scholarly journals Lamina Cribrosa Microarchitecture in Monkey Early Experimental Glaucoma: Global Change

2016 ◽  
Vol 57 (7) ◽  
pp. 3451 ◽  
Author(s):  
Juan Reynaud ◽  
Howard Lockwood ◽  
Stuart K. Gardiner ◽  
Galen Williams ◽  
Hongli Yang ◽  
...  
Keyword(s):  
Global Change ◽  
Lamina Cribrosa ◽  
Experimental Glaucoma

scholarly journals Posterior (Outward) Migration of the Lamina Cribrosa and Early Cupping in Monkey Experimental Glaucoma

2011 ◽  
Vol 52 (10) ◽  
pp. 7109 ◽  
Author(s):  
Hongli Yang ◽  
Galen Williams ◽  
J. Crawford Downs ◽  
Ian A. Sigal ◽  
Michael D. Roberts ◽  
...  
Keyword(s):  
Lamina Cribrosa ◽  
Experimental Glaucoma ◽  
Outward Migration

scholarly journals In Vivo Changes in Lamina Cribrosa Microarchitecture and Optic Nerve Head Structure in Early Experimental Glaucoma

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0134223 ◽  
Author(s):  
Kevin M. Ivers ◽  
Nripun Sredar ◽  
Nimesh B. Patel ◽  
Lakshmi Rajagopalan ◽  
Hope M. Queener ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Optic Nerve Head ◽  
Lamina Cribrosa ◽  
Experimental Glaucoma

scholarly journals The Connective Tissue Components of Optic Nerve Head Cupping in Monkey Experimental Glaucoma Part 1: Global Change

2015 ◽  
Vol 56 (13) ◽  
pp. 7661 ◽  
Author(s):  
Hongli Yang ◽  
Ruojin Ren ◽  
Howard Lockwood ◽  
Galen Williams ◽  
Vincent Libertiaux ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Global Change ◽  
Connective Tissue ◽  
Optic Nerve Head ◽  
Experimental Glaucoma

scholarly journals Remodeling of the Connective Tissue Microarchitecture of the Lamina Cribrosa in Early Experimental Glaucoma

2009 ◽  
Vol 50 (2) ◽  
pp. 681 ◽  
Author(s):  
Michael D. Roberts ◽  
Vicente Grau ◽  
Jonathan Grimm ◽  
Juan Reynaud ◽  
Anthony J. Bellezza ◽  
...  
Keyword(s):  
Connective Tissue ◽  
Lamina Cribrosa ◽  
Experimental Glaucoma

Microstructure Motivated Growth and Remodeling of the Lamina Cribrosa in Early Glaucoma

2011 ◽  
Author(s):  
Rafael Grytz ◽  
Ian A. Sigal ◽  
Jeffrey W. Ruberti ◽  
J. Crawford Downs
Keyword(s):  
Connective Tissue ◽  
Structural Changes ◽  
Lamina Cribrosa ◽  
Posterior Pole ◽  
Retinal Ganglion ◽  
Experimental Glaucoma ◽  
Relevant Risk Factor ◽  
Orbital Space ◽  
Iop Elevation ◽  
Pass Through

Glaucoma is a leading cause of blindness in the world and is due to the loss of retinal ganglion cell axons. These axons deteriorate in a region in the posterior pole of the eye known as the optic nerve head (ONH). The axons pass through the lamina cribrosa (LC) as they exit the eye at the ONH. The LC is characterized by a porous, connective tissue structure composed of laminar beams. The function of the LC is unclear, but is believed to include providing mechanical support to the axons as they transition from inside the pressurized globe to the lower pressure orbital space. Early experimental glaucoma studies have shown that the LC remodels into a thicker, more posterior structure which incorporates more connective tissue after chronic IOP elevation [1,2]. The process by which this occurs is unknown. These structural changes are assumed to play an important role in the pathophysiology of the ocular disease glaucoma, where elevated IOP is known to be the most relevant risk factor.

