Tombran-Tink / Barnstable / Shields Mechanisms of the Glaucomas

Disease Processes and Therapeutic Modalities
1. Auflage 2008
ISBN: 978-1-59745-373-8
Verlag: Humana Press
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 762 Seiten

Reihe: Ophthalmology Research

The purpose of this important new book is to provide basic scientists working in the field of glaucoma with a current understanding of the clinical aspects of glaucoma. The authors comprehensively review the most current knowledge available in the field and provide a basis in which researchers can effectively study the glaucomas. The multidisciplinary book will be of great value as its contents will aid the reader in prevention of blindness from glaucoma.

Autoren/Hrsg.

Tombran-Tink, Joyce

Barnstable, Colin J.

Shields, M. Bruce

Inhaltsverzeichnis

1;Preface;7
2;Contents;11
3;Contributors;15
4;Companion CD;19
5;I EPIDEMIOLOGY OF GLAUCOMA;21
5.1;Age and Racial Variation in the Prevalence of Open- Angle Glaucoma in the USA;22
5.1.1;INTRODUCTION;22
5.1.2;PREVALENCE OF OAG;23
5.1.3;EFFECT OF AGE;25
5.1.4;EFFECT OF RACE;29
5.1.5;ESTIMATING THE NUMBERS OF INDIVIDUALS IN THE USA WITH GLAUCOMA;32
5.1.6;PREVALENCE OF BLINDNESS DUE TO GLAUCOMA;32
5.1.7;IMPACT OF NEW TECHNOLOGY;33
5.1.8;POLICY IMPLICATIONS;34
5.1.9;CONCLUSION;34
5.1.10;REFERENCES;34
5.2;Epidemiology of and Risk Factors for Primary Open- Angle Glaucoma;38
5.2.1;INTRODUCTION;38
5.2.2;DEFINITIONS OF GLAUCOMA;39
5.2.3;STUDY DESIGN;40
5.2.4;PREVALENCE OF PRIMARY OPEN-ANGLE GLAUCOMA;42
5.2.5;INCIDENCE OF OPEN-ANGLE GLAUCOMA FROM POPULATION- BASED STUDIES;45
5.2.6;RISK FACTORS FOR GLAUCOMA;46
5.2.7;REFERENCES;47
5.3;The Reykjavik Eye Study on Prevalence of Glaucoma in Iceland and Identi . ed Risk Factors;54
5.3.1;INTRODUCTION;54
5.3.2;MATERIAL AND METHODS;55
5.3.3;EXAMINATION;55
5.3.4;DEFINITIONS;56
5.3.5;RESULTS;57
5.3.6;DISCUSSION;62
5.3.7;REFERENCES;64
5.4;Defined Glaucoma in Chinese Population;68
5.4.1;INTRODUCTION;68
5.4.2;PRIMARY GLAUCOMA;70
5.4.3;Demographic Indices;72
5.4.4;Age.;72
5.4.5;Sex.;73
5.4.6;Race.;73
5.4.7;Ocular Factors;73
5.4.8;Other risk factors;74
5.4.9;Demographic Indices;75
5.4.10;Age.;75
5.4.11;Sex.;75
5.4.12;Race.;75
5.4.13;Ocular Factors;75
5.4.14;Other Risk Factors;76
5.4.15;SECONDARY GLAUCOMA;76
5.4.16;CONGENITAL GLAUCOMA;77
5.4.17;SUMMARY;78
5.4.18;REFERENCES;78
5.5;The Wroclaw Epidemiological Study;82
5.5.1;INTRODUCTION;82
5.5.2;SCREENING FOR GLAUCOMA;83
5.5.3;THE WROCLAW EPIDEMIOLOGICAL STUDY;86
5.5.4;REFERENCES;96
