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Clinical Sciences |

Relationship Between Central Corneal Thickness and Changes of Optic Nerve Head Topography and Blood Flow After Intraocular Pressure Reduction in Open-angle Glaucoma and Ocular Hypertension FREE

Mark R. Lesk, MSc, MD; Ali S. Hafez, MD, PhD; Denise Descovich, MD
[+] Author Affiliations

Author Affiliations: Department of Ophthalmology, University of Montreal, and Ophthalmology Research Unit, Centre de Recherche Guy-Bernier, Maisonneuve-Rosemont Hospital, Montreal, Quebec.


Arch Ophthalmol. 2006;124(11):1568-1572. doi:10.1001/archopht.124.11.1568.
Text Size: A A A
Published online

Objectives  To investigate changes in optic nerve head topography and blood flow after therapeutic intraocular pressure reduction and to correlate them with central corneal thickness.

Methods  Sixteen patients with open-angle glaucoma and 16 patients with ocular hypertension underwent Heidelberg retina tomography and scanning laser Doppler flowmetry in 1 eye before and at least 2 months after a mean 35% sustained therapeutic reduction in intraocular pressure. Patients were assigned to a thin or thick group based on their median central corneal thickness.

Results  Compared with 16 patients with thick corneas (mean ± SD central corneal thickness, 587 ± 31 μm), the 16 patients with thin corneas (518 ± 32 μm) had greater reductions in mean (36 ± 32 vs 4 ± 36 μm, P = .003) and in maximum cup depth (73 ± 107 vs 4 ± 89 μm, P = .02). These changes were not statistically significantly different between the patients with open-angle glaucoma and those with ocular hypertension. Smaller mean ± SD improvements in neuroretinal rim blood flow were seen in patients with thinner corneas compared with those with thicker corneas (35 ± 80 vs 110 ± 111 arbitrary units, P = .04).

Conclusion  Patients with open-angle glaucoma and ocular hypertension with thinner corneas show significantly greater shallowing of the cup, a surrogate marker for lamina cribrosa displacement (compliance), and smaller improvements of neuroretinal rim blood flow after intraocular pressure reduction.

Figures in this Article

Altered lamina cribrosa compliance has long been postulated to have a role in the development of open-angle glaucoma (OAG). Lamina cribrosa mobility has been studied in ex vivo human16and monkey7,8eyes, in living human913and monkey14,15eyes, and in histological studies.1,8,1618Findings from some studies8,15,19suggest that there may be an initial hypercompliance in early glaucoma followed by reduced compliance (ie, increased rigidity) later in the course of the disease. In most patients with glaucoma, the central lamina cribrosa is covered by little or no neural or glial tissue. Therefore, lamina cribrosa compliance can be readily estimated using scanning confocal laser tomography by examining the position of the base of the cup relative to the retinal surface after intraocular pressure (IOP) changes.9,1113

Considerable evidence suggests that abnormal optic nerve blood flow has a role in the development of glaucomatous optic neuropathy.20Recent data indicate that optic nerve head neuroretinal rim blood flow improves significantly in patients with OAG after sustained therapeutic IOP reduction.21Among patients with ocular hypertension (OHT), such improvements were limited to vasospastic subjects.22The prognostic significance of these blood flow changes remains to be determined.

Findings suggest that the presence of a thin cornea is linked to the development of glaucoma among patients with OHT,23as well as to the severity of OHT24,25and OAG.26,27In OHT and OAG, a thin cornea is more strongly associated with disease severity than IOP.23,27Underestimated Goldmann tonometric pressures seem to only partly explain the relationship between thin corneas and increased glaucoma risk. The other mechanisms underlying this relationship are unknown. Corneal thickness has been linked to scleral thickness.2830In this study, we examined the relationship between central corneal thickness and lamina cribrosa compliance. Because the blood vessels that feed the optic nerve head run through the lamina cribrosa, we also examined changes in neuroretinal rim blood flow that occur with IOP-dependent lamina changes.

