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Outlook on Therapeutic Strategies for Primary Open-Angle Glaucoma Based on the Theory of Translamina-Pressure Difference

  • Weiwei Chen
  • Ningli WangEmail author
Chapter
Part of the Advances in Visual Science and Eye Diseases book series (AVSED, volume 1)

Abstract

Glaucoma is a group of optic nerve lesions characterized by progressive loss of retinal ganglion cells (RGCs) and their axons and primarily manifested by progressive optic nerve damage, atrophy, and visual field defects, with increased intraocular pressure (IOP) being the main risk factor [1]. Generally, glaucoma is classified into two types: primary angle-closure glaucoma (PACG) and primary open-angle glaucoma (POAG). PACG is mainly a result of optic nerve damage caused by blockage of aqueous humor outflow and elevated intraocular pressure due to mechanical angle closure, and its pathogenesis has been clearly known. Along with the economic development and lifestyle changes in the country, the disease profiles have changed greatly. Currently, primary open-angle glaucoma (POAG) has become the most common irreversible eye disease that results in blindness and disability, accounting for 74% of the patients with glaucoma, with its pathogenesis yet remaining unknown so far [2].

References

  1. 1.
    Kwon YH, Fingert JH, Kuehn MH, Alward WL. Primary open-angle glaucoma. N Engl J Med. 2009;360(11):1113–24.CrossRefGoogle Scholar
  2. 2.
    Quigley HA, Broman AT. The number of people with glaucoma worldwide in 2010 and 2020. Br J Ophthalmol. 2006;90(3):262–7.CrossRefGoogle Scholar
  3. 3.
    Shields MB. Normal-tension glaucoma: is it different from primary open-angle glaucoma? Curr Opin Ophthalmol. 2008;19(2):85–8.CrossRefGoogle Scholar
  4. 4.
    Wang N, Xie X, Yang D, Xian J, Li Y, Ren R, Peng X, Jonas JB, Weinreb RN. Orbital cerebrospinal fluid space in glaucoma: the Beijing intracranial and intraocular pressure (iCOP) study. Ophthalmology. 2012;119(10):2065–73. e2061CrossRefGoogle Scholar
  5. 5.
    Burgoyne CF, Downs JC. Premise and prediction-how optic nerve head biomechanics underlies the susceptibility and clinical behavior of the aged optic nerve head. J Glaucoma. 2008;17(4):318–28.CrossRefGoogle Scholar
  6. 6.
    Fechtner RD, Weinreb RN. Mechanisms of optic nerve damage in primary open angle glaucoma. Surv Ophthalmol. 1994;39(1):23–42.CrossRefGoogle Scholar
  7. 7.
    Yamamoto T, Kitazawa Y. Vascular pathogenesis of normal-tension glaucoma: a possible pathogenetic factor, other than intraocular pressure, of glaucomatous optic neuropathy. Prog Retin Eye Res. 1998;17(1):127–43.CrossRefGoogle Scholar
  8. 8.
    Band LR, Hall CL, Richardson G, Jensen OE, Siggers JH, Foss AJ. Intracellular flow in optic nerve axons: a mechanism for cell death in glaucoma. Invest Ophthalmol Vis Sci. 2009;50(8):3750–8.CrossRefGoogle Scholar
  9. 9.
    Zhang Z, Wang X, Jonas JB, Wang H, Zhang X, Peng X, Ritch R, Tian G, Yang D, Li L, et al. Valsalva manoeuver, intra-ocular pressure, cerebrospinal fluid pressure, optic disc topography: Beijing intracranial and intra-ocular pressure study. Acta Ophthalmol. 2013;Google Scholar
  10. 10.
    Sakka SG. The patient with intra-abdominal hypertension. Anasthesiol Intensivmed Notfallmed Schmerzther. 2016;51(1):8–16.CrossRefGoogle Scholar
  11. 11.
    Youssef AM, Hamidian Jahromi A, Vijay CG, Granger DN, Alexander JS. Intra-abdominal hypertension causes reversible blood-brain barrier disruption. J Trauma Acute Care Surg. 2012;72(1):183–8.PubMedGoogle Scholar
  12. 12.
    Sinclair AJ, Walker EA, Burdon MA, van Beek AP, Kema IP, Hughes BA, Murray PI, Nightingale PG, Stewart PM, Rauz S, Tomlinson JW. Cerebrospinal fluid corticosteroid levels and cortisol metabolism in patients with idiopathic intracranial hypertension: a link between 11beta-HSD1 and intracranial pressure regulation? J Clin Endocrinol Metab. 2010;95(12):5348–56.CrossRefGoogle Scholar
  13. 13.
    Jacobson DM, Wall IM, Digre KB, Corbett J. Serum vitamin A concentrate is elevated in idiopathic intracranial hypertension. Neurology. 1999;53:1114–8.CrossRefGoogle Scholar
  14. 14.
    Warner JEA, Bernstein PS, Yemelyanov A, Alder SC, Farnsworth ST, Digre KB. Vitamin A in the cerebrospinal fluid of patients with and without idiopathic intracranial hypertension. Ann Neurol. 2002;52:647–50.CrossRefGoogle Scholar
  15. 15.
    Selhorst J, Kulkantrakorn K, Corbett JJ, Leira EC, Chung SM. Retinol- binding protein in idiopathic intracranial hypertension (IIH). J Neuroophthalmol. 2000;20:250–2.CrossRefGoogle Scholar
  16. 16.
    Wang YX, Jonas JB, Wang N, You QS, Yang D, Xie XB, Xu L. Intraocular pressure and estimated cerebrospinal fluid pressure. The Beijing Eye Study 2011. PLoS One. 2014;9(8):e104267.CrossRefGoogle Scholar
  17. 17.
    Xu L, Wang YX, Wang S, Jonas JB. Neuroretinal rim area and body mass index. PLoS One. 2012;7(1):e30104.CrossRefGoogle Scholar
  18. 18.
    Ren R, Wang N, Zhang X, Tian G, Jonas JB. Cerebrospinal fluid pressure correlated with body mass index. Graefes Arch Clin Exp Ophthalmol. 2012;250(3):445–6.CrossRefGoogle Scholar

Copyright information

© Springer Nature Singapore Pte Ltd. 2019

Authors and Affiliations

  1. 1.Beijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren HospitalCapital Medical UniversityBeijingChina
  2. 2.Beijing Ophthalmology & Visual Sciences Key LaboratoryBeijingChina

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