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LEE R. WOLIN, PhD; L. C. MASSOPUST, JR., PhD; J. MEDER, RN

Arch Ophthalmol. 1964;72(4):521-524.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

A number of physiologic factors which affect the electroretinogram (ERG) have been reported, including hypoxia,^1,13 glucose deprivation,¹ reduced retinal blood supply,^7,9 increase in intraocular pressure,^6,9,10 retinal edema,^7,8 and toxic effects of drugs.^2,11,13,14 Many clinical conditions such as various retinopathies, glaucoma, papilledema, and optic neuritis appear to affect the ERG as a result of circulatory changes, often associated with sclerotic processes (see also reviews by Crescitelli⁵ and Henkes⁸).

While there is general agreement that the ERG appears to originate somewhere within the retina, there is far from a perfect correlation between ERG potentials and visual functioning, normal vision persisting in the presence of abnormal ERG's, and normal ERG's being found in cases of seriously impaired vision. In this regard it is of interest to note that Tepas and Armington¹⁵ report that "At low luminance levels, where a summed electroretinogram could no . . . [Full Text PDF of this Article]

Author Affiliations
Cleveland

Laboratory of Neurophysiology, Cleveland Psychiatric Institute.

Footnotes
Submitted for publication March 25, 1964.

Conducted in conjunction with Dr. Maurice Albin of Cleveland Metropolitan General Hospital.

This research was supported in part by grants M-05756 and NB-04393 from the National Institutes of Health.

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