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Evaluation of coexisting optic nerve head drusen and glaucoma with optical coherence tomography [Case Report]
Roh, S; Noecker, R J; Schuman, J S
OBJECTIVE: Optic nerve head drusen often make evaluation of the nerve head difficult to interpret. In addition, visual field defects are known to occur in patients with optic disk drusen, resembling glaucomatous damage. The authors report two cases of coincident optic nerve head drusen and glaucoma, in which the use of optical coherence tomography (OCT) in evaluating the nerve fiber layer was beneficial. PARTICIPANTS: Two patients with both optic nerve head drusen and glaucoma, one with primary open angle glaucoma, the other with pseudoexfoliation glaucoma were evaluated. Both patients had asymmetric optic disk drusen, with clinically visible drusen only in one eye. INTERVENTION: Ophthalmologic examination, color and red-free photography, automated Humphrey visual field testing and OCT were performed. RESULTS: Nerve fiber layer loss as measured by OCT was found to be greater than expected by the appearance of the optic nerve head and red-free photography, with visual fields consistent with findings in case 1. In case 2, visual fields were full, despite nerve fiber layer thinning seen by OCT and red-free photography. CONCLUSIONS: There can be significant nerve fiber layer thinning in patients with both glaucoma and optic disk drusen, despite the appearance of the optic nerve head in these patients. The cup margin may be obscured by the drusen, giving rise to a falsely full-appearing disk. In such cases, OCT may provide a useful means to quantitatively measure the nerve fiber layer thickness and to aid in the management of these patients by detecting nerve fiber layer thinning earlier than would otherwise be possible.
PMCID:2917009
PMID: 9224467
ISSN: 0161-6420
CID: 1889232
A 1-year study of brimonidine twice daily in glaucoma and ocular hypertension. A controlled, randomized, multicenter clinical trial. Chronic Brimonidine Study Group
Schuman, J S; Horwitz, B; Choplin, N T; David, R; Albracht, D; Chen, K
OBJECTIVE: Brimonidin tartrate is a highly selective alpha 2-agonist. This study investigates the safety and efficacy of 0.2% brimonidine administered twice daily for 1 year in patients with glaucoma or ocular hypertension. METHODS: The study design was a multicenter, double-masked, randomized, parallel-group, active-controlled comparison clinical trial. Subjects instilled 0.2% brimonidine or 0.5% timolol maleate twice daily for 12 months. Subjects were examined at baseline, week 1, and months 1, 2, 3, 6, 9, and 12. A subset of subjects was examined at week 2. RESULTS: Of 443 subjects enrolled in this study, 374 met the entry criteria; 186 received brimonidine and 188 received timolol. Brimonidine-treated subjects showed an overall mean peak reduction in intraocular pressure (IOP) of 6.5 mm Hg; timolol-treated subjects had a mean peak reduction in IOP of 6.1 mm Hg. Brimonidine lowered mean peak IOP significantly more than timolol at week 2 and month 3 (P < .03); no significant difference was observed between the groups for this variable at other visits throughout the 1-year course of the study. No evidence of tachyphylaxis was seen in either group. Allergy was seen in 9% of subjects treated with brimonidine. Dry mouth was more common in the brimonidine-treated group than in the timolol-treated group (33.0% vs 19.4%), but complaints of burning and stinging were more common in the timolol-treated group (41.9%) than in the brimonidine-treated patients (28.1%). Headache, fatigue, and drowsiness were similar in the 2 groups. In general, the tolerance to medication was acceptable. CONCLUSIONS: Brimonidine is safe and effective in lowering IOP in glaucomatous eyes. Brimonidine provides a sustained long-term ocular hypotensive effect, is well tolerated, and has a low rate of allergic response.
PMID: 9230823
ISSN: 0003-9950
CID: 1889242
A gene responsible for the pigment dispersion syndrome maps to chromosome 7q35-q36
Andersen, J S; Pralea, A M; DelBono, E A; Haines, J L; Gorin, M B; Schuman, J S; Mattox, C G; Wiggs, J L
OBJECTIVES: To demonstrate the inheritance of the pigment dispersion syndrome in 4 families and to determine the location of a gene responsible for this syndrome. PATIENTS: Fifty-four members of 4 families affected by the pigment dispersion syndrome and pigmentary glaucoma. All 4 families are white. Two of the pedigrees are of Irish descent, and 2 are of mixed western European descent that includes some Irish ancestry. INTERVENTIONS: Individuals from 4 pedigrees affected by the pigment dispersion syndrome and their spouses were clinically examined for evidence of the pigment dispersion syndrome. DNA samples from patients and appropriate family members were used for a genome screen using microsatellite repeat markers distributed throughout the human genome. Genotypes were used for linkage analysis to identify markers segregating with the disease trait. RESULTS: Twenty-eight patients showed clinical evidence of the pigment dispersion syndrome. Of these, 14 also had elevated intraocular pressures requiring medical or surgical treatment or both. Significant linkage was observed between the disease phenotype and markers located on the telomere of the long arm of human chromosome 7 (i.e., 7q35-q36). The maximum 2-point lod score (i.e., Zmax) for a single pedigree (i.e., PDS5) was 5.72 at theta = 0 for markers D7S2546 and D7S550. An analysis of affected recombinant individuals demonstrated that the responsible gene is located in a 10-centimorgan interval between markers D7S2462 and D7S2423. CONCLUSIONS: The pigment dispersion syndrome was found to be inherited as an autosomal dominant trait in 4 affected pedigrees. The gene responsible for the syndrome in these 4 families maps to the telomeric end of the long arm of chromosome 7 (i.e., 7q35-q36). Locating a gene responsible for this condition is the first step toward the isolation of the gene itself. Characterization of the responsible gene will help elucidate the pathophysiology of this disease and potentially will lead to new methods of diagnosis and treatment.
