1. EYE - Dr. Chintan

12. Cause Myopia Hypermetropia
Axial Eyeball length more Eyeball length less
Curvatural Lens, Cornea more
convex
Lens, Cornea more
flatter
Positional Lens anterior Lens posterior
Index Refractive index more Refractive index less
Missel. Spasm of
accommodation
Aphakia

13. LASIK
-

14. -

17. Mechanism of “Accommodation”
- In children, the refractive power of the lens of the eye
can be increased voluntarily from 20 diopters to about
34 diopters; this in an “accommodation” of 14 diopters
- The shape of the lens is changed from that of a
moderately convex lens to that of a very convex lens
- In a young person, the lens is composed of a strong
elastic capsule filled with viscous, proteinaceous,
transparent fluid
- When the lens is in a relaxed state with no tension on its
capsule, it assumes an almost spherical shape, owing
mainly to the elastic retraction of the lens capsule

18. -

19. Accommodation
- Suspensory ligaments are constantly tensed by their
attachments at the anterior border of the choroid
and retina.
- The tension on the ligaments causes the lens to
remain relatively flat under normal conditions of
the eye
- Ciliary muscle - meridional fibers and circular
fibers
- when they contract - releasing the ligaments’
tension on the lens

20. Accommodation
- The ciliary muscle is controlled almost entirely by
parasympathetic nerve signals transmitted to the eye through
the third cranial nerve from the third nerve nucleus in the
brain stem
- Presbyopia - lens grows larger and thicker and becomes far
less elastic, partly because of progressive denaturation of the
lens proteins – weak ciliary muscle
- The power of accommodation decreases from about 14
diopters in a child to less than 2 diopters by the time a person
reaches 45 to 50 years; it then decreases to essentially 0
diopters at age 70 years
- no longer accommodate for both near and far vision - bifocal
glasses

22. Lens
- Contact lens - abnormally shaped cornea - bulging
cornea — keratoconus
- the lens turns with the eye and gives a broader field
of clear vision than glasses do
- Cataracts - older people – opacity in lens
- Denaturation of proteins – coagulation of proteins –
normal transparent protein fibers replaced
- Rx - surgical removal of the lens

23. -

24. Visual Acuity
- Maximum at fovea centralis – maximum number of
cones
- Depth perception – binocular vision
- Far vision
- Near vision
- Color vision
- VEP

25. Intraocular Fluid
- aqueous humor, which lies in front of the lens
- vitreous humor, which is between the posterior
surface of the lens and the retina
- The aqueous humor is a freely flowing fluid
- vitreous body, is a gelatinous mass held together
by a fine fibrillar network composed primarily
of greatly elongated proteoglycan molecules

26. Intraocular Fluid
- Aqueous humor is continually being formed and
reabsorbed. The balance between formation and
reabsorption of aqueous humor regulates the total
volume and pressure of the intraocular fluid
- Aqueous humor is formed in the eye at an average
rate of 2 to 3 microliters each minute - secreted by
the ciliary processes - projecting from the ciliary
body into the space behind the iris
- Aqueous humor is formed almost entirely as an
active secretion by the epithelium of the ciliary
processes - active transport of Na ions + Cl + HCO3
+ water + nutrients

27. -

28. Outflow of Aqueous Humor
- After aqueous humor is formed by the ciliary
processes
- anterior to the lens
- through the pupil
- the anterior chamber of the eye, ant. to iris
- the angle between the cornea and the iris
- meshwork of trabeculae
- canal of Schlemm
- extraocular veins

30. IOP
- The average normal intraocular pressure is about
15 mm Hg, with a range from 12 to 20 mm Hg
- Tonometry
- The rate of fluid flow into the canal increases
markedly as the pressure rises.
- At about 15 mm Hg in the normal eye, the amount
of fluid leaving the eye by way of the canal of
Schlemm usually averages 2.5 micro l/min and
equals the inflow of fluid from the ciliary body

