Following the first recording of electroretinographic responses in man to a barred pattern by Riggs and associates (1964) in normal and by Lawwill (1973Lawwill ( , 1974) ) in clinical cases, the first striking observation of a complete loss of pattern electroretinogram (PERG) after injurious section of the optic nerve by Groneberg & Teping (I 980) has led to the conclusion that the PERG originates from proximal retinal structures different from those responsible for the luminance electroretinogram (LERG). Typical changes of the PERG are seen during branch occlusion of the central retinal artery and vein. In ocular hypertension without visual field loss and glaucoma-related papillary changes the PERG is decreased at intraocular pressures above 26 mm Hg. In cases of primary glaucoma with regulated intraocular tension and without using miotics the amplitude of the PERG reflects the damage to the inner retinal layers. This favorably compares with the P100 latencies of the visual evoked cortical potential (VECP) which in primary glaucoma were partly within, partly outside the normal range. Other retinal diseases showing amplitude changes in the PERG are primary macular dystrophy, diabetic retinopathy, and the acute stage of optic neuritis. In all these cases the Ganzfeld LERG may be normal or nearly normal, whereas the PERG undergoes typical changes. On the contrary a highly preserved PERG can be recorded in cases of retinitis pigmentosa where the electrooculogram light rise and the LERG are already missing. In light of these findings the recording of PERG constitutes a new promising method of clinical electroretinography reflecting the activity of the hitherto omitted innermost retinal layers. It thereby contributes essentially to the location of disturbances within the visual system.