- •PROGRESS IN BRAIN RESEARCH
- •List of Contributors
- •Preface
- •Epidemiology of primary glaucoma: prevalence, incidence, and blinding effects
- •Introduction
- •Prevalence of glaucoma
- •PAC suspect
- •PACG
- •Incidence of glaucoma
- •Blinding effects of glaucoma
- •Abbreviations
- •Acknowledgment
- •References
- •Predictive models to estimate the risk of glaucoma development and progression
- •Risk assessment in ocular hypertension and glaucoma
- •Risk factors for glaucoma development
- •Intraocular pressure
- •Corneal thickness
- •Cup/disc ratio and pattern standard deviation
- •The need for predictive models
- •Predictive models for glaucoma development
- •Predictive models for glaucoma progression
- •Limitations of predictive models
- •References
- •Intraocular pressure and central corneal thickness
- •Main text
- •References
- •Angle-closure: risk factors, diagnosis and treatment
- •Introduction
- •Mechanism
- •Other causes of angle closure
- •Risk factors
- •Age and gender
- •Ethnicity
- •Ocular biometry
- •Genetics
- •Diagnosis
- •Acute primary angle closure
- •Angle assessment in angle closure
- •Gonioscopy technique
- •Ultrasound biomicroscopy (UBM)
- •Scanning peripheral anterior chamber depth analyzer (SPAC)
- •Management
- •Acute primary angle closure
- •Medical therapy
- •Argon laser peripheral iridoplasty (ALPI)
- •Laser peripheral iridotomy (PI)
- •Lens extraction
- •Monitoring for subsequent IOP rise in eyes with APAC
- •Fellow eye of APAC
- •Chronic primary angle-closure glaucoma (CACG)
- •Laser peripheral iridotomy
- •Laser iridoplasty
- •Medical therapy
- •Trabeculectomy
- •Lens extraction
- •Combined lens extraction and trabeculectomy surgery
- •Goniosynechialysis
- •Summary
- •List of abbreviations
- •References
- •Early diagnosis in glaucoma
- •Introduction
- •History and examination
- •Quantitative tests and the diagnostic process
- •Pretest probability
- •Test validity
- •Diagnostic test performance
- •Posttest probability
- •Combing test results
- •Selective tests of visual function
- •Early glaucoma diagnosis from quantitative test results
- •Progression to make a diagnosis
- •Conclusions
- •Abbreviations
- •References
- •Monitoring glaucoma progression
- •Introduction
- •Monitoring structural damage progression
- •Monitoring functional damage progression
- •Abbreviations
- •References
- •Standard automated perimetry and algorithms for monitoring glaucoma progression
- •Standard automated perimetry
- •Global indices
- •HFA: MD, SF, PSD, CPSD
- •Octopus indices: MD, SF, CLV
- •OCTOPUS seven-in-one report (Fig. 2)
- •SAP VF assessment: full-threshold strategy
- •SAP VF defects assessment: OHTS criteria
- •SAP VF defects assessment: AGIS criteria
- •SAP VF defects assessment: CIGTS
- •Fastpac
- •Swedish interactive threshold algorithm
- •SAP VF assessment: the glaucoma staging system
- •SAP: interocular asymmetries in OHTS
- •SAP, VF progression
- •SAP: the relationship to other functional and structural diagnostic tests in glaucoma
- •SAP, FDP-Matrix
- •SAP, SWAP, HPRP, FDT
- •SAP: the relationship between function and structure
- •SAP, confocal scanning laser ophthalmoscopy, SLP-VCC
- •SAP, optical coherence tomography
- •SAP and functional magnetic resonance imaging
- •References
- •Introduction
- •Retinal ganglion cells: anatomy and function
- •Is glaucoma damage selective for any subgroup of RGCs?
