3-D Histomorphometry of the Normal and Early Glaucomatous Monkey Optic Nerve Head: Lamina Cribrosa and Peripapillary Scleral Position and Thickness

Yang, Hongli; Downs, J. Crawford; Girkin, Christopher A.; Sakata, Lisandro M.; Bellezza, Anthony J.; Thompson, Hilary W.; Burgoyne, Claude F.

doi:10.1167/iovs.07-0349

Cited by 235 publications

(252 citation statements)

References 26 publications

Supporting

Mentioning

241

Contrasting

Unclassified

Order By: Relevance

“…Hayreh, et al 96,97 has argued that primary ischemia to the retrolaminar optic nerve could cause a fibrotic response that pulls the lamina posteriorly into a form that is indistinguishable from glaucomatous cupping. However, we see no evidence for this in early experimental glaucoma monkeys (16 -30% axon loss) that demonstrate profound posterior deformation of the lamina and expansion of the scleral portion of the neural canal 45,46,[48][49][50] . These deformations occur after four to eight weeks of minimal to moderate IOP elevations.…”

contrasting

confidence: 58%

“…"Laminar deformation" is that portion of cup enlargement that results from lamina cribrosa and peripapillary scleral connective tissue damage followed by permanent, IOP-induced deformation 45,46,48,49,64 . Laminar deformation results in a clinically deeper form of cupping that occurs only in those optic neuropathies in which the ONH connective tissues have been damaged and have become susceptible to permanent, IOP-induced deformation.…”

Section: Onh Biomechanics and Onh Cuppingmentioning

confidence: 99%

“…Recent studies in the monkey [45][46][47][48][49][50] and rat [51][52][53] support the importance of the ONH, by describing profound alterations within the prelaminar, laminar and peripapillary scleral tissues of the ONH at the earliest detectable stage of experimental glaucoma.…”

Section: The Optic Nerve Head (Onh)mentioning

confidence: 99%

“…"Prelaminar thinning" is that portion of cup enlargement that results from net thinning of the prelaminar tissues due to physical compression and/or loss of RGC axons even in the presence of gliosis [90][91][92][93] . In this paradigm, prelaminar thinning results in a clinically shallow form of cupping 94,95 (being limited to the prelaminar tissues) that occurs in all forms of RGC axon loss (including aging) and is therefore nonspecific."Laminar deformation" is that portion of cup enlargement that results from lamina cribrosa and peripapillary scleral connective tissue damage followed by permanent, IOP-induced deformation 45,46,48,49,64 . Laminar deformation results in a clinically deeper form of cupping that occurs only in those optic neuropathies in which the ONH connective tissues have been damaged and have become susceptible to permanent, IOP-induced deformation.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Premise and Prediction???How Optic Nerve Head Biomechanics Underlies the Susceptibility and Clinical Behavior of the Aged Optic Nerve Head

Burgoyne¹,

Downs²

2008

Journal of Glaucoma

Self Cite

194

169

View full text Add to dashboard Cite

We propose that age-related alterations in optic nerve head (ONH) biomechanics underlie the clinical behavior and increased susceptibility of the aged ONH to glaucomatous damage. The literature which suggests that the aged ONH is more susceptible to glaucomatous damage at all levels of intraocular pressure is reviewed. The relevant biomechanics of the aged ONH are discussed and a biomechanical explanation for why, on average, the stiffened peripapillary scleral and lamina cribrosa connective tissues of the aged eye should lead to a shallow (senile sclerotic) form of cupping is proposed. A logic for why age-related axon loss and the optic neuropathy of glaucoma in the aged eye may overlap is discussed. Finally, we argue for a need to characterize all forms of clinical cupping into prelaminar and laminar components so as to add precision to the discussion of clinical cupping which does not currently exist. Such characterization may lead to the early detection of ONH axonal and connective tissue pathology in ocular hypertension and eventually aid in the assessment of etiology in all forms of optic neuropathy including those that may be purely age-related. The Susceptibility of the Aged Optic Nerve Head (ONH)A variety of data suggest that the ONH becomes more susceptible to progressive glaucomatous damage as it ages, though this concept remains unproven through direct experimentation, and may not be true for every aged eye. These data can be summarized as follows. First, in most [1][2][3][4][5] , but not all 6,7 , population based studies, intraocular pressure (IOP) either does not increase with age or if it does, the magnitude of increase is not likely to be clinically important. Thus, the fact that the prevalence of the neuropathy increases with age 8 is likely explained by a greater susceptibility to IOP and other non-IOP-related risk factors, rather than a higher prevalence of IOP elevation, with increasing age. Second, in an extensive review of the literature, we can find only a few reports of the onset and progression of normal tension glaucoma (NTG) in infants, children and young adults 9 . While we acknowledge that accurate NTG prevalence estimates require long-term telemetric characterization of untreated IOP and rigorous population based ONH and visual field examinations, all existing studies suggest that NTG is most commonly a disease of the elderly [10][11][12][13][14][15] in the young 9 . Third, age is an independent risk factor for both the prevalence 16 and progression of the neuropathy at all stages of damage [17][18][19] . The Clinical Behavior of the Aged ONHApart from the issue of ONH susceptibility, we predict that if all aspects of insult are equal (alterations in IOP, the volume flow of blood and nutrient transfer from the laminar capillary to the ONH astrocyte are all of the same magnitude, duration and fluctuation), the aged eye will demonstrate clinical cupping that is on average shallow and pale (at all stages of field loss) compared to the eye of a child or young adult. This clini...