PMID: 9076212
ISSN: 0003-9950
CID: 1889222
Erbium:YAG laser sclerectomy with a sapphire optical fiber
McHam, M L; Eisenberg, D L; Schuman, J S; Wang, N
BACKGROUND AND OBJECTIVE/OBJECTIVE:Laser sclerectomy may offer advantages to conventional glaucoma filtering surgery by minimizing conjunctival manipulation and subsequent subconjunctival scarring and by providing easier access to difficult locations. It has been theorized that minimizing collateral thermal damage may enhance the success rate and reduce complications associated with laser sclerectomy. The thermal damage induced by the pulsed erbium:yttrium aluminum garnet (Er:YAG) laser is notably less than that of other laser modalities, including neodymium:YAG (1.06 microns), Er:YSGG (2.79 microns), holmium: YAG (2.10 microns), and holmium: YSGG (2.10 microns). A major obstacle to the clinical use of the Er:YAG laser has been the lack of an efficient and reliable delivery system. The single-crystal sapphire optical fiber has an acceptable attenuation rate and favorable characteristics for delivery of the Er:YAG wave-length in a clinical setting. MATERIALS AND METHODS/METHODS:An Er:YAG laser (2.94 microns) focused into a 300-micron, single-crystal sapphire fiber was used to create ab-externo sclerectomies with varying energy levels and pulse rates in each eye of six anesthetized rabbits and six human cadaver eyes. Specimens then underwent histopathologic analysis and determination of the thermal damage zone. RESULTS:For the rabbit sclerectomies, there was a significant positive correlation between energy per pulse and the diameter of the thermal damage zone, which averaged 22.0 +/- 12.7 microns for all energy levels. For the human sclerectomies, a positive correlation existed between the total energy delivered (mJ/pulse x total pulses) and the thermal damage zone, with the mean thermal damage zone, being 25.0 +/- 9.0 microns. CONCLUSION/CONCLUSIONS:The Er:YAG laser with a sapphire optical fiber delivery system is an effective means of creating ab-externo sclerectomies with minimal thermal damage.
PMID: 9031306
ISSN: 1082-3069
CID: 3894242
A gene responsible for the pigment dispersion syndrome maps to chromosome 7q35-36. [Meeting Abstract]
Andersen, JS; Wiggs, JL; Pralea, AM; DelBono, EA; Haines, JL; Gorin, MB; Schuman, JS; Mattox, CG; Small, KW
ISI:000071446000147
ISSN: 0002-9297
CID: 1888222
ELAM-1 and interleukin-1 alpha mRNA expression in trabecular meshwork cells [Meeting Abstract]
Wang, N; Schuman, JS; Terraciano, AJ; Cook, JR; Fini, ME; Sadow, PM; Zhang, X; Cai, J; Haffner, GM
ISI:A1997WN18602614
ISSN: 0146-0404
CID: 1888902
A gene responsible for the pigment dispersion syndrome maps to chromosome 7q35-36 [Meeting Abstract]
Wiggs, JL; Andersen, JS; Pralea, AM; DelBono, EA; Haines, JL; Gorin, MB; Schuman, JS; Mattox, CG
ISI:A1997WN18602670
ISSN: 0146-0404
CID: 1888912
The comparison of nerve fiber layer thickness in glaucomatous monkey eyes measured by optical coherence tomography and histomorphometry [Meeting Abstract]
Huang, LN; Schuman, JS; PKloizman, T; Pieroth, L; Hee, MR; Coker, JG; Puliafito, CA; Fujimoto, JG; Swanson, EA
ISI:A1997WN21500737
ISSN: 0146-0404
CID: 1888922
Comparison of the nerve fiber layer by optical coherence tomography before and after intraocular pressure lowering procedures [Meeting Abstract]
Pieroth, L; Schuman, JS; Hertzmark, E; Hee, MR; Coker, JG; Chung, PY; PedutKloizman, T; Puliafito, CA; Mattox, C; Fujimoto, JG; Swanson, EA
ISI:A1997WN21500740
ISSN: 0146-0404
CID: 1888932
Goldmann and pneumatic tonometry in a normal pediatric population. [Meeting Abstract]
Eisenberg, DL; Sherman, BG; McKeown, CA; Schuman, JS
ISI:A1997WN21501744
ISSN: 0146-0404
CID: 1888942