Abstract
Glaucoma is a multifactorial disease with progressive loss of retinal ganglion cells (RGCs). Optic nerve head (ONH) is the main site of glaucomatous damage, with inferotemporal part being especially vulnerable to any mechanical force, because a dense bundle of RGCs axons enter ONH. Lamina cribrosa movement, distortion and collapse results in axonal damage. Loss of RGCs cause typical glaucomatous visual field defects. Continuous progression of the disease negatively affects a broad spectrum of everyday life activities, like good postural and balance control, walking, reading and driving. Ongoing structural glaucomatous changes negatively impact functional patients’ outcome, thus exacerbating their quality of life.
Therefore, the assessment of relationship between structure and function is one of the most important aspects to provide patients with best care. By evaluating the severity and progression of the disease in a timely manner, appropriate treatment regimen can be initiated for glaucoma patients.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
Ogden T, Duggan JDK, et al. Morphometry of nerve bundle pores in the optic nerve head of the human. Exp Eye Res. 1988;46:559–68.
Grytz R, Fazio MA, Libertiaux V, Bruno L, Gardiner S, Girkin CA, et al. Age-and race-related differences in human scleral material properties. Investig Ophthalmol Vis Sci. 2014;55(12):8163–72.
Girard MJA, Suh JF, Bottlang M, Burgoyne CF, Downs JC. Scleral biomechanics in the aging monkey eye. Invest Ophthalmol Vis Sci. 2009;50(11):5226–37.
Yang H, He L, Gardiner SK, Reynaud J, Williams G, Hardin C, et al. Age-related differences in longitudinal structural change by spectral-domain optical coherence tomography in early experimental glaucoma. Invest Opthalmol Vis Sci. 2014;55(10):6409.
Downs JC, Girkin CA. Lamina cribrosa in glaucoma. Curr Opin Ophthalmol. 2017;28(2):113–9.
Strouthidis NG, Fortune B, Yang H, Sigal IA, Burgoyne CF. Longitudinal change detected by spectral domain optical coherence tomography in the optic nerve head and peripapillary retina in experimental glaucoma. Invest Ophthalmol Vis Sci. 2011;52:1206–19.
Yang H. 3-D histomorphometry of the normal and early glaucomatous monkey optic nerve head: lamina cribrosa and peripapillary scleral position and thickness. Invest Ophthalmol Vis Sci. 2007;48:4597–607.
Kim JA, Kim TW, Weinreb RN, Lee EJ, Girard MJA, Mari JM. Lamina Cribrosa morphology predicts progressive retinal nerve fiber layer loss in eyes with suspected Glaucoma. Sci Rep. 2018;8(1):1–10.
Radius RL, Anderson DR. The course of axons through the retina and optic nerve head. Arch Ophthalmol. 1979;97:1154–8.
Quigley H, Addicks EM. Regional differences in the structure of the lamina cribrosa and their relation to glaucomatous optic nerve damage. Arch Ophthalmol. 1981;99:137–43.
Hood DC, Raza AS, de Moraes CG, et al. Glaucomatous damage of the macula. Prog Retin Eye Res. 2013;32:1–21.
Hood DC, Raza AS, de Moraes CG, et al. The nature of macular damage in glaucoma as revealed by averaging optical coherence tomography data. Transl Vis Sci Technol. 2012;1:3.
Dandona L, Quigley HA, Brown AE, et al. Quantitative regional structure of the normal human lamina cribrosa. A racial comparison. Arch Ophthalmol. 1990;108:393–8.
Sung MS, Kang BW, Kim HG, et al. Clinical validity of macular ganglion cell complex by spectral domain-optical coherence tomography in advanced glaucoma. J Glaucoma. 2014;23:341–6.
Nouri-Mahdavi K, Hoffmann D, Coleman AL, et al. Predictive factors for glaucomatous visual field progression in the Advanced Glaucoma Intervention Study. Ophthalmology. 2004;111:1627–35.
Siaudvytyte L, Januleviciene I, Ragauskas A, Bartusis L, Meiliuniene ISB, et al. The difference in translaminar pressure gradient and neuroretinal rim area in glaucoma and healthy subjects. J Ophthalmol. 2014;2014:937360.
Feola AJ, Coudrillier B, Mulvihill J, Geraldes DM, Vo NT, Albon J, et al. Deformation of the lamina cribrosa and optic nerve due to changes in cerebrospinal fluid pressure. Invest Ophthalmol Vis Sci. 2017;58(4):2070–8.
Hayreh SS, Zimmerman MB, Podhajsky PAW. Nocturnal arterial hypotension and its role in optic nerve head and ocular ischemic disorders. Am J Ophthalmol. 1994;117:603–24.
Flammer J, Haefliger IO, Orgül SRT. Vascular dysregulation: a principal risk factor for glaucomatous damage? J Glaucoma. 1999;8:212–9.
Drance S, Anderson DR, Schulzer M, Collaborative Normal-Tension Glaucoma Study Group. Risk factors for progression of visual field abnormalities in normal-tension glaucoma. Am J Ophthalmol. 2001;131:699–708.
Nicolela MT, Ferrier SN, Morrison CA, et al. Effects of coldinduced vasospasm in glaucoma: the role of endothelin-1. Invest Ophthalmol Vis Sci. 2003;44:2565–72.
Emre M, Orgül S, Haufschild T, Shaw SG, Flammer J. Increased plasma endothelin-1 levels in patients with progressive open angle glaucoma. Br J Ophthalmol. 2005;89:60–3.
Cioffi GA. Ischemic model of optic nerve injury. Trans Am Ophthalmol Soc. 2005;103:592–613.
