Editors Selection IGR 21-1

Anatomical Structures: Corneal Hysteresis as a Risk Factor for Progression

Crawford Downs

Comment by Crawford Downs on:

84612 Relationship of Corneal Hysteresis and Anterior Lamina Cribrosa Displacement in Glaucoma, Wong BJ; Moghimi S; Zangwill LM et al., American Journal of Ophthalmology, 2020; 212: 134-143

See also comment(s) by Julian Garcia Feijoo & Frances SaenzTony Realini

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Optic nerve head (ONH) biomechanics has been hypothesized to play an important role in the development and progression of glaucoma, but it is not well understood. The dearth of available data is due to the technical challenges involved in the measurement of ONH tissue mechanical properties (stiffness) and the complexity of the ONH and scleral geometry. Further complicating the study of ONH biomechanics is the biologic variability in the load-bearing structure, which includes geometry (regional scleral thickness, neural canal shape and size, regional laminar pore size and beam thickness, etc.), and tissue stiffness, which may change with age, pathology, extracellular matrix composition, and connective tissue remodeling. Fortunately, recent advances in OCT and other imaging technologies are leading to more accurate and comprehensive clinical assessments of ONH biomechanical behavior in vivo.

Wong, Weinreb and coworkers studied the association of the longitudinal change in the position of the anterior lamina cribrosa surface (ALCS, measured with OCT) to corneal hysteresis (CH), plus other factors, in 147 eyes from 96 glaucoma or glaucoma suspect patients followed for 3.5 years and 7.9 visits on average. Results show that the ALCS migrated posteriorly on average at 0.78 µm/yr. Only 17 of the 196 eyes showed a significant ALCS posterior migration over time, while 22 eyes showed anterior migration; 74% of the eyes showed no change in ALCS position. Choroidal thinning, a smaller IOP increase over time, and lower CH were significantly associated with posterior ALCS migration. Only 6% of eyes showed visual field progression during the study term, and so glaucoma progression was not significantly associated with ALCS migration (or CH indirectly).

This study is important because it adds weight to the available evidence that lower CH is associated with glaucoma progression, and the study shows that CH is also associated with posterior ALCS migration

This study is important because it adds weight to the available evidence that lower CH is associated with glaucoma progression, and the primary finding in the present study shows that CH is also associated with posterior ALCS migration. This study links CH to ONH morphological change and remodeling for the first time, which is thought to be one of the mechanisms underlying glaucoma pathophysiology. The authors discuss the hypothesis that CH is related to (or somehow reflects) ONH biomechanics, although most experimental evidence has not shown a relationship between anterior and posterior pole biomechanics. There is another plausible hypothesis that could explain their findings. Experiments have shown that the cornea acts as a shock absorber of sorts and hysteresis allows the cornea to damp and absorb transient IOP fluctuations. Hence, a lower CH would be associated with larger, more energetic transient IOP fluctuations, which may be associated with larger laminar strain fluctuations that drive greater posterior migration and remodeling of the lamina cribrosa. In this scenario, lower CH drives greater biomechanical insult to the ONH and lamina cribrosa, leading to greater axonal damage and loss. Future studies will be required to tease out the relationships that are emerging from this area of study, but the present work pushes the field further down the path to understanding the complex mechanisms underlying glaucomatous axon damage.

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