| Peer-Reviewed

Ocular Hypertension and Glaucoma: A Review and Current Perspectives

Received: 7 March 2017     Accepted: 27 March 2017     Published: 14 April 2017
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Abstract

Hypertension of the eye fundamentally results from an imbalance between the production and extrusion of aqueous humor (AQH) within the anterior segment of the eye. Vitreous humor (VH) (in the posterior segment of the eye) and AQH are responsible for maintaining the shape of the eye-ball in order that light is correctly focused on the retina for good vision. However, as we age, cells of the AQH drainage system (trabecular meshwork, TM) die and cellular debris accumulates within the TM and the canal of Schlemm thereby slowing, and in some cases, preventing AQH efflux. This results in increased resistance and elevation of hydrostatic pressure within the anterior segment, also termed as elevated intraocular pressure (IOP) or ocular hypertension (OHT). Sustained OHT exerts mechanical pressure on the retinal ganglion cells (RGCs) and the optic nerve fibers at the back of the eye leading to their progressive demise by apoptosis, thereby distorting and diminishing visual acuity over time, and eventually leading to irreversible blindness. In some patients even “normal” IOP is destructive because their RGCs and their axons projecting to the brain are genetically or chemically predisposed to early cell death. These pathologies are termed “glaucomatous optic neuropathy (GON)” and OHT is often associated with glaucoma, especially primary open-angle glaucoma (POAG). Today, there are several pharmacological and minimally invasive surgical interventions / devices that constitute therapeutic modalities to treat OHT and glaucoma. OHT etiology and treatments will be discussed in more detail in this review article.

Published in International Journal of Ophthalmology & Visual Science (Volume 2, Issue 2)
DOI 10.11648/j.ijovs.20170202.11
Page(s) 22-36
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2017. Published by Science Publishing Group

Keywords

Glaucoma, Ocular Hypertension, Neuroprotection, Pharmacology, Aqueous Humor

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    Najam A. Sharif. (2017). Ocular Hypertension and Glaucoma: A Review and Current Perspectives. International Journal of Ophthalmology & Visual Science, 2(2), 22-36. https://doi.org/10.11648/j.ijovs.20170202.11

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    Najam A. Sharif. Ocular Hypertension and Glaucoma: A Review and Current Perspectives. Int. J. Ophthalmol. Vis. Sci. 2017, 2(2), 22-36. doi: 10.11648/j.ijovs.20170202.11

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    AMA Style

    Najam A. Sharif. Ocular Hypertension and Glaucoma: A Review and Current Perspectives. Int J Ophthalmol Vis Sci. 2017;2(2):22-36. doi: 10.11648/j.ijovs.20170202.11

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  • @article{10.11648/j.ijovs.20170202.11,
      author = {Najam A. Sharif},
      title = {Ocular Hypertension and Glaucoma: A Review and Current Perspectives},
      journal = {International Journal of Ophthalmology & Visual Science},
      volume = {2},
      number = {2},
      pages = {22-36},
      doi = {10.11648/j.ijovs.20170202.11},
      url = {https://doi.org/10.11648/j.ijovs.20170202.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijovs.20170202.11},
      abstract = {Hypertension of the eye fundamentally results from an imbalance between the production and extrusion of aqueous humor (AQH) within the anterior segment of the eye. Vitreous humor (VH) (in the posterior segment of the eye) and AQH are responsible for maintaining the shape of the eye-ball in order that light is correctly focused on the retina for good vision. However, as we age, cells of the AQH drainage system (trabecular meshwork, TM) die and cellular debris accumulates within the TM and the canal of Schlemm thereby slowing, and in some cases, preventing AQH efflux. This results in increased resistance and elevation of hydrostatic pressure within the anterior segment, also termed as elevated intraocular pressure (IOP) or ocular hypertension (OHT). Sustained OHT exerts mechanical pressure on the retinal ganglion cells (RGCs) and the optic nerve fibers at the back of the eye leading to their progressive demise by apoptosis, thereby distorting and diminishing visual acuity over time, and eventually leading to irreversible blindness. In some patients even “normal” IOP is destructive because their RGCs and their axons projecting to the brain are genetically or chemically predisposed to early cell death. These pathologies are termed “glaucomatous optic neuropathy (GON)” and OHT is often associated with glaucoma, especially primary open-angle glaucoma (POAG). Today, there are several pharmacological and minimally invasive surgical interventions / devices that constitute therapeutic modalities to treat OHT and glaucoma. OHT etiology and treatments will be discussed in more detail in this review article.},
     year = {2017}
    }
    

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  • TY  - JOUR
    T1  - Ocular Hypertension and Glaucoma: A Review and Current Perspectives
    AU  - Najam A. Sharif
    Y1  - 2017/04/14
    PY  - 2017
    N1  - https://doi.org/10.11648/j.ijovs.20170202.11
    DO  - 10.11648/j.ijovs.20170202.11
    T2  - International Journal of Ophthalmology & Visual Science
    JF  - International Journal of Ophthalmology & Visual Science
    JO  - International Journal of Ophthalmology & Visual Science
    SP  - 22
    EP  - 36
    PB  - Science Publishing Group
    SN  - 2637-3858
    UR  - https://doi.org/10.11648/j.ijovs.20170202.11
    AB  - Hypertension of the eye fundamentally results from an imbalance between the production and extrusion of aqueous humor (AQH) within the anterior segment of the eye. Vitreous humor (VH) (in the posterior segment of the eye) and AQH are responsible for maintaining the shape of the eye-ball in order that light is correctly focused on the retina for good vision. However, as we age, cells of the AQH drainage system (trabecular meshwork, TM) die and cellular debris accumulates within the TM and the canal of Schlemm thereby slowing, and in some cases, preventing AQH efflux. This results in increased resistance and elevation of hydrostatic pressure within the anterior segment, also termed as elevated intraocular pressure (IOP) or ocular hypertension (OHT). Sustained OHT exerts mechanical pressure on the retinal ganglion cells (RGCs) and the optic nerve fibers at the back of the eye leading to their progressive demise by apoptosis, thereby distorting and diminishing visual acuity over time, and eventually leading to irreversible blindness. In some patients even “normal” IOP is destructive because their RGCs and their axons projecting to the brain are genetically or chemically predisposed to early cell death. These pathologies are termed “glaucomatous optic neuropathy (GON)” and OHT is often associated with glaucoma, especially primary open-angle glaucoma (POAG). Today, there are several pharmacological and minimally invasive surgical interventions / devices that constitute therapeutic modalities to treat OHT and glaucoma. OHT etiology and treatments will be discussed in more detail in this review article.
    VL  - 2
    IS  - 2
    ER  - 

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  • Global Alliances and External Research, Global Research & Development, Santen Incorporated, Emeryville, USA

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