Ординатура / Офтальмология / Английские материалы / Shields Textbook of Glaucoma, 6th edition_Allingham, Damji, Freedman_2010

algorithm” (SITA) [in German]. Klin Monatsbl Augenheilkd. 2000;216(3):143-147.

184.Lachkar Y, Barrault O, Lefrancois A, et al. Rapid Tendency Oriented Perimeter (TOP) with the Octopus visual field analyzer [in French].J Fr Ophtalmol. 1998;21(3):180-184.

185.Maeda H, Nakaura M, Negi A. New perimetric threshold test algorithm with dynamic strategy and tendency oriented perimetry (TOP) in glaucomatous eyes. Eye. 2000;14(pt 5):747-751.

186.King AJ, Taguri A, Wadood AC, et al. Comparison of two fast strategies, SITA Fast and TOP, for the assessment of visual fields in glaucoma patients. Graefes Arch Clin Exp Ophthalmol. 2002;240 (6):481-487.

187.Anderson AJ. Spatial resolution of the tendency-oriented perimetry algorithm. Invest Ophthalmol Vis Sci. 2003;44(5):1962-1968.

188.Demirel S, Vingrys AJ. Eye movements during perimetry and the effect that fixational instability has on perimetric outcomes. J Glaucoma. 1994;3(1):28-35.

189.Li Y, Mills RP. Kinetic fixation improves threshold sensitivity in the central visual field. J Glaucoma. 1992;1(2):108-116.

190.Katz J, Sommer A. Reliability indexes of automated perimetric tests. Arch Ophthalmol. 1988;106 (9):1252-1254.

191.Bickler-Bluth M, Trick GL, Kolker AE, et al. Assessing the utility of reliability indices for automated visual fields. Testing ocular hypertensives. Ophthalmology. 1989;96(5):616-619.

192.Nelson-Quigg JM, Twelker JD, Johnson CA. Response properties of normal observers and patients during automated perimetry. Arch Ophthalmol. 1989;107(11):1612-1615.

193.Schulzer M, Mills RP, Hopp RH, et al. Estimation of the short-term fluctuation from a single determination of the visual field. Invest Ophthalmol Vis Sci. 1990;31(4):730-735.

194.Johnson LN, Aminlari A, Sassani JW. Effect of intermittent versus continuous patient monitoring on reliability indices during automated perimetry. Ophthalmology. 1993;100(1):76-84.

195.Lee M, Zulauf M, Caprioli J. A new reliability parameter for automated perimetry: inconsistent responses. J Glaucoma. 1993;2(4):279-284.

196.Jacobs NA, Patterson IH. Variability of the hill of vision and its significance in automated perimetry. Br J Ophthalmol. 1985;69(11): 824-826.

197.Katz J, Sommer A. Asymmetry and variation in the normal hill of vision. Arch Ophthalmol. 1986;104(1):65-68.

198.Heijl A, Lindgren G, Olsson J. Normal variability of static perimetric threshold values across the central visual field. Arch Ophthalmol. 1987;105(11):1544-1549.

199.Werner EB, Petrig B, Krupin T, et al. Variability of automated visual fields in clinically stable glaucoma patients. Invest Ophthalmol Vis Sci. 1989;30(6):1083-1089.

200.Heijl A, Lindgren A, Lindgren G. Test-retest variability in glaucomatous visual fields. Am J Ophthalmol. 1989;108(2):130-135.

201.Haefliger IO, Flammer J. Increase of the short-term fluctuation of the differential light threshold around a physiologic scotoma. Am J Ophthalmol. 1989;107(4):417-420.

202.Diestelhorst M, Kullenberg C, Krieglstein GK. Short-term fluctuation of light discrimination sensitivity at the borders of glaucomatous visual field defects [in German]. Klin Monatsbl Augenheilkd. 1987;191(6): 439-442.

203.Katz J, Sommer A. A longitudinal study of the age-adjusted variability of automated visual fields. Arch Ophthalmol. 1987;105(8):1083-1086.

204.Werner EB, Adelson A, Krupin T. Effect of patient experience on the results of automated perimetry in clinically stable glaucoma patients. Ophthalmology. 1988;95(6):764-767.

205.Hoskins HD, Magee SD, Drake MV, et al. Confidence intervals for change in automated visual fields. Br J Ophthalmol. 1988;72(8):591-597.

206.Weber J, Krieglstein GK, Papoulis C. Graphic analysis of topographic trends in perimetry followup of glaucoma [in German]. Klin Monatsbl Augenheilkd. 1989;195(5):319-322.

207.Werner EB, Drance SM. Early visual field disturbances in glaucoma. Arch Ophthalmol. 1977;95 (7):1173-1175.

208.Werner EB, Saheb N, Thomas D. Variability of static visual threshold responses in patients with elevated IOPs. Arch Ophthalmol. 1982; 100(10):1627-1631.

209.Werner EB, Drance SM. Increased scatter of responses as a precursor of visual field changes in glaucoma. Can J Ophthalmol. 1977;12(2):140-142.

210.Flammer J, Drance SM, Zulauf M. Differential light threshold. Shortand long-term fluctuation in patients with glaucoma, normal controls, and patients with suspected glaucoma. Arch Ophthalmol. 1984;102(5): 704-706.