Pache M, Flammer J. A sick eye in a sick body? Systemic findings in patients with primary open-angle glaucoma. Surv Ophthalmol. 2006;51:179–212.
Gherghel D, Hosking SL, Cunliffe IA. Abnormal systemic and ocular vascular response to temperature provocation in primary open-angle glaucoma patients: a case for autonomic failure? Invest Ophthalmol Vis Sci. 2004;45:3546–54.
Mackenzie PJ, Cioffi GA. Vascular anatomy of the optic nerve head. Can J Ophthalmol/J Can d’Ophtalmologie. 2008;43(3):308–12.
Jia Y, Morrison JC, Tokayer J, et al. Quantitative OCT angiography of optic nerve head blood flow. Biomed Opt Express. 2012;3:3127–37.
Liu L, Jia Y, Takusagawa HL, et al. Optical coherence tomography angiography of the peripapillary retina in glaucoma. JAMA Ophthalmol. 2015;133:1045–52.
Yarmohammadi A, Zangwill LM, Diniz-Filho A, et al. Optical coherence tomography angiography vessel density in healthy, glaucoma suspect, and glaucoma eyes. Invest Ophthalmol Vis Sci. 2016;57:OCT451–9.
Yoles E, Schwartz M. Degeneration of spared axons following partial white matter lesion: implications for optic nerve neuropathies. Exp Neurol. 1988;153(1):1–7.
Hernandez MR. The optic nerve head in glaucoma: role of astrocytes in tissues remodeling. Prog Retin Eye Res. 2000;19:297–321.
Qu J, Jakobs TC. The time course of gene expression during reactive gliosis in the optic nerve. PLoS One. 2013;8(6):e67094.
Liu B, Neufeld AH. Expression of nitric oxide synthase-2 (NOS-2) in reactive astrocytesof the human glaucomatous optic nerve head. Glia. 2000;30:78–86.
Jourdain P, Bergersen LH, Bhaukaurally K, et al. Glutamate exocytosis from astrocytes controls synaptic strength. Nat Neurosci. 2007;10(3):331–9.
Ramirez AI, de Hoz R, Salobrar-Garcia E, Salazar JJ, Rojas B, Ajoy D, et al. The role of microglia in retinal neurodegeneration: Alzheimer’s disease, Parkinson, and glaucoma. Front Aging Neurosci. 2017;9(JUL):1–21.
Leaver SG, Cui Q, Plant GW, Arulpragasam A, Hisheh S, Verhaagen J, Harvey AR. AAV-mediated expression of CNTF promotes long-term survival and regeneration of adult rat retinal ganglion cells. Gene Ther. 2006;13:1328–41.
Leaver SG, Cui Q, Bernard O, Harvey AR. Cooperative effects of bcl-2 and AAV-mediated expression of CNTF on retinal ganglion cell survival and axonal regeneration in adult transgenic mice. Eur J Neurosci. 2006;24:3323–32.
Di Polo A, Aigner LJ, Dunn RJ, Bray GM, Aguayo AJ. Prolonged delivery of brain-derived neurotrophic factor by adenovirus-infected Muller cells temporarily rescues injured retinal ganglion cells. Proc Natl Acad Sci U S A. 1998;95:3978–83.
Quigley HA, Nickells RW, Kerrigan LA, et al. Retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis. Invest Ophthalmol Vis Sci. 1995;36:774–86.
Gupta N, Ang LC, Noel de Tilly L, et al. Human glaucoma and neural degeneration in intracranial optic nerve, lateral geniculate nucleus, and visual cortex. Br J Ophthalmol. 2006;90:674–8.
Yamamoto T, Kitazawa Y. Vascular pathogenesis of normal-tension glaucoma: a possible pathogenic factor, other than intraocular pressure, of glaucomatous optic neuropathy. Prog Retin Eye Res. 1998;17:127–43.
Hare WA, Wheeler L. Experimental glutamatergic excitotoxicity in rabbit retinal ganglion cells: block by memantine. Invest Ophthalmol Vis Sci. 2009;50(6):2940–8.
Vorwerk CK, Lipton SA, Zurakowski D, et al. Chronic low-dose glutamate is toxic to retinal ganglion cells. Toxicity blocked by memantine. Invest Ophthalmol Vis Sci. 1996;37(8):1618–24.
Lipton SA, Rosenberg PA. Mechanisms of disease: excitatory amino acids as a final common pathway in neurologic disorders. N Engl J Med. 1994;330(9):613–22.
Meldrum B, Garthwaite J. Excitatory amino acid neurotoxicity and neurodegenerative disease. Trends Pharmacol Sci. 1990;11(9):379–87.
Hartwick AT, Zhang X, Chauhan BC, et al. Functional assessment of glutamate clearance mechanisms in chronic rat glaucomamodel using retinal ganglion cell calcium imaging. J Neurochem. 2005;94:794–807.
Levkovitch-Verbin H, Quigley HA, Kerrigan-Baumrind LA, et al. Optic nerve transection in monkeys may result in secondary degeneration of retinal ganglion cells. Invest Ophthalmol Vis Sci. 2001;42:975–82.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2019 Springer Nature Switzerland AG
About this chapter
Cite this chapter
Maciulaitiene, R., Januleviciene, I. (2019). Structure Loss. In: Januleviciene, I., Harris, A. (eds) Biophysical Properties in Glaucoma. Springer, Cham. https://doi.org/10.1007/978-3-319-98198-7_18
Download citation
DOI: https://doi.org/10.1007/978-3-319-98198-7_18
Published:
Publisher Name: Springer, Cham
Print ISBN: 978-3-319-98197-0
Online ISBN: 978-3-319-98198-7
eBook Packages: MedicineMedicine (R0)