Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:
Ординатура / Офтальмология / Английские материалы / Clinical Anatomy and Physiology of the Visual System 3rd edition_Remington_2012.pdf
Скачиваний:
0
Добавлен:
28.03.2026
Размер:
25.17 Mб
Скачать

106 Clinical Anatomy of the Visual System

seen in senile nuclear sclerosis.92 The color changes that often accompany nuclear cataracts are usually seen as various hues of yellow or brown; this pigmentation is primarily protein-bound.91

Posterior Subcapsular Cataract (PSC)

The opacity in the posterior subcapsular region is formed by epithelial-like cells that migrate from the equatorial region. These cells accumulate at the posterior pole forming an opacity.96 It is speculated that radiation damage is one causative factor as patients undergoing radiation therapy for cancer treatments also develop PSCs and/or cortical cataracts.62 There are some sutural congenital cataracts that occur at this location, but they are caused by swelling of the basal ends of cortical fibers.62

Steroid-Induced Cataract

Steroid-induced cataracts are also located in the posterior subcapsular region. Dosage and the duration of steroid use appear to be controlling factors, although individuals may have varying levels of susceptibility. Children develop such cataracts at a faster rate than do adults. Reversal of the cataract can occur but this is rare.5,37,66 The opacity appears to be formed of undifferentiated epithelial cells at the interface of the posterior cortex and capsule. These misplaced cells (which should only be present in the lens epithelium) display aberrant behavior. The undifferentiated cells may have migrated from the preequatorial area, influenced by a change in the concentration of growth factors.66 The growth factors governing mitosis, migration, and differentiation are obtained from aqueous and reside in the lens capsule. If steroids influence production of these growth factors that are present in the aqueous, and the concentration and location in the capsule is altered, cellular processes can be affected.66

REFERENCES

1.Patterson CA, Delamere NA: The lens. In Hart WM, editor: Adler’s physiology of the eye, ed 9, St Louis, 1992, Mosby, p 348.

2.Dubbelman M, van der Heijde GL, Weeber HA: The thickness of the aging human lens obtained from corrected Scheimpflug images, Optom Vis Sci 78(6):411, 2001.

3.Koretz JE, Strenk SA, Strenk LM, et al: Scheimpflug and high resolution­ magnetic resonance imaging of the anterior segment: a comparative study, J Opt Soc Am A Opt Image Sci Vis 21:346–354, 2004.

4.Hogan MJ, Alvarado JA, Weddell JE: Histology of the human eye, Philadelphia, 1971, Saunders, p 638.

5.Strenk SA, Semmlow JL, Strenk LM, et al: Age-related changes in ciliary muscle and lens: a magnetic resonance imaging study,

Invest Ophthalmol Vis Sci 40:1162, 1999.

6.Jones CE, Atchison DA, Pope JM: Changes in lens dimensions and refractive index with age and accommodation, Optom Vis Sci 84:990–995, 2007.

7.Rosen AM, Denham DB, Fernandez V, et al: in vitro dimensions and curvatures of human lenses, Vision Res 46:1002–1009, 2006.

8.Glasser A, Kaufman PL: Accommodation and presbyopia. In Kaufman PL, Alm A, editors: Adler’s physiology of the eye, ed 10, St Louis, 2003, Mosby, p 197.

9.Smith G, Pierscionek BK: The optical structure of the lens and its contribution to the refractive status of the eye, Ophthalmic Physiol Opt 18(1):21, 1998.

10.Pierscionek BK: Refractive index contours in the human lens, Exp Eye Res 64:887, 1997.

11.Borish IM: Clinical refraction, ed 3, Chicago, 1975, Professional Press, p 169.

12.Koretz JF, Handelman GH, Brown NP: Analysis of human crystalline lens curvature as a function of accommodative state and age, Vision Res 24:1141, 1984.

13.Kuszak JR, Brown HG: Embryology and anatomy of the lens. In Albert DM, Jakobiec FA, editors: Principles and practice of ophthalmology, Philadelphia, 1994, Saunders, p 82.

14.Barraquer RI, Michael R, Abreu R, et al: Human lens capsule thickness as a function of age and location along the sagittal lens perimeter, Invest Ophthalmol Vis Sci 47:2053–2060, 2006.

15.Alexander RA, Garner A: Elastic and precursor fibres in the normal human eye, Exp Eye Res 36:305, 1983.

