eye. The second step evaluates pupil size, pupil reaction, and fixation movement of the eyes on "successive" illumination of one eye at a time. This is useful in detecting amblyopia.

Amblyopia↗
PubMed1980

Endophthalmitis complicating Haemophilus influenzae type B meningitis.

In two children, pyogenic endophthalmitis developed simultaneously with Haemophilus influenzae type b meningitis. The eye of one of the patients recovered fully; the eye of the other became phthisical and was enucleated. Culturable or pathologically identifiable organisms were not found in either eye; nevertheless, it is suggested that these cases represented metastatic H influenzae type b endophthalmitis from a primary site of infection in the meninges.

Chloramphenicol↗
PubMed1980

Glaucoma due to endothelialization of the anterior chamber angle. A comparison of posterior polymorphous dystrophy of the cornea and Chandler's syndrome.

Posteroir polymorphous dystrophy (PPMD) and Chandler's syndrome are separate ocular diseases with certain clinical features in common. Both may cause endothelial dystrophy, corneal edema, iridocorneal adhesions, and glaucoma. Differences between the two disorders include the morphology of the endothelial dystrophy, hereditary transmission, laterality, and rate of progression. Histopathologic examination of trabeculectomy and iridectomy specimens from two patients with Pmd and one patient with Chandler's syndrome disclosed a common basic pathologic process--endothelialization of the anterior chamber angle. Ectopic corneal endothelium and abnormal Descemet's membrane extended across the trabecular meshwork and onto the anterior surface of the iris. The appearance of the endothelial cells, however, was strikingly different in the two conditions. The endothelial cells in PPMD had ultrastructural characteristics of epithelial cells. Those in Chandler's syndrome were degenerated but retained ultrastructural features of endothelial cells.

Anterior Chamber↗
PubMed1980

Dominantly inherited macular dystrophy with flecks (Stargardt).

A family had dominantly inherited macular dystrophy with flecks and without evidence of major cone dysfunction. This family shows that the clinical picture of Stargardt's disease can result from at least two different genes: one with dominant and another with recessive heredity. Some patients had fundus flavimaculatus flecks of Stargardt's disease; others did not. In our opinion progressive atrophic macular (foveal) dystrophy as Stargardt's disease without flecks is not a separate clinical entity but part of the same genetic defect. Furthermore, a dominant hereditary pattern in patients without flecks or major cone dysfunction is insufficient evidence for classification of such patients as having cone dystrophy.

Adolescent↗
PubMed1980

Lowe's syndrome.

The histopathological manifestations in four eyes from two male patients with the oculo-cerebro-renal syndrome of Lowe included a small, discoid, cataractous lens, peculiar capsular and epithelial changes with aberrant formation of collagenous fibrous tissue, polar lenticular changes with anterior vitreous condensation, embryonic anterior chamber angle with anterior displacement of rudimentary ciliary processes, segmental hypoplasia of iris dilator muscle, and Lange's folds with peripheral retinal cystoid changes. Additional findings in one of the cases included bilateral corneal keloids, vitreous organization, hyalinized retinal vessels, and mild gliosis. We suggest that the congenital ocular abnormalities in Lowe's syndrome are related to an as yet unidentified, inherited enzymatic and/or biochemical defect, and that they progress further because of an abnormal aqueous humour environment. The role of aminoaciduria and mucopolysaccharidosis in the pathogenesis of systemic and ocular defects is discussed in the light of recent investigations.

Anterior Chamber↗
PubMed1979

Nasolacrimal duct probing in infants.

Use of a fiberoptic endoscope to visualize the vault of the inferior turbinate during lacrimal duct probing and irrigation revealed a high incidence of false passages. This was confirmed on dacryocystofluoroscopy. The creation of false passages as documented by us can help explain clinical probing failure in apparently successful probings in which "metal on metal" is felt in the nose.

Endoscopy↗
PubMed1978

Herpes simplex retinitis.

Fatal encephalitis with accompanying retinitis developed in a previously healthy 18-month-old infant. Clinically the disease appeared as whitish-yellow punctate lesions, perivascular cuffing, and hemorrhage. The antibody titer to herpes simplex rose from 1:8 on the day of admission to 1:256 on the day of death. Postmortem, intranuclear inclusion bodies that were typical of those found with herpesvirus were seen in the brain and retina. Viral particles consistent with those of herpesvirus were found by electron microscopy in the brain and in the inner-nuclear and ganglion-nerve fiber layers of the retina. This demonstrates the direct infectious nature of herpetic retinitis. Hematogenous spread of the virus to the retina is presumed.

Brain Stem↗
PubMed1978

Traumatic corneal endothelial rings.

Nonpenetrating "blast injuries" to the eye in two patients resulted in multiple, small, corneal epithelial foreign bodies that were associated with characteristic ring-shaped opacities of the corneal endothelium. These endothelial lesions were clinically visible immediately after injury and became more pronounced during the next several hours. They disappeared within days and resulted in no permanent loss of visual acuity. This communication describes and illustrates the appearance of these endothelial lesions both clinically and in an animal model. Light and electron microscopic observations of an experimental model, with the use of monkey and rabbit eyes, revealed that the ring-shaped opacities resulted from swelling of the corneal endothelium, as well as accumulation of fibrin and leukocytes on the injured cells. Except for the epithelial impact site and the concussion injury of the endothelium, the cornea was uninvolved, and the stroma remained clear.

Adolescent↗
PubMed1977

The clinical spectrum of posterior polymorphous dystrophy.

We examined 61 affected members of eight families with an inherited corneal dystrophy. The corneal abnormalities varied greatly from one member of a family to another. Some patients had only a few isolated endothelial vesicles, while others in the same family had severe secondary stromal and epithelial edema. In some patients edema was present at birth or in early childhood; in others it developed later in life. The wide variation of corneal abnormalities suggests the possibility that several conditions previously described as separate disease entities, such as grouped vesicles, Schnyder's posterior herpes, posterior polymorphous dystrophy, and congenital hereditary endothelial dystrophy, are part of the clinical spectrum of expression of a single familial corneal dystrophy. Some affected family members also had ocular hypertension or open-angle glaucoma. Broad iridocorneal adhesions were present in some of the patients with glaucoma and in others with normal intraocular pressures. Other ocular abnormalities present in a few patients include pupillary ectropion, "glass membranes" on the anterior iris surface, and bands in Descemet's membrane. The transmission in most of the families was autosomal dominant. In two families it appeared to be autosomal recessive.

Adolescent↗