The study protocol was approved by the Ethics Committee of Maisonneuve-Rosemont Hospital, Montreal, Quebec, and all patients signed an informed consent form. Patients with OAG had gonioscopically confirmed open angles and manifested at least 2 of the following 3 criteria: characteristic nerve fiber bundle visual field defects, glaucomatous optic neuropathy, and a history of IOP greater than 21 mm Hg. Patients with OHT had a history of IOP greater than 24 mm Hg on at least 2 occasions, normal visual fields, and normal or suspect optic nerve head appearance based on slitlamp biomicroscopy. Subjects were excluded if any abnormal ocular findings were present other than pseudophakia, if significant media opacities precluded scanning laser Doppler flowmetry (SLDF) imaging, and if they were unable to comply with the study protocol.

Medical and ocular histories were recorded, and IOP, refractive errors, and best-corrected visual acuity were measured before the baseline study visit. A basic ophthalmologic examination, including biomicroscopy, ophthalmoscopy, and gonioscopy, was performed, and the visual field was assessed using automated perimetry (Humphrey Field Analyzer, program 24-2; Humphrey Instruments, San Leandro, Calif).

Thirty-two patients having clinical indications for IOP reduction were recruited from the hospital glaucoma clinics and underwent confocal scanning laser tomography with the Heidelberg retina tomograph (version 2.01; Heidelberg Engineering, Heidelberg, Germany) and SLDF of the optic nerve head with the Heidelberg retina flowmeter and SLDF software version 3.3 (Heidelberg Engineering)31before and at least 2 months after a minimum IOP reduction of 20%. For Heidelberg retina tomographic imaging, the mean topographies were derived from 3 high-quality images. The SLDF values for neuroretinal rim blood flow were derived from the mean of 5 high-quality images as described previously.21

As indicated clinically, IOP was reduced using topical hypotensive medications, argon laser trabeculoplasty, or filtration surgery. All patients were treated by one of us (M.R.L.). One eye was studied in each patient. If both eyes required therapy, the eye with the clearest media was chosen. We used the Heidelberg retina tomography stereometric variables of mean cup depth and maximum cup depth to estimate lamina cribrosa position in micrometers before and after IOP reduction. We used the SLDF variable of flow in all pixels overlying the neuroretinal rim to determine neuroretinal rim blood flow in arbitrary units before and after IOP reduction. Central corneal pachymetry was determined using an ultrasound pachymeter (DGH 500 Pachette; DGH Technology, Fraser, Pa) using the mean of the 3 closest of 5 consecutive measurements. Values are given as mean ± SD. Statistical evaluations were performed using Pearson product moment correlation test and t test. Statistical significance was set at P<.05. Analysis of covariance (ANCOVA) was used to control for covariables.

Patient characteristics are given in Table 1. There were 16 patients with OAG and 16 patients with OHT. Patients were assigned to the thin group or to the thick group based on their median central corneal thickness (CCT). To keep the groups balanced with respect to diagnosis, the 8 patients with OAG with the thinnest corneas were grouped with the 8 patients with OHT with the thinnest corneas to form the thin group. Clinical variables other than CCT did not differ significantly between the thin (n = 16) and thick (n = 16) groups.

Table Graphic Jump LocationTable 1. Characteristics of Patients With Open-angle Glaucoma and Ocular Hypertension*

The optic nerve head stereometric variable of mean cup depth was reduced by a mean value of 36 ± 32 μm in the thin CCT group and by 4 ± 36 μm in the thick CCT group, a difference that was statistically significant (P = .003, ANCOVA controlling for percentage IOP reduction) (Table 2 and Figure 1). The maximum cup depth was reduced by 73 ± 107 μm in the thin CCT group and by 4 ± 89 μm in the thick CCT group, a difference that was statistically significant (P = .02, ANCOVA). The relationship between corneal thickness and shallowing of the cup was present in the OAG and OHT groups and was not significantly different between the groups (P = .29 and P = .18 for mean and maximum cup depths, respectively, ANCOVA) (Table 3).

