Editors Selection IGR 14-1

Optical Coherence Tomography: In-vivo evaluation of focal lamina cribrosa defects in glaucoma

Tae-Woo Kim
Eun Ji Lee

Comment by Tae-Woo Kim & Eun Ji Lee on:

48881 In Vivo Evaluation of Focal Lamina Cribrosa Defects in Glaucoma, Kiumehr S; Park SC; Dorairaj S et al., Archives of Ophthalmology, 2012; 130: 552-559

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The lamina cribrosa (LC) is implicated as the primary site of damage to the retinal ganglion cell axons in glaucoma. Considering inhomogeneity and anisotrophy of the LC connective tissue structure, investigating the localized structural changes of the LC should help identifying precise pathogenic mechanisms of glaucomatous optic nerve damage. Although spectral-domain optical coherence tomog- raphy (SD-OCT) has recently been used to evaluate the LC in vivo, previous studies described general morphologic changes of the LC such as thinning or displacement of the LC in glaucoma, not focal defects or deformation of the LC. In an attempt to identify if the LC undergoes localized deformation in glaucoma in addition to the general morphologic change, Kiumehr et al. evaluated focal LC defects in 92 healthy eyes and 45 glaucomatous eyes using enhanced depth imaging SD-OCT images obtained by their robust imaging algorithm. The authors demonstrated that focal LC defects were found in 34 of 38 eyes with glaucoma (89%), while such change was not detected in any of the healthy eyes. They found that in the area with focal LC defects, the LC appeared to have focal loss of laminar beams, probably as a result of physical collapse, disruption or remodeling, and the anterior laminar surface had irregularity violating the smooth curvilinear contour observed in healthy eyes. The location of focal LC defects correlated well with the location of structural and functional glaucomatous damage. They mostly occurred in the inferior or inferotemporal far periphery of the LC and presented clinically as neuroretinal rim thinning and notching. In addition, the location corresponded to the visual field hemifield with greater mean loss of sensitivity in the pattern deviation plot. These findings suggest that mechanisms of LC deformation in glaucoma include focal loss of laminar beams in addition to the general changes in its thickness or position. Although the study is partly limited by an imperfect image quality (i.e., vascular shadow or thick neuroretinal rim which obscure the LC), and a lack of histologic confirmation, their findings underscore the importance of LC evaluation in glaucoma in addition to the conventional structural assessment of the optic nerve head. Further studies that will identify the pathophysiological course of focal LC defects and their relationship with glaucoma progression are greatly anticipated.

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