211.Flammer J, Drance SM, Fankhauser F, et al. Differential light threshold in automated static perimetry. Factors influencing short-term fluctuation. Arch Ophthalmol. 1984;102(6):876-879.

212.Chauhan BC, Drance SM, Lai C. A cluster analysis for threshold perimetry. Graefes Arch Clin Exp Ophthalmol. 1989;227(3):216-220.

213.Mandava S, Zulauf M, Zeyen T, et al. An evaluation of clusters in the glaucomatous visual field. Am J Ophthalmol. 1993; 116(6):684-691.

214.Fankhauser F, Fankhauser F 2nd, Giger H. A cluster and scotoma analysis based on empiric criteria. Graefes Arch Clin Exp Ophthalmol. 1993; 231(12):697-703.

215.Asman P, Heijl A, Olsson J, et al. Spatial analyses of glaucomatous visual fields; a comparison with traditional visual field indices. Acta Ophthalmol. 1992;70(5):679-686.

216.Asman P, Heijl A. Glaucoma Hemifield Test. Automated visual field evaluation. Arch Ophthalmol. 1992;110(6):812-819.

217.Duggan C, Sommer A, Auer C, et al. Automated differential threshold perimetry for detecting glaucomatous visual field loss. Am J Ophthalmol. 1985;100(3):420-423.

218.Sommer A, Enger C, Witt K. Screening for glaucomatous visual field loss with automated threshold perimetry. Am J Ophthalmol. 1987;103(5): 681-684.

219.Asman P, Heijl A. Evaluation of methods for automated Hemifield analysis in perimetry. Arch Ophthalmol. 1992;110(6):820-826.

P.118

220.Susanna R Jr, Nicolela MT, Soriano DS, et al. Automated perimetry: a study of the glaucoma hemifield test for the detection of early glaucomatous visual field loss. J Glaucoma. 1994;3(1):12-16.

221.Katz J, Quigley HA, Sommer A. Repeatability of the Glaucoma Hemifield Test in automated perimetry. Invest Ophthalmol Vis Sci. 1995;36(8): 1658-1664.

222.Johnson CA, Sample PA, Cioffi GA, et al. Structure and function evaluation (SAFE): I. criteria for glaucomatous visual field loss using standard automated perimetry (SAP) and short wavelength automated perimetry (SWAP). Am J Ophthalmol. 2002;134(2):177-185.

223.The AGIS Investigators. The advanced glaucoma intervention study, 2: visual field test scoring and reliability. Ophthalmology. 1994;101(8): 1445-1455.

224.Musch DC, Lichter PR, Guire KE, et al. The Collaborative Initial Glaucoma Treatment Study: study design, methods, and baseline characteristics of enrolled patients. Ophthalmology. 1999;106 (4):653-662.

225.Hills JF, Johnson CA. Evaluation of the t test as a method of detecting visual field changes. Ophthalmology. 1988;95(2):261-266.

226.Enger C, Sommer A. Recognizing glaucomatous field loss with the Humphrey STATPAC. Arch Ophthalmol. 1987;105(10):1355-1357.

227.Heijl A, Lindgren G, Olsson J, et al. Visual field interpretation with empiric probability maps. Arch Ophthalmol. 1989;107(2):204-208.

228.Heijl A, Asman P. A clinical study of perimetric probability maps. Arch Ophthalmol. 1989;107 (2):199-203.

229.Birch MK, Wishart PK, O'Donnell NP. Determining progressive visual field loss in serial Humphrey visual fields. Ophthalmology. 1995;102(8):1227-1234; discussion 34-35.

230.Fitzke FW, Hitchings RA, Poinoosawmy D, et al. Analysis of visual field progression in glaucoma. Br J Ophthalmol. 1996;80(1):40-48.

231.Werner EB, Bishop KI, Koelle J, et al. A comparison of experienced clinical observers and statistical tests in detection of progressive visual field loss in glaucoma using automated perimetry. Arch Ophthalmol. 1988; 106(5):619-623.

232.Chauhan BC, Drance SM, Douglas GR. The use of visual field indices in detecting changes in the visual field in glaucoma. Invest Ophthalmol Vis Sci. 1990;31(3):512-520.

233.Viswanathan AC, Fitzke FW, Hitchings RA. Early detection of visual field progression in glaucoma: a comparison of PROGRESSOR and STATPAC 2. Br J Ophthalmol. 1997;81(12):10371042.

234.Armaly MF. The visual field defect and ocular pressure level in open angle glaucoma. Invest Ophthalmol Vis Sci. 1969;8(1):105-1024.

235.Heilmann K. On the reversibility of visual field defects in glaucomas. Trans Am Acad Ophthalmol Otolaryngol. 1974;78(2):OP304-OP308.

236.Flammer J, Drance SM. Reversibility of a glaucomatous visual field defect after acetazolamide therapy. Can J Ophthalmol. 1983;18(3):139-141.

237.Katz LJ, Spaeth GL, Cantor LB, et al. Reversible optic disk cupping and visual field improvement in adults with glaucoma. Am J Ophthalmol. 1989;107(5):485-492.

