**1. Introduction**

[58] Toris, C. B, Gabelt, B. T, & Kaufman, P. L. Update on the mechanism of action of top‐ ical prostaglandins for intraocular pressure reduction. Surv. Ophthalmol. (2008).

[59] Tripathi, B. J, Tripathi, R. C, Chen, J, Gotsis, S, & Li, J. Trabecular cell expression of fibronectin and MMP-3 is modulated by aqueous humor growth factors. Exp. Eye

[60] Vesaluoma, M, Mertaniemi, P, Mannonen, S, Lehto, I, Uusitalo, R, Sarna, S, Tarkka‐ nen, A, & Tervo, T. Cellular and plasma fibronectin in the aqueous humour of pri‐ mary open-angle glaucoma, exfoliative glaucoma and cataract patients. Eye (Lond).

[61] Vessey, K, Lencses, K, Rushforth, D, Hruby, V, & Stell, W. Glucagon receptor ago‐ nists and antagonists affect the growth of the chick eye: a role for glucagonergic reg‐ ulation of emmetropization? Invest. Ophthalmol. Vis. Sci. (2005). , 46(11), 3922-3931.

[62] Weinstein, B, Gordon, G, & Southren, A. Potentiation of glucocorticoid activity by 5 beta-dihydrocortisol: its role in glaucoma. Science. (1983). , 222(4620), 172-173.

[63] Wilbanks, G, Mammoli, M, & Streilen, J. Studies on the induction of anterior cham‐ ber-associated immune deviation (ACAID). III. Induction of ACAID depends upon intraocular transforming growth factor-beta. Eur. J. Immunol. (1992). , 22(1), 165-173.

[64] Wordinger, R. J, Fleenor, D. L, Hellberg, P. E, Pang, I. H, Tovar, T. O, Zode, G. S, Fuller, J. A, & Clark, A. F. Effects of TGF-beta2, BMP-4, and gremlin in the trabecular meshwork: implications for glaucoma. Invest. Ophthalmol. Vis. Sci. (2007). Mar; ,

[65] Yamada, N, Yanai, R, Inui, M, & Nishida, T. Sensitizing effect of substance P on cor‐ neal epithelial migration induced by IGF-1, fibronectin, or interleukin-6. Invest. Oph‐

[66] Yanai, R, Yamada, N, Inui, M, & Nishida, T. Correlation of proliferative and antiapoptotic effects of HGF, insulin, IGF-1, IGF-2, and EGF in SV40-transformed human corneal epithelial cells. Exp. Eye Res. (2006). Jul; Epub 2006 Mar 10., 83(1), 76-83.

[67] Zilfyan, A. A. Shifts in content of fibronectin, insulin-like growth factor-1 and E2 prostaglandins in aqueous humour in case of senile and complicated cataracts. The

[68] Zilfyan, A. A. The role of cortisol, prolactin, CD4 and CD8 in induction of anterior chamber associated immune deviation (ACAID) in case of cataracts. The New Arme‐

Nov; 53 (Suppl. 1): S, 107-120.

102 Glaucoma - Basic and Clinical Aspects

Res. (2004). Mar; , 78(3), 653-660.

(1998). Pt 5): 886-890.

48(3), 1191-1200.

thalmol. Vis. Sci. (2005). Mar; , 46(3), 833-839.

New Armenian Medical Journal. (2012). , 6(3), 34-41.

nian Medical Journal. (2009). , 3(1), 59-67.

Glaucomas are a heterogeneous group of optic neuropathies characterized by progressive loss of retinal ganglion cells (RGCs) leading to visual field defects. The distinctive pattern of optic nerve degeneration results in glaucomatous cupping. The atrophy of optic nerve cells initially leads to loss of peripheral vision and visual field loss increases with increased dam‐ age to optic nerve. Worldwide glaucoma is the second leading cause of blindness affecting more than 70 million people [1, 2]. Traditionally elevated intraocular pressure (IOP) is con‐ sidered as a major risk factor for glaucomatous neuropathy. In addition to increased IOP, other risk factors include age, genetic and environmental factors, myopia, primary vascular dysregulation and hypertension [3, 4].

Glaucoma has been classified into different types based on various criteria. One of the wide‐ ly used classifications depends on the nature of iridio-corneal angle [5]. Primary open angle glaucomas (POAGs) are the most common and clinically well defined subsets of glaucomas among Caucasians [6]. As its name suggests, in POAG there is no anatomical hindrance to the flow of aqueous humor as the angle structures remain 'open'. However, the drainage of humor is still inefficient resulting in an increase in IOP. Based on the age of onset, POAG can be juvenile (5-35 years) or adult onset (onset after 45 years) [6]. POAGs are usually chronic and largely asymptomatic, with gradual elevation of IOP and consequent visual field loss. In a significant fraction of POAG, glaucoma occurs even in the absence of eleva‐ tion of IOP. These are recognized as normal tension glaucomas (NTG) [7].

© 2013 Swarup et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Angle closure glaucomas (ACGs) are relatively rare among Caucasians and usually are acute. It is the most common form of glaucoma in Asian population [8, 9]. In ACGs, the iri‐ diocorneal angle is closed, blocking the drainage of aqueous humor and resulting in eleva‐ tion of IOP. People with shallower anterior chamber, with hypermetropia and hence narrower angles, are more susceptible to ACGs. Unlike POAG, ACG can be associated with symptoms like eye pain, blurred vision, headache, nausea, and hence is usually detected earlier [10].

In developmental or congenital glaucoma, developmental anomalies in tissues like trabecu‐ lar meshwork and Schlemm's canal cause optic neuropathies [5].
