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Central Visual Fields for Short Wavelength Sensitive Pathways in Glaucoma and Ocular Hypertension

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Central Visual Fields for Short Wavelength Sensitive Pathways in Glaucoma and Ocular Hypertension Investigative Ophthalmology & Visual Science, Vol. 29, No. 1, January 1988 Copyright © Association for Research in Vision and Ophthalmology Central Visual Fields For Short Wavelength Sensitive Pathways in Glaucoma and Ocular Hypertension Gordon Heron,*j- Anthony J. Adorns,* and Roger Husred^:§ While conventional clinical visual acuity and kinetic visual fields may be essentially normal in ocular hypertension and early stages of glaucoma, other foveal aspects of vision (eg color, spatial and temporal contrast sensitivity) may be quite abnormal. Specifically, a selective vulnerability of the short wavelength sensitive (SWS) visual pathways in these conditions has previously been noted. Here we studied the central visual fields of 33 primary open angle glaucoma (POAG) patients, 32 ocular hypertensives (OHT), and 24 age-matched normal controls using blue and yellow test flashes on bright yellow backgrounds. SWS cone and MWS and/or LWS cone pathway sensitivities were measured at the fovea and at 2.5°, 5°, 10° and 15° eccentricities, in either the inferior temporal (for OHT) or horizontal nasal retina (for POAG). As expected, all groups had normal sensitivity to yellow flashes —detected by LWS and/or MWS cones—in these meridians. By comparison, for the blue flashes— detected by the SWS cones—the POAG and OHT groups had sensitivity deficits, uniformly across the central visual field, of about 6X and 1.8X, respectively, compared to normals. While six of 31 (19%) OHT subjects had localized glaucomatous field defects (>0.4 log units) in the non-foveal inferior temporal retina, none of the 12 OHT subjects who were also tested in the horizontal nasal retina showed loss in this meridian. Finally, while no POAG subjects had localized sensitivity loss for yellow flashes in the horizontal nasal retina, four did show local field defects with blue test flashes. These results are consistent with significant local and diffuse ganglion cell loss involving the blue- sensitive visual pathways in both OHT and POAG patients. Invest Ophthalmol Vis Sci 29:64-72,1988 The loss of nerve fibers in glaucoma is thought to Traditionally, greater emphasis has been placed on occur in two ways. A localized loss of axons, usually evaluating the localized loss of nerve fibers, using vi- occurring at the poles of the optic nerve head,1 pro- sual field evaluation. The earliest localized visual duces the familiar changes of asymmetric cupping of field loss typically occurs outside of the central macu- the disk and notching of the neuroretinal rim. This lar area and, in recent times, much work has been loss may be evident as a defect of the retinal nerve carried out on improving methods of visual field ex- fiber layer2"4 and give rise to the typical nerve fiber amination to provide increasingly more sensitive bundle defects found in the Bjerrum areas of the vi- tests of the earliest signs of functional loss. Whether sual fields. The second type of axon loss produces a the localized loss of nerve fibers can first be detected generalized reduction in retinal sensitivity, and may functionally by the visual fields, or structurally by ex- be observed at the nerve head as an overall enlarge- amination of the optic nerve head and retinal nerve ment of the optic cup with a reduction in the neuro- fiber layer, is currently a matter of some debate.7'8 retinal rim area.4"6 The recent reports by Quigley1'8"10 which suggest that patients with mild or moderate visual field defects From the "School of Optometry, University of California at may have lost as many as 50% of their axons at the Berkeley, Berkeley, California, and the ^Ophthalmology Clinic, optic nerve head have stimulated interest in identify- Silas Hayes Hospital, Fort Ord, California. ing the earliest possible changes in glaucoma. More f On leave from Glasgow College of Technology, Glasgow, provocative is the evidence from Quigley's studies Scotland. § Lt. Col., MC, USA. The views expressed in this article are those suggesting that even ocular hypertensive eyes, with of the authors and do not reflect official United States Army or no clinically manifested visual field loss or change in Department of Defense policy. the appearance of the nerve head, may have as many Supported by NIH giant EY-02271 to AJA. as 35% of the axons of the nerve head missing. Submitted for publication: December 3, 1986; accepted July 6, 1987. A generalized reduction of retinal sensitivity from Reprint requests: Anthony J. Adams, School of Optometry, Uni- the diffuse loss of axons, although present, is difficult 4 5 versity of California, Berkeley, CA 94720. to demonstrate by visual field examination. - How- 64 Downloaded from iovs.arvojournals.org on 09/23/2021 No. 1 SWS CONE FIELDS IN GLAUCOMA AND OCULAR HYPERTENSION / Heron er ol. 65 ever, a