- •Segregation
- •Isolation
- •FDT: rationale and perimetric techniques
- •SWAP: rationale and perimetric techniques
- •FDT: clinical data
- •SWAP: clinical data
- •Clinical data comparing FDT and SWAP
- •Conclusions
- •References
- •Scanning laser polarimetry and confocal scanning laser ophthalmoscopy: technical notes on their use in glaucoma
- •The GDx scanning laser polarimeter
- •Serial analysis
- •Limits
- •The Heidelberg retinal tomograph
- •Limits
- •Conclusions
- •References
- •The role of OCT in glaucoma management
- •Introduction
- •How OCT works
- •How OCT is performed
- •Evaluation of RNFL thickness
- •Evaluation of optic disc
- •OCT in glaucoma management
- •New perspective
- •Abbreviations
- •References
- •Introduction
- •Technology
- •Visual stimulation
- •Reproducibility and habituation of RFonh
- •Retinal neural activity as assessed from the electroretinogram (ERG)
- •The Parvo (P)- and Magno (M)-cellular pathways
- •Physiology
- •Magnitude and time course of RFonh in humans
- •Varying the parameters of the stimulus on RFonh
- •Luminance versus chromatic modulation
- •Frequency
- •Effect of pattern stimulation
- •Neurovascular coupling in humans
- •Clinical application
- •RFonh in OHT and glaucoma patients
- •Discussion
- •FLDF and neurovascular coupling in humans
- •Comments on clinical application of FLDF in glaucoma
- •Conclusions and futures directions
- •Acknowledgements
- •References
- •Advances in neuroimaging of the visual pathways and their use in glaucoma
- •Introduction
- •Conventional MR imaging and the visual pathways
- •Diffusion MR imaging
- •Functional MR imaging
- •Proton MR spectroscopy
- •References
- •Primary open angle glaucoma: an overview on medical therapy
- •Introduction
- •When to treat
- •Whom to treat
- •Genetics
- •Race
- •Ocular and systemic abnormalities
- •Tonometry and pachymetry
- •How to treat
- •Beta-blockers
- •Prostaglandins
- •Alpha-agonists
- •Carbonic anhydrase inhibitors (CAIs)
- •Myotics
- •Fixed combinations
- •References
- •The treatment of normal-tension glaucoma
- •Introduction
- •Epidemiology
- •Clinical features
- •Optic disk
- •Central corneal thickness
- •Disease course
- •Risk factors
- •Intraocular pressure
- •Local vascular factors
- •Immune mechanisms
- •Differential diagnosis
- •Diagnostic evaluation
- •Therapy
- •IOP reduction
- •Systemic medications
- •Neuroprotection
- •Noncompliance
- •Genetics of NTG
- •Abbreviations
- •References
- •The management of exfoliative glaucoma
- •Introduction
- •Epidemiology
- •Ocular and systemic associations
- •Ocular associations
- •Systemic associations
- •Pathogenesis of exfoliation syndrome
- •Mechanisms of glaucoma development
- •Management
- •Medical therapy
- •Laser surgery
- •Operative surgery
- •Future treatment of exfoliation syndrome and exfoliative glaucoma
- •Treatment directed at exfoliation material
- •References
- •Laser therapies for glaucoma: new frontiers
- •Background
- •Laser iridotomy
- •Indications
- •Contraindications
- •Patient preparation
- •Technique
- •Nd:YAG laser iridectomy
- •Argon laser iridectomy
- •Complications
- •LASER trabeculoplasty
- •Treatment technique
- •Mechanism of action
- •Indications for treatment
- •Contraindications to treatment
- •Patient preparation and postoperative follow-up
- •Complications of the treatment
- •Selective laser trabeculoplasty
- •Results
- •LASER iridoplasty
- •Indications
- •Contraindications
- •Treatment technique
- •Complications
- •LASER cyclophotocoagulation
- •Introduction
- •Indications and contraindications
- •Patient preparation
- •Transpupillary cyclophotocoagulation
- •Endoscopic cyclophotocoagulation
- •Transscleral cyclophotocoagulation
- •Transscleral noncontact cyclophotocoagulation
- •Transscleral contact cyclophotocoagulation
- •Complications
- •Excimer laser trabeculotomy
- •References
- •Modulation of wound healing during and after glaucoma surgery
- •The process of wound healing
- •Using surgical and anatomical principles to modify therapy
- •Growth factors
- •Cellular proliferation and vascularization
- •Cell motility, matrix contraction and synthesis
- •Drug delivery