Biomechanics of the Posterior Pole During the Remodeling Progression From Normal to Early Experimental Glaucoma

2009 ◽  
Author(s):  
Ian A. Sigal ◽  
Hongli Yang ◽  
Michael D. Roberts ◽  
Claude F. Burgoyne ◽  
J. Crawford Downs
Keyword(s):  
Visual Information ◽  
Lamina Cribrosa ◽  
Posterior Pole ◽  
Glaucomatous Optic Neuropathy ◽  
Retinal Ganglion ◽  
Experimental Glaucoma ◽  
Pass Through ◽  
Mechanical Insult ◽  
The Brain ◽  
Connective Tissue Structure

Glaucoma is one of the leading causes of blindness worldwide. The loss of vision associated with glaucoma is due to damage to the retinal ganglion cell axons, which transmit visual information to the brain. Damage to these axons is believed to occur as the axons pass through the lamina cribrosa (LC), a connective tissue structure in the optic nerve head at the back of the eye. Elevated intraocular pressure (IOP) has been identified as the main risk factor for the development of the neuropathy, but the mechanism(s) by which a mechanical insult (elevated IOP) is translated into a biological effect (glaucomatous optic neuropathy) is not well understood.

Deformation of the Lamina Cribrosa and Anterior Scleral Canal Wall in Early Experimental Glaucoma

2003 ◽  
Vol 44 (2) ◽  
pp. 623 ◽  
Author(s):  
Anthony J. Bellezza ◽  
Christopher J. Rintalan ◽  
Hilary W. Thompson ◽  
J. Crawford Downs ◽  
Richard T. Hart ◽  
...  
Keyword(s):  
Lamina Cribrosa ◽  
Canal Wall ◽  
Experimental Glaucoma

scholarly journals Longitudinal in vivo changes in radial peripapillary capillaries and optic nerve head structure in non-human primates with early experimental glaucoma

2021 ◽  
Author(s):  
Gwen Musial ◽  
Suman Adhikari ◽  
Hanieh Mirhajianmoghadam ◽  
Hope M Queener ◽  
Alexander W Schill ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Adaptive Optics ◽  
Optic Nerve Head ◽  
Time Course ◽  
Neuronal Loss ◽  
Lamina Cribrosa ◽  
Fiber Layer ◽  
Experimental Glaucoma ◽  
Nerve Fiber Layer Thickness

Purpose: There is conflicting evidence as to whether a loss of radial peripapillary capillaries (RPCs) precedes neuronal loss in glaucoma. We examined the time-course of in vivo changes in RPCs, optic nerve head (ONH) structure, and retinal nerve fiber layer thickness (RNFLT) in experimental glaucoma (EG). Methods: Spectral domain optical coherence tomography images were acquired before and approximately every 2 weeks after inducing unilateral EG in 9 rhesus monkeys to quantify mean anterior lamina cribrosa surface depth (ALCSD), minimum rim width (MRW), and RNFLT. Perfused RPC density was measured from adaptive optics scanning laser ophthalmoscope images acquired on the temporal half of the ONH. The time of first significant change was quantified as when values fell and remained outside of the 95% confidence interval established from control eyes. Results: Mean ALCSD and/or MRW were the first parameters to change in 8 EG eyes. RPC density changed first in the 9th. At their first points of change, mean ALCSD posteriorly deformed by 100.2 +- 101.2 microns, MRW thinned by 82.3 +- 65.9 microns, RNFLT decreased by 25 +- 14 microns, and RPC density decreased by 4.5 +- 2.1%. RPC density decreased before RNFL thinning in 5 EG eyes. RNFLT decreased before RPC density decreased in 2 EG eyes, while 2 EG eyes had simultaneous changes. Conclusions: In most EG eyes, RPC density decreased before (or simultaneous with) a change in RNFLT, suggesting that vascular factors may play a role in axonal loss in some eyes in early glaucoma.

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