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Electroretinal responses in ocular vascular occlusions due to temporal arteritis.

Temporal arteritis is a potentially blinding disease of the elderly; its effects are principally due to inflammatory obliteration of the arterial supply to the retina and the optic nerve head. The ophthalmic artery and the extraocular course of the central retinal and posterior ciliary arteries may be involved singly or in combination. The usual presenting feature in these cases is acute ischaemic optic neuropathy due to diminished posterior ciliary artery perfusion; central retinal artery occlusion is less frequently seen. The central retinal artery (CRA) and cilio-retinal arteries, when present, supply the inner layers of the retina by capillary plexus (Michaelson, I954). In experimental CRA occlusion, with generalized ischaemic necrosis of the ganglion cells and most of the inner nuclear layer, the positive b-wave of the electroretinogram (ERG) is diminished, and an augmented negative a-wave results from unmasking of the PIII component of Granit (I933) which is generated in the receptor layer (Brown, I968). Granit's PII component, responsible for the b-wave of the ERG, is generally considered to originate in the inner nuclear layer, possibly from the Muller cells (Dowling, 1970). The posterior ciliary arteries (PCAs), usually two or three in number, supply the optic nerve head, the choroid posterior to the equator, and the overlying pigment epithelium and outer retina (visual receptors and outer nuclear layer) by diffusion from the choriocapillaris (Hayreh, I97Ia). Experimental PCA occlusions in monkeys cause ischaemic optic neuropathy, patches ofchorioretinal atrophy, and a subnormal ERG,with proportionate reduction in aand b-waves (Hayreh and Baines, 1972b, c; McLeod and Hayreh,