Biomechanical changes of the optic disc

Sigal, Ian A.; Roberts, Michael D.; Girard, M; Burgoyne, Claude F.; Downs, J. Crawford

doi:10.1016/b978-0-7020-2983-7.00020-6

Cited by 22 publications

(30 citation statements)

References 43 publications

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“…The first interaction can be interpreted as the structural stiffness of the scleral shell (i.e., a combination of scleral material properties and geometry), as discussed elsewhere. 3,13,21,23,41,46,47 The second interaction can be interpreted as the role of laminar stiffness in the expansion of the scleral canal: increased lamina modulus (stiffer) reducing canal expansion, more so when the sclera was compliant than when it was stiff (Fig. 6).…”

Section: There Were Influential Factor Interactions For Both Lcd and Scementioning

confidence: 98%

“…12,13 In describing the effects of IOP on the LC, a useful conceptual framework has emerged in the past few years: that of the balance between the direct effects of IOP "pushing" the lamina posteriorly and the indirect effects of IOP deforming the sclera, expanding the canal, which in turn "pulls" the lamina taut from the sides. 3,12,23,25,47,48 Within this framework, a stiff sclera would deform little, with a small canal expansion (i.e., not pulling the lamina taut), resulting in the LC displacing posteriorly. Conversely, a compliant sclera would deform more, pull the lamina taut from the sides, and result in a shift of LCD anteriorly (less posteriorly or more anteriorly).…”

Section: There Were Influential Factor Interactions For Both Lcd and Scementioning

confidence: 98%

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IOP-Induced Lamina Cribrosa Displacement and Scleral Canal Expansion: An Analysis of Factor Interactions Using Parameterized Eye-Specific Models

Sigal

Yang

Roberts

et al. 2011

Invest. Ophthalmol. Vis. Sci.

147

120

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Section: There Were Influential Factor Interactions For Both Lcd and Scementioning

confidence: 98%

Section: There Were Influential Factor Interactions For Both Lcd and Scementioning

confidence: 98%

IOP-Induced Lamina Cribrosa Displacement and Scleral Canal Expansion: An Analysis of Factor Interactions Using Parameterized Eye-Specific Models

Sigal

Yang

Roberts

et al. 2011

Invest. Ophthalmol. Vis. Sci.

147

120

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“…These changes in the ONH connective tissues alter their geometries and mechanical responses to loading, which feeds back directly into the mechanical effects of IOP on the ONH. Adapted from Figure 1 in (Sigal, Roberts et al, 2010). …”

Section: Figuresmentioning

confidence: 99%

Glaucomatous cupping of the lamina cribrosa: A review of the evidence for active progressive remodeling as a mechanism

Downs

Roberts

Sigal

2011

Experimental Eye Research

193

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The purpose of this review is to examine the literature in an attempt to elucidate a biomechanical basis for glaucomatous cupping. In particular, this work focuses on the role of biomechanics in driving connective tissue remodeling in the progression of laminar morphology from a normal state to that of an excavated glaucomatous state. While there are multiple contributing factors to the pathogenesis of glaucoma, we focus on laminar extracellular matrix (ECM) remodeling in glaucoma and the feedback mechanisms and signals that may guide progressive laminar cupping. We review the literature on the potential mechanisms of glaucomatous changes in the laminar ECM at the anatomic, structural, cellular and subcellular levels in the context of the biomechanical paradigm of glaucomatous onset and progression. From this review several conclusions can be drawn. First, extensive remodeling of the lamina cribrosa ECM occurs in primary open angle glaucoma. Second, there is surprisingly little evidence to support acute mechanical damage to the lamina as the principal mechanism of cupping. Third, ONH astrocytes and lamina cribrosa cells can sense their mechanical environment and respond to mechanical stimuli by remodeling the ECM. Fourth, there is evidence suggesting that chronic remodeling of the lamina results in a progressive posterior migration of the laminar insertion into the canal wall, which eventually results in the posterior lamina inserting into the pia mater. Finally, modeling studies suggest that laminar remodeling may be a biomechanical feedback mechanism through which cells modify their environment in an attempt to return to a homeostatic mechanical environment. It is plausible that biomechanics-driven connective tissue remodeling is a mechanism in the progression of laminar morphology from a normal state to that of a cupped, excavated glaucomatous state.

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“…It is thought that tissue deformation is one of the main contributors to ONH damage in glaucoma. 4 Our data, then, would be the first suggesting that such deformation occurs in relation to the cardiac cycle.…”

Section: Discussionmentioning

confidence: 71%

“…Clinical, epidemiological, 3 experimental, and mathematical modeling data 4 suggest that factors such as intraocular pressure (IOP), low ocular perfusion pressure, age, ethnicity, greater scleral elasticity, and myopia contribute to the development of glaucoma; however, it is not known how, mechanistically, such factors might combine to cause the pattern of axonal loss and optic disc morphological change that clinicians recognize as glaucoma.…”

mentioning

confidence: 98%

Pulsatile Movement of the Optic Nerve Head and the Peripapillary Retina in Normal Subjects and in Glaucoma

Singh¹,

Dion

Godin

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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Biomechanical changes of the optic disc

Cited by 22 publications

References 43 publications

IOP-Induced Lamina Cribrosa Displacement and Scleral Canal Expansion: An Analysis of Factor Interactions Using Parameterized Eye-Specific Models

IOP-Induced Lamina Cribrosa Displacement and Scleral Canal Expansion: An Analysis of Factor Interactions Using Parameterized Eye-Specific Models

Glaucomatous cupping of the lamina cribrosa: A review of the evidence for active progressive remodeling as a mechanism

Pulsatile Movement of the Optic Nerve Head and the Peripapillary Retina in Normal Subjects and in Glaucoma

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