16.Krag S, Olsen T, Andreassen TT: Biomechanical characteristics of the human anterior lens capsule in relation to age, Invest Ophthalmol Vis Sci 38(2):357, 1997.

17.Kuwabara T: The maturation of the lens cell: a morphologic study, Exp Eye Res 20:427, 1975.

18.Kuszak JR, Peterson KL, Brown HG: Electron microscopic observations of the crystalline lens, Microsc Res Tech 33:441, 1996.

19.Bassnett S, Kuszak JR, Reinisch L, et al: Intercellular communication between epithelial and fiber cells of the eye lens, J Cell Sci 107:799, 1994.

20.Rae J: Physiology of the lens. In Albert DM, Jakobiec FA, editors: Principles and practice of ophthalmology, Philadelphia, 1994, Saunders,­ p 123.

21.Kuszak JR, Novak LA, Brown HG: An ultrastructural analysis of the epithelial-fiber interface (EFI) in primate lenses, Exp Eye Res 61:579, 1995.

22.Lo WK, Harding CV: Structure and distribution of gap junctions in lens epithelium and fiber cells, Cell Tissue Res 244(2):253, 1986.

23.Lo WK, Harding CV: Tight junctions in the lens epithelia of human and frog: freeze-fracture and protein tracer studies, Invest Ophthalmol Vis Sci 24(4):396, 1983.

24.Mathias RT, Kistler J, Donaldson P: The lens circulation, J Membr Biol 216:1–16, 2007.

25.Vavvas D, Azar NF, Azar DT: Mechanisms of disease: cataracts,

Ophthalmol Clin North Am 15:49, 2002.

26.Clark JI: Development and maintenance of lens transparency. In Albert DM, Jakobiec FA, editors: Principles and practice of ophthalmology, Philadelphia, 1994, Saunders, p 114.

27.Mathias RT, Rae JL: Transport properties of the lens, Am J Physiol 249(3):181, 1985.

28.Dahm R, van Marle J, Prescott AR, et al: Gap junctions containing alpha8-connexin (MP70) in the adult mammalian lens epithelium suggests a re-evaluation of its role in the lens, Exp Eye Res 69:45, 1999.

29.Kuszak JR, Peterson KL, Sivak JG, et al: The interrelationship of lens anatomy and optical quality. II. Primate lenses, Exp Eye Res 59(5):521, 1994.

30.Streeten BW, Licari PA: The zonules and the elastic microfibrillar system in the ciliary body, Invest Ophthalmol Vis Sci 24(6):667, 1983.

31.Bourge JL, Robert AM, Renard G: Zonular fibers, multimolecular composition as related to function (elasticity) and pathology,

Pathol Biol (Paris) 55:347–359, 2007.

CHAPTER 5  t  Crystalline Lens 107

32.Rohen JW: Scanning electron microscopic studies of the zonular apparatus in human and monkey eyes, Invest Ophthalmol Vis Sci 18:133, 1979.

33.Von Helmholtz HH: Treatise on physiologic optics, Mineola, NY, 1962, Dover (Translated by JPC Southhall), p 143.

34.Von Noorden G: Burien and von Noorden’s binocular vision and ocular­ motility, ed 5, St Louis, 1996, Mosby, p 85.

35.Johnson CA: Effects of luminance and stimulus distance on accommodation and visual resolution, J Opt Soc Am 66:138–142, 1976.

36.Garner LF, Smith G: Changes in equivalent and gradient refractive index of the crystalline lens with accommodation, Optom Vis Sci 74(2):114, 1997.

37.Garner LF, Yap MK: Changes in ocular dimensions and refraction with accommodation, Ophthalmic Physiol Opt 17(1):12, 1997.

38.Drexler W, Baumgartner A, Findl O, et al: Biometric investigation of changes in the anterior eye segment during accommodation, Vision Res 37:2789, 1997.

39.Drexler W, Findl O, Schmetterer L, et al: Eye elongation during accommodation in humans: differences between emmetropes and myopes, Invest Ophthalmol Vis Sci 39(11):2140, 1998.

40.Koretz JF, Bertasso AM, Neider MW, et al: Slit-lamp studies of the rhesus monkey eye. II. Changes in crystalline lens shape, thickness and position during accommodation and aging, Exp Eye Res 45:317, 1987.