Place holder to copy figure label and caption
Figure 1.

Change in topography.

Graphic Jump Location
Table Graphic Jump LocationTable 2. Change in Topography After Sustained Intraocular Pressure (IOP) Reduction Among Combined Patients With Open-angle Glaucoma and Ocular Hypertension*
Table Graphic Jump LocationTable 3. Change in Topography After Sustained Intraocular Pressure Reduction Among Patients With Open-angle Glaucoma (OAG) vs Ocular Hypertension (OHT)*

We also looked for significant changes of cup depth in individual eyes. The standard deviation of cup depth for the 3 images performed at each of 2 sessions (before and after IOP reduction) was calculated. Then, the number of eyes in which the cup depth changed by more than 4 SDs for that eye was calculated. One eye for which we were unable to locate the original images was excluded from this analysis. For mean cup depth, 8 of 15 eyes showed significant shallowing in the thin CCT group, while 3 of 16 eyes showed significant shallowing in the thick CCT group, a difference that was significant by χ2 analysis (P = .04). The same analysis for maximum cup depth yielded 4 of 15 eyes showing at least 4-SD shallowing in the thin CCT group compared with 1 of 16 eyes in the thick CCT group, a difference that was not significant (P = .1). We further confirmed the difference in topographical changes by performing the Mann-Whitney rank order test for changes of mean and maximum cup depth. This test confirmed that, compared with the thick CCT group, the thin CCT group had significantly greater reductions in mean cup depth (P = .02), while the greater reduction in maximum cup depth in the thin CCT group did not reach statistical significance (P = .13).

Smaller improvements in neuroretinal rim blood flow were seen in patients with OAG and OHT with thinner corneas compared with those with thicker corneas. This difference was statistically significant in the patients with OAG and OHT and remained significant after controlling for percentage IOP reduction (P = .04, ANCOVA). This difference was significant in the OAG group but not in the OHT group (Table 4 and Figure 2). We also looked for significant changes of rim flow in individual eyes. The standard deviation of rim flow for the 5 images performed at each of 2 sessions was calculated. Then, the number of eyes in which the rim flow changed by more than 4 SDs for that eye was calculated. Seven of 16 eyes showed significant increases in rim flow in the thick CCT group, while 2 of 16 eyes showed such increases in the thin CCT group, a difference that was significant by χ2 analysis at P = .05. Using a cutoff of 3 SDs gave a more significant χ2 result of P = .01 (9 of 16 in the thick CCT group vs 2 of 16 in the thin CCT group).

Place holder to copy figure label and caption
Figure 2.

Change in neuroretinal rim blood flow. AU indicates arbitrary units; OAG, open-angle glaucoma; and OHT, ocular hypertension.

Graphic Jump Location
Table Graphic Jump LocationTable 4. Change in Neuroretinal Rim Blood Flow After Sustained Intraocular Pressure Reduction*

The results of this preliminary study suggest that patients with OHT and OAG with thin central corneas have greater forward displacement of the base of the cup, a surrogate marker for lamina cribrosa position, following IOP reduction than their cohorts with thicker central corneas. Patients with thin central corneas also seem to have smaller improvements in neuroretinal rim blood flow after IOP reduction than patients with thicker central corneas.

A thin central cornea is emerging as a major risk factor for severity of OHT and OAG.2327Diurnal and long-term IOP fluctuations are also a major risk factor for progression in OAG.3234These results suggest that a thin central cornea may be a marker for physiological differences in the biomechanical properties of the lamina cribrosa. In other words, it may be that a thin central cornea is connected to a thin sclera, which, in turn, is connected to a thin lamina. Assuming identical material properties, a thin lamina should demonstrate greater compliance (less rigidity) than a thick lamina. A thin lamina should then manifest greater displacement in response to diurnal or therapeutic IOP fluctuations. Greater laminar displacement could lead to increased damage to adjacent axons by different mechanisms.35

