Lamina cribrosa measurements for glaucomatous eyes: a new focus point in optical coherence tomography

Submit Manuscript | http://medcraveonline.com network of collagen fibers. It has been considered that LC maintains the pressure gradient between intraocular pressure (IOP) and the periocular pressure and it structurally supports RGC axons. As LC is structurally weaker than other parts of sclera which are thicker and denser, it is highly sensitive to the effects of the IOP elevation.1,2 LC is a dynamic structure responding with thinning or thickening to IOP changes. Following sudden IOP increase, optic cup excavation associates with thinning in prelaminary tissue. The IOP elevation causes the compression, posterior displacement or bulging of the LC, deformation of the pores, kinking and pinching of the RGC axons and blood vessels traversing through the laminar pores. It has been thought that the blockade of axoplasmic flow within RGC or ischemic damage to RGC axons due to compressional LC deformation caused by the distortion or posterior displacement of the LC might lead to glaucomatous optic neuropathy (GON). Additionally, it has been demonstrated in experimental studies that posterior displacement of LC precedes early surface-detected structural damage and retinal nerve fiber layer (RNFL) loss. Thus, LC is the putative primary region of the axonal injury in RGC in GON.1,2