6;II MECHANISMS OF INTRAOCULAR PRESSURE ELEVATION IN THE GLAUCOMAS;100
6.1;Pretrabecular Mechanisms of Intraocular Pressure Elevation;102
6.1.1;INTRODUCTION;102
6.1.2;NEOVASCULAR GLAUCOMA;102
6.1.3;IRIDOCORNEAL ENDOTHELIAL SYNDROME;108
6.1.4;EPITHELIAL AND FIBROUS MEMBRANES;111
6.1.5;INFLAMMATORY MEMBRANES;114
6.1.6;REFERENCES;115
6.2;Glaucomatous Changes in the Trabecular Meshwork;118
6.2.1;INTRODUCTION;118
6.2.2;ANATOMY;119
6.2.3;AGING CHANGES;123
6.2.4;PRIMARY OPEN-ANGLE GLAUCOMA;124
6.2.5;PSEUDOEXFOLIATION SYNDROME;126
6.2.6;PIGMENTARY GLAUCOMA;128
6.2.7;CORTICOSTEROID-INDUCED GLAUCOMA;131
6.2.8;SUMMARY;132
6.2.9;REFERENCES;133
6.3;Trabecular Mechanisms of Intraocular Pressure Elevation;136
6.3.1;INTRODUCTION;136
6.3.2;PATHOBIOLOGY OF PEX SYNDROME;138
6.3.3;OPEN-ANGLE GLAUCOMA ASSOCIATED WITH PEX SYNDROME;142
6.3.4;MANAGEMENT OF GLAUCOMAS ASSOCIATED WITH PEX SYNDROME;148
6.3.5;SUMMARY AND PERSPECTIVES;150
6.3.6;REFERENCES;151
6.4;Post-Trabecular Glaucomas with Elevated Episcleral Venous Pressure;158
6.4.1;INTRODUCTION;158
6.4.2;OBSTRUCTIVE MECHANISMS OF ELEVATED EPISCLERAL VENOUS PRESSURE;159
6.4.3;ARTERIO-VENOUS SHUNT MECHANISMS OF ELEVATED EPISCLERAL VENOUS PRESSURE;163
6.4.4;IDIOPATHIC ELEVATED EPISCLERAL VENOUS PRESSURE;169
6.4.5;REFERENCES;170
6.5;Angle-Closure Glaucomas;178
6.5.1;INTRODUCTION;178
6.5.2;POST-INFLAMMATORY ANGLE-CLOSURE GLAUCOMA;179
6.5.3;PROLIFERATIVE CAUSES OF ANGLE-CLOSURE GLAUCOMA;180
6.5.4;CONCLUSION;182
6.5.5;REFERENCES;182
6.6;Angle-Closure Glaucomas;186
6.6.1;MECHANISM OF PUPILLARY BLOCK ANGLE CLOSURE;186
6.6.2;CLINICAL FINDINGS;187
6.6.3;PROVOCATIVE TESTS;187
6.6.4;MANAGEMENT;188
6.6.5;LENS-INDUCED MECHANISMS OF PUPILLARY BLOCK ANGLE CLOSURE;188
6.6.6;POSTERIOR SYNECHIA;190
6.6.7;REFERENCES;191
6.7;Angle-Closure Glaucomas;192
6.7.1;INTRODUCTION;192
6.7.2;ANGLE CLOSURE ORIGINATING AT THE LEVEL OF THE CILIARY BODY;194
6.7.3;ANGLE CLOSURE ORIGINATING AT THE LEVEL OF THE LENS;197
6.7.4;ANGLE CLOSURE ORIGINATING POSTERIOR TO THE LENS;200
6.7.5;ACKNOWLEDGMENTS;202
6.7.6;REFERENCES;202
7;III GENETICS OF GLAUCOMA;208
7.1;Genetics and Glaucoma Susceptibility;210
7.1.1;RELEVANCE OF GENETICS;210
7.1.2;GENETIC SUSCEPTIBILITY AND PROGRESS IN GENE LOCALIZATION AND IDENTIFICATION;211
7.1.3;COLLABORATION BETWEEN CLINICAL AND BASIC RESEARCHERS;219
7.1.4;CONCLUSION;219
7.1.5;REFERENCES;219
7.2;Myocilin Mutations and Their Role in Open- Angle Glaucoma;224
7.2.1;INTRODUCTION;224
7.2.2;IDENTIFICATION OF THE MYOCILIN GENE;225
7.2.3;MUTATION ANALYSIS OF THE MYOC GENE IN OAG;225
7.2.4;THE Q368STOP MUTATION;227