41.Ludwig K, Wegscheider E, Hoops JP, et al: in vivo imaging of the human zonular apparatus with high-resolution ultrasound biomicroscopy, Graefes Arch Clin Exp Ophthalmol 237:361–371, 1999.

42.Fisher RF: The vitreous and lens in accommodation, Trans Ophthalmol­ Soc U K 102:318, 1982.

43.Mauger RR, Likens CP, Applebaum M: Effects of accommodation and repeated applanation tonometry on intraocular pressure, Am J Optom Physiol Opt 6(1):28, 1984.

44.Hamasaki D, Ong J, Marg E: The amplitude of accommodation in presbyopia, Am J Optom Arch Am Acad Optom 33:3–14, 1956.

45.Pardue MT, Sivak JG: Age-related changes in human ciliary muscle, Optom Vis Sci 77:204, 2000.

46.Hermans EA, Dubbelman M, van der Heijde GL, et al: Change in the accommodative force on the lens of the human eye with age, Vision Res 48:119–126, 2008.

47.Strenk SA, Strenk LM, Guo S: Magnetic resonance imaging of aging, accommodating, phakic, and pseudophakic ciliary muscle diameters, J Cataract Refract Surg 32:1792–1798, 2006.

48.Sakabe I, Oshika T, Lim SJ, et al: Anterior shift of zonular insertion onto the anterior surface of human crystalline lens with age, Ophthalmology 105(2):295, 1998.

49.Assia EI, Apple DJ, Morgan RC, et al: The relationship between stretching capability of the anterior capsule and zonules, Invest Ophthalmol Vis Sci 32:2835–2839, 1991.

50.Fisher RF: The influence of age on some ocular basement membranes, Eye 1:184–189, 1987.

51.Krag S, Andreassen TT: Mechanical properties of the human posterior lens capsule, Invest Ophthalmol Vis Sci 44:691, 2003.

52.Seland JH: Ultrastructural changes in the normal human lens capsule­ from birth to old age, Acta Ophthalmol 52:688, 1974.

53.Glasser A, Campbell MC: Biometric, optical and physical changes in the isolated human crystalline lens with age in relation to presbyopia, Vision Res 39:1991, 1999.

54.Beers AP, van der Heijde GL: Age-related changes in the accommodation mechanism, Optom Vis Sci 73(4):235, 1996.

55.Brown N: The change in lens curvature with age, Exp Eye Res 19:175, 1974.

56.Brandreth RH: Clinical slit lamp biomicroscopy, Berkeley, Calif, 1978, Brandreth.

57.Sasaki K, Kojirna M, Hara T: in vivo observation of the crystalline lens capsule, Ophthalmic Res 20(3):154, 1988.

58.Trokel S: The physical basis for transparency of the crystalline lens, Invest Ophthalmol 1:493, 1962.

59.Danysh BP, Duncan MK: The lens capsule, Exp Eye Res 88:151–164, 2009.

60.Hejtmancik JF: Congenital cataracts and their molecular genetics,

Semin Cell Dev Biol 19:134–149, 2008.

61.Chong HNV: Clinical ocular physiology, Butterworth Heinemann,

Linacre House, Oxford, UK, 1996, Jordan Hill, p 41.

62.Beebe DC: The lens. In Kaufman PL, Alm A, editors: Adler’s physiology of the eye, ed 10, St Louis, 2003, Mosby, p 117.

63.Truscott RJ: Presbyopia. Emerging from a blur towards an understanding of the molecular basis for this most common eye condition, Exp Eye Res 88:241–247, 2009.

64.Takemoto L, Sorensen CM: Protein-protein interactions and lens transparency, Exp Eye Res 87:496–501, 2008.

65.Zelenka PS, Arpitha P: Coordinating cell proliferation and migration in the lens and cornea, Sem Cell Develop Bio 19:113–124, 2008.

66.Jobling AI, Augusteyn RC: What induces steroid cataracts? A review of steroid-induced posterior subcapsular cataracts, Clin Exp Optom 85:61–75, 2002.

67.Rao PV, Maddala R: The role of the lens actin cytoskeleton in fiber cell elongation and differentiation, Sem Cell Dev Bio 17:698–711, 2006.

68.Donaldson PJ, Chee KS, Lim JC, et al: Regulation of lens volume: Implication for lens transparency, Exp Eye Res 88:144–150, 2009.