238.Tsai CS, Shin DH, Wan JY, et al. Visual field global indices in patients with reversal of glaucomatous cupping after intraocular pressure reduction. Ophthalmology. 1991;98(9):1412-1419.

239.Gandolfi SA. Improvement of visual field indices after surgical reduction of intraocular pressure. Ophthalmic Surg. 1995;26(2):121-126.

240.Heijl A, Bengtsson B. The short-term effect of laser trabeculoplasty on the glaucomatous visual field. A prospective study using computerized perimetry. Acta Ophthalmol. 1984;62(5):705-714.

241.Holmin C, Krakau CE. Trabeculoplasty and visual field decay: a followup study using computerized perimetry. Curr Eye Res. 1984;3(9): 1101-1105.

242.Salim S, Paranhos A, Lima M, et al. Influence of surgical reduction of intraocular pressure on regions of the visual field with different levels of sensitivity. Am J Ophthalmol. 2001;132(4):496-500.

243.Hart WM Jr. Computer processing of visual data. II. Automated pattern analysis of glaucomatous visual fields. Arch Ophthalmol. 1981;99(1): 133-136.

244.Weleber RG, Tobler WR. Computerized quantitative analysis of kinetic visual fields. Am J Ophthalmol. 1986;101(4):461-468.

245.Esterman B. Grid for scoring visual fields. I. Tangent screen. Arch Ophthalmol. 1967;77(6):780-

246.Esterman B. Grid for scoring visual fields. II. Perimeter. Arch Ophthalmol. 1968;79(4):400-406.

247.Esterman B. Functional scoring of the binocular field. Ophthalmology. 1982;89(11):1226-1234.

248.American Medical Association. Impairment of visual field. In: Cocchiarella L, Andersson G, eds. Guides to the Evaluation of Permanent Impairment. 5th ed. Chicago: American Medical Association; 2000:287-295.

249.Mills RP, Drance SM. Esterman disability rating in severe glaucoma. Ophthalmology. 1986;93 (3):371-378.

250.Delgado MF, Nguyen NT, Cox TA, et al. Automated perimetry: a report by the American Academy of Ophthalmology. Ophthalmology. 2002; 109(12):2362-2374.

251.Johnson CA. Recent developments in automated perimetry in glaucoma diagnosis and management. Curr Opin Ophthalmol. 2002;13(2): 77-84.

252.Hart WM, Jr., Hartz RK, Hagen RW, et al. Color contrast perimetry. Invest Ophthalmol Vis Sci. 1984;25(4):400-413.

253.Hart WM Jr, Gordon MO. Color perimetry of glaucomatous visual field defects. Ophthalmology. 1984;91(4):338-346.

254.Hart WM Jr, Silverman SE, Trick GL, et al. Glaucomatous visual field damage. Luminance and color-contrast sensitivities. Invest Ophthalmol Vis Sci. 1990;31 (2):359-367.

255.Logan N, Anderson DR. Detecting early glaucomatous visual field changes with a blue stimulus. Am J Ophthalmol. 1983;95(4): 432-434.

256.Mindel JS, Safir A, Schare PW. Visual field testing with red targets. Arch Ophthalmol. 1983;101 (6):927-929.

257.Hart WM Jr, Burde RM. Color contrast perimetry. The spatial distribution of color defects in optic nerve and retinal diseases. Ophthalmology. 1985;92(6):768-776.

258.Sample PA. Short-wavelength automated perimetry: it's role in the clinic and for understanding ganglion cell function. Prog Retin Eye Res. 2000;19(4):369-383.

259.Sample PA, Weinreb RN. Color perimetry for assessment of primary open-angle glaucoma. Invest Ophthalmol Vis Sci. 1990;31 (9):1869-1875.

260.Wild JM. Short wavelength automated perimetry. Acta Ophthalmol Scand. 2001;79(6):546-559.

261.Lewis RA, Johnson CA, Adams AJ. Automated perimetry and short wavelength sensitivity in patients with asymmetric intraocular pressures. Graefes Arch Clin Exp Ophthalmol. 1993;231(5):274-

262.Johnson CA, Brandt JD, Khong AM, et al. Short-wavelength automated perimetry in low-, medium-, and high-risk ocular hypertensive eyes. Initial baseline results. Arch Ophthalmol. 1995;113 (1):70-76.

263.Girkin CA, Emdadi A, Sample PA, et al. Short-wavelength automated perimetry and standard perimetry in the detection of progressive optic disc cupping. Arch Ophthalmol. 2000;118(9):1231-1236.

264.Demirel S, Johnson CA. Incidence and prevalence of short wavelength automated perimetry deficits in ocular hypertensive patients. Am J Ophthalmol. 2001;131(6):709-715.

265.Sample PA, Weinreb RN. Progressive color visual field loss in glaucoma. Invest Ophthalmol Vis Sci. 1992;33(6):2068-2071.

266.Johnson CA, Adams AJ, Casson EJ, et al. Blue-on-yellow perimetry can predict the development of glaucomatous visual field loss. Arch Ophthalmol. 1993;111(5):645-650.

267.Sample PA, Taylor JD, Martinez GA, et al. Short-wavelength color visual fields in glaucoma suspects at risk. Am J Ophthalmol. 1993;115(2):225-233.