7.2.5;EVIDENCE OF A FOUNDER EFFECT FOR THE Q368STOP MUTATION IN MYOC;227
7.2.6;THE Q368STOP AND GLAUCOMA PHENOTYPE;228
7.2.7;THE Q368STOP IN UNAFFECTED INDIVIDUALS;230
7.2.8;THE Q368STOP AND MODIFIER GENES;231
7.2.9;CONCLUSION;232
7.2.10;REFERENCES;232
7.3;The Functional Role of Myocilin in Glaucoma;238
7.3.1;INTRODUCTION;238
7.3.2;THE NATURE OF MYOCILIN;239
7.3.3;THE ROLE OF NORMAL OR WILDTYPE MYOCILIN FOR GLAUCOMA;241
7.3.4;THE ROLE OF MUTANT MYOCILIN FOR GLAUCOMA;242
7.3.5;REFERENCES;245
7.4;Roles of CYP1B1, Optineurin, and WDR36 Gene Mutations in Glaucoma;252
7.4.1;INTRODUCTION;252
7.4.2;CYTOCHROME P4501B1 (;254
7.4.3;OPTINEURIN (;264
7.4.4;WD REPEAT DOMAIN 36 (;272
7.4.5;SUMMARIES AND CONCLUSION;279
7.4.6;REFERENCES;280
7.5;Genetic Association in the Open-Angle Glaucomas;294
7.5.1;INTRODUCTION;294
7.5.2;GLAUCOMA AND APOPTOSIS;296
7.5.3;GLAUCOMA AND AUTOIMMUNITY;297
7.5.4;GLAUCOMA AND CYTOKINES;297
7.5.5;GLAUCOMA AND INTERLEUKIN-1;297
7.5.6;GLAUCOMA AND TUMOR NECROSIS FACTOR-ALPHA;298
7.5.7;GLAUCOMA AND TRANSPORT OF ANTIGENIC PEPTIDES;298
7.5.8;GLAUCOMA AND TISSUE MORPHOGENESIS;300
7.5.9;GLAUCOMA AND OXIDATIVE STRESS;301
7.5.10;SUMMARY;302
7.5.11;REFERENCES;303
7.6;ApoE Polymorphisms and Severity of Open- Angle Glaucoma;308
7.6.1;INTRODUCTION;308
7.6.2;CLINICAL PRESENTATIONS OF PRIMARY OPEN-ANGLE GLAUCOMA;310
7.6.3;RISK FACTORS AND PROGNOSTIC FACTORS FOR PRIMARY OPEN- ANGLE GLAUCOMA;311
7.6.4;THE;312
7.6.5;GENE;312
7.6.6;PATHOPHYSIOLOGICAL ROLES OF APOE;315
7.6.7;POLYMORPHISMS AND GLAUCOMA;317
7.6.8;CONTRIBUTIONS OF;318
7.6.9;TO OPTIC NERVE DEGENERATION;318
7.6.10;IN GLAUCOMA;318
7.6.11;CONCLUDING REMARKS;319
7.6.12;ACKNOWLEDGMENTS;319
7.6.13;REFERENCES;320
8;IV MOLECULAR AND CELLULAR RESPONSES IN THE EYE TO GLAUCOMA;328
8.1;Changes in Aqueous Humor Dynamics with Age and Glaucoma;330
8.1.1;INTRODUCTION: AGEING AND AGE-RELATED DISEASE;330
8.1.2;CHANGES IN AQUEOUS HUMOR DYNAMICS;331
8.1.3;ULTRASTRUCTURAL CHANGES WITH AGE AND GLAUCOMA;333
8.1.4;PUTATIVE MECHANISMS UNDERLYING AGEING AND AGE- RELATED DISEASE;336
8.1.5;CONCLUSIONS;340
8.1.6;REFERENCES;341
8.2;Mechanosensitive Genes in the Trabecular Meshwork at Homeostasis;348
8.2.1;INTRODUCTION;348
8.2.2;TECHNOLOGIES TO EVALUATE CHANGES IN GENE EXPRESSION;349
8.2.3;MODELS TO STUDY GENE RESPONSE TO MECHANICAL STRESS: ELEVATED IOP AND STRETCH;353
8.2.4;HOW PRESSURE AFFECTS THE TRABECULAR MESHWORK: HOMEOSTASIS AND GLOBAL GENE EXPRESSION;357
8.2.5;EFFECTS OF MECHANICAL STRESS ON SINGLE GENES;365
