The purpose ofthis study was to determine the mechanical response of the lamina cribrosa (LC) to elevated intraocular pressure (IOP) so as to identify possible mechanisms of optic nerve damage in early glaucoma. Ten In this paper, we seek to complement previous work by a direct morphometric study of the response of the LC in normal human eyes to acute changes in IOP. We feel that this approach has several advantages. Firstly, a morphometric approach allows both the overall shape and the internal architecture of the LC to be evaluated as a function of pressure. This is in contrast with previous studies of the effects of pressure on the LC which focused on positional changes of the anterior surface of the retina at the ONH or on the topography ofthe ONH. Secondly, the use of normal eyes in acute experiments permits potential assessment of the factors initiating axonal damage, since the effect of IOP on a presumably normal ONH can be studied. This is important since ONH architecture in glaucomatous eyes will be substantially different from that ofnormal eyes, owing to degenerative optic neuropathy.The goals of the present work were: (i) to characterise and quantify acute deformations of the LC as a result of elevated IOP; (ii) to formulate a mechanical model of the stress distribution within the LC which is consistent with clinically and experimentally observed patterns of axonal damage in glaucoma; and (iii) to identify features of the LC which might increase the susceptibility of some eyes to glaucomatous damage. The experimental approach was to fix normal human eyes at either high or low pressure and then to compare morphometrically the LC from the low and high pressure groups.Materials and methods Ten pairs of ostensibly normal human eyes (average age 69 years) from which the corneas had been removed for transplantation were obtained within 24 hours post mortem from the Eye Bank of Ontario. The eyes were hemisected at the equator and the vitreous was carefully removed under an operating microscope. This dissection was performed while suspending the eye in a saline bath to prevent the retina from detaching. Each posterior hemisphere was then mounted onto a plastic perfusion dish'4 which sealed it at the equator and allowed it to be pressurised. Briefly, this dish had a small discshaped elevated region with bevelled edges which effectively matched the inner diameter of the globe at the equator. The eye was then clamped in position by a ring whose inner
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