- •Future directions: total scarring control and tissue regeneration
- •Acknowledgments
- •References
- •Surgical alternative to trabeculectomy
- •Introduction
- •Deep sclerectomy
- •Viscocanalostomy
- •Conclusions
- •References
- •Modern aqueous shunt implantation: future challenges
- •Background
- •Current shunts and factors affecting their function
- •Shunt-related factors
- •Surface area
- •Plate material
- •Valved versus non-valved
- •Commercially available devices
- •Comparative studies
- •Patient and ocular factors
- •Severity of glaucoma damage
- •Tolerance of topical ocular hypotensive medications
- •Aqueous hyposecretion
- •Previous ocular surgery
- •Scleral thinning
- •Patient cooperation for and tolerance of potential slit-lamp interventions
- •Future challenges
- •Predictability
- •Cataract formation
- •The long-term effect on the cornea
- •References
- •Model systems for experimental studies: retinal ganglion cells in culture
- •Mixed RGCs in culture
- •Retinal explants
- •Glial cultures
- •RGC-5 cells
- •Differentiation of RGC-5 cells
- •RGC-5 cell neurites
- •Advantages and disadvantages of culture models
- •References
- •Rat models for glaucoma research
- •Rat models for glaucoma research
- •Use of animal models for POAG
- •Suitability of the rat for models of optic nerve damage in POAG
- •Methods for measuring IOP in rats
- •General considerations for measuring IOP in rats
- •Assessing optic nerve and retina damage
- •Experimental methods of producing elevated IOP
- •Laser treatment of limbal tissues
- •Episcleral vein cautery
- •Conclusions
- •Abbreviations
- •Acknowledgements
- •References
- •Mouse genetic models: an ideal system for understanding glaucomatous neurodegeneration and neuroprotection
- •Introduction
- •The mouse as a model system
- •Mice are suitable models for studying IOP elevation in glaucoma
- •Tools for glaucoma research
- •Accurate IOP measurements are fundamental to the study of glaucoma
- •The future of IOP assessment
- •Assessment of RGC function
- •Mouse models of glaucoma
- •Primary open-angle glaucoma
- •MYOC
- •OPTN
- •Strategies for developing new models of POAG
- •Developmental glaucoma
- •Pigmentary glaucoma
- •Experimentally induced models of glaucoma
- •Mouse models to characterize processes involved in glaucomatous neurodegeneration
- •Similar patterns of glaucomatous damage occur in humans and mice
- •The lamina cribrosa is an important site of early glaucomatous damage
- •An insult occurs to the axons of RGCs within the lamina in glaucoma
- •What is the nature of the insult at the lamina?
- •Other changes occur in the retina in glaucoma
- •PERG and complement
- •Using mouse models to develop neuroprotective strategies
- •Somal protection
- •Axonal protection
- •Erythropoietin administration
- •Radiation-based treatment
- •References
- •Clinical trials in neuroprotection
- •Introduction
- •Methods of clinical studies
- •Issues in the design and conduct of clinical trials
- •Clinical trials of neuroprotection
- •Clinical trials of neuroprotection in ophthalmology
- •Endpoints
- •Neuroprotection and glaucoma
- •Conclusions
- •Abbreviations
- •References
- •Pathogenesis of ganglion ‘‘cell death’’ in glaucoma and neuroprotection: focus on ganglion cell axonal mitochondria
- •Introduction
- •Retinal ganglion cells and mitochondria
- •Possible causes for ganglion cell death in glaucoma
- •Mitochondrial functions and apoptosis
- •Mitochondrial function enhancement and the attenuation of ganglion cell death
- •Creatine
- •Nicotinamide
- •Epigallocatechin gallate
- •Conclusion
- •References
- •Astrocytes in glaucomatous optic neuropathy
- •Introduction
- •Quiescent astrocytes
- •Reactive astrocytes in glaucoma
- •Signal transduction in glaucomatous astrocytes
- •Protein tyrosine kinases (PTKs)
- •Serine/threonine protein mitogen-activated kinases (MAPKs)
- •G protein-coupled receptors
- •Ras superfamily of small G proteins
- •Astrocyte migration in the glaucomatous optic nerve head
- •Cell adhesion of ONH astrocytes
- •Connective tissue changes in the glaucomatous optic nerve head
- •Extracellular matrix synthesis by ONH astrocytes
- •Extracellular matrix degradation by reactive astrocytes