show abstract

contrasting

confidence: 58%

Section: Onh Biomechanics and Onh Cuppingmentioning

confidence: 99%

Section: The Optic Nerve Head (Onh)mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Premise and Prediction???How Optic Nerve Head Biomechanics Underlies the Susceptibility and Clinical Behavior of the Aged Optic Nerve Head

Burgoyne¹,

Downs²

2008

Journal of Glaucoma

Self Cite

194

169

View full text Add to dashboard Cite

show abstract

“…6,[22][23][24][25][26] Previous studies have suggested that systemic and ocular factors, such as ageing, [27][28][29] chronically elevated IOP, [30][31][32] level of glaucomatous damage, 1,17,33 and disc size (scleral canal diameter), 34 could influence the susceptibility of an individual ONH to a given level of IOP. More recently, it has been suggested that other factors could be either directly or indirectly related to ONH response to pressure-induced damage, such as corneal parameters (both CCT and CH) 13,[35][36][37] and diabetes.…”

Section: Introductionmentioning

confidence: 99%

Factors associated with topographic changes of the optic nerve head induced by acute intraocular pressure reduction in glaucoma patients

Prata

Lima

Moraes

et al. 2010

Eye

View full text Add to dashboard Cite

Purpose To investigate factors associated with changes in optic nerve head (ONH) topography after acute intraocular pressure (IOP) reduction in patients with primary open-angle glaucoma (POAG). Methods Untreated POAG patients (IOP 421 mm Hg) were prospectively enrolled. Systemic and ocular information were collected, including central corneal thickness (CCT) and corneal hysteresis (CH). All patients underwent confocal scanning laser ophthalmoscopy and tonometry (Goldmann) before and 1 h after pharmacological IOP reduction. The mean of three measurements was considered for analysis. Changes in each ONH topographic parameter were assessed (one eye was randomly selected), and those that changed significantly were correlated with patient's systemic and ocular characteristics. Results A total of 42 patients were included (mean age, 66.7 ± 11.8 years). After a mean IOP reduction of 47.3±11.9%, significant changes were observed in cup area and volume, and in rim area and volume (Po0.01), but not in mean cup depth (P ¼ 0.80). Multiple regression analysis (controlling for baseline IOP and magnitude of IOP reduction) showed that CH (r 2 ¼ 0.17, Po0.01) and diabetes diagnosis (r 2 X0.21, Po0.01) were negatively correlated with the magnitude of changes in ONH parameters, whereas the cup-to-disc ratio was positively correlated (r 2 ¼ 0.30, Po0.01). Age, race, disc area, and CCT were not significant (PX0.12). Including all significant factors in a multivariable model, only the presence of diabetes remained significantly associated with all ONH parameters evaluated (Po0.01). Conclusions Different systemic and ocular factors, such as diabetes, CH, and the relative size of the cup, seem to be associated with the magnitude of changes in ONH topography after acute IOP reduction in POAG patients. These associations partially explain the ONH changes observed in these patients and suggest that other factors are possibly implicated in an individual susceptibility to IOP.

show abstract

In Vivo Evaluation of Focal Lamina Cribrosa Defects in Glaucoma

et al. 2012

View full text Add to dashboard Cite

show abstract

3-D Histomorphometry of the Normal and Early Glaucomatous Monkey Optic Nerve Head: Lamina Cribrosa and Peripapillary Scleral Position and Thickness

Cited by 235 publications

References 26 publications

Premise and Prediction???How Optic Nerve Head Biomechanics Underlies the Susceptibility and Clinical Behavior of the Aged Optic Nerve Head

Premise and Prediction???How Optic Nerve Head Biomechanics Underlies the Susceptibility and Clinical Behavior of the Aged Optic Nerve Head

Factors associated with topographic changes of the optic nerve head induced by acute intraocular pressure reduction in glaucoma patients

In Vivo Evaluation of Focal Lamina Cribrosa Defects in Glaucoma

Contact Info

Product

Resources

About