Electrophysiological evidence that early glaucoma affects foveal vision

Abstract

The pattern electroretinogram (PERG) and visual evoked potential (PVEP) were recorded simultaneously using a 1.1 cpd pattern which was counterphase modulated at 1 Hz. The responses of ocular hypertensive (OHT) eyes (with normal visual fields) and eyes with early glaucoma (with early visual field defects and/or early cupping of the optic nervehead) were compared to age-matched normal observers. All patients (26 eyes) and normal observers (14 eyes) had normal transient flash electroretinograms. Delays were seen in mean PERG latency in both OHT and early glaucoma eyes, while mean PERG amplitude was significantly reduced only in the early glaucoma eyes. The PVEP responses were 'unmeasurable' in 11/26 patient eyes because the waveforms were grossly abnormal in shape, making it impossible to identify the N- and P-components. The data were categorized in this manner: a patient response was considered abnormal if latency or amplitude exceeded normal limits (PERG or PVEP) or if the waveform was 'unmeasurable' due to its shape (PVEP only). Of the 26 patient eyes, we found that 8 eyes had normal PERG and PVEP, 11 eyes had abnormal PERG and PVEP, one eye had an abnormal PERG and a normal PVEP, and 6 eyes (3 patients) had a normal PERG and an abnormal PVEP. These data support the proposition that foveal vision (as assessed by the PVEP) may be affected by early glaucomatous damage. The relationship between the PERG and PVEP also was evaluated using a new measurement which we call the 'latency window'. Using this measurement, 15/26 patient eyes were abnormal-9 of these had 'unmeasurable' PVEPs. This measurement could be useful in classifying 'W'-shaped PVEPs as normal or abnormal.

Pattern electroretinograms for the detection of neural loss in patients with permanent temporal visual field defect from chiasmal compression

“…The origin of P50 is even more uncertain, but it is probably generated by the ganglion cell bodies and/or by structures distal to the ganglion cells [5]. Several clinical studies have indicated that damage to the retinal ganglion cells and their fibers can be revealed by PERG recordings in patients with glaucoma [6][7][8][9] as well as in many neuro-ophthalmic conditions including demyelinating optic neuritis [10], ischemic optic neuropathy, and compressive anterior optic pathway dysfunction [4,11,12].…”

Comparative evaluation of Optical Coherence Tomography (OCT) with Pattern Reversal Visual Evoked Potential (PRVEP) in early primary open angle glaucoma

“…Previous electrophysiologic evidence [17,18,19] indicated that the impaired PRVEP responses observed in POAG patients could be ascribed to impaired neural conduction in the optic nerve and in the whole post retinal visual pathways as a consequence of the dysfunction of the innermost retinal layers.…”

Clinical impact of migraine for the management of glaucoma patients

“…The N95 component displays spatial tuning and is considered a contrast-related component originating in the retinal ganglion cells (Berninger and Schuurmans, 1985;Hess and Baker, 1984;Korth, 1983;Luo and Frishman, 2011;Viswanathan et al, 2000), whereas the P50 is partly derived from ganglion cells but also has an additional luminance component that is believed to arise in the outer retina (Korth, 1983;Luo and Frishman, 2011;Trick and Wintermeyer, 1982). Reduced P50 and/or N95 amplitude and delays in timing of these major components of the transient pattern ERG have been reported in patients with early glaucoma (Hood et al, 2005;Marx et al, 1987;Parisi, 2001;Parisi et al, 2006). To investigate whether similar deficits are present in people with migraine, we adopted the ISCEV standard approach to measure the transient pattern ERG (1 Hz, 0.8 checks, 31 field, high contrast > 95%) in a group of 45 migraine sufferers (26 MO, 19 MA) and 30 nonheadache controls.…”