Abstract
PurposeTo determine the factors influencing the anterior lamina cribrosa (LC) surface depth (LCD) in patients with open-angle glaucoma (OAG), focusing on the association between LCD and the position of the central retinal vessel trunk (CRVT) at the anterior LC surface.MethodsOptic nerve heads of 205 OAG eyes were scanned using swept-source optical coherence tomography (SS-OCT). After processing the images using adaptive compensation, the LCD was determined from 11 horizontal B-scan images that divided the optic disc vertically into 12 equal parts. Eyes were divided into two groups (central or peripheral) according to where the CRVT exits from the anterior LC surface. The influence of CRVT position on LCD was evaluated, taking into account age, gender, untreated intraocular pressure (IOP), IOP at optic-disc scanning, retinal nerve fiber layer (RNFL) thickness, visual-field mean deviation, central corneal thickness, and axial length.ResultsPatients in the peripheral CRVT group were younger and more myopic, and had a larger mean LCD and thinner global RNFL than those in the central CRVT group (all P≤0.023). On multivariate analysis, the peripheral CRVT location was significantly associated with a larger LCD (P = 0.002), together with the significant association of younger age (P<0.001), higher untreated IOP (P = 0.010), and thinner RNFL (P = 0.003) on the larger LCD.ConclusionIn OAG, CRVT location was an independent factor influencing the LCD, together with age, untreated IOP, and global RNFL thickness. The data indicate that the CRVT may contribute to the resistance of the LC against deformation. A longitudinal prospective observation is required to clarify this relationship.
Highlights
The lamina cribrosa (LC) is the primary site of glaucomatous optic nerve damage
The peripheral central retinal vessel trunk (CRVT) location was significantly associated with a larger LC surface depth (LCD) (P = 0.002), together with the significant association of younger age (P
The results revealed an association between a greater LCD and a peripherally located CRVT, younger age, higher untreated IOP, and thinner global RNFL
Summary
Histologic studies have demonstrated that compression and posterior displacement of the LC underlies glaucomatous cupping [1, 2]. LC deformation may compress the laminar capillaries, thereby causing ischemic insult to the axons [1, 6]. Experimental studies have shown that displacement of the LC precedes early surface-detected structural damage and retinal nerve fiber layer (RNFL) loss [7,8,9,10]. This finding further suggests that LC deformation is the primary event underlying axonal damage in glaucoma
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