Mechanical Strain and Restructuring of the Optic Nerve Head

Downs, J. Crawford; Burgoyne, Claude F.; Grytz, Rafael

doi:10.1016/b978-0-7020-5193-7.00008-x

Cited by 8 publications

(7 citation statements)

References 52 publications

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“…The current findings are consistent with previous studies suggesting that focal LC defects and impaired ocular hemodynamics may be etiologically related, and that mechanical and vascular mechanisms of glaucomatous optic nerve injury are inseparably intertwined. 12, 13 …”

Section: Discussionmentioning

confidence: 99%

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Optical Coherence Tomography Angiography Vessel Density in Glaucomatous Eyes with Focal Lamina Cribrosa Defects

et al. 2016

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Purpose To investigate whether vessel density assessed by optical coherence tomography angiography (OCT-A) is reduced in glaucomatous eyes with focal lamina cribrosa (LC) defects. Design Cross-sectional case-control study. Participants Eighty-two primary open angle glaucoma (POAG) patients from the Diagnostic Innovations in Glaucoma Study (DIGS) with and without focal LC defects (41 eyes of 41 patients in each group) matched by severity of visual field (VF) damage. Methods OCT-A-derived circumpapillary vessel density (cpVD) was calculated as the percentage area occupied by vessels in the measured region extracted from the retinal nerve fiber layer (RNFL) in a 750-μm-wide elliptical annulus around the disc. Focal LC defects were detected using swept-source OCT images. Main Outcome Measures Comparison of global and sectoral (eight 45 degree sectors) cpVDs and circumpapillary retinal nerve fiber layer (cpRNFL) thicknesses in eyes with and without LC defects. Results Age, global and sectoral cpRNFL thicknesses, visual field mean deviation and pattern standard deviation, presence of the optic disc hemorrhage, and mean ocular perfusion pressure did not differ between the patients with and without LC defects (P > 0.05, for all comparisons). Mean cpVDs of eyes with LC defects were significantly lower than those without a defect globally (52.9 ± 5.6 vs. 56.8 ± 7.7 %, P = 0.013), and in the inferotemporal (IT) (49.5 ± 10.3 vs. 56.8 ± 12.2 %, P = 0.004), superotemporal (ST) (54.3 ± 8.8 vs. 58.8 ± 9.6 %, P = 0.030), and inferonasal (IN) (52.4 ± 9.0 vs. 57.6 ± 9.1 %, P = 0.009) sectors. Eyes with LC defects in the IT sector (n = 33) had significantly lower cpVDs than those without a defect in the corresponding IT and IN sectors (P < 0.05, respectively). Eyes with LC defects in the ST sector (n = 19) had lower cpVDs in ST, IT, and IN sectors (P < 0.05, respectively). Conclusions In eyes with similar severity of glaucoma, OCT-A-measured vessel density was significantly lower in POAG eyes with focal LC defects than those without a LC defect. Moreover, reduction of vessel density was spatially correlated with the location of the LC defect.

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Section: Discussionmentioning

confidence: 99%

“…10, 11 However, little is known about the association between the retinal microvasculature and the presence of focal LC defects, an issue relevant to pathogenesis of glaucomatous optic neuropathy. 12, 13 …”

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confidence: 99%

Optical Coherence Tomography Angiography Vessel Density in Glaucomatous Eyes with Focal Lamina Cribrosa Defects

et al. 2016

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“…The difference between intraocular and orbital pressure establishes “engineering” or “mechanical” stresses (force/cross-sectional area of the tissue bearing the load) within the ONH neural and connective tissues, the magnitude of which is determined by the level of IOP and the 3-dimensional (3D) geometry or architecture of the tissues that carry them (45, 51, 56). These mechanical stresses are separate from physiologic stress which we define as physical and metabolic changes within a cell in response to alterations in its environment.…”

Section: Optic Nerve Head Biomechanicsmentioning

confidence: 99%

“…These mechanical stresses are separate from physiologic stress which we define as physical and metabolic changes within a cell in response to alterations in its environment. The direct (outward) effect of IOP on the internal limiting membrane of the ONH prelaminar tissues is resisted by the pressure within the retrolaminar optic nerve tissues (retrolaminar tissue pressure) and the outward expansion of the scleral canal which pulls the lamina cribrosa “tight” within the canal, effectively increasing its resistance to outward deformation (56, 57). …”

Section: Optic Nerve Head Biomechanicsmentioning

confidence: 99%

“…The important concept for this discussion is that engineering models suggest that the stresses generated by the IOP/orbital pressure difference within the scleral connective tissues are far higher than the direct (outward) stresses on the neural and connective tissues of the lamina (Fig 2) (54, 56, 58). How the ONH connective tissues respond to a given distribution of mechanical stress is determined by their material properties.…”

Section: Optic Nerve Head Biomechanicsmentioning

confidence: 99%

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The Morphological Difference Between Glaucoma and Other Optic Neuropathies

Burgoyne

2015

Journal of Neuro-Ophthalmology

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The clinical phenomenon of cupping has two principal pathophysiologic components in all optic neuropathies: prelaminar thinning and laminar deformation. We define prelaminar thinning to be the portion of cup enlargement that results from thinning of the prelaminar tissues due to physical compression and/or loss of Retinal Ganglion Cell axons. We define laminar deformation or laminar cupping to be the portion of cup enlargement that results from permanent, intraocular pressure-(IOP) induced deformation of the lamina cribrosa and peripapillary scleral connective tissues following damage and/or remodeling. We propose that the defining phenomenon of glaucomatous cupping is deformation and/or remodeling of the neural and connective tissues of the optic nerve head (ONH), which is governed by the distribution of IOP-related connective tissue stress and strain, regardless of the mechanism of insult or the level of IOP at which that deformation and/or remodeling occurs. Said in another way, “glaucomatous cupping” is the term clinicians use to describe the clinical appearance and behavior the ONH assumes as its neural and connective tissues deform, remodel or mechanically fail: 1) in a pattern and 2) by the several pathophysiologic processes governed by IOP-related connective tissue stress and strain. ONH Biomechanics explains why a given optic nerve head will demonstrate a certain form of “cupping” and at what level of IOP that might happen. Animal models are allowing us to tease apart the important components of cupping in IOP-related and non-IOP-related forms of optic neuropathy. A paradigm change in spectral domain optical coherence tomography ONH, retinal nerve fiber layer and Macular imaging should improve our ability to phenotype all forms of damage to the visual system including glaucoma.

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