Physiologic significance of steady-state pattern electroretinogram losses in glaucoma: clues from simulation of abnormalities in normal subjects
Related Experiment Video
Updated: Jun 20, 2026
Assessing Early Stage Open-Angle Glaucoma in Patients by Isolated-Check Visual Evoked Potential
Published on: May 25, 2020
Vittorio Porciatti1, Lori M Ventura
1Bascom Palmer Eye Institute, Department of Ophthalmology, University of Miami Miller School of Medicine, 900 N.W. 17th Street, Miami, FL 33136, USA. vporciatti@med.miami.edu
Purpose:
To better understand pathophysiologic mechanisms underlying pattern electroretinogram (PERG) losses in glaucoma by simulating either retinal ganglion cell (RGC) dysfunction or RGC loss in normal subjects.
Materials And Methods:
The steady-state PERG has been recorded in 10 normal subjects (mean age: 31+/-8 y) according to the PERGLA paradigm by means of skin electrodes in response to horizontal gratings (1.7 cycles/degree, 99% contrast, 40 cd/m mean luminance, circular field size 25 degree diameter) alternating 16.28 times/seconds. Simulated RGC dysfunction has been obtained by reducing either contrast and mean luminance or blurring the visual stimulus. Simulated RGC loss has been obtained by reducing stimulus area. Outcome measures were PERG amplitude and phase obtained by discrete Fourier transform of PERG waveforms.
Results:
Progressive PERG amplitude reductions spanning the entire dynamic range of PERG response could be obtained by progressively reducing stimulus contrast and luminance, blurring the stimulus, and reducing stimulus area. The same variations in stimulus conditions caused phase changes of disparate sign and magnitude. Phase advanced (latency shortened) by reducing stimulus contrast or blurring the stimulus; phase lagged (latency increased) by reducing stimulus luminance; phase remained constant by reducing stimulus area.
Conclusions:
PERG amplitude and phase are essentially uncoupled, implying that these measures reflect distinct aspects of RGC activity. On the basis of our results and known PERG physiology, we propose a model in which both RGC dendrites and RGC axons contribute to the PERG signal. PERG delays may represent an indication of synaptic dysfunction that is potentially reversible.
