Abstract
ABSTRACTThe lamina cribrosa (LC) is the presumed site of axonal injury in glaucoma. Its deformation has been suggested to contribute to optic neuropathy by impeding axoplasmic flow within the optic nerve fibers, leading to apoptosis of retinal ganglion cells. To visualize the LC in vivo, optical coherence tomography (OCT) has been applied. Spectral domain (SD)-OCT, used in conjunction with recently introduced enhanced depth imaging (EDI)-OCT, has improved visualization of deeper ocular layers, but in many individuals it is still limited by inadequate resolution, poor image contrast and insufficient depth penetrance. The posterior laminar surface especially is not viewed clearly using these methods. New generation high-penetration (HP)-OCTs, also known as swept-source (SS)-OCT, are capable to evaluate the choroid in vivo to a remarkable level of detail. SS-OCTs use a longer wavelength (1,050 nm instead of 840 nm) compared to the conventional techniques. We review current knowledge of the LC, findings from trials that use SD-OCT and EDI-OCT, and our experience with a prototype SS-OCT to visualize the LC in its entirety.Key PointsWhat is known?• The LC is the presumed site of axonal injury in glaucoma• Compared to spectral domain-OCT, enhanced depth imaging-OCT improves imaging of the LC• Even so, currently used SD-OCT techniques are restricted by poor wavelength penetrance of the deeper ocular layersWhat our findings add?• SS-OCT may be a superior imaging modality for deep ocular structures• Prior studies used SS-OCT to evaluate choroidal thickness in both healthy and ‘normal tension glaucoma’ eyes• SS-OCT enables good evaluation of three-dimension (3D) lamina cribrosa morphology.How to cite this article: Nuyen B, Mansouri K, Weinreb RN. Imaging of the Lamina Cribrosa using Swept-Source Optical Coherence Tomography. J Current Glau Prac 2012;6(3): 113-119.
Highlights
A leading cause of blindness worldwide,[1] glaucoma comprises a group of progressive optic neuropathies with characteristic optic disk damage and a concomitant pattern of visual field loss.[2]
The convergence of the axons forms the neuroretinal rim of the nerve before exiting the eye through the lamina cribrosa (LC), a scleral structure that is characterized by sheets of porous connective tissue
In the past, limited visualization of the LC on clinical examination has made its evaluation challenging to the extent that most available information about this structure has been gathered from postmortem analysis of human eyes with glaucoma[20,21] or animal eyes with experimental glaucoma.[22,23]
Summary
A leading cause of blindness worldwide,[1] glaucoma comprises a group of progressive optic neuropathies with characteristic optic disk damage and a concomitant pattern of visual field loss.[2]. Glaucoma is characterized by the progressive degeneration of the retinal ganglion cells, axons, soma and dendrites.[7,8] On the basis of histopathologic studies, the LC has been implicated as the site of original optic nerve damage in glaucoma.[9] Changes in the LC, especially deformation and compression, have been related to a decrease in connective tissue, resulting in structural thinning that is linked to glaucomatous axonal damage.[10,11] Morphological changes in the LC pore shape and size have been correlated with the severity and progression of glaucoma.[12,13,14] In monkey eyes, chronic ocular hypertension has been shown to result in particular changes in the LC, including outward migration of the posterior lamina insertion point.[6] Overall, the structural thinning, pore deformities and posterior displacement of the LC cause the pores to deform.[15] This deformation likely impedes axoplasmic flow and disrupts transport of trophic factors important to the survival of retinal ganglion cells.[16,17] structural changes in the LC may play a role in neuronal death characteristic of glaucoma. In the past, limited visualization of the LC on clinical examination has made its evaluation challenging to the extent that most available information about this structure has been gathered from postmortem analysis of human eyes with glaucoma[20,21] or animal eyes with experimental glaucoma.[22,23] Such studies are prone to the distorting effects of fixation, and it is largely unknown how changes in IOP affect enucleated eyes.[20,24,25] in vivo characterization of the LC, including features such as its thickness and average pore shape and size, is an essential part of studying glaucomatous disease
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