268.Johnson CA, Adams AJ, Casson EJ, et al. Progression of early glaucomatous visual field loss as detected by blue-on-yellow and standard white-on-white automated perimetry. Arch Ophthalmol. 1993; 111(5): 651-656.

269.Johnson CA, Sample PA, Zangwill LM, et al. Structure and function evaluation (SAFE): II. Comparison of optic disk and visual field characteristics. Am J Ophthalmol. 2003;135(2):148-154.

270.Moss ID, Wild JM, Whitaker DJ. The influence of age-related cataract on blue-on-yellow perimetry. Invest Ophthalmol Vis Sci. 1995;36(5): 764-773.

271.Wild JM, Moss ID, Whitaker D, et al. The statistical interpretation of blue-on-yellow visual field loss. Invest Ophthalmol Vis Sci. 1995; 36(7):1398-1410.

272.Sample PA, Martinez GA, Weinreb RN. Short-wavelength automated perimetry without lens density testing. Am J Ophthalmol. 1994; 118(5):632-641.

273.Kim YY, Kim JS, Shin DH, et al. Effect of cataract extraction on blue-on-yellow visual field. Am J Ophthalmol. 2001;132(2):217-220.

274.Kara-Junior N, Jardim JL, de Oliveira Leme E, et al. Effect of the AcrySof Natural intraocular lens on blue-yellow perimetry. J Cataract Refract Surg 2006;32(8):1328-1330.

275.Maeda H, Tanaka Y, Nakamura M, et al. Blue-on-yellow perimetry using an Armaly glaucoma screening program. Ophthalmologica. 1999;213(2): 71-75.

276.Ugurlu S, Hoffman D, Garway-Heath DF, et al. Relationship between structural abnormalities and short-wavelength perimetric defects in eyes at risk of glaucoma. Am J Ophthalmol. 2000;129(5):592-

P.119

277.Bengtsson B. A new rapid threshold algorithm for short-wavelength automated perimetry. Invest Ophthalmol Vis Sci. 2003;44(3):1388-1394.

278.Bengtsson B, Heijl A. Normal intersubject threshold variability and normal limits of the SITA SWAP and full threshold SWAP perimetric programs. Invest Ophthalmol Vis Sci. 2003;44(11):5029-

5034.

279.Bengtsson B, Heijl A. Diagnostic sensitivity of fast blue-yellow and standard automated perimetry in early glaucoma: a comparison between different test programs. Ophthalmology. 2006;113(7):10921097.

280.Landers J, Sharma A, Goldberg I, et al. Topography of the frequency doubling perimetry visual field compared with that of short wavelength and achromatic automated perimetry visual fields. Br J Ophthalmol. 2006; 90(1):70-74.

281.Rossetti L, Fogagnolo P, Miglior S, et al. Learning effect of short-wavelength automated perimetry in patients with ocular hypertension. J Glaucoma 2006;15(5):399-404.

282.Hutchings N, Hosking SL, Wild JM, et al. Long-term fluctuation in short-wavelength automated perimetry in glaucoma suspects and glaucoma patients. Invest Ophthalmol Vis Sci. 2001;42(10):23322337.

283.Rosli Y, Maddess T, Dawel A, et al. Multifocal frequency-doubling pattern visual evoked responses to dichoptic stimulation. Clin Neurophysiol. 2009;120(12):2100-2108.

284.Alward WL. Frequency doubling technology perimetry for the detection of glaucomatous visual field loss. Am J Ophthalmol. 2000;129(3): 376-378.

285.Maddess T, Goldberg I, Dobinson J, et al. Testing for glaucoma with the spatial frequency doubling illusion. Vision Res. 1999;39(25): 4258-4273.

286.Quigley HA. Neuronal death in glaucoma. Prog Retin Eye Res. 1999; 18(1):39-57.

287.Harwerth RS, Crawford ML, Frishman LJ, et al. Visual field defects and neural losses from experimental glaucoma. Prog Retin Eye Res. 2002; 21(1):91-125.

288.Morgan JE. Retinal ganglion cell shrinkage in glaucoma. J Glaucoma. 2002;11(4):365-370.

289.Morgan JE. Selective cell death in glaucoma: does it really occur? Br J Ophthalmol. 1994;78 (11):875-879; discussion 9-80.

290.Martin L, Wanger P, Vancea L, et al. Concordance of high-pass resolution perimetry and frequency-doubling technology perimetry results in glaucoma: no support for selective ganglion cell damage. J Glaucoma. 2003;12(1):40-44.

291.Quigley HA. Identification of glaucoma-related visual field abnormality with the screening protocol of frequency doubling technology. Am J Ophthalmol. 1998;125(6):819-829.

292.Johnson CA, Samuels SJ. Screening for glaucomatous visual field loss with frequency-doubling perimetry. Invest Ophthalmol Vis Sci. 1997; 38(2):413-425.

293.Cioffi GA, Mansberger S, Spry P, et al. Frequency doubling perimetry and the detection of eye disease in the community. Trans Am Ophthalmol Soc. 2000;98:195-199; discussion 9-202.