Larger increases in rim blood flow after IOP reduction were observed in the thick CCT group. Because patients with thick central corneas may have a reduced risk of progressing or of reaching an advanced state of glaucoma,2327this finding suggests that improved blood flow in response to therapy may be a good prognostic sign in glaucoma. In patients with thin central corneas, it is conceivable that the vasculature has become more damaged due to repetitive movements of the more compliant lamina. In these patients, the vasculature may be less able to respond to IOP reduction with a beneficial increase in blood flow. Smaller increases in optic nerve head blood flow may also be present on IOP reduction because the microvasculature passing through the lamina cribrosa may become compressed by the large forward displacement of the laminar sheets. Laminar sheet compression is common in glaucoma.16These data suggest an interrelationship between the mechanical and vascular properties of the optic nerve head.

However, our data on neuroretinal rim blood flow may, in fact, be misleading. In the eyes with more compliant laminas, it is possible that laminar (as opposed to neuroretinal rim) blood flow after IOP reduction was greatly increased. This increase in laminar blood flow (not measured by our method) may have manifested as a less impressive increase in neuroretinal rim blood flow because of shunting. Future research should examine lamina cribrosa blood flow and neuroretinal rim blood flow.

A review of the literature suggests that, after an initial hypercompliant phase, the lamina cribrosa becomes more rigid in glaucoma.19,14,15,35,36One interpretation of these findings is that increased laminar rigidity contributes to axonal loss. Another interpretation is that increased laminar rigidity follows axonal loss. Findings from the present study suggest that patients with thick central corneas have a more rigid lamina cribrosa. Because other studies2327have demonstrated a lower risk of progression in patients with thick central corneas, increased laminar rigidity may be a biological response that is protective to axons in this disease. Although the mechanisms of this protection remain unknown, the results of our study suggest that improved blood flow to the neuroretinal rim after IOP reduction may be involved in this protective effect.

Our findings also suggest a potential method for determining the risk level for an individual patient with glaucoma. Patients with high lamina cribrosa mobility or poor vascular response to IOP reduction may be at greater risk of progressive disease and may be targeted for more aggressive or alternate therapies. Although the results presented herein are preliminary and the mechanistic links are speculative, they serve as a conceptual framework for more detailed future studies.

Correspondence: Mark R. Lesk, MSc, MD, Ophthalmology Research Unit, Centre de Recherche Guy-Bernier, Maisonneuve-Rosemont Hospital, 5415 Boulevard Assomption, Montreal, Quebec, Canada H1T 2M4 (lesk@videotron.ca).

Submitted for Publication: February 9, 2005; final revision received May 31, 2006; accepted June 5, 2006.

Financial Disclosure: None reported.

Funding/Support: This study was supported by Fonds de Recherché en Santé Quebec, by E. A. Baker Foundation of the Canadian National Institute for the Blind, by Fonds de Recherché en Ophtalmologie de l’Université de Montreal, and by unrestricted funds from Merck-Frosst Canada, Alcon Canada, and Allergan Canada (all to Dr Lesk). Dr Lesk is a Fonds de Recherché en Santé Quebec research scholar.

Previous Presentation: This study was presented at the Association for Research in Vision and Ophthalmology annual meeting; April 28, 2004; Fort Lauderdale, Fla.

Acknowledgment: We thank Miguel Chagnon, MSc, for his statistical analysis.