- •Oxidative stress in ONH astrocytes
- •Conclusions
- •Acknowledgments
- •References
- •Glaucoma as a neuropathy amenable to neuroprotection and immune manipulation
- •Glaucoma as a neurodegenerative disease
- •Oxidative stress and free radicals
- •Excessive glutamate, increased calcium levels, and excitotoxicity
- •Deprivation of neurotrophins and growth factors
- •Abnormal accumulation of proteins
- •Pharmacological neuroprotection for glaucoma
- •Protection of the retinal ganglion cells involves the immune system
- •Searching for an antigen for potential glaucoma therapy
- •Concluding remarks
- •References
- •Oxidative stress and glaucoma: injury in the anterior segment of the eye
- •Introduction
- •Oxidative stress
- •Trabecular meshwork
- •IOP increase and free radicals
- •Glaucomatous cascade
- •Nitric oxide and endothelins
- •Extracellular matrix
- •Metalloproteinases
- •Other factors of interest
- •Therapeutic and preventive substances of interest in glaucoma
- •Ginkgo biloba extract
- •Green tea
- •Ginseng
- •Memantine and its derivates
- •Conclusions
- •Abbreviations
- •References
- •Conclusions on neuroprotective treatment targets in glaucoma
- •Acknowledgments
- •References
- •Involvement of the Bcl2 gene family in the signaling and control of retinal ganglion cell death
- •Introduction
- •Intrinsic apoptosis vs. extrinsic apoptosis
- •The Bcl2 family of proteins
- •The requirement of BAX for RGC soma death
- •BH3-only proteins and the early signaling of ganglion cell apoptosis
- •Conclusion
- •Abbreviations
- •Acknowledgments
- •References
- •Assessment of neuroprotection in the retina with DARC
- •Introduction
- •DARC
- •Introducing the DARC technique
- •Annexin 5-labeled apoptosis and ophthalmoloscopy
- •Detection of RGC apoptosis in glaucoma-related animal models with DARC
- •Assessment of glutamate modulation with DARC
- •Glutamate at synaptic endings
- •Glutamate excitotoxicity in glaucoma
- •Assessment of coenzyme Q10 in glaucoma-related models with DARC
- •Summary
- •Abbreviations
- •Acknowledgment
- •References
- •Potential roles of (endo)cannabinoids in the treatment of glaucoma: from intraocular pressure control to neuroprotection
- •Introduction
- •The endocannabinoid system in the eye
- •The IOP-lowering effects of endocannabinoids
- •Endocannabinoids and neuroprotection
- •Conclusions
- •References
- •Glaucoma of the brain: a disease model for the study of transsynaptic neural degeneration
- •Retinal ganglion cells, retino-geniculate neurons
- •Lateral geniculate nucleus
- •Mechanisms of RGC injury in glaucoma
- •Transsynaptic degeneration of the lateral geniculate nucleus in glaucoma
- •Neural degeneration in magno-, parvo-, and koniocellular LGN layers
- •Visual cortex in glaucoma
- •Neuropathology of glaucoma in the visual pathways in the human brain
- •Mechanisms of glaucoma damage in the central visual pathways
- •Implications of central visual system injury in glaucoma
- •Conclusion
- •Acknowledgments
- •References
- •Clinical relevance of optic neuropathy
- •Is there a remodeling of retinal circuitry?
- •Behavioral consequences of glaucoma
- •Glaucoma as a neurodegenerative disease versus neuroplasticity and adaptive changes
- •Future directions
- •Acknowledgment
- •References
- •Targeting excitotoxic/free radical signaling pathways for therapeutic intervention in glaucoma
- •Introduction
- •Channel properties of NMDA receptors correlated with excitotoxicity
- •Downstream signaling cascades after overactivation of NMDA receptors
- •Relevance of excitotoxicity to glaucoma
- •Therapeutic approaches to prevent RGC death by targeting the pathways involved in NMDA excitotoxicity
- •Drugs targeting NMDA receptors
- •Kinetics of NMDA receptor antagonists
- •Memantine
- •NitroMemantines
- •Drugs targeting downstream signaling molecules in NMDA-induced cell death pathways
- •p38 MAPK inhibitors
- •Averting caspase-mediated neurodegeneration
- •Abbreviations
- •Acknowledgments
- •References
- •Stem cells for neuroprotection in glaucoma
- •Introduction
- •Glaucoma as a model of neurodegenerative disease
- •Why use stem cells for neuroprotective therapy?