294.Tatemichi M, Nakano T, Tanaka K, et al. Performance of glaucoma mass screening with only a visual field test using frequency-doubling technology perimetry. Am J Ophthalmol. 2002;134(4):529-

295.Sample PA, Bosworth CF, Blumenthal EZ, et al. Visual function-specific perimetry for indirect comparison of different ganglion cell populations in glaucoma. Invest Ophthalmol Vis Sci. 2000;41 (7):1783-1790.

296.Cello KE, Nelson-Quigg JM, Johnson CA. Frequency doubling technology perimetry for detection of glaucomatous visual field loss. Am J Ophthalmol. 2000;129(3):314-322.

297.Quinn LM, Gardiner SK, Wheeler DT, et al. Frequency doubling technology perimetry in normal children. Am J Ophthalmol. 2006; 142(6):983-989.

298.Wall M, Neahring RK, Woodward KR. Sensitivity and specificity of frequency doubling perimetry in neuro-ophthalmic disorders: a comparison with conventional automated perimetry. Invest Ophthalmol Vis Sci. 2002;43(4):1277-1283.

299.Anderson AJ, Johnson CA. Effect of dichoptic adaptation on frequency-doubling perimetry. Optom Vis Sci. 2002;79(2):88-92.

300.Johnson CA, Cioffi GA, Van Buskirk EM. Frequency doubling technology perimetry using a 24-2 stimulus presentation pattern. Optom Vis Sci. 1999;76(8):571-581.

301.Spry PG, Johnson CA. Within-test variability of frequency-doubling perimetry using a 24-2 test

pattern. J Glaucoma. 2002;11(4):315-320.

302.Racette L, Medeiros FA, Zangwill LM, et al. Diagnostic accuracy of the Matrix 24-2 and original N-30 frequency-doubling technology tests compared with standard automated perimetry. Invest Ophthalmol Vis Sci. 2008;49(3):954-960.

303.Centofanti M, Fogagnolo P, Oddone F, et al. Learning effect of Humphrey matrix frequency doubling technology perimetry in patients with ocular hypertension. J Glaucoma. 2008;17(6):436-441.

304.Gonzalez-Hernandez M, de la Rosa MG, de la Vega RR, et al. Long-term fluctuation of standard automatic perimetry, pulsar perimetry and frequency-doubling technology in early glaucoma diagnosis. Ophthalmic Res. 2007;39(6):338-343.

305.Iester M, Capris P, Pandolfo A, et al. Learning effect, short-term fluctuation, and long-term fluctuation in frequency doubling technique. Am J Ophthalmol. 2000;130(2):160-164.

306.Bullimore MA, Wood JM, Swenson K. Motion perception in glaucoma. Invest Ophthalmol Vis Sci. 1993;34(13):3526-3533.

307.Fahle M, Wehrhahn C. Motion perception in the peripheral visual field. Graefes Arch Clin Exp Ophthalmol. 1991;229(5):430-436.

308.Ruben S, Fitzke F. Correlation of peripheral displacement thresholds and optic disc parameters in ocular hypertension. Br J Ophthalmol. 1994; 78(4):291-294.

309.Piltz JR, Swindale NV, Drance SM. Vernier thresholds and alignment bias in control, suspect, and glaucomatous eyes. J Glaucoma. 1993;2(2): 87-95.

310.Arden GB, Jacobson JJ. A simple grating test for contrast sensitivity: preliminary results indicate value in screening for glaucoma. Invest Ophthalmol Vis Sci. 1978;17(1):23-32.

311.McKendrick AM, Johnson CA, Anderson AJ, et al. Elevated vernier acuity thresholds in glaucoma. Invest Ophthalmol Vis Sci. 2002;43 (5):1393-1399.

312.Anderson AJ, Vingrys AJ. Multiple processes mediate flicker sensitivity. Vision Res. 2001;41 (19):2449-2455.

313.Rota-Bartelink A. The diagnostic value of automated flicker threshold perimetry. Curr Opin Ophthalmol. 1999;10(2):135-139.

314.Frisen L. High-pass resolution perimetry. A clinical review. Doc Ophthalmol. 1993;83(1):1-25.

315.Wall M, Ketoff KM. Random dot motion perimetry in patients with glaucoma and in normal subjects. Am J Ophthalmol. 1995;120(5): 587-596.

316.House P, Schulzer M, Drance S, et al. Characteristics of the normal central visual field measured with resolution perimetry. Graefes Arch Clin Exp Ophthalmol. 1991;229(1):8-12.

317.Chauhan BC, Mohandas RN, Whelan JH, et al. Comparison of reliability indices in conventional and high-pass resolution perimetry. Ophthalmology. 1993;100(7):1089-1094.

318.Sample PA, Ahn DS, Lee PC, et al. High-pass resolution perimetry in eyes with ocular hypertension and primary open-angle glaucoma. Am J Ophthalmol. 1992;113(3):309-316.

319.Martinez GA, Sample PA, Weinreb RN. Comparison of high-pass resolution perimetry and standard automated perimetry in glaucoma. Am J Ophthalmol. 1995;119(2):195-201.

320.Chauhan BC, LeBlanc RP, McCormick TA, et al. Comparison of highpass resolution perimetry and pattern discrimination perimetry to conventional perimetry in glaucoma. Can J Ophthalmol. 1993;28(7): 306-311.