Yan  DBColoma  FMMetheetrairut  ATrope  GEHeathcote  JGEthier  CR Deformation of the lamina cribrosa by elevated intraocular pressure. Br J Ophthalmol 1994;78643- 648
PubMed Link to Article
Yan  DBFlanagan  JGFarra  T Study of regional deformation of the optic nerve head using scanning laser tomography. Curr Eye Res 1998;17903- 916
PubMed Link to Article
Albon  JPurslow  PPKarwatowski  WSEasty  DL Age related compliance of the lamina cribrosa in human eyes. Br J Ophthalmol 2000;84318- 323
PubMed Link to Article
Levy  NSCrapps  EE Displacement of optic nerve head in response to short-term intraocular pressure elevation in human eyes. Arch Ophthalmol 1984;102782- 786
PubMed Link to Article
Zeimer  RCOgura  Y The relationship between glaucomatous damage and optic nerve head mechanical compliance. Arch Ophthalmol 1989;1071232- 1234
PubMed Link to Article
Zeimer  R Biomechanical properties of the optic nerve head. In:Drance  SMed.Optic Nerve in Glaucoma. Amsterdam, the Netherlands Kugler Publications1995;107- 121
Levy  NSCrapps  EEBonney  RC Displacement of the optic nerve head: response to acute intraocular pressure elevation in primate eyes. Arch Ophthalmol 1981;992166- 2174
PubMed Link to Article
Bellezza  AJRintalan  CJThompson  HW Deformation of the lamina cribrosa and anterior scleral canal wall in early experimental glaucoma. Invest Ophthalmol Vis Sci 2003;44623- 637
PubMed Link to Article
Azuara-Blanco  AHarris  ACantor  LB  et al.  Effects of short term increase of intraocular pressure on optic disc cupping. Br J Ophthalmol 1998;82880- 883
PubMed Link to Article
Bowd  CWeinreb  RNLee  BEmdadi  AZangwill  LM Optic disk topography after medical treatment to reduce intraocular pressure. Am J Ophthalmol 2000;130280- 286
PubMed Link to Article
Irak  IZangwill  LMGarden  V  et al.  Change in optic disk topography after trabeculectomy. Am J Ophthalmol 1996;122690- 695
PubMed
Lesk  MRSpaeth  GLAzuara-Blanco  A  et al.  Reversal of optic disc cupping after glaucoma surgery analyzed with a scanning laser tomograph. Ophthalmology 1999;1061013- 1018
PubMed Link to Article
Raitta  CTomita  GVesti  E  et al.  Optic disc topography before and after trabeculectomy in advanced glaucoma. Ophthalmic Surg Lasers 1996;27349- 354
PubMed
Burgoyne  CFQuigley  HAThompson  HW  et al.  Early changes in optic disc compliance and surface position in experimental glaucoma. Ophthalmology 1995;1021800- 1809
PubMed Link to Article
Heickell  AGBellezza  AJThompson  HWBurgoyne  CF Optic disc surface compliance testing using confocal scanning laser tomography in the normal monkey eye. J Glaucoma 2001;10369- 382
PubMed Link to Article
Quigley  HAHohmann  RMAddicks  EM  et al.  Morphological changes in the lamina cribrosa correlated with neural loss in open-angle glaucoma. Am J Ophthalmol 1983;95673- 691
PubMed
Quigley  HAAddicks  EM Regional differences in the structure of the lamina cribrosa and their relation to glaucomatous optic nerve damage. Arch Ophthalmol 1981;99137- 143
PubMed Link to Article
Jonas  JBBerenshtein  EHolbach  L Anatomic relationship between lamina cribrosa, intraocular space, and cerebrospinal fluid space. Invest Ophthalmol Vis Sci 2003;445189- 5195
PubMed Link to Article