- •Stem cell sources
- •Neuroprotection by transplanted stem cells
- •Endogenous stem cells
- •Key challenges
- •Conclusion
- •Abbreviations
- •Acknowledgments
- •References
- •The relationship between neurotrophic factors and CaMKII in the death and survival of retinal ganglion cells
- •Introduction
- •Glaucoma and the RGCs
- •Are other retinal cells affected in glaucoma?
- •Retinal ischemia related glaucoma
- •Excitotoxicity and the retina
- •Signal transduction
- •NMDA receptor antagonists and CaMKII
- •Caspase-3 activation in NMDA-induced retinal cell death and its inhibition by m-AIP
- •BDNF and neuroprotection of RGCs
- •Summary and conclusions
- •Abbreviations
- •Acknowledgments
- •References
- •Evidence of the neuroprotective role of citicoline in glaucoma patients
- •Introduction
- •Patients: selection and recruitment criteria
- •Pharmacological treatment protocol
- •Methodology of visual function evaluation: electrophysiological examinations
- •PERG recordings
- •VEP recordings
- •Statistic evaluation of electrophysiological results
- •Electrophysiological (PERG and VEP) responses in OAG patients after the second period of evaluation
- •Effects of citicoline on retinal function in glaucoma patients: neurophysiological implications
- •Effects of citicoline on neural conduction along the visual pathways in glaucoma patients: neurophysiological implications
- •Possibility of neuroprotective role of citicoline in glaucoma patients
- •Conclusive remarks
- •Abbreviations
- •References
- •Neuroprotection: VEGF, IL-6, and clusterin: the dark side of the moon
- •Neuroprotection: VEGF-A, a shared growth factor
- •VEGF-A isoforms
- •VEGF-A receptors
- •Angiogenesis, mitogenesis, and endothelial survival
- •Neurotrophic and neuroprotective effect
- •Intravitreal VEGF inhibition therapy and neuroretina toxicity
- •Neuroprotection: clusterin, a multifunctional protein
- •Clusterin/ApoJ: a debated physiological role
- •Clusterin and diseases
- •Clusterin and the nervous system
- •Neuroprotection: IL-6, VEGF, clusterin, and glaucoma
- •Rational basis for the development of coenzyme Q10 as a neurotherapeutic agent for retinal protection
- •Introduction
- •Ischemia model
- •Neuroprotective effect of Coenzyme Q10 against cell loss yielded by transient ischemia in the RGC layer
- •Retinal ischemia and glutamate
- •Coenzyme Q10 minimizes glutamate increase induced by ischemia/reperfusion
- •Summary
- •Acknowledgment
- •References
- •17beta-Estradiol prevents retinal ganglion cell loss induced by acute rise of intraocular pressure in rat
- •Methods
- •Morphometric analysis
- •Microdialysis
- •Drug application
- •Statistical analysis
- •Results
- •17beta-Estradiol pretreatment minimizes RGC loss
- •Discussion
- •Acknowledgment
advantage of DCT relative to CCT independence may not hold true for patients with POAG.
The answer to the clinical questions of whether CCT measurement is useful in the clinical practice and how the pachimetric data should influence the clinical decision process in the management of glaucoma suspects, established glaucomas, or OHT is all but straightforward.
The evidence that CCT is a reliable indicator of risk for progression of OHT to glaucoma is consistent, as shown by the OHTS and EGPS results. The decision to treat a patient with OHT depends on an assessment of risk, and CCT is an important and necessary part of that determination while there is little evidence that CCT is useful in predicting progression of glaucoma as shown by the results of EMGT. Besides the hypothesis that CCT might influence the underlying biological risk to develop glaucoma, there is the universally acknowledged influence of CCT on IOP measurements, and the fact that IOP is an important parameter for diagnosing glaucoma and represents the only risk factor modifiable with therapy.
As previously discussed, a correction formula for CCT would be useful to improve the accuracy of GAT readings, but considering the variety and inconsistency of the published correction algorithms, the arbitrary selection of one algorithm carries the risk of introducing further errors rather than removing them.
Moreover, the accuracy in measuring true IOP might not be absolutely necessary in every stage of glaucoma management and the error induced in an individual case is likely to be constant, not impairing monitoring of IOP changes over time.