31. IOP
When large amounts of debris are present in the
aqueous humor, as occurs after hemorrhage into
the eye or during intraocular infection,
the debris is likely to accumulate in the trabecular
spaces leading from the anterior chamber to the
canal of Schlemm;
this debris can prevent adequate reabsorption of
fluid from the anterior chamber, sometimes
causing glaucoma

32. IOP
- on the surfaces of the trabecular plates are large
numbers of phagocytic cells
- Immediately outside the canal of Schlemm is a layer
of interstitial gel that contains large numbers of
reticuloendothelial cells that have an extremely
high capacity for engulfing debris and digesting it
into small molecular substances that can then be
absorbed.
- The surface of the iris and other surfaces of the eye
behind the iris are covered with an epithelium that
is capable of phagocytizing proteins and small
particles from the aqueous humor

33. Glaucoma
- Principal Cause of Blindness
- IOP becomes pathologically high, sometimes
rising acutely to 60 to 70 mm Hg
- Pressures above 25 to 30 mm Hg can cause loss
of vision when maintained for long periods
- Extremely high pressures can cause blindness
within days or even hours

34. Glaucoma
- As the pressure rises, the axons of the optic nerve are
compressed where they leave the eyeball at the optic
disc.
- This compression block axonal flow of cytoplasm from
the retinal neuronal cell bodies into the optic nerve
fibers leading to the brain
- The result is lack of appropriate nutrition of the fibers,
which eventually causes death of the involved fibers.
- compression of the retinal artery, which enters the
eyeball at the optic disc, also adds to the neuronal
damage by reducing nutrition to the retina.

35. Glaucoma
- the abnormally high pressure results from
increased resistance to fluid outflow through the
trabecular spaces into the canal of Schlemm at the
iridocorneal junction
- in acute eye inflammation, WBC and tissue debris
can block these trabecular spaces and cause an
acute increase in IOP
- In chronic conditions, especially in older
individuals, fibrous occlusion of the trabecular
spaces
- Rx – medical (Drops), surgical

42. Pigment Layer of the Retina
- The black pigment melanin in the pigment layer prevents
light reflection throughout the globe of the eyeball -
important for clear vision
- its absence in albinos - people who are hereditarily
lacking in melanin pigment in all parts of their bodies
- When an albino enters a bright room, light that impinges
on the retina is reflected in all directions inside the
eyeball by the unpigmented surfaces of the retina
- A single discrete spot of light that would normally excite
only a few rods or cones is reflected everywhere and
excites many receptors - visual acuity of albinos

44. Retina
- The pigment layer also stores large quantities of
vitamin A - this vitamin A is exchanged back and
forth through the cell membranes of the outer
segments of the rods and cones
- Inner layers of retina – central retinal artery
- outer segments of the rods and cones, depend
mainly on diffusion from the choroid blood vessels
for their nutrition, oxygen
- Retinal Detachment

45. Photochemistry of Vision
- Both rods and cones contain chemicals that
decompose on exposure to light and, in the
process, excite the nerve fibers leading from the
eye.
- The light-sensitive chemical in the rods is called
rhodopsin (visual purple: scotopsin + 11-cis
retinal); the light sensitive chemicals in the
cones, called cone pigments or color pigments.
- Rhodopsin-Retinal Visual Cycle

47. Night Blindness & Vitamin A
- Night blindness occurs in any person with severe vitamin A
deficiency - the amounts of retinal and rhodopsin that can
be formed are severely depressed.
- The amount of light available at night is too little to permit
adequate vision
- For night blindness to occur, a person usually must remain
on a vitamin A–deficient diet for months, because large
quantities of vitamin A are normally stored in the liver
- Once night blindness develops, it can sometimes be
reversed in less than 1 hour by IV injection of vitamin A

51. Photochemistry of Color Vision
- photopsins in the cones are slightly different
from the scotopsin of the rods
- color pigments are called
- blue-sensitive pigment - cyanolabe,
- green-sensitive pigment - chlorolabe, and
- red-sensitive pigment - erythrolabe
- light wavelengths of 445, 535 & 570 nanometers

53. Colour Blindness
- Normal vision – trichromatic
- Abnormal – dichromatic, monochromatic
- Triatanomaly – defective blue Colour
- Protanomaