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Intro; Preface; Contents; Contributors; Part I: Review of the Study of Trans-laminar Cribrosa Pressure Difference; 1: Road Map for the Pathogenesis of Glaucomatous Optic Neuropathy; References; 2: Time to Eliminate "Normal Tension" in Primary Open-Angle Glaucoma; 2.1 Introduction; 2.2 Origin of Normal-Tension Glaucoma; 2.3 Pathogenesis of Primary Open-Angle Glaucoma; 2.4 Genetics of POAG; 2.5 Is NTG Clinically Distinguishable from POAG?; 2.6 Conclusion; References; 3: Intracranial and Intraocular Pressure-Related Diseases; 3.1 Anatomy; 3.2 Epidemiology
3.3 IOP: A Dilemma in Glaucoma Diagnosis and Treatment3.4 Cerebrospinal Fluid Pressure: The New Dangerous Factor; 3.5 Trans-laminar Cribrosa Pressure Difference (TLPD): The Pathogenesis for Glaucoma?; 3.6 Mechanisms and Clinical Implications; 3.7 Conclusion; References; 4: Conciliation of Discrepancy of Hypertensive Glaucoma and Normal-Tension Glaucoma Through Intraocular-Intracranial Pressure Gradient; 4.1 The Historical Evolution of the Definition of Glaucoma; 4.2 The Transitions of the Definition of Primary Glaucoma in Recent Guidelines and Expert Consensuses
4.2.1 Transitions of the Definition of Primary Open-Angle Glaucoma (POAG)4.2.1.1 POAG Definition in the Expert Consensuses in China; 4.2.1.2 POAG Definition by the American Academy of Ophthalmology (AAO); 4.2.1.3 Contrast of POAG Definitions Between China and America; 4.2.2 Transitions of the Definition of Primary Angle-Closure Glaucoma (PACG); 4.2.2.1 The Classification System by the International Society of Geographical and Epidemiological Ophthalmology (ISGEO); 4.2.2.2 PACG Definition in China; 4.2.2.3 Contrast of PACG Definitions and Classifications Between China and America
4.3 New Hypotheses and Theories About the Relationship Between Pressure and Glaucoma4.3.1 "Safe IOP Hypothesis"; 4.3.2 "Ocular-Cranial Pressure Gradient Theory"; 4.4 Summary; References; 5: Primary Open-Angle Glaucoma, Trans-Lamina Cribrosa Pressure Difference, and Central Nerve System; 5.1 The Relationship Between POAG and CNS Diseases; 5.2 The Relationship Between POAG and TLPD; 5.3 DBA/2 Mouse Model of Glaucoma; 5.3.1 Obstruction of Axoplasmic Transport in Glaucoma Was Developed from the Proximal to the Distal Axon
5.3.2 Obstruction of Distal Axonal Transport in Glaucoma Owns Characteristics of Age-Dependent and Retinal Localization5.3.3 The Axonal Structure of RGC Cells in Glaucoma Is Still Preserved After the Obstruction of Axonal Transport; 5.4 The Visual Pathway Damage Induced by POAG; 5.4.1 The Damage of the Anterior Visual Pathway of POAG; 5.4.2 The Damage of Posterior Visual Pathway in POAG; 5.4.3 Other Glaucomatous Damage in CNS; 5.5 Mechanism of Action (MOA) Study of CNS Damage in Glaucoma; 5.6 Summary; References; 6: The Role of CSFP in Glaucoma: A View in Retrospect; References
3.3 IOP: A Dilemma in Glaucoma Diagnosis and Treatment3.4 Cerebrospinal Fluid Pressure: The New Dangerous Factor; 3.5 Trans-laminar Cribrosa Pressure Difference (TLPD): The Pathogenesis for Glaucoma?; 3.6 Mechanisms and Clinical Implications; 3.7 Conclusion; References; 4: Conciliation of Discrepancy of Hypertensive Glaucoma and Normal-Tension Glaucoma Through Intraocular-Intracranial Pressure Gradient; 4.1 The Historical Evolution of the Definition of Glaucoma; 4.2 The Transitions of the Definition of Primary Glaucoma in Recent Guidelines and Expert Consensuses
4.2.1 Transitions of the Definition of Primary Open-Angle Glaucoma (POAG)4.2.1.1 POAG Definition in the Expert Consensuses in China; 4.2.1.2 POAG Definition by the American Academy of Ophthalmology (AAO); 4.2.1.3 Contrast of POAG Definitions Between China and America; 4.2.2 Transitions of the Definition of Primary Angle-Closure Glaucoma (PACG); 4.2.2.1 The Classification System by the International Society of Geographical and Epidemiological Ophthalmology (ISGEO); 4.2.2.2 PACG Definition in China; 4.2.2.3 Contrast of PACG Definitions and Classifications Between China and America
4.3 New Hypotheses and Theories About the Relationship Between Pressure and Glaucoma4.3.1 "Safe IOP Hypothesis"; 4.3.2 "Ocular-Cranial Pressure Gradient Theory"; 4.4 Summary; References; 5: Primary Open-Angle Glaucoma, Trans-Lamina Cribrosa Pressure Difference, and Central Nerve System; 5.1 The Relationship Between POAG and CNS Diseases; 5.2 The Relationship Between POAG and TLPD; 5.3 DBA/2 Mouse Model of Glaucoma; 5.3.1 Obstruction of Axoplasmic Transport in Glaucoma Was Developed from the Proximal to the Distal Axon
5.3.2 Obstruction of Distal Axonal Transport in Glaucoma Owns Characteristics of Age-Dependent and Retinal Localization5.3.3 The Axonal Structure of RGC Cells in Glaucoma Is Still Preserved After the Obstruction of Axonal Transport; 5.4 The Visual Pathway Damage Induced by POAG; 5.4.1 The Damage of the Anterior Visual Pathway of POAG; 5.4.2 The Damage of Posterior Visual Pathway in POAG; 5.4.3 Other Glaucomatous Damage in CNS; 5.5 Mechanism of Action (MOA) Study of CNS Damage in Glaucoma; 5.6 Summary; References; 6: The Role of CSFP in Glaucoma: A View in Retrospect; References