A hundred years ago Holmgren1 first reported that an electrical change was produced when the eye was exposed to light, and in 1877 Dewar2 recorded such potentials from the human eye. Kahn and Löwenstein3 attempted to develop electroretinography as a clinical technique in 1924, but not until 1941, when Riggs4 successfully developed a contact-lens electrode, did a simple method become available for studying this response in man. During this time, important contributions to the understanding of the various components of the electroretinogram (ERG) appeared from the laboratory of Granit.5 In 1945, Adrian6 showed that the human ERG could be separated into specific rod- and cone-mediated responses. The clinical usefulness of the ERG became most apparent after the pioneering studies of Karpe7 in Sweden.
The ERG can be defined simply as the record of the transient electrical response produced by the retina following light