321.Chauhan BC. The value of high-pass resolution perimetry in glaucoma. Curr Opin Ophthalmol. 2000;11(2):85-89.

322.Iester M, Altieri M, Vittone P, et al. Detection of glaucomatous visual field defect by nonconventional perimetry. Am J Ophthalmol. 2003; 135(1):35-39.

323.Silverman SE, Trick GL, Hart WM Jr. Motion perception is abnormal in primary open-angle glaucoma and ocular hypertension. Invest Ophthalmol Vis Sci. 1990;31(4):722-729.

324.Bosworth CF, Sample PA, Gupta N, et al. Motion automated perimetry identifies early glaucomatous field defects. Arch Ophthalmol. 1998; 116(9):1153-1158.

325.Bosworth CF, Sample PA, Williams JM, et al. Spatial relationship of motion automated perimetry and optic disc topography in patients with glaucomatous optic neuropathy. J Glaucoma. 1999;8(5):281-

289.

326.Bowd C, Zangwill LM, Berry CC, et al. Detecting early glaucoma by assessment of retinal nerve fiber layer thickness and visual function. Invest Ophthalmol Vis Sci. 2001;42(9):1993-2003.

327.Goldmann H. Fundamentals of exact perimetry. 1945. Optom Vis Sci. 1999;76(8):599-604.

328.Portney GL, Hanible JE. A comparison of four projection perimeters. Am J Ophthalmol. 1976;81 (5):678-681.

329.Wohlrab TM, Erb C, Rohrbach JM, et al. Age-adjusted normal values with the Tubingen Automatic Perimeter TAP 2000 CC [in German]. Ophthalmologe. 1996;93(4):428-432.

330.Harms H. Entwicklungsmoglichkeiten der Perimetrie [in German]. Graefes Arch Clin Exp Ophthalmol. 1950;150:28-57.

P.120

331.Armaly MF. Ocular pressure and visual fields. A ten-year follow-up study. Arch Ophthalmol. 1969;81(1):25-40.

332.Rock WJ, Drance SM, Morgan RW. Visual field screening in glaucoma. An evaluation of the Armaly technique for screening glaucomatous visual fields. Arch Ophthalmol. 1973;89(4):287-290.

333.Drance SM, Brais P, Fairclough M, et al. A screening method for temporal visual defects in chronic simple glaucoma. Can J Ophthalmol. 1972;7(4): 428-429.

334.Rock WJ, Drance SM, Morgan RW. A modification of the Armaly visual field screening technique for glaucoma. Can J Ophthalmol. 1971;6(4): 283-292.

335.Fischer FW. Threshold-adjusted supraliminal pattern perimetry with the Goldmann perimeter [in German]. Klin Monbl Augenheilkd. 1984; 185(3):204-211.

336.Rabin S, Kolesar P, Podos SM, et al. A visual field screening protocol for glaucoma. Am J Ophthalmol. 1981;92(4):630-635.

337.Stepanik J. Diagnosis of glaucoma with the Goldmann perimeter [in German]. Klin Monatsbl Augenheilkd. 1983;183:330-332.

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Shields > SECTION I - The Basic Aspects of Glaucoma >

6 - Glaucomatous Influence on Visual Function

Authors: Allingham, R. Rand

Title: Shields Textbook of Glaucoma, 6th Edition Copyright ©2011 Lippincott Williams & Wilkins

> Table of Contents > SECTION I - The Basic Aspects of Glaucoma > 6 - Glaucomatous Influence on Visual Function

6

Glaucomatous Influence on Visual Function

In addition to the previously discussed visual field changes in glaucoma (see Chapter 5), other visual function tests may have abnormal results early in glaucoma. Some of these tests may one day prove useful in detecting the presence and progression of glaucoma and in judging the efficacy of glaucoma therapy.

BRIGHTNESS SENSITIVITY

Patients with glaucomatous optic atrophy have decreased light sensitivity when dark adapted, which correlates with the degree of nerve damage (1), and dark adaptation, tested with chromatic stimuli, has been reported to be abnormal in patients with ocular hypertension (2). The results of some studies provided little evidence for photoreceptor abnormalities in glaucoma (3, 4), but other studies suggested that the photoreceptors may be involved in glaucomatous damage (5, 6). Light sensitivity can also be evaluated with a brightness ratio test, in which the patient discriminates the difference in sensitivity of

the two eyes to light, and it has been suggested that tests of this type may be useful in glaucoma screening (7, 8). In preliminary studies, patients with open-angle glaucoma had abnormal responses on dichoptic testing, in which one half of a test object is presented to one eye, and the other half to the fellow eye, to help determine the location of a defect in the visual pathway (9).

