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 ◽  
...  
PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0134223 ◽  
Author(s):  
Kevin M. Ivers ◽  
Nripun Sredar ◽  
Nimesh B. Patel ◽  
Lakshmi Rajagopalan ◽  
Hope M. Queener ◽  
...  

2009 ◽  
Vol 50 (2) ◽  
pp. 681 ◽  
Author(s):  
Michael D. Roberts ◽  
Vicente Grau ◽  
Jonathan Grimm ◽  
Juan Reynaud ◽  
Anthony J. Bellezza ◽  
...  

Author(s):  
Rafael Grytz ◽  
Ian A. Sigal ◽  
Jeffrey W. Ruberti ◽  
J. Crawford Downs

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.


Author(s):  
Ian A. Sigal ◽  
Hongli Yang ◽  
Michael D. Roberts ◽  
Claude F. Burgoyne ◽  
J. Crawford Downs

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.


2016 ◽  
Vol 57 (7) ◽  
pp. 3451 ◽  
Author(s):  
Juan Reynaud ◽  
Howard Lockwood ◽  
Stuart K. Gardiner ◽  
Galen Williams ◽  
Hongli Yang ◽  
...  

2003 ◽  
Vol 44 (2) ◽  
pp. 623 ◽  
Author(s):  
Anthony J. Bellezza ◽  
Christopher J. Rintalan ◽  
Hilary W. Thompson ◽  
J. Crawford Downs ◽  
Richard T. Hart ◽  
...  

2021 ◽  
Author(s):  
Gwen Musial ◽  
Suman Adhikari ◽  
Hanieh Mirhajianmoghadam ◽  
Hope M Queener ◽  
Alexander W Schill ◽  
...  

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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