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At least 703 records · Page 39Linked to original sources
PubMed2000

Molecular genetics of Oguchi disease, fundus albipunctatus, and other forms of stationary night blindness: LVII Edward Jackson Memorial Lecture.

PURPOSE: To compare the clinical findings of the various forms of stationary night blindness caused by mutations in identified genes encoding proteins of photoreceptors or the retinal pigment epithelium. METHODS: Review of the visual acuities, visual fields, fundi, dark-adaptation curves, and electroretinograms from patients with stationary night blindness caused by mutations in the genes RHO, GNAT1, PDE6B, RHOK, SAG, RDH5, and CACNA1F, respectively encoding rhodopsin, the alpha subunit of rod transducin, the beta subunit of rod cGMP-phosphodiesterase, rhodopsin kinase, arrestin, 11-cis retinol dehydrogenase, and a retinal L-type calcium channel. RESULTS: In the evaluated forms of stationary night blindness, the time course of dark adaptation and the characteristics of the electroretinogram indicate that rod photoreceptors are present and that they function, although abnormally. In night blindness resulting from defects in rhodopsin, the alpha subunit of rod transducin, or the beta subunit of rod cGMP phosphodiesterase, rod photoreceptors respond only to light intensities far brighter than normal, and the sensitivity of rods to light is similar to that of normal individuals who are not dark adapted. In fundus albipunctatus and in Oguchi disease, the rod photoreceptors can achieve normal sensitivity to dim light but only after 2 or more hours of dark adaptation, compared with approximately 0.5 hours for normal individuals. In each of these forms of stationary night blindness, the poor rod sensitivity and the time course of dark adaptation correlate with the known or presumed physiologic abnormalities caused by the identified gene defects. Patients with some forms of stationary night blindness, such as fundus albipunctatus and Oguchi disease, may develop degeneration of the retina leading to severe loss of vision in later life. CONCLUSIONS: The identification of the mutant genes causing forms of stationary night blindness refines the classification of these diseases and enhances our understanding of the underlying physiologic defects. Ophthalmologists must be aware that although these diseases are traditionally categorized as "stationary," some of them lead to reduced visual acuity or constricted visual fields, especially in older patients. Efforts to develop therapies for these diseases should concentrate on these more severe forms.

Amino Acid Sequence↗
PubMed2001

Clinical variations and complications of Coats disease in 150 cases: the 2000 Sanford Gifford Memorial Lecture.

PURPOSE: The purpose of this report is to review the clinical variations and natural course of Coats disease, using strict diagnostic guidelines. METHODS: In a retrospective, consecutive series, Coats disease was defined as idiopathic retinal telangiectasia with intraretinal or subretinal exudation without appreciable signs of retinal or vitreal traction. We reviewed our experience with the clinical features, complications, and diagnostic approaches to Coats disease. RESULTS: In 150 consecutive patients (158 eyes), Coats disease was diagnosed at a median age of 5 years (range, 1 month to 63 years), occurred in 114 males (76%), and was unilateral in 142 patients (95%). There was no predilection for race or laterality. The most common referral diagnoses were Coats disease in 64 cases (41%) and retinoblastoma in 43 (27%). The first symptom or sign was decreased visual acuity in 68 cases (34%), strabismus in 37 (23%), leukocoria in 31 (20%), and 13 patients (8%) were asymptomatic. Visual acuity at presentation was 20/200 to no light perception in 121 eyes (76%). The anterior segment was normal in 142 eyes (90%). The retinal telangiectasia involved the midperipheral or peripheral fundus in 156 of the 158 eyes (99%) and was restricted to the macular area in two eyes (1%); involved mainly the temporal fundus in 66 eyes (42%), inferior fundus in 41 eyes (26%), and more than one sector in 34 eyes (22%). Retinal exudation was present in all 12 clock hours in 86 eyes (55%) and six or more clock hours in 115 eyes (73%). There was a total retinal detachment in 74 eyes (47%) and neovascular glaucoma in 12 (8%). Retinal macrocysts were present in 18 eyes (11%), a vasoproliferative tumor in nine eyes (6%) and retinal neovascularization in four eyes (3%). Fluorescein angiography in 49 of the 158 eyes (37%) disclosed early hyperfluorescence of the telangiectasias and macular edema in 18 of eyes (37%). Ultrasonography typically showed a retinal detachment but no solid mass. CONCLUSIONS: Coats disease is a distinct clinical entity characterized by idiopathic retinal telangiectasia and retinal exudation. It is usually unilateral, occurs mostly in young males, and can cause severe visual loss resulting from exudative retinal detachment. The clinician should follow strict criteria in making the diagnosis, to avoid confusing Coats disease with other forms of exudative retinopathy.

Adolescent↗
PubMed2001

Classification and management of Coats disease: the 2000 Proctor Lecture.