COLOR VISION

Reduced sensitivity to colors has been described in patients with ocular hypertension, tilted discs, and various forms of glaucoma, and may precede any detectable loss of peripheral or central vision by standard acuity or visual field testing (10). Compared with achromatic sensitivity, color sensitivity was found to be more affected in glaucoma (11). Most studies agree that the color vision deficit is associated primarily with blue-sensitive pathways (12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24 and 25). This is consistent with the observation that blue signals are detected by the short-wavelength cones, and then processed by the blue-yellow bistratified ganglion cells, which are different from the midget ganglion cells (26, 27). These cells project their axons to the interlaminar koniocellular layers of the lateral geniculate nucleus (28). Blue cones contribute little to the sensation of brightness or to visual acuity, which may account for why standard visual

acuity tests, perimetry, or contrast sensitivity studies might miss an associated visual deficit. The color visual dysfunction is strongly related to elevated intraocular pressure (IOP) levels (22, 23), suggesting that the damage is pressure induced. Selective loss of red-green sensitivity has been observed in some patients with glaucoma (29). However, chromatic visualevoked potential (VEP), which utilizes redgreen flicker, was found to be altered in nonglaucomatous optic neuropathies, but not glaucoma (30). It is unclear whether the loss of color vision and the visual field changes associated with nerve fiber bundle loss share the same mechanism. Ocular hypertensive eyes with yellow-blue and blue-green defects were found to have diffuse early changes in visual field sensitivity (17) and an increased risk of glaucomatous visual field loss, compared with similar eyes that did not have these color vision

disturbances (14). The same color abnormalities in patients with early glaucoma correlated significantly with diffuse retinal nerve fiber loss (24). However, no significant correlation between color vision scores and visual field performance was found among patients with ocular hypertension when age correction was applied to the color variable (31), and another study revealed no clear association between early glaucomatous cupping and color vision anomalies (18). Specificity is limited by the fact that the tritan deficit is also the one most frequently seen with age-related changes. When study populations were matched for age and lens density, however, color vision loss in glaucoma was still attributable in part to the disease process (21).

In most reported studies, the color vision testing was performed with the Farnsworth-Munsell 100-hue test, dichotomous (D-15) tests, or variants of these, all of which are laborious and of questionable precision. One study has shown that halogen lighting is preferable for the Farnsworth-Munsell 100-hue test in glaucoma and confirmed the presence of blue-yellow pathway deficiency in glaucoma (32). Another study has shown that although the error scores on the Farnsworth-Munsell 100-hue test were elevated in glaucomatous eyes, the test did not always discriminate well and seemed to lack a high diagnostic value (33).

Various tests have been devised to overcome limitations of the Farnsworth-Munsell test, including computer-driven monitors that present flickering color contrasts or peripheral color contrasts, an automatic anomaloscope, a color contrast sensitivity test in which the target and surround have the same luminance but different chromaticity, and a personal computer (34, 35, 36, 37 and 38). Even with the most sensitive, precise system, however,

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glaucoma is not always detected, suggesting that some patients with glaucoma have true preservation of color vision (37, 39, 40).

As discussed in Chapter 5, short-wavelength automated perimetry (SWAP), which projects a blue target on a yellow background, has been shown to detect glaucoma damage earlier than conventional white-on- white perimetry (41, 42, 43 and 44). SWAP has also been found to be more sensitive to progression of

visual field loss and to progression of glaucomatous disc cupping (45, 46). Contrast Sensitivity

Subtle loss of both central and peripheral vision can be demonstrated in some patients with glaucoma, before visual field changes are detectable with standard techniques, by measuring the amount of contrast required for a patient to discriminate between adjacent visual stimuli (47, 48, 49, 50, 51 and 52). In some studies, the contrast sensitivity impairment correlates with visual field (48, 49 and 50, 53), especially with the central visual field and optic nerve head (50, 54) damage. The yield of detecting glaucoma may be increased by measuring peripheral contrast sensitivity, 20 to 25 degrees eccentrically (55, 56). Tests to measure contrast sensitivity may use spatial or temporal strategies. Although spatial contrast sensitivity may be a useful adjunct, caution has been advised in interpreting the results without considering additional clinical data (52). The overlap with other causes of reduced spatial contrast sensitivity, including age, creates high false-negative and false-positive rates (50, 51, 57, 58). Spatial contrast sensitivity has been shown to decrease in persons with healthy eyes after 50 years of age, which appears to be independent of the crystalline lens (59, 60). Although spatial summation properties differ between M- and P-mediated pathways, the underlying spatial summation properties associated with these pathways are similar in control patients and those with glaucoma (61). In a study comparing the decrease in contrast sensitivity between normal aging and glaucoma, aging decreased low-spatial frequencysensitive components of both the M and P pathways. Glaucoma results in a further reduction of sensitivity that does not seem to be selective for M or P functions, which the investigators presumed were mediated by cells with larger receptive fields (62). For reference, frequency doubling technology (FDT) measures the contrast threshold to low spatial frequency, high temporal frequency sinusoidal luminance profile bars (63).

Sine-wave gratings of parallel light and dark bands (Arden gratings), in which the patient must detect the striped pattern at various levels of contrast and spatial frequencies, have been evaluated extensively in this group of psychophysical tests (47). The original Arden gratings were limited by the subjectivity of the required responses (64, 65). A modification, in which the patient must indicate the orientation of the gratings, has been reported to minimize this limitation (65). The testing methods include computercontrolled video displays and photographically reproduced grating patterns, both of which have given good approximations of the spatial contrast sensitivity function (66). One of these tests uses sine-wave gratings of low spatial frequency and laser interference fringes to increase sensitivity to peripheral defects (67, 68 and 69).