8.2.6;COMPREHENSIVE SELECTION OF POTENTIALLY RELEVANT MECHANOSENSITIVE GENES;369
8.2.7;CONCLUDING THOUGHTS FOR FUTURE DIRECTIONS;371
8.2.8;ACKNOWLEDGMENTS;371
8.2.9;REFERENCES;371
8.3;Reactive Astrocytes in the Glaucomatous Optic Nerve Head;382
8.3.1;PRIMARY OPEN-ANGLE GLAUCOMA AND ELEVATED INTRAOCULAR PRESSURE;382
8.3.2;ONH ASTROCYTES IN POAG;383
8.3.3;CELL CULTURE MODELS OF MECHANOTRANSDUCTION IN ONH ASTROCYTES;384
8.3.4;SIGNAL TRANSDUCTION PATHWAYS INVOLVED IN THE TRANSITION OF QUIESCENT TO REACTIVE ASTROCYTES;385
8.3.5;FUNCTIONS OF REACTIVE ASTROCYTES;390
8.3.6;CONCLUSIONS;401
8.3.7;ACKNOWLEDGMENTS;402
8.3.8;REFERENCES;402
8.4;Optic Neuropathy and Ganglion Cell Degeneration in Glaucoma;412
8.4.1;INTRODUCTION;412
8.4.2;DIVERSE CELLULAR EVENTS ASSOCIATED WITH GLAUCOMA;413
8.4.3;MOLECULAR MECHANISMS ASSOCIATED WITH GLAUCOMATOUS NEURONAL DAMAGE;417
8.4.4;CONTROLLING THE GLAUCOMATOUS DAMAGE: NEURONAL PROTECTION, PLASTICITY, AND REGENERATION;423
8.4.5;CONCLUSION;429
8.4.6;REFERENCES;429
8.5;Proteomics in Defining Pathogenic Processes Involved in Glaucomatous Neurodegeneration;444
8.5.1;IMPORTANCE OF THE COMPREHENSIVE ANALYSIS OF PROTEIN EXPRESSION TO IDENTIFY PATHOGENIC MECHANISMS OF GLAUCOMATOUS NEURODEGENERATION;444
8.5.2;CURRENT APPLICATIONS OF PROTEOMICS IN GLAUCOMATOUS NEURODEGENERATION;445
8.5.3;REFERENCES;457
8.6;Proteomic Advances Toward Understanding Mechanisms of Glaucoma Pathology;462
8.6.1;INTRODUCTION;462
8.6.2;COCHLIN;463
8.6.3;PEPTIDYL ARGININE DEIMINASE 2;467
8.6.4;SUMMARY AND PROSPECTS;473
8.6.5;ACKNOWLEDGMENTS;474
8.6.6;REFERENCES;474
8.7;Molecular and Cellular Responses in the Eye to Glaucoma;478
8.7.1;ANIMAL MODELS FOR GLAUCOMA RESEARCH;478
8.7.2;ANALYSIS OF GENE EXPRESSION USING THE MICROARRAY SYSTEM;482
8.7.3;REFERENCES;484
9;V OCULAR TISSUE AND PSYCHOPHYSIOLOGICAL RESPONSES IN GLAUCOMA;488
9.1;Ocular Biomechanics in Glaucoma;490
9.1.1;INTRODUCTION;490
9.1.2;BIOMECHANICS OF AQUEOUS HUMOR DRAINAGE;491
9.1.3;BIOMECHANICS OF THE AQUEOUS HUMOR AND IRIS;494
9.1.4;BIOMECHANICS OF THE OPTIC NERVE HEAD IN GLAUCOMA;497
9.1.5;REFERENCES;502
9.2;Intraocular Pressure, Perfusion Pressure, and Optic Nerve Energy Metabolism;510
9.2.1;INTRODUCTION;510
9.2.2;OCULAR BLOOD FLOW AND AUTOREGULATION;511
9.2.3;OPTIC NERVE OXYGEN TENSION AND ITS REGULATION;513
9.2.4;IOP AND OPTIC NERVE HEAD OXIDATIVE METABOLISM;518
9.2.5;OPTIC NERVE OXYGEN PHYSIOLOGY AND GLAUCOMA;520
9.2.6;OCULAR BLOOD FLOW IN GLAUCOMA;522
9.2.7;CARBONIC ANHYDRASE INHIBITORS AND OCULAR BLOOD FLOW;523
9.2.8;CARBONIC ANHYDRASE INHIBITORS AND OPTIC NERVE OXYGEN TENSION;525