69.Delamere NA, Tamiya S: Lens Na+, K+-ATPase. In Tombran-Tink J, Barnstable CJ, editors: Ophthalmology research: ocular transporters in ophthalmic diseases and drug delivery, Totowa, NJ, 2008, Humana Press, pp 111–123.

70.Bassnett S, Beebe DC: Coincident loss of mitochondria and nuclei during lens fiber cell differentiation, Dev Dyn 194:85–92, 1992.

71.Delamere NA, Tamiya S: Lens ion transport: from basic concepts to regulation of Na+, K-ATPase activity, Exp Eye Res 88:140–143, 2009.

72.Zampighi GA: The lens. In Fischbarg J, editor: The biology of the eye, Amsterdam, 2006, Elsevier, pp 149–179.

73.Young RW: The family of sunlight-related eye diseases, Optom Vis Sci 71(2):125, 1994.

74.Hightower KR, Reddan JR, McCready JP, et al: Lens epithelium: a primary target of UVB irradiation, Exp Eye Res 59:557, 1994.

75.Hightower KR: The role of the lens epithelium in development of UV cataract, Curr Eye Res 14:71, 1995.

76.West SK, Duncan DD, Muñoz B, et al: Sunlight exposure and risk of lens opacities in a population-based study, Arch Ophthalmol 116:1666, 1998.

77.Berthoud VM, Beyer EC: Oxidative stress, lens gap junctions, and cataracts, Antioxid Redox Signal 11:339–353, 2009.

78.Reddy VN: Glutathione and its function in the lens—an overview, Exp Eye Res 50:771–778, 1990.

79.Reddy VN, Giblin FJ, Lin LR, et al: The effect of aqueous humor ascorbate on ultraviolet-B-induced DNA damage in lens epithelium, Invest Ophthalmol Vis Sci 39(2):344, 1998.

80.Alió JL, Schimchak P, Negri HP, et al: Crystalline lens optical dysfunction through aging, Ophthalmology 112:2022–2029, 2005.

81.Moffat BA, Landman KA, Truscott RJ, et al: Age-related changes in the kinetics of water transport in normal human lenses, Exp Eye Res 69(6):663, 1999.

82.Korlimbinis A, Berry Y, Thibault D, et al: Protein aging: truncation of aquaporin 0 in human lens regions is a continuous agedependent process, Exp Eye Res 88:966–973, 2009.

83.Friedrich MG, Truscott RJ: Membrane association of proteins in the aging human lens: Profound changes take place in the fifth decade of life, Invest Ophthalmol Vis Sci 50:4786–4793, 2009.

84.Pierscionek BK: Age-related response of human lenses to stretching forces, Exp Eye Res 60:325, 1995.

108 Clinical Anatomy of the Visual System

85.Moffat BA, Atchison DA, Pope JM: Age-related changes in refractive index distribution and power of the human lens as measured by magnetic resonance micro-imaging in vitro, Vis Res 42:1683, 2002.

86.Dubbelman M, van der Heijde GL: The shape of the aging human lens: curvature, equivalent refractive index and the lens paradox, Vision Res 41:1867, 2001.

87.Charman WN: The eye in focus: accommodation and presbyopia, Clin Exp Optom 91:207–225, 2008.

88.Cruickshanks KJ, Klein BE, Klein R: Ultraviolet light exposure and lens opacities: the Beaver Dam Eye Study, Am J Public Health 82(12):1658, 1992.

89.Brown NP, Harris ML, Shun-Shin GA, et al: Is cortical spoke cataract due to lens fibre breaks? The relationship between fibre folds, fibre breaks, waterclefts and spoke cataract, Eye 7:672, 1993.

90.Vrensen G, Willekens B: Biomicroscopy and scanning electron microscopy of early opacities in the aging human lens, Invest Ophthalmol­ Vis Sci 31(8):1582, 1990.

91.Truscott RJ: Age-related nuclear cataract-oxidation is the key, Exp Eye Res 80:709–725, 2005.

92.Sweeney MH, Truscott RJ: An impediment to glutathione diffusion in older normal human lenses: a possible precondition for nuclear cataract, Exp Eye Res 67:587, 1998.

93.Truscott RJ: Age-related nuclear cataract: a lens transport problem,

Ophthalmol Res 32:185, 2000.

