1978
DOI: 10.1159/000264930
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Electrophysiological Evidence for Glaucomatous Lesions in the Optic Nerve

Abstract: Under stimulation with pattern reversal the visual-evoked potentials in glaucoma patients are shown to be delayed compared to a group of normals. This latency increase is due neither to age nor reduction in visual acuity. The glaucomatous lesion in the optic nerve can in some cases be demonstrated in the absence of visual field defect. The electrophysiological delays are similar to those measured in mild cases of neuritis in multiple sclerosis.

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Cited by 30 publications
(9 citation statements)
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“…This examination became especially practical and simple to perform with the introduction of checkerboard pattern stimulation. These potentials are significantly delayed in demyelinating diseases, in compressive lesions of the anterior visual pathways (Halliday et al, 1973(Halliday et al, , 1976, and in glaucoma (Huber & Wagner, 1978), whereas in our experience, they are usually not delayed in optic atrophies, in which condition they are more often characterized by amplitude reduction. We supposed that this would probably also be the case in defects of the optic nerve.…”
Section: Introductionmentioning
confidence: 41%
“…This examination became especially practical and simple to perform with the introduction of checkerboard pattern stimulation. These potentials are significantly delayed in demyelinating diseases, in compressive lesions of the anterior visual pathways (Halliday et al, 1973(Halliday et al, , 1976, and in glaucoma (Huber & Wagner, 1978), whereas in our experience, they are usually not delayed in optic atrophies, in which condition they are more often characterized by amplitude reduction. We supposed that this would probably also be the case in defects of the optic nerve.…”
Section: Introductionmentioning
confidence: 41%
“…Pattern visual evoked cortical potential (VECP) investigations in patients with chronic simple glaucoma (CSG) have shown reductions in amplitude (Ermers et al, 1974;Bartl, 1978;Galloway and Barber, 1981;Czobor and Marosfi, 1984), increased phase (Cappin and Nissim, 1975;Abe and Iwata, 1976;Towle et al, 1983;Howe and Mitchell, 1984a), latency (Huber andWagner, 1978, Sokol et al, 1981;Mitchell and Howe, 1981;Atkin et al, 1983;Bobak et al, 1983;Ponte et al, 1984), and electrophysiologically determined contrast sensitivity . Some have shown quite impressive detection rates, but as Sokol and colleagues (1981) and Towle and colleagues (1983) have pointed out, not all have corrected for the confounding effects on the VECP of pupil size, age, and the presence of cataract.…”
Section: Introductionmentioning
confidence: 99%
“…Most authors agree, that the pathogenesis of glaucoma damage of the optic nerve is related to the balance between local blood pressure and IOP (Hayreh 1978). The zJisuaZ rzwked response (VER) is sensitive to many types of optic nerve affections and indeed, several reports have delt with VER abnormalities in well-established cases of OAG (Ermers et al 1974;Cappin & Nissim 1975;Bart1 1978;Huber & Wagner This paper briefly presents the results of an investigation of the VER in a sample of persons with long-term observation of untreated intraocular hypertension. The effect of a 15-20 mmHg artificial IOP increase is evaluated.…”
Section: Intraocular Hvpertensionmentioning
confidence: 99%