05866nam 2201429z- 450 991059507890332120231214133136.0(CKB)5680000000080736(oapen)https://directory.doabooks.org/handle/20.500.12854/92136(EXLCZ)99568000000008073620202209d2022 |y 0engurmn|---annantxtrdacontentcrdamediacrrdacarrierIntraocular Pressure and Ocular HypertensionBaselMDPI Books20221 electronic 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.Medicinebicsscintraocular pressureserum calciumfemaleab interno trabeculotomyglaucomaincision in the Schlemm's canal in degreespost-surgical complicationneuroretinal rim reversalBruch's membrane opening-minimum rim widthtrabeculectomyrefractive errorneuroretinamyopiaintraocular pressure (IOP)tonometryGoldmann applanation tonometer (GAT)central corneal thickness (CCT)ocular hypertensionhigher-order aberrationsKahook Dual Bladeagecentral corneal thicknessGoldmann Applanation tonometernon-contact tonometerrebound tonometeriCareopen angle glaucoma (OAG)Schlemm's canal viscodilationOMNI viscosurgical systemminimally invasive glaucoma surgeries (MIGS)trabeculotomycataract extractionaqueous humorGDF15serumintravitreal injectionanti-VEGF agentstrabecular meshworkMatrigel3D cultureoutflowcytoskeletonrho-kinase inhibitorprostaglandin analogchildhood glaucomaaphakiapseudophakiacataract surgerylensectomymanagement (or therapy)glaucoma drainage devicecyclodestructioncorneal biomechanicsocular response analyzerORAcorneal hysteresisnon-penetrating deep sclerectomyEsnoper V-2000 implantglucocorticoidssafety profileintranasal administrationinhaled administrationsystemic administrationsteroid responsecanaloplastynon-perforating surgical procedurespseudoexfoliation glaucoma (PEXG)Schlemm's canalphase-sensitive optical coherent tomographypulsatile motionIOP fluctuationprimary open-angle glaucomaintraocular pressure measurementiCare tonometryPerkins tonometrystandardized anaesthesiacorneal thicknessprogressionrisk stratificationXEN GelStentcorneal resistance factoropen-angle glaucomalaser treatmentdropless treatmentthyroid-associated ophthalmopathyextraocular musclemagnetic resonance imagingT2 relaxation timeMedicineBrusini Paoloedt1328476Salvetat Maria LetiziaedtZeppieri MarcoedtBrusini PaoloothSalvetat Maria LetiziaothZeppieri MarcoothBOOK9910595078903321Intraocular Pressure and Ocular Hypertension3038588UNINA