05887nam 2201453z- 450 991059507890332120220916(CKB)5680000000080736(oapen)https://directory.doabooks.org/handle/20.500.12854/92136(oapen)doab92136(EXLCZ)99568000000008073620202209d2022 |y 0engurmn|---annantxtrdacontentcrdamediacrrdacarrierIntraocular Pressure and Ocular HypertensionBasel20221 online resource (288 p.)3-0365-5100-X 3-0365-5099-2 Primary open-angle glaucoma (POAG) is a multi-factorial progressive optic neuropathy characterized by retinal ganglion cell degeneration and progressive visual field loss which, if left untreated, may lead to blindness. Increased intraocular pressure (IOP) is considered to be the main risk factor for developing POAG, and its reduction has been shown to correlate with a decrease in glaucoma incidence and progression. Considering that fewer than 10% of the subjects with ocular hypertension (OHT) will develop morphological and/or functional glaucomatous damage within 5 years if not treated, glaucoma causes and molecular changes leading to ocular tissue damage in glaucoma are still largely unknown. The contemporary treatment of POAG is mainly oriented towards reducing IOP; the importance of the IOP reduction in other types of glaucoma, such as the "normal pressure glaucoma", is still discussed. The IOP value is maintained by balancing the amount of fluid contained within the anterior and posterior chambers of the eye; our comprehension of the mechanisms underlying the secretion and active and passive outflow of the aqueous humor is extremely important for improving the treatment of glaucoma. Innovative pharmacological approaches, and laser and surgical procedures aiming to reduce IOP, have been developed in recent years. This book provides a compendium of topics regarding IOP, aqueous humor dynamics, tonometry, and medical and surgical techniques developed to reduce the IOP in subjects with ocular hypertension or glaucoma.Medicinebicssc3D cultureab interno trabeculotomyageanti-VEGF agentsaphakiaaqueous humorBruch's membrane opening-minimum rim widthcanaloplastycataract extractioncataract surgerycentral corneal thicknesscentral corneal thickness (CCT)childhood glaucomacorneal biomechanicscorneal hysteresiscorneal resistance factorcorneal thicknesscyclodestructioncytoskeletondropless treatmentEsnoper V-2000 implantextraocular musclefemaleGDF15glaucomaglaucoma drainage deviceglucocorticoidsGoldmann Applanation tonometerGoldmann applanation tonometer (GAT)higher-order aberrationsiCareiCare tonometryincision in the Schlemm's canal in degreesinhaled administrationintranasal administrationintraocular pressureintraocular pressure (IOP)intraocular pressure measurementintravitreal injectionIOP fluctuationKahook Dual Bladelaser treatmentlensectomymagnetic resonance imagingmanagement (or therapy)Matrigelminimally invasive glaucoma surgeries (MIGS)myopian/aneuroretinaneuroretinal rim reversalnon-contact tonometernon-penetrating deep sclerectomynon-perforating surgical proceduresocular hypertensionocular response analyzerOMNI viscosurgical systemopen angle glaucoma (OAG)open-angle glaucomaORAoutflowPerkins tonometryphase-sensitive optical coherent tomographypost-surgical complicationprimary open-angle glaucomaprogressionprostaglandin analogpseudoexfoliation glaucoma (PEXG)pseudophakiapulsatile motionrebound tonometerrefractive errorrho-kinase inhibitorrisk stratificationsafety profileSchlemm's canalSchlemm's canal viscodilationserumserum calciumstandardized anaesthesiasteroid responsesystemic administrationT2 relaxation timethyroid-associated ophthalmopathytonometrytrabecular meshworktrabeculectomytrabeculotomyXEN GelStentMedicineBrusini Paoloedt1328476Salvetat Maria LetiziaedtZeppieri MarcoedtBrusini PaoloothSalvetat Maria LetiziaothZeppieri MarcoothBOOK9910595078903321Intraocular Pressure and Ocular Hypertension3038588UNINA