Biomedical subjects
A R Frederick
Publications and source records attributed to A R Frederick.
Melanoma arising de novo over a 16-month period.
Choroidal melanoma is widely regarded as a slow-growing tumor. We report herein the first documented case, to our knowledge, of a choroidal melanoma present in an eye in which examination 16 months earlier disclosed no tumor. On gross examination following enucleation, the largest tumor diameter at the base was 19 mm and the height was 11 mm. The implications as to the growth rate and the precursor lesions of choroidal melanomas are discussed.
Idiopathic retinal gliosis mimicking a choroidal melanoma.
A 37-year-old woman has followed for more than 10 years with an amelanotic peripheral intraocular tumor. This solitary lesion grew slowly and, because of the possibility of an amelanotic melanoma, the eye was enucleated. Histopathology revealed a localized "massive" retinal gliosis (MRG). Immunohistochemical staining for S-100 protein and glial fibrillary acidic protein (GFAP) were positive. Electron microscopy showed a highly fibrillar component and basement membrane formation in the extracellular space. Proliferating cells contained abundant fine filaments. These findings confirmed the glial origin of the proliferating cells. The previously undefined relationship of these localized forms of MRG with solitary astrocytomas is discussed.
Multifocal and recurrent (serous) choroidopathy (MARC) syndrome: a new variety of idiopathic central serous choroidopathy.
Presented is a group of 110 patients with patches of granular atrophy of the retinal pigment epithelium which I believe represents a new subtype of idiopathic central serous choroidopathy (ICSC). It is designated as multifocal and recurrent (serous) choroidopathy (MARC) syndrome. Such patients are the 'older' ICSC patients and they usually have bilateral involvement which may show marked asymmetry. The history is seldom helpful in defining previous episodes of leaking. The fundus changes are thought to represent the sequelae of multiple, recurrent, or chronic choroidopathy in the form of serous detachments of the retinal pigment epithelium and/or neurosensory retina. Such detachments may not be present at the time of a single examination, and thus the fundus picture may be puzzling without an awareness of this syndrome which exhibits a wide spectrum of severity. Difficulties in detecting the low detachments and fluorescein leaking are emphasized. There is often a marked disparity between the ophthalmoscopic and the fluorescein angiographic pictures, and examination by the latter technique is urged. I do not believe this entity progresses to senile disciform disease, but can result in marked visual loss. If extrafoveal leaking is found in the presence of decreased acuity and a macular detachment, and if there is evidence of previous attacks, photocoagulation can effectively flatten the retina. I believe photocoagulation therapy under these conditions is justifiable.
Intraocular hemangiopericytoma.
A 40-year-old woman had an intraocular lesion consistent with a choroidal hemangioma. Xenon arc photocoagulation was applied to reduce subretinal fluid, and the lesion remained stationary until the patient's death eight years later. The lesion was composed of spindle-shaped and ovoid cells with numerous inconspicuous capillaries. The tumor cells were surrounded by reticulin-positive fibers. The diagnosis of hemangiopericytoma was confirmed by electron microscopy, which demonstrated proliferating pericytes associated with basal lamina. Although hemangiopericytomas are occasionally found in the orbit, to our knowledge this report is the first of an intraocular hemangiopericytoma. Because the pericyte is an integral component of the choroidal vasculature, the origin of this tumor in the choroid is not unexpected. The diagnosis of hemangiopericytoma should be considered when evaluating vascular choroidal lesions.
Vogt-Koyanagi-Harada syndrome with focal neurologic signs.
The Vogt-Koyanagi-Harada syndrome includes inflammation of the uveal tract, retina, and meninges. Integumentary and auditory signs are common. Neurologic involvement has been reported. We studied two patients who manifested many of the varied clinical signs of Vogt-Koyanagi-Harada syndrome, but who also showed focal neurologic involvement, including acute transverse myelitis and ciliary ganglionitis. Both patients responded well to corticosteroid therapy. The findings in these patients and the results of previous studies suggest that Vogt-Koyanagi-Harada syndrome is a cell-mediated autoimmune disorder in which a component of myelin acts as an inciting antigen.
A new needle design for scleral buckling procedures.
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The results of retinal detachment surgery. Analysis of 268 operations with a broad scleral buckle.
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