It is generally accepted and consistent in most reports in the literature that thicker corneas are associated with an overestimation of the true IOP and thinner corneas are associated with an underestimation of the true IOP although it is likely that for the majority of patients the inaccuracy would be small with little clinical impact.
On the basis of the scientific knowledge available so far, it is likely that a reasonable approach is, as proposed by James D. Brandt, to ‘‘take care of patients simply by categorizing corneas as thin, average or thick, just as it is important to recognize that optic discs come in small, medium,
29
and large, allowing the clinician to interpret the configurations accordingly’’ (Brandt, 2007).
References
Aghaian, E., Choe, J.E., Lin, S. and Stamper, R.L. (2004) Central corneal thickness of Caucasians, Chinese, Hispanics, Filipinos, African Americans, and Japanese in a glaucoma clinic. Ophthalmology, 111(12): 2211–2219.
Anderson, D.R.Normal Tension Glaucoma Study. (2003) Collaborative normal tension glaucoma study. Curr. Opin. Ophthalmol., 14(2): 86–90.
Brandt, J.D. (2007) Central corneal thickness, tonometry, and glaucoma risk — a guide for the perplexed. Can. J. Ophthalmol., 42(4): 562–566.
Ceruti, P., Morbio, R., Marraffa, M. and Marchini, G. (2008) Comparison of Goldmann applanation tonometry and dynamic contour tonometry in healthy and glaucomatous eyes. Eye, 25(1):
Congdon, N.G., Broman, A.T., Bandeen-Roche, K., Grover, D. and Quigley, H.A. (2006) Central corneal thickness and corneal hysteresis associated with glaucoma damage. Am. J. Ophthalmol., 141: 868–875.
Ehlers, N., Bramsen, T. and Sperling, S. (1975) Applanation tonometry and central corneal thickness. Acta Ophthalmol. (Copenh.), 53: 34–43.
Foster, P.J., Baasanhu, J., Alsbirk, P.H., Munkhbayar, D., Uranchimeg, D. and Johnson, G.J. (1998) Central corneal thickness and intraocular pressure in a Mongolian population. Ophthalmology, 105: 969–973.
Foster, P.J., Machin, D., Wong, T.Y., Ng, T.P., Kirwan, J.F., Johnson, G.J., Khaw, P.T. and Seah, S.K. (2003) Determinants of intraocular pressure and its association with glaucomatous optic neuropathy in Chinese Singaporeans: the Tanjong Pagar Study. Invest. Ophthalmol. Vis. Sci., 44(3): 885–891.
Francis, B.A., Hsieh, A., Lai, M.Y., Chopra, V., Pena, F., Azen, S. and Varma, R.Los Angeles Latino Eye Study Group. (2007) Effects of corneal thickness, corneal curvature, and intraocular pressure level on Goldmann applanation tonometry and dynamic contour tonometry. Ophthalmology, 114(1): 20–26.
Goldmann, H. and Schmidt, T. (1957) Applanation tonometry. Ophthalmologica, 134(4): 221–242.
Gordon, M.O., Beiser, J.A., Brandt, J.D., Heuer, D.K., Higginbotham, E.J., Johnson, C.A., Keltner, J.L., Miller, J.P., Parrish II, R.K., Wilson, M.R. and Kass, M.A. (2002) The ocular hypertension treatment study: baseline factors that predict the onset of primary open-angle glaucomaArch. Ophthalmol., 120: 714–720. discussion 829–830
Grieshaber, M.C., Schoetzau, A., Zawinka, C., Flammer, J. and Orgul, S. (2007) Effect of central corneal thickness on dynamic contour tonometry and Goldmann applanation tonometry in primary open-angle glaucoma. Arch. Ophthalmol., 125(6): 740–744.
30
Herdener, S., Hafizovic, D., Pache, M., Lautebach, S. and Funk, J. (2008) Is the PASCAL-tonometer suitable for measuring intraocular pressure in clinical routine? Longand short-term reproducibility of dynamic contour tonometry. Eur. J. Ophthalmol., 18(1): 39–43.
Ito, T., Ohguro, H., Mamiya, K., Ohguro, I. and Nakazawa, M. (2006) Effects of antiglaucoma drops on MMP and TIMP balance in conjunctival and subconjunctival tissue. Invest. Ophthalmol. Vis. Sci., 47(3): 823–830.