9.2.9;CONCLUSION;529
9.2.10;REFERENCES;530
9.3;Optic Nerve;536
9.3.1;GLAUCOMATOUS OPTIC NEUROPATHY AND ITS IOP-INDUCED MECHANISM;536
9.3.2;HISTOLOGICAL CHANGE OF THE ONH IN GLAUCOMA;537
9.3.3;CELL-BIOLOGICAL CHANGES OF THE ONH IN GLAUCOMA;538
9.3.4;ONH AS A BIOMECHANICAL STRUCTURE;539
9.3.5;APPLICATION OF OCULAR HYPERTENSION ANIMAL MODELS FOR GON;540
9.3.6;FUTURE DIRECTIONS;541
9.3.7;REFERENCES;541
9.4;Psychophysiology of Glaucoma;546
9.4.1;INTRODUCTION;546
9.4.2;FORM (STRUCTURE);547
9.4.3;FUNCTION;553
9.4.4;STRUCTURE/FUNCTION RELATIONSHIPS;561
9.4.5;REFERENCES;563
10;VI MODELS OF GLAUCOMA;568
10.1;The Primate Model of Experimental Glaucoma;570
10.1.1;INTRODUCTION;570
10.1.2;BACKGROUND;571
10.1.3;APPLICATIONS OF THE PRIMATE MODEL OF GLAUCOMA;574
10.1.4;NON-INVASIVE ASSESSMENT OF GLAUCOMA ONSET AND PROGRESSION;581
10.1.5;SUMMARY;584
10.1.6;REFERENCES;585
10.2;Involvement of Inflammation in a Mouse Model of Inherited Pigmentary Glaucoma;598
10.2.1;INTRODUCTION;598
10.2.2;PDS AND PIGMENTARY GLAUCOMA;599
10.2.3;THE DBA/2J MOUSE IS A MODEL OF PROGRESSIVE PIGMENTARY GLAUCOMA;600
10.2.4;GENETIC MUTATIONS IN THE DBA/2J MOUSE;603
10.2.5;IMMUNE DYSFUNCTION IN THE DBA/2J MOUSE;605
10.2.6;INVOLVEMENT OF IL-18 IN THE PATHOGENESIS OF GLAUCOMA IN THE DBA/ 2J MOUSE;606
10.2.7;OTHER BIOCHEMICAL ALTERATIONS IN THE IRIS OF THE DBA/ 2J MOUSE;608
10.2.8;IL-18-DEFICIENT DBA/2J MICE;610
10.2.9;CONCLUSION;615
10.2.10;ACKNOWLEDGMENTS;615
10.2.11;REFERENCES;615
10.3;Use of Purified Retinal Ganglion Cells for an In Vitro Model to Study Glaucoma;620
10.3.1;INTRODUCTION;620
10.3.2;DEVELOPMENT OF RGCS;621
10.3.3;PURIFICATION OF RGCS;621
10.3.4;PROCEDURE;622
10.3.5;CONTROVERSY CONCERNING NMDA EXCITOTOXICITY IN RGCS;624
10.3.6;CONCLUSIONS;625
10.3.7;REFERENCES;626
10.3.8;INTRODUCTION;628
11;VII THERAPEUTIC MODALITIES;628
11.1;Pharmacological Therapies for Managing Glaucoma;630
11.1.1;INTRODUCTION;630
11.1.2;BIOAVAILABILITY OF TOPICAL DRUGS;632
11.1.3;GUIDELINES FOR THE MEDICAL THERAPY OF GLAUCOMA;633
11.1.4;ADRENERGIC AGONISTS;635
11.1.5;-ADRENERGIC ANTAGONISTS;637
11.1.6;CARBONIC ANHYDRASE INHIBITORS;639
11.1.7;CHOLINERGICS;640
11.1.8;PROSTAGLANDIN ANALOGUES;642
11.1.9;FIXED COMBINATION AGENTS;645
11.1.10;HYPEROSMOTIC AGENTS;647
11.1.11;FUTURE DIRECTIONS;648
11.1.12;CONCLUSION;649
11.1.13;REFERENCES;649
11.2;Redox-Based Therapies for Neuroprotection;664
11.2.1;RETINAL GANGLION CELL DEATH IS THE FINAL COMMON PATHWAY OF VIRTUALLY ALL OPTIC NEUROPATHIES;664
11.2.2;THERE ARE MULTIPLE MECHANISMS BY WHICH AXONAL DAMAGE CAN TRANSDUCE AN INJURY SIGNAL;665
