- •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
imaging equipment, such as AS-OCT, and noncontact specular microscopy that the mechanical contribution to the influence of shunts on corneal endothelium will eventually be resolved.
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