number of changes of visual function at the inferior retina with about 30% of them also tested fovea have been reported and are usually cited as along the nasal horizontal retina. Here we were inter- evidence of diffuse loss. Much of this evidence comes ested in revealing diffuse or localized field loss that from color vision studies, although studies of spa- clearly had not been identified by conventional clini- tial""13 and temporal14 contrast sensitivity in the cal field testing. (The 40° meridian in the temporal central macula also contribute to this conclusion. In inferior retina is thought to represent one of the earli- fact, even though visual acuity is normally thought to est locations for localized loss in the development of be unaffected in the earlier stages of glaucoma, care- glaucoma.) A similar sized group of age-matched ful assessment often shows that it may be mildly re- control subjects was used for measurements in both duced.5 meridians. A number of studies of foveal color vision can now be cited as showing that, in glaucoma, hue discrimi- Materials and Methods nation is reduced selectively in the blue-yellow axis of Glaucoma and ocular hypertensive patients were color discrimination.15"23 More specifically, both recruited for this study from the Eye Clinic of the achromatic and chromatic sensitivity is reduced, with Silas Hayes Hospital at Fort Ord, California. Glau- the greatest sensitivity loss occurring in the blue end coma patients (n = 33) were of the primary open of the spectrum.24"30 Surprisingly, similar results have angle type (POAG), had visual acuities of 20/40 or been reported among many ocular hypertensive pa- better in the tested eye (all except two had 20/30 or tients where no localized loss of axons has been pre- better), were under reasonable control and had not sumed.20-23'24'28'31 Now there is evidence linking fo- undergone any laser or filtration surgery. Seventeen veal color vision loss to diffuse retinal nerve fiber of the POAG patients had small paracentral or ar- loss.32 Such findings, along with reports of loss of cuate scotomas only or an isolated nasal step, five had other central vision function in many ocular hyper- large paracentral or arcuate scotomas including nasal tensives, raises the possibility that diffuse loss may steps, six had marked nasal or temporal depression precede localized loss in the evolution of glaucoma- with large paracentral or arcuate scotomas, and five tous field loss. Of course such a conclusion must were categorized as endstage with small temporal or always be tempered by the fact that the relative sensi- central islands of vision. All subjects consented to tivity of a particular test paradigm can confound any participation after details of the study and its proce- conclusions about whether central diffuse loss of vi- dures were explained. sion precedes or follows localized field defects in The ocular hypertensives (OHT, n = 32) were de- glaucoma. fined as having IOP (by applanation) of greater than Against bright yellow backgrounds, which depress 22 mm Hg on two or more occasions, no visual field the sensitivity of MWS and LWS cones, SWS cones defects (Humphrey Instruments, San Leandro, CA; are responsible for the detection of deep blue flashes Central Threshold Test: Stimulus III white and back- of light in the normal eye. We have shown pre- ground 31.5 apostilbs), normal appearance of the viously33 that the actual conditions we used in this optic nerve head, and acuity better than 20/30 in the study isolate short wavelength sensitive (SWS) cones tested eye. in just this way. SWS cones play no role in detection The age-matched normal control group (n = 24) of yellow flashes superimposed on a bright yellow had acuity better than 20/30, pressures less than 21 background; this is done by MWS and/or LWS mm Hg, no glaucomatous visual field defects, no field cones. In this study we use the test of SWS cone loss, and no pathological cupping, pallor, or edema of thresholds to examine the foveal and central visual the disk. All of the subjects in the study had only field sensitivity in groups of glaucoma, ocular hyper- minor cortical and nuclear lens changes, and were tension and age-matched normal subjects. We were free of retinal disease by fundus examination and particularly interested in identifying both local and fundus photography. diffuse sensitivity loss. In the glaucoma patients sensi- SWS cone thresholds were determined using an tivity profiles were determined primarily along the 11° yellow (Schott, Jena, East Germany; filter nasal retina horizontal raphe with about 30% of the OG530) background onto which a 1° blue (Kodak, subjects also being tested along the 40° meridian in Rochester, NY; Wratten filter 47B) test spot was pro- the temporal inferior retina. The nasal retina hori- jected. For comparison, a threshold was obtained zontal meridian was chosen as representative of a using a 1 ° yellow spot projected onto the same back- "low risk" site for glaucomatous field loss by conven- ground.
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