While elevated intraocular pressure (IOP) undoubtedly plays a crucial role in many
glaucoma patients, vascular dysregulation and chronic regional
ischemia are also thought to contribute to the pathophysiology of
glaucoma. In an effort to critically evaluate hypotheses involving vascular abnormalities in
glaucoma, Cioffi, Van Buskirk and co-workers have developed a model of
optic neuropathy based on chronic regional
ischemia. The multifocal electroretinogram (
MERG) has previously been used to assess function in non-human primates with experimental
glaucoma induced by high-IOP. In this study, the
MERG was used to monitor function in macaque monkeys with experimental
glaucoma induced by chronic anterior
optic nerve ischemia. Initial recordings from experimental eyes, which were later documented histologically to have moderate axon loss, revealed little difference from recordings of control eyes. This suggested that many of the signal components in the macaque
MERG, which are known (from other studies) to be eliminated by
intravitreal injections of
NMDA/TTX or by high-IOP experimental
glaucoma, may also be affected by the choice of
anesthetic agents and
MERG recording parameters. Subsequent experiments were performed to specifically evaluate the effects of bipolar versus monopolar signal derivation,
anesthetic agents,
MERG stimulus design and spatial scale. The results demonstrate that successful measurement of inner
retinal and optic nerve head
MERG components, especially those which have been shown by other investigators to originate with
ganglion cell spiking activity, will depend critically upon the choice of
anesthetic agents and recording parameters. One of the most important parameters seems to be use of a monopolar signal derivation, with the contralateral cornea serving as the reference position.