PURPOSE: To review the methods and results of management in a large series of patients with Coats disease, to determine risk factors for poor visual outcome and enucleation, and to propose a practical classification of Coats disease. METHODS: In a retrospective consecutive series in 150 patients, Coats disease was defined as idiopathic retinal telangiectasia with intraretinal or subretinal exudation without appreciable signs of retinal or vitreal traction. We reviewed our experience with management, including observation, laser photocoagulation, cryotherapy, and various techniques of retinal detachment surgery and enucleation. The anatomic outcome, complications of treatment, visual results, and reasons for enucleation were tabulated. Factors predictive of poor visual outcome (20/200 or worse) and enucleation were determined using Cox proportional hazards regression models. Based on these observations, a staging classification of Coats disease, applicable to treatment selection and ocular prognosis, is proposed. RESULTS: In 117 patients (124 eyes) with a mean follow up of 55 months (range, 6 months to 25 years) primary management was observation in 22 eyes (18%), cryotherapy in 52 (42%), laser photocoagulation in 16 (13%), various methods of retinal detachment surgery in 20 (17%), and enucleation in 14 (11%). Anatomic improvement or stability was achieved in 76% of eyes, and final visual acuity was 20/50 or better in 17 eyes (14%), 20/60 to 20/100 in eight (6%), 20/200 to finger counting in 30 (24%), and hand motion to no light perception in 49 (40%) Enucleation was ultimately necessary in 20 eyes (16%). Risk factors predictive of poor visual outcome (20/200 or worse) included postequatorial (P =.01), diffuse (P =.01), or superior (P =.04) location of the telangiectasias and exudation, failed resolution of subretinal fluid after treatment (P =.02), and presence of retinal macrocysts (P =.02). The main risk factors for enucleation were elevated intraocular pressure (greater than 22 mm Hg; P less than or equal to.001) and iris neovascularization (P less than or equal to.001). Coats disease was classified into stage 1, telangiectasia only; stage 2, telangiectasia and exudation (2A, extrafoveal exudation; 2B, foveal exudation) stage 3, exudative retinal detachment (3A, subtotal; 3B, total); stage 4, total detachment and secondary glaucoma; and stage 5, advanced end-stage disease. Poor visual outcome (20/200 or worse) was found in 0% of eyes with stage 1, 53% with stage 2, 74% with stage 3, and 100% of stages 4 and 5 Coats disease. Enucleation was ultimately necessary in 0% of stages 1 and 2, 7% of stage 3, 78% of stage 4, and 0% of stage 5 disease. CONCLUSIONS: Carefully selected treatment can anatomically stabilize or improve the eye with Coats disease in 76% of eyes. However, poor visual outcome of 20/200 or worse commonly results. Patients who present with stages 1 to 3 Coats disease have the best visual prognosis, and patients with stages 4 and 5 have a poor visual prognosis.

Cryosurgery↗
PubMed2001

Optic nerve protection, regeneration, and repair in the 21st century: LVIII Edward Jackson Memorial lecture.

PURPOSE: To present the current status and clinical implications of optic nerve protection, repair, and regeneration after experimental injury in mammals, including nonhuman primates. DESIGN: Optic nerve and neuro-ophthalmology experimental study review. METHOD: Synthesis of experimental data regarding experimental studies of optic nerve protection, repair, and regeneration. RESULTS: Under certain conditions, mammalian retinal ganglion cells can be prevented from dying despite injury to the cell bodies or their axons, injured mammalian retinal ganglion cells whose axons have degenerated can be induced to extend new axons, and regenerating axons can reach their correct targets in the central nervous system. In addition, stem cells can be induced to become retinal ganglion cells. CONCLUSIONS: It may soon be possible to preserve and restore vision in persons whose sight is threatened or has been lost from disease or damage to the optic nerve.

Animals↗
PubMed1997

The ocular melanoma story. LIII Edward Jackson Memorial Lecture: Part II.

PURPOSE: To trace the evolution and status of our knowledge of choroidal melanoma with regard to the nature, cause, and treatment of this tumor. METHODS: Historical materials beginning with Georg Bartisch's contributions in 1583 through to the Collaborative Ocular Melanoma Study and recent basic research are reviewed. RESULTS: Many individuals have made important contributions to our knowledge about this tumor. Basic information, however, regarding the natural history of the tumor, the most effective treatment, and its cause is lacking. CONCLUSION: The Collaborative Ocular Melanoma Study will provide important information regarding the choice of treatment between enucleation and radiotherapy as well as natural history information, quality of life, and definitive pathology findings. Definitive treatment of choroidal melanoma will depend on knowledge of the genetic defects that cause the tumor. Within the next 25 years, it is predicted that genetic defects will be determined and tumor samples will be obtained using small-needle aspiration and DNA probes located on microchips. In addition, treatment will then be based on drugs designed to inhibit molecules related to the genetic defect in the tumor.

Choroid Neoplasms↗
PubMed1996

Edward Jackson in 1896: a man and his specialty at a crossroads. LIII Edward Jackson Memorial Lecture: Part 1.

PURPOSE: To review the life of Dr. Edward Jackson and his contributions to American medicine and ophthalmology, using as a reference point 1896, the year of the founding of the American Academy of Ophthalmology. METHODS: Review of published materials by and about Edward Jackson and other historical materials to evaluate Dr. Jackson's contributions to and the status of American ophthalmology during the late nineteenth and early twentieth centuries. RESULTS: Eighteen ninety-six was a seminal year for Dr. Jackson. He assumed a leadership role in American ophthalmology and medicine while overcoming personal tragedy and the difficult transition from being part of the Eastern establishment to becoming "a great champion of the West." CONCLUSION: The issues and events of 1896, and their evolution and repercussions in subsequent decades, confirm that Edward Jackson was a major figure in shaping modern American ophthalmology.

History, 19th Century↗
PubMed1999

Health, medicine, and ophthalmology: facing the facts and paying the piper LVI Edward Jackson Memorial Lecture.

PURPOSE: To describe the sources of tension within the health care system and methods for pursuing their solution. METHODS: Presentation of observations pertinent to patient, provider, and payer perspectives relevant to the cost, delivery, and quality of care and their impact on health. RESULTS: Societal forces, not just wealth, are major determinants of both health and the costs of health care. CONCLUSIONS: Tensions created by rising health care costs in the face of finite societal resources will increase in the years ahead. These can be resolved only by realizing new efficiencies in care, and prioritizing, through an explicit process, the care that is to be provided.

Cost Control↗