11.2.3;SUPEROXIDE IS AN INTRACELLULAR SIGNALING MOLECULE FOR RGC DEATH;666
11.2.4;REDUCTION OF OXIDIZED THIOLS INHIBITS RGC DEATH AFTER AXOTOMY IN VITRO AND IN VIVO;667
11.2.5;NOVEL AGENTS THAT REDUCE OXIDIZED THIOLS PROTECT;668
11.2.6;RGCS IN VITRO AT LOW CONCENTRATIONS;668
11.2.7;SUMMARY AND OUTLOOK FOR THE FUTURE;669
11.2.8;ACKNOWLEDGMENTS;670
11.2.9;REFERENCES;671
11.3;Neuroprotective Signaling Pathways in Glaucoma;676
11.3.1;INTRODUCTION;676
11.3.2;THE NEUROTROPHINS;678
11.3.3;CILIARY NEUROTROPHIC FACTOR;682
11.3.4;BASIC FIBROBLAST GROWTH FACTOR;684
11.3.5;GLIAL CELL LINE-DERIVED NEUROTROPHIC FACTOR;685
11.3.6;PEPTIDOMIMETIC LIGANDS;686
11.3.7;ANTI-APOPTOTIC SIGNALING;687
11.3.8;SUMMARY AND FUTURE DIRECTIONS;689
11.3.9;ACKNOWLEDGMENTS;689
11.3.10;REFERENCES;690
11.4;Role of Selective Laser Trabeculoplasty in the Management of Glaucoma;702
11.4.1;PRINCIPLE;702
11.4.2;HISTOPATHOLOGY;703
11.4.3;MECHANISMS;705
11.4.4;TREATMENT TECHNIQUE;707
11.4.5;REFERENCES;709
11.5;Mechanisms and Mechanics of Incisional Surgery for Glaucoma;712
11.5.1;INTRODUCTION;712
11.5.2;THE MECHANISMS OF GLAUCOMA SURGERY;713
11.5.3;PREOPERATIVE PLANNING;715
11.5.4;ANESTHESIA;716
11.5.5;MECHANICS OF TRABECULECTOMY;716
11.5.6;MECHANICS OF NON-PENETRATING DEEP SCLERECTOMY;729
11.5.7;SUMMARY;730
11.5.8;REFERENCES;731
11.6;Aqueous Shunts;734
11.6.1;THE EVOLVING CONCEPT;734
11.6.2;PATHOPHYSIOLOGY;737
11.6.3;EXPLANT ENCAPSULATION AND CORRELATIONS WITH IOP AND FUNCTION;738
11.6.4;EXPLANT SURFACE AREA;740
11.6.5;VALVED VERSUS NON-VALVED DEVICES;740
11.6.6;ULTRASOUND AND AQUEOUS SHUNTS;743
11.6.7;ANTERIOR CHAMBER VERSUS PARS PLANA TUBE INSERTION;743
11.6.8;SCHOCKET AND MODIFIED SCHOCKET;743
11.6.9;ONE- VERSUS TWO-QUADRANT SURGERY—SUPERIOR OR INFERIOR LOCATION;744
11.6.10;TUBE INSERTION AND METHODS OF TEMPORARY LIGATURE FOR NON- VALVED DEVICES;744
11.6.11;CLINICAL INDICATIONS FOR SHUNTS;746
11.6.12;ANTIFIBROTICS (5-FU AND MITOMYCIN) AND AQUEOUS SHUNTS;747
11.6.13;COMPLICATIONS OF SHUNTS;747
11.6.14;PEDIATRIC GLAUCOMAS;750
11.6.15;CLINICAL FAILURE AND ITS MANAGEMENT;750
11.6.16;RANDOMIZED TRIALS INVOLVING AQUEOUS SHUNTS;751
11.6.17;NEW CONCEPTS AND INNOVATIONS;751
11.6.18;SUMMARY;751
11.6.19;REFERENCES;751
11.7;New Approaches to the Surgical Management of the Glaucomas;758
11.7.1;INTRODUCTION;758
11.7.2;SHORTCOMINGS OF CURRENT GLAUCOMA SURGERY;759
11.7.3;AREAS OF RESEARCH FOR NEW GLAUCOMA SURGERY;761
11.7.4;CONCLUSIONS;766
11.7.5;ACKNOWLEDGMENTS;766
11.7.6;REFERENCES;766
12;Index;772