May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Simultaneous Assessment of Pattern Evoked Potentials From Retinal Ganglion Cells and Visual Cortex (PERG and VEP) in Normal Eyes and in Compressive Optic Neuropathy
Author Affiliations & Notes
  • R.H. Kardon
    Ophthalmology and Visual Sciences, Univ of Iowa Hospital & Clinic and VA, Iowa City, IA
  • P. Spanheimer
    Ophthalmology and Visual Sciences, Univ of Iowa Hospital & Clinic and VA, Iowa City, IA
  • Footnotes
    Commercial Relationships  R.H. Kardon, None; P. Spanheimer, None.
  • Footnotes
    Support  VA Rehabilitation R&D Service, unrestricted grant from Research to Prevent Blindness
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 649. doi:
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      R.H. Kardon, P. Spanheimer; Simultaneous Assessment of Pattern Evoked Potentials From Retinal Ganglion Cells and Visual Cortex (PERG and VEP) in Normal Eyes and in Compressive Optic Neuropathy . Invest. Ophthalmol. Vis. Sci. 2005;46(13):649.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: The relationship between the pattern electroretinogram (PERG) and visual evoked potential (VEP) was characterized in normal eyes and in eyes with compressive optic neuropathy to simultaneously assess the status of retinal ganglion cells and their transmission of visual evoked responses to visual cortex . Methods: 27 normal subjects and 13 patients with compressive optic neuropathy were tested using a clinical PERG/VEP instrument in which pattern evoked potentials were simultaneously recorded from lower eyelid and scalp surface skin electrodes during a 4 minute test for each eye. The effect of compressive optic neuropathy on evoked potentials proximal and distal to the site of compression was studied by comparing the amplitude and latency of the PERG and VEP, respectively. Results: In normal eyes, decreases in stimulus contrast caused proportional decrements in mean amplitude of the simultaneously recorded PERG and VEP but without change in phase delay. Eyes with active compressive optic neuropathy on imaging showed three patterns; 1) disproportionate delay in phase of the VEP compared to amplitude of the PERG with or without thinning of the retinal nerve fiber layer, indicating conduction block 2) proportionately abnormal VEP phase and PERG amplitude with thinning of the retinal nerve fiber layer, indicating axonal loss 3) significantly abnormal PERG amplitude and VEP phase, but normal retinal nerve fiber layer thickness, indicating dysfunction of retinal ganglion cells proximal to the compression, without significant axon loss. One patient with complete recovery of temporal field loss on automated perimetry after neurosurgical decompression of a pituitary tumor despite thinning of the retinal nerve fiber layer showed a significant decrease in PERG, with an unexpected increase in VEP, indicating possible compensatory increase in gain at the level of visual cortex. Conclusions: Simultaneous recording of pattern evoked pattern potentials from the retinal ganglion cells and visual cortex allows the status of the visual pathway to be objectively assessed proximal and distal to the site of insult. This may provide information on whether dysfunction is permanent or reversible as well as compensatory gain control mechanisms in the visual pathway.

Keywords: neuro-ophthalmology: cortical function/rehabilitation • neuro-ophthalmology: optic nerve • electroretinography: clinical 
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