Lamina Cribrosa in Glaucoma: Diagnosis and Monitoring

Abstract

The lamina cribrosa is the putative site of retinal ganglion cell axonal injury in glaucoma. Although histological studies have provided evidence of structural changes to the lamina cribrosa, even in early stages of glaucoma, until recently, the ability to evaluate the lamina cribrosa in vivo has been limited. Recent advances in optical coherence tomography, including enhanced depth and swept-source imaging, have changed this, providing a means to image the lamina cribrosa. Imaging has identified general and localized configurational changes in the lamina of glaucomatous eyes, including posterior laminar displacement, altered laminar thickness, and focal laminar defects with spatial association with conventional structural and functional losses. In addition, although the temporal relationship between changes to the lamina cribrosa and glaucomatous retinal ganglion cell loss is yet to be elucidated, quantitative measurements of laminar microarchitecture have good reproducibility and offer the potential to serve as biomarkers for glaucoma diagnosis and progression.

Spectral domain optical coherence tomography evaluation of the feline optic nerve and peripapillary retina

“…In the future it would be of great value to determine if the cup depth is of clinical value in the diagnosis and evaluation of the progression of glaucoma in feline patients as it is in humans. Finally, assessment of the lamina cribrosa such as to determine laminar displacement and thickness can be of additional diagnostic value when evaluating the optic cup of patients affected with glaucoma and other optic neuropathies …”

Neuroprotection in glaucoma: recent advances and clinical translation

“…98 Impaired axonal transport of mitochondria has been linked to RGC death and, given that the unmyelinated axons of RGCs in the pre-laminar retinal nerve fibre layer (RNFL) require a higher energy input, this may in part explain their vulnerability to metabolic injury. 103 Structural differences in the lamina cribrosa and interindividual variation in the blood supply to the ONH may also explain individual susceptibility to IOPmediated damage, and the difference in rates of progression between individuals with glaucoma. 10, 14 The blood supply of the ONH is primarily derived from the choroid, with the inner (RNFL) and outermost (retrolaminar) regions also receiving input from retinal arteries.…”

“…14,107 Apart from production via mitochondrial respiratory chain reactions, there is also a simultaneous increase in extra-mitochondrial production of ROS in the cytosol. 103,104 However, dysfunctional, but not dead, RGCs may be amenable to neurorecovery with early intervention that targets potential mitochondrial dysfunction and elevated oxidative stress, via minimizing the generation or accumulation of ROS. 108 Rhodopsin and other photosensitizers also augment the production of ROS in the retina during photopic vision, which, by definition, involves exposure of the retina to light.…”

Pearls for Correct Assessment of Optic Disc at Glaucoma Diagnosis

“…It has been considered that the LC is a structure which maintains the pressure gradient between IOP and the periocular pressure. [1][2][3][4][5]41,42 The LC is very sensitive to the effects of the IOP because it is structurally weaker compared with the thicker and denser scleral parts. The elevation of IOP causes the posterior displacement or bulging of the LC, deformation of the pores and compression of the nerve fibres and blood vessels traversing though laminar pores.…”

“…It has been reported that the size and shape of LC pores may predict glaucomatous VF loss (Figure 2A and D). [1][2][3][4][5]41,42 Parapapillary atrophy, zones alpha and beta PPA refers to the thinning and degeneration of the chorioretinal tissue just outside of the optic disc and the exposure of the retinal pigment epithelium (RPE), which gives the tissue a moth-eaten appearance. It is considered that PPA occurs due to ischemia in the peripapillary choroidal circulation and/ or vascular deficiency in the ONH.…”