Varma  RMinckler  DS Anatomy and pathophysiology of the retinal optic nerve. In:Ritch  RShields  MBKrupin  Teds.The Glaucomas. St Louis, Mo Mosby–Yearbook1996- 168
Flammer  JOrgul  SCosta  VP  et al.  The impact of ocular blood flow in glaucoma. Prog Retin Eye Res 2002;21359- 393
PubMed Link to Article
Hafez  ASBizzaro  RLGRivard  MLesk  MR Changes in optic nerve head blood flow after therapeutic intraocular pressure reduction in glaucoma patients and ocular hypertensives. Ophthalmology 2003;110201- 210
PubMed Link to Article
Hafez  ASBizzaro  RLGDescovich  DLesk  MR Correlation between finger blood flow and changes in optic nerve blood flow following therapeutic intraocular pressure reduction. J Glaucoma 2005;14448- 454
PubMed Link to Article
Gordon  MOBeiser  JABrandt  JD  et al.  The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol 2002;120714- 720
PubMed Link to Article
Medeiros  FASample  PAWeinreb  RN Corneal thickness measurements and frequency doubling technology perimetry abnormalities in ocular hypertensive eyes. Ophthalmology 2003;1101903- 1908
PubMed Link to Article
Medeiros  FASample  PAWeinreb  RN Corneal thickness measurements and visual function abnormalities in ocular hypertensive patients. Am J Ophthalmol 2003;135131- 137
PubMed Link to Article
Medeiros  FASample  PAZangwill  LM  et al.  Corneal thickness as a risk factor for visual field loss in patients with preperimetric glaucomatous optic neuropathy. Am J Ophthalmol 2003;136805- 813
PubMed Link to Article
Herndon  LWWeizer  JSStinnett  SS Central corneal thickness as a risk factor for advanced glaucoma damage. Arch Ophthalmol 2004;12217- 21
PubMed Link to Article
Albekioni  ZJoson  PTello  CLiebmann  JMRitch  R Correlation between central corneal thickness and scleral thickness [ARVO abstract]. Invest Ophthalmol Vis Sci 2003;44e-abstract103
PubMed
Oliviera  CTello  CRitch  RLiebmann  JM Correlation between central corneal thickness, scleral thickness, and refractive error. [ARVO abstract]. Invest Ophthalmol Vis Sci 2004;44e-abstract- 963
Rolle  TLo Presti Constantino  LMorgese  A  et al.  Structural glaucomatous damage and ocular biometric parameters [ARVO abstract]. Invest Ophthalmol Vis Sci 2004;45e-abstract- 3335
Michelson  GWelzenbach  JPal  IHarazny  J Functional imaging of the retinal microvasculature by scanning laser Doppler flowmetry. Int Ophthalmol 2001;23327- 335
PubMed Link to Article
Asrani  SZeimer  RWilensky  JGieser  DVitale  SLindenmuth  K Large diurnal fluctuations in intraocular pressure are an independent risk factor in patients with glaucoma. J Glaucoma 2000;9134- 142
PubMed Link to Article
Werner  EBDrance  SMSchulzer  M Trabeculectomy and the progression of glaucomatous visual field loss. Arch Ophthalmol 1977;951374- 1377
PubMed Link to Article
Nouri-Mahdavi  KHoffman  DColeman  AL  et al.  Predictive factors for glaucomatous visual field progression in the Advanced Glaucoma Intervention Study. Ophthalmology 2004;1111627- 1635
PubMed Link to Article
Burgoyne  CFMorrison  JC The anatomy and pathophysiology of the optic nerve head in glaucoma. J Glaucoma 2001;10 ((suppl 1)) S16- S18
PubMed Link to Article
Quigley  HA Overview and introduction to session on connective tissue of the optic nerve in glaucoma. In:Drance  SMed.Optic Nerve in Glaucoma. Amsterdam, the Netherlands Kugler Publications1995;15- 36

Figures

Place holder to copy figure label and caption
Figure 1.

Change in topography.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.

Change in neuroretinal rim blood flow. AU indicates arbitrary units; OAG, open-angle glaucoma; and OHT, ocular hypertension.

Graphic Jump Location

Tables

Table Graphic Jump LocationTable 1. Characteristics of Patients With Open-angle Glaucoma and Ocular Hypertension*
Table Graphic Jump LocationTable 2. Change in Topography After Sustained Intraocular Pressure (IOP) Reduction Among Combined Patients With Open-angle Glaucoma and Ocular Hypertension*
Table Graphic Jump LocationTable 3. Change in Topography After Sustained Intraocular Pressure Reduction Among Patients With Open-angle Glaucoma (OAG) vs Ocular Hypertension (OHT)*
Table Graphic Jump LocationTable 4. Change in Neuroretinal Rim Blood Flow After Sustained Intraocular Pressure Reduction*

References

Yan  DBColoma  FMMetheetrairut  ATrope  GEHeathcote  JGEthier  CR Deformation of the lamina cribrosa by elevated intraocular pressure. Br J Ophthalmol 1994;78643- 648
PubMed Link to Article
Yan  DBFlanagan  JGFarra  T Study of regional deformation of the optic nerve head using scanning laser tomography. Curr Eye Res 1998;17903- 916
PubMed Link to Article
Albon  JPurslow  PPKarwatowski  WSEasty  DL Age related compliance of the lamina cribrosa in human eyes. Br J Ophthalmol 2000;84318- 323
PubMed Link to Article
Levy  NSCrapps  EE Displacement of optic nerve head in response to short-term intraocular pressure elevation in human eyes. Arch Ophthalmol 1984;102782- 786
PubMed Link to Article
Zeimer  RCOgura  Y The relationship between glaucomatous damage and optic nerve head mechanical compliance. Arch Ophthalmol 1989;1071232- 1234
PubMed Link to Article
Zeimer  R Biomechanical properties of the optic nerve head. In:Drance  SMed.Optic Nerve in Glaucoma. Amsterdam, the Netherlands Kugler Publications1995;107- 121
Levy  NSCrapps  EEBonney  RC Displacement of the optic nerve head: response to acute intraocular pressure elevation in primate eyes. Arch Ophthalmol 1981;992166- 2174
PubMed Link to Article
Bellezza  AJRintalan  CJThompson  HW Deformation of the lamina cribrosa and anterior scleral canal wall in early experimental glaucoma. Invest Ophthalmol Vis Sci 2003;44623- 637
PubMed Link to Article
Azuara-Blanco  AHarris  ACantor  LB  et al.  Effects of short term increase of intraocular pressure on optic disc cupping. Br J Ophthalmol 1998;82880- 883
PubMed Link to Article
Bowd  CWeinreb  RNLee  BEmdadi  AZangwill  LM Optic disk topography after medical treatment to reduce intraocular pressure. Am J Ophthalmol 2000;130280- 286
PubMed Link to Article
Irak  IZangwill  LMGarden  V  et al.  Change in optic disk topography after trabeculectomy. Am J Ophthalmol 1996;122690- 695
PubMed
Lesk  MRSpaeth  GLAzuara-Blanco  A  et al.  Reversal of optic disc cupping after glaucoma surgery analyzed with a scanning laser tomograph. Ophthalmology 1999;1061013- 1018
PubMed Link to Article
Raitta  CTomita  GVesti  E  et al.  Optic disc topography before and after trabeculectomy in advanced glaucoma. Ophthalmic Surg Lasers 1996;27349- 354
PubMed
Burgoyne  CFQuigley  HAThompson  HW  et al.  Early changes in optic disc compliance and surface position in experimental glaucoma. Ophthalmology 1995;1021800- 1809
PubMed Link to Article
Heickell  AGBellezza  AJThompson  HWBurgoyne  CF Optic disc surface compliance testing using confocal scanning laser tomography in the normal monkey eye. J Glaucoma 2001;10369- 382
PubMed Link to Article
Quigley  HAHohmann  RMAddicks  EM  et al.  Morphological changes in the lamina cribrosa correlated with neural loss in open-angle glaucoma. Am J Ophthalmol 1983;95673- 691
PubMed
Quigley  HAAddicks  EM Regional differences in the structure of the lamina cribrosa and their relation to glaucomatous optic nerve damage. Arch Ophthalmol 1981;99137- 143
PubMed Link to Article
Jonas  JBBerenshtein  EHolbach  L Anatomic relationship between lamina cribrosa, intraocular space, and cerebrospinal fluid space. Invest Ophthalmol Vis Sci 2003;445189- 5195
PubMed Link to Article
Varma  RMinckler  DS Anatomy and pathophysiology of the retinal optic nerve. In:Ritch  RShields  MBKrupin  Teds.The Glaucomas. St Louis, Mo Mosby–Yearbook1996- 168
Flammer  JOrgul  SCosta  VP  et al.  The impact of ocular blood flow in glaucoma. Prog Retin Eye Res 2002;21359- 393
PubMed Link to Article
Hafez  ASBizzaro  RLGRivard  MLesk  MR Changes in optic nerve head blood flow after therapeutic intraocular pressure reduction in glaucoma patients and ocular hypertensives. Ophthalmology 2003;110201- 210
PubMed Link to Article
Hafez  ASBizzaro  RLGDescovich  DLesk  MR Correlation between finger blood flow and changes in optic nerve blood flow following therapeutic intraocular pressure reduction. J Glaucoma 2005;14448- 454
PubMed Link to Article
Gordon  MOBeiser  JABrandt  JD  et al.  The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol 2002;120714- 720
PubMed Link to Article
Medeiros  FASample  PAWeinreb  RN Corneal thickness measurements and frequency doubling technology perimetry abnormalities in ocular hypertensive eyes. Ophthalmology 2003;1101903- 1908
PubMed Link to Article
Medeiros  FASample  PAWeinreb  RN Corneal thickness measurements and visual function abnormalities in ocular hypertensive patients. Am J Ophthalmol 2003;135131- 137
PubMed Link to Article
Medeiros  FASample  PAZangwill  LM  et al.  Corneal thickness as a risk factor for visual field loss in patients with preperimetric glaucomatous optic neuropathy. Am J Ophthalmol 2003;136805- 813
PubMed Link to Article
Herndon  LWWeizer  JSStinnett  SS Central corneal thickness as a risk factor for advanced glaucoma damage. Arch Ophthalmol 2004;12217- 21
PubMed Link to Article
Albekioni  ZJoson  PTello  CLiebmann  JMRitch  R Correlation between central corneal thickness and scleral thickness [ARVO abstract]. Invest Ophthalmol Vis Sci 2003;44e-abstract103
PubMed
Oliviera  CTello  CRitch  RLiebmann  JM Correlation between central corneal thickness, scleral thickness, and refractive error. [ARVO abstract]. Invest Ophthalmol Vis Sci 2004;44e-abstract- 963
Rolle  TLo Presti Constantino  LMorgese  A  et al.  Structural glaucomatous damage and ocular biometric parameters [ARVO abstract]. Invest Ophthalmol Vis Sci 2004;45e-abstract- 3335
Michelson  GWelzenbach  JPal  IHarazny  J Functional imaging of the retinal microvasculature by scanning laser Doppler flowmetry. Int Ophthalmol 2001;23327- 335
PubMed Link to Article
Asrani  SZeimer  RWilensky  JGieser  DVitale  SLindenmuth  K Large diurnal fluctuations in intraocular pressure are an independent risk factor in patients with glaucoma. J Glaucoma 2000;9134- 142
PubMed Link to Article
Werner  EBDrance  SMSchulzer  M Trabeculectomy and the progression of glaucomatous visual field loss. Arch Ophthalmol 1977;951374- 1377
PubMed Link to Article
Nouri-Mahdavi  KHoffman  DColeman  AL  et al.  Predictive factors for glaucomatous visual field progression in the Advanced Glaucoma Intervention Study. Ophthalmology 2004;1111627- 1635
PubMed Link to Article
Burgoyne  CFMorrison  JC The anatomy and pathophysiology of the optic nerve head in glaucoma. J Glaucoma 2001;10 ((suppl 1)) S16- S18
PubMed Link to Article
Quigley  HA Overview and introduction to session on connective tissue of the optic nerve in glaucoma. In:Drance  SMed.Optic Nerve in Glaucoma. Amsterdam, the Netherlands Kugler Publications1995;15- 36

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