Performing these techniques, including sinusoidal grating targets, is difficult and time consuming. An effort to minimize these limitations has led to the development of high-pass resolution perimetry (discussed in Chapter 5).

Temporal contrast sensitivity, in which the patient must detect a visual stimulus flickering at various frequencies, provides another measure of contrast sensitivity and appears to be more useful than spatial contrast sensitivity in patients with glaucoma. The stimulus may be presented as a homogeneous flickering field (flicker fusion frequency) or as a counterphase flickering grating of low spatial frequency (spatiotemporal contrast sensitivity) (59, 70, 71). Patients with glaucoma may have reduced function with either method, although the latter appears to be a more sensitive test (71, 72). Spatiotemporal contrast sensitivity was also found to be more useful in detecting glaucoma than spatial contrast sensitivity testing of the central retina was, although, again, the usefulness of the test is limited to those younger than 50 years (59). Other studies have found age to be a less significant factor in sensitivity loss, although one study suggested that cardiovascular disease may be associated with foveal dysfunction (73, 74 and 75). There is also a question as to whether temporal contrast sensitivity loss among patients with ocular hypertension represents early glaucomatous damage or a transient effect of raised IOP. One study suggested that either mechanism may be found within subsets of this population (76). Reducing the IOP in patients with glaucoma may improve contrast sensitivity at high frequencies of 18 cycles/degree (77).

Several techniques have been evaluated to improve the usefulness of contrast sensitivity testing. One study suggested that the determination of a ratio between spatial contrast sensitivity and flicker

sensitivity measures visual pathology more precisely than the absolute value of either test does (78). Another test of temporal contrast sensitivity, in which the patient must discriminate two rapidly successive pulses of light from a single pulse, is reported to be highly sensitive and specific in distinguishing glaucomatous eyes from healthy ones (79). Another test, the whole-field scotopic retinal sensitivity test, uses a flashlight-sized device in which the patient views a white light in the entire visual field and is asked to detect alternating illuminated and dark fields at 1-second intervals (80). This test may be useful as a screening tool (80, 81), although one study found too much overlap between healthy persons and individuals with ocular hypertension (82).

Another attempt to use a temporal contrast or flickering target has been called temporal modulation perimetry or flicker perimetry (83, 84 and 85). In healthy eyes there is an age-related loss of temporal modulation sensitivity (83). It appears to be less affected by visual acuity or retinal degradation than either light-sense or resolution perimetry, and it is more sensitive than light-sense perimetry to increasing IOP (84, 85 and 86).

Different target shapes and patterns, which the patient must distinguish, are also reported to be of particular value

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in detecting optic nerve disease (87). In one study with pattern discrimination perimetry, long-term and short-term fluctuations were clinically significant but did not prevent adequate separation between normal and abnormal measurements (88). Visual function in glaucomatous eyes, as measured by contrast sensitivity, has been shown to improve after (3-ßblocker therapy (89). ELECTROPHYSIOLOGIC STUDIES

Most measures of visual fields and other visual functions are dependent on the patient's subjective response. A significant amount of work is also being done on alternative, objective methods of evaluating the visual field. The pattern electroretinogram, the photopic negative response of the electroretinogram, and the multifocal VEP (mfVEP) appear to have the most potential to detect early glaucomatous damage that may not be detected by standard automated perimetry (90, 91, 92, 93, 94, 95 and 96). Of the currently available electrophysiologic tests, the mfVEP is the only one that can provide topographic information about the visual field defects. The relation between electrophysiologic tests and the underlying damage to ganglion cells is still not completely understood, but it has been suggested that the signal in the mfVEP response may be linearly related to the ganglion cells loss (93). Patients with glaucoma were also found in one study to have increased baseline values with electro-oculography (97), but a subsequent study did not confirm that finding (98).

Electroretinograms

Electroretinograms (ERGs) evoked by reversing checkerboard or grating patterns, referred to as pattern ERGs (PERGs), are sensitive to retinal ganglion cell and optic nerve dysfunction and have reduced amplitudes in patients with glaucoma (92, 99, 100, 101, 102, 103, 104, 105 and 106). PERG may detect early damage to ganglion cells (91), which may explain why reduced PERG amplitudes appear in the early stages of glaucoma and in some eyes with ocular hypertension, especially those at elevated risk for glaucoma (101, 105, 106, 107, 108, 109 and 110). These findings suggest that PERG may be useful in discriminating between those patients with ocular hypertension who will develop visual field loss and those who will not.

Studies differ on whether PERG correlates with IOP and disc topography, with one study showing no correlation and others showing an association with IOP control, computed optic nerve head analysis, or the retinal nerve fiber layer thickness (108, 111, 112 and 113). The PERG has been shown to correlate with visual field indices (114), and visual field defects are associated with PERG reduction in the corresponding hemisphere (115). However, no precise correlation was found with color vision deficits (116). Decreased amplitude and an increase in peak latency were found to correlate with increasing age (104), paralleling the estimated normal loss of ganglion cells. Indeed, reduction in PERG was directly related to histologically defined optic nerve damage in a monkey model (117). PERG in combination with SWAP was shown in one study to improve the power to predict progression of visual field loss