Abstract
Chronic glaucoma has been shown preferentially to damage larger retinal cells and optic nerve fibres that provide the input to the magnocellular visual pathway. We compared the motion-onset visual evoked potentials (primarily the magnocellular system) with those to standard pattern reversal in 20 patients with bilateral chronic glaucoma. For motion-onset visual evoked potentials, the pattern (isolated 40′ checks of 10% contrast) moved in four cardinal directions (varied randomly from trial to trial) at a velocity of 10 deg/s for 20 ms, with an interstimulus interval of 1 s. In pattern-reversal stimulation, the checkerboard reversed at a rate of 2 reversals per second. In 60% of the eyes investigated, the results of both types of visual evoked potentials correlated, showing either normal (27.5%) or increased (32.5%) latencies. In the remaining 40% of the eyes, the normal pattern-reversal visual evoked potential latencies were accompanied by prolonged motion-onset visual evoked potentials. The high occurrence of delayed motion-onset visual evoked potentials in our patients confirms the primary magnocellular loss in chronic glaucoma and suggests that the motion-onset VEPs are suitable for detection of glaucomatous changes.
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References
Quigley HA, Dunkelberger GR, Green WR. Chronic human glaucoma causing selectively greater loss of large optic nerve fibres. Ophthalmology 1988; 95: 357–63.
Quigley HA, Sanchez RM, Dunkelberger GR, L'Hermaut NL, Baginski TA. Chronic glaucoma selectively damages large optic nerve fibres. Invest Ophthalmol Vis Sci 1981; 28: 913–20.
Livingstone M, Hubel D. Segregation of form, color, movement and depth: anatomy, physiology and perception. Science 1988; 240: 740–9.
Fitzke FW, Poinoosawmy D, Nagassubramanian S., Hitchings RA. Peripheral displacement thresholds in glaucoma and ocular hypertension. In: Heil A, ed. Perimetric update. Amsterdam: Kugler & Ghedini Publications, 1989: 399–452.
Silverman SE, Trick GL, Hart WM. Motion perception is abnormal in primary open-angle glaucoma and ocular hypertension. Invest Ophthalmol Vis Sci 1990; 31: 722–9.
Joffe KM, Raymond JE, Crichton A. Motion perimetry in glaucoma. Invest Ophthalmol Vis Sci 1991; 32: 1103.
Bullimore MA, Wood JM, Swenson K. Motion perception in glaucoma. Invest Ophthalmol Vis Sci 1993; 34: 3526–33.
Kubová Z, Kuba M, Spekreijse H, Blakemore C. Contrast dependence of motion-onset and pattern-reversal evoked potentials. Vision Res 1995; 35: 197–205.
Kuba M, Kubová Z. Visual evoked potentials specific for motion-onset. Doc Ophthalmol 1992; 80: 83–9.
Kuba M, Toyonaga N, Kubová Z. Motion-reversal visual evoked responses. Physiol Res 1992; 41: 369–73.
National Academy of Sciences-National Research Council Committee on Vision. Report of Working Group 39: recommended standard procedures for the clinical measurement and specification of visual acuity. Adv Ophthalmol 1980; 41: 103–48.
Towle VL, Moskowitz A, Sokol S, Schwartz B. The visual evoked potential in glaucoma and ocular hypertension: effects of check size, field size, and stimulation rate. Invest Ophthalmol Vis Sci 1983; 24: 175–83.
Göpfert E, Schlykowa L, Müller R. Zur topographie des Bewegungs-VEP am Menschen. Z EBG-BMG 1988; 19: 14–8.
Sokol S, Domar A, Moskowitz A, Schwartz H. Pattern evoked potential latency and contrast sensitivity in glaucoma and ocular hypertension. Doc Ophthalmol Proc Ser 1981; 27: 79–86.
Howe JW, Mitchell KW. Simultaneous recording of pattern electroretinogram and visual evoked cortical potential in group of patients with glaucoma. Doc Ophthalmol Proc Ser 1984; 40: 101–7.
Howe JW, Mitchell KW. Visual evoked cortical potential to paracentral retinal stimulation in chronic glaucoma, ocular hypertension, and an age-matched group of normals. Doc Ophthalmol 1986; 63: 37–44.
Fernández-Tirado FJ, Ucles P, Pablo L, Honrubia FM. Electrophysiological methods in early glaucoma detection. Acta Ophthalmol 1994; 72: 168–74.
Regan D. Steady-state evoked potentials. J Opt Soc Am 1977; 67: 1475–89.
Tobimatsu S, Tashima-Kurita S, Nakayama-Hiromatsu M, Kato M. Clinical relevance of phase of steady-state VEPs to P100 latency of transient VEPs. Electroencephalogr Clin Neurophysiol 1991; 80: 89–93.
Strasburger H. The analysis of steady-state evoked potentials revisited. Clin Vision Sci 1987; 1: 245–56.
Bray LCH, Mitchell KW, Howe JH, Gashau A. Visual function in glaucoma: a comparative evaluation of computerised static perimetry and the pattern visual evoked potential. Clin Vision Sci 1992; 7: 21–9.
Baez KA, McNaught AI, Dowler JGF, Poinoosawy D, Fitzke FW, Hitchins RA. Motion detection threshold and field progression in normal tension glaucoma. Br J Ophthalmol 1995; 79: 125–8.
Kubová Z, Kuba M, Juran J, Blakemore C. Is the motion system relatively spared in amblyopia? Evidence from cortical evoked responses. Vision Res 1996; 36: 181–90.
Kubová Z, Kuba M. Clinical application of motion-onset visual evoked potentials. Doc Ophthalmol 1992; 81: 209–18.
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Kubová, Z., Kuba, M., Hrochová, J. et al. Motion-onset visual evoked potentials improve the diagnosis of glaucoma. Doc Ophthalmol 92, 211–221 (1996). https://doi.org/10.1007/BF02583292
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DOI: https://doi.org/10.1007/BF02583292