Cysticercosis of the orbit.
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Acute Disease↗
Biomedical subjects
J H Antoszyk
Publications and source records attributed to J H Antoszyk.
Interlocking Crawford triangles in frontalis suspension.
In Crawford's pattern of frontalis suspension, two bands are passed, one nasally and the other temporally, forming two base-down triangles with their apexes attached at the brow incisions. Over time, opposing vector forces in the center of the eyelid can cause "cheese-wiring" of the bands with resultant shortening of the inferior bases of both triangles and loosening of the suspensory loops. We modified the standard pattern by interlocking the bands centrally in the lid. A mathematical model was developed that demonstrates neutralization of these opposing forces, resulting in a symmetrical and flexible redistribution of the lifting forces. In support of this mathematical model, a retrospective analysis of 42 consecutive cases using this technique revealed good aesthetic results in terms of lid height, contour, and symmetry, with no important complications from this modification.
Adolescent↗
Orbital decompression for Graves' disease: exposure through a modified blepharoplasty incision.
A "transorbital" three-wall decompression through a modified blepharoplasty incision was used to treat 19 orbits for either cosmetic disfigurement or optic neuropathy. In the 14 orbits with disfigurement, surgical retroplacement averaged 5.2 mm; vision improved to 20/40 or better in four of five eyes with optic neuropathy. Complications attributed to the surgery included: acquired strabismus (two transient, one permanent) and infraorbital hypesthesia (one transient, one permanent). This technique's advantages are: 1) a single incision with wide exposure, 2) a low incidence of permanent strabismus, 3) a lateral orbital rim and canthal tendon preservation, and 4) a large reduction in proptosis.
Adult↗
Unilateral peripapillary myelinated nerve fibers with myopia and/or amblyopia.
This report describes 12 patients with unilateral peripapillary myelinated nerve fibers associated with myopia and/or amblyopia. Seven patients had myopia with a mean of -13.00 diopters of anisometropia and abnormal maculae varying from a decreased reflex to pigment dispersion. These patients had final visual acuities of 20/200 or less following conventional amblyopia therapy. In contrast, five patients had myopia with a mean of -3.75 diopters of anisometropia and normal maculae. These patients had final visual acuities of 20/30 or greater with identical therapy. There was a statistically significant difference between the mean diopters of anisometropia of these two groups. However, the range of diopters of anisometropia overlapped, and the critical feature that determined which patients could achieve good vision was the macular appearance. This condition is distinct from simple unilateral myopia with amblyopia and from myelinated nerve fibers without myopia or amblyopia.
Amblyopia↗
Traumatic hyphema in children. Treatment with epsilon-aminocaproic acid.
Forty-nine patients, ages 3 to 18 years, who sustained nonpenetrating unilateral trauma with hyphemas were assigned randomly to receive either 100 mg/kg of epsilon-aminocaproic acid (EACA), an antifibrinolytic agent, orally every 4 hours for 5 days (maximum 30 g/day) or a placebo. No patients ingested acetylsalicylic acid (ASA)-containing compounds before or during admission. Two patients of 24 treated with EACA and 1 of 25 given placebo had rebleeds. The hyphemas in the EACA-treated group took significantly longer to clear (mean, 5.3 versus 2.6 days; P less than 0.001). Because of the low incidence of rebleeds in the placebo group, the efficacy of EACA in reducing the rate of rebleeds could not be determined. Further studies with this drug, controlling for age, race, sickle trait, and pre-admission antiplatelet agents should be undertaken before its routine use in traumatic hyphema management can be recommended.
Adolescent↗
Linkage of atypical vitelliform macular dystrophy (VMD-1) to the soluble glutamate pyruvate transaminase (GPT1) locus.
One hundred twenty-eight blood samples were drawn from members of a single family with atypical vitelliform macular dystrophy (VMD-1) characterized by variable expressivity in affected members of at least 5 generations. Because of the late onset of detectable retinal lesions in most family members, phenotype data from only 93 individuals who were at least 14 years of age were analyzed for linkage. Phenotype data from the remaining 35 members of the family who were under age 14 were excluded from the analysis. Maximum-likelihood analysis for linkage between VMD-1 and 13 biochemical and serological markers in the family demonstrated linkage between VMD-1 and the soluble glutamate pyruvate transaminase (GPT1) locus, which has been tentatively assigned to the short arm of chromosome 16. A maximum lod score of Z = 4.34 (odds favoring linkage of approximately 22,000 to 1) was obtained at a recombination fraction of theta = .05.
Adolescent↗
Variable expressivity of autosomal dominant anterior segment mesenchymal dysgenesis in six generations.
Of 58 members in a six-generation family with anterior segment mesenchymal dysgenesis with variable expressivity, 21 of 35 members (60%) at risk were affected. Of the 15 living affected family members, nine (60%) had visual acuities of 6/12 (20/40) or better in at least one eye, five (33%) had visual acuities between 6/15 and 6/60 (20/50 and 20/200) in at least one eye, and one (7%) had a visual acuity of less than counting fingers at one foot in both eyes. All nine affected patients who underwent slit-lamp examinations had corneal abnormalities with and without synechiae. All 15 affected patients also had cataracts, and three of the 15 (20%) had optic nerve abnormalities. In a corneal button from the severely affected proband, Descemet's layer and endothelial cells were absent even in the periphery. Other corneal and lenticular changes were secondary to the primary endothelial defect. Anterior segment mesenchymal dysgenesis in this family appeared to be caused by an aberration of the first wave of mesenchyme from the rim of the optic cup.
Adolescent↗
Anterior segment mesenchymal dysgenesis: probable linkage to the MNS blood group on chromosome 4.
Thirty-seven blood samples were analyzed for linkage from members of a single family with an anterior segment mesenchymal dysgenesis (ASMD1) with variable expressivity affecting members of at least six generations. Maximum-likelihood analysis for linkage between ASMD1 and 14 biochemical and serological markers in the family showed a probable linkage between ASMD1 and the MNS blood group on the long arm of chromosome 4 (Z = 2.36 at a recombination fraction of .09).
Chromosome Mapping↗