94.Sweeney MH, Truscott RJ: An impediment to glutathione diffu­ sion in older normal human lenses: a possible precondition for nuclear cataract, Exp Eye Res 67:587–595, 1998.

95.Moffat BA, Landman KA, Truscott RJ, et al: Age-related changes in the kinetics of water transport in normal human lenses, Exp Eye Res 69:663–669, 1999.

96.Streeten BW, Eshaghian J: Human posterior subcapsular cataract. A gross and flat preparation study, Arch Ophthalmol 96:1653– 1658, 1978.

C H A P T E R

6 Aqueous and Vitreous Humors

The aqueous and vitreous are contained in three chambers within the eye. The anterior and posterior chambers contain aqueous humor, and the vitreous chamber contains the vitreous gel. A description of each chamber will be followed by an explanation of the formation, composition, and function of the aqueous and the vitreous.

A N T E R I O R C H A M B E R

The anterior chamber is bounded anteriorly by the corneal endothelium; peripherally by the trabecular meshwork, a portion of the ciliary body, and the iris root; and posteriorly by the anterior iris surface and the pupillary area of the anterior lens (Figure 6-1). The center of the anterior chamber is deeper than the periphery. The anterior chamber angle is formed at the periphery of the chamber, where the corneoscleral and uveal coats meet. The aqueous humor exits the anterior chamber through the structures located in this angle.

ANTERIOR CHAMBER ANGLE

STRUCTURES

The structures through which aqueous exits, collectively called the filtration apparatus, consist of the trabecular meshwork and Schlemm’s canal. These structures and the scleral spur occupy the excavated area located at the internal corneoscleral junction known as the internal scleral sulcus.

Scleral Spur

The scleral spur lies at the posterior edge of the internal scleral sulcus (see Chapter 2). The posterior portion of the scleral spur is the attachment site for the tendon of the longitudinal ciliary muscle fibers, whereas many of the trabecular meshwork sheets attach to the spur’s anterior aspect, such that the collagen of the spur is continuous with that of the trabeculae1 (Figure 6-2).

Trabecular Meshwork

The trabecular meshwork encircles the circumference of the anterior chamber, occupying most of the inner aspect of the internal scleral sulcus. In cross section it

has a triangular shape, with its apex at the termination of Descemet’s membrane (Schwalbe’s line) and its base at the scleral spur (Figure 6-3). The inner face borders the anterior chamber, and the outer side lies against corneal stroma, sclera, and Schlemm’s canal. The meshwork is composed of flattened perforated sheets, with three to five sheets at the apex. These sheets branch into 15 to 20 sheets as they extend posteriorly from Schwalbe’s line to the scleral spur.2 The trabecular meshwork is an open latticework, the branches of which interlace. The intertrabecular spaces between the sheets are connected through pores, or openings within the sheets (historically called the “spaces of Fontana”).3 The openings are of varying sizes and become smaller near Schlemm’s canal. No apertures directly join the meshwork with the canal.2 A small aspect of the meshwork at the most anterior location is adjacent to connective tissue of the limbus and differs in structure from the filtering portion. Some believe that this is a niche where cells reside that have properties similar to stem cells. These cells may be capable of replacing the endothelial cells of the trabecular meshwork after injury.4

The meshwork can be separated into two anatomic divisions. The corneoscleral meshwork is the outer region; its sheets attach to the scleral spur. The inner sheets, which lie inner to the spur and attach to the ciliary stroma and longitudinal muscle fibers, make up the uveal meshwork; some of these sheets may attach to the iris root.3,5 The two portions differ slightly in structure; the corneoscleral meshwork is sheetlike, and the uveal meshwork is cordlike2 (Figure 6-4). The pores in the uveal meshwork are the largest, and pore size diminishes in the sheets closer to the canal. Projections from the surface layer of the iris, known as iris processes, connect to the trabeculae, usually projecting no farther forward than the midpoint of the meshwork.2

The meshwork trabeculae consist of an inner core of collagen and elastic fibers6 embedded in ground substance and covered by basement membrane and endothelium.7 The endothelial cells are a continuation of the corneal endothelium.5,8 The endothelial cells contain the cellular organelles for protein synthesis and apparently are capable of replacing the connective tissue components. These cells also contain lysosomes, which give them the capacity for phagocytosis.5 Gap junctions and short areas of tight junctions join the endothelial

109