Johnson, M., Kass, M.A., Moses, R.A. and Grodzki, W.J. (1978) Increased corneal thickness simulating elevated intraocular pressure. Arch. Ophthalmol., 96: 664–665.
Kamppeter, B.A. and Jonas, J.B. (2005) Dynamic contour tonometry for intraocular pressure measurement. Am. J. Ophthalmol., 140(2): 318–320.
Kirwan, C. and O’Keefe, M. (2007) Corneal hysteresis using the Reichert ocular response analyser: findings preand postLASIK and LASEK. Acta Ophthalmol. Scand., 21.
Kirwan, C., O’Keefe, M. and Lanigan, B. (2006) Corneal hysteresis and intraocular pressure measurement in children using the Reichert ocular response analyzer. Am. J. Ophthalmol., 142(6): 990–992.
Kotecha, A. (2007) What biomechanical properties of the cornea are relevant for the clinician? Surv. Ophthalmol., 52(Suppl 2): 109–114.
La Rosa, F.A., Gross, R.L. and Orengo, N.S. (2001) Central corneal thickness of Caucasians and African Americans in glaucomatous and nonglaucomatous populations. Arch. Ophthalmol., 119: 23–27.
Leske, M.C., Heijl, A., Hyman, L., Bengtsson, B., Dong, L. and Yang, Z. (1999) Early manifest glaucoma trial: design and baseline data. Ophthalmology, 106: 2144–2153.
Leske, M.C., Heijl, A., Hussein, M., Bengtsson, B., Hyman, L. and Komaroff, E.Early Manifest Glaucoma Trial Group. (2003) Factors for glaucoma progression and the effect of treatment: the early manifest glaucoma trial. Arch. Ophthalmol., 121(1): 48–56.
Liu, J. and Roberts, C.J. (2005) Influence of corneal biomechanical properties on intraocular pressure measurement: quantitative analysis. J. Cataract Refract. Surg., 31: 146–155.
Luce, D.A. (2005) Determining in vivo biomechanical properties of the cornea with an ocular response analyzer. J. Cataract Refract. Surg., 31(1): 156–162.
Martinez de la Casa, J.M., Garcia Feijoo, J., Vico, E., Fernandez Vidal, A., Benitez del Castillo, J.M., Wasfi, M. and Garcia Sanchez, J. (2006) Effect of corneal thickness on dynamic contour, rebound, and Goldmann tonometry. Ophthalmology, 113(12): 2156–2162.
Medeiros, F.A., Sample, P.A. and Weinreb, R.N. (2007) Comparison of dynamic contour tonometry and Goldmann applanation tonometry in African American subjects. Ophthalmology, 114(4): 658–665.
Miglior, S., Pfeiffer, N., Torri, V., Zeyen, T., Cunha Vaz, J. and Adamsons, I. (2007) Predictive factors for open-angle glaucoma among patients with ocular hypertension in the European glaucoma prevention study. Ophthalmology, 114(1): 3–9.
Nicolela, M.T., Soares, A.S., Carrillo, M.M., Chauhan, B.C., LeBlanc, R.P. and Artes, P.H. (2006) Effect of moderate intraocular pression changes on topographic measurement with confocal scanning laser tomography in patients with glaucoma. Arch. Ophthalmol., 124(5): 633–640.
Orssengo, G.J. and Pye, D.C. |
(1999) Determination of |
the true intraocular pressure |
and modulus of elasticity |
of the human cornea in vivo. Bull. Mathematical Biol., 61: 551–572.
Ortiz, D., Pin˜ero, D., Shabayek, M.H., Arnalich Montiel, F. and Alio´, J.L. (2007) Corneal biomechanical properties in normal, post-laser in situ keratomileusis, and keratoconic eyes. J. Cataract Refract. Surg., 33(8): 1371–1375.
Pfeiffer, N., Torri, V., Miglior, S., Zeyen, T., Adamsons, I. and Cunha Vaz, J. (2007) Central corneal thickness in the European glaucoma prevention study. Ophthalmology, 114(3): 454–459.
Shah, S., Laiquzzaman, M., Bhojwani, R., Mantry, S. and Cunliffe, I. (2007) Assessment of the biomechanical properties of the cornea with the ocular response analyzer in normal and keratoconic eyes. Invest. Ophthalmol. Vis. Sci., 48(7): 3026–3031.