Faculty Bibliography

PURPOSE: To detect glaucomatous damage to the inner retina using the multifocal electroretinogram (mERG). METHODS: The stimulus array consisted of 103 hexagons with a mean luminance of 100 cd/m2 and a contrast of 50%. The mERG was recorded from 13 control subjects, 18 patients with open-angle glaucoma (OAG), 4 glaucoma suspects, and one patient with ischemic optic neuropathy (ION). Individual responses, as well as responses summed within quadrants or across the entire array, were measured in a number of ways. Humphrey visual fields were obtained for all patients, and the mean total deviation (MD) values for the 18 patients with OAG ranged from -2.2 to -18.2 with a mean (SD) of -7.3 (4.5). RESULTS: The mERG measure that best discriminated between the patients and the control subjects was the ratio of the amplitude at 8 msec after the peak response to the amplitude at the peak. Although the value of this ratio fell below the median of the control group for 16 of the 18 OAG patients, only 6 of these patients had ratios that fell below the normal range. Other measures of first- and second-order kernels did not do as well. Both within and across patients, the correlation between local field loss and the mERG ratio measure was poor. Furthermore, although in some patients the mERG waveform is clearly different from normal, in other patients (including the patient with ION) the waveform approximates the normal even in visual field areas with substantial sensitivity loss. CONCLUSIONS: Because glaucomatous damage is known to affect the ganglion cell axon, these data suggest that damage to ganglion cell axons is not a sufficient condition to produce changes in the mERG as measured here and that in patients with clear changes in mERG waveforms, these changes do not appear to be well localized and local waveforms are poorly correlated with local changes in field sensitivity

PURPOSE: To develop a quantitative measure of local damage to the ganglion cells/optic nerve based on an interocular comparison of multifocal visual evoked potentials (mVEP). METHODS: Multifocal VEPs were recorded from both eyes of six normal subjects and four patients; each eye was stimulated separately. Two of the patients had glaucoma, one had ischemic optic neuropathy, and one had unilateral optic neuritis. All four patients had considerably more damage in one eye than in the other, as indicated by their Humphrey visual fields. The multi-input procedure of Sutter was used to obtain 60 VEP responses to a scaled checkerboard pattern. The amplitude in each response was obtained using a root mean square measure of response magnitude. For each of the 60 pairs of responses, a ratio between the amplitude of the responses from the two eyes was obtained as a measure of the relative health of one eye compared with the other. The mean and SD of this ratio measure for the control group were used to specify confidence intervals for each of the 60 locations. All patients had Humphrey 24-2 visual fields performed. To allow a comparison of the mVEPs to the visual fields, a procedure was developed for displaying the results of both tests on a common set of coordinates. RESULTS: Except for a small interocular difference in timing attributable to nasotemporal retinal differences, the pairs of mVEP responses from the two eyes of the control subjects were essentially identical. Many of the pairs of responses from the patients were significantly different. In general, there was reasonably good agreement with the Humphrey 24-2 visual field data. Although some regions with visual field defects were not detected in the mVEP due to small responses from the better eye, other abnormalities were detected that were hard to discern in the visual fields. CONCLUSIONS: Local monocular damage to the ganglion cell/optic nerve can be quantitatively measured by an interocular comparison of the mVEP

PURPOSE: Electroretinograms to high-intensity flashes were obtained to determine the extent of rod and cone photoreceptor and postreceptor dysfunction in patients with primary open-angle glaucoma. METHODS: Full-field flash electroretinograms were obtained using brief high-intensity flashes. Dark-adapted (rod-dominated) and light-adapted (cone-dominated) electroretinogram responses were recorded to a 'white' light as a function of flash intensity. The a-wave data were fitted with a model based on photopigment transduction to obtain values for the parameters of log Rmax (the maximum response) and log S (sensitivity). Oscillatory potentials were measured to the cone-dominated high-intensity flashes. Standard clinical 30 Hz flicker electroretinogram responses were recorded using a Grass photostimulator. RESULTS: Analysis of rod and cone a-wave data showed that log Rmax and log S values were within the normal range in nearly all of the patients. For some patients, oscillatory potentials were delayed beyond the normal range. CONCLUSION: Our results provide little evidence for widespread photoreceptor abnormalities in primary open-angle glaucoma

Contributions to the multifocal electroretinogram (ERG) from the inner retina (i.e. ganglion and amacrine cells) were identified by recording from monkeys before and after intravitreal injections of n-methyl DL aspartate (NMDLA) and/or tetrodotoxin (TTX). Components similar in waveform to those removed by the drugs were identified in the human multifocal ERG if the stimulus contrast was set at 50% rather than the typically employed 100% contrast. These components were found to be missing or diminished in the records from some patients with glaucoma and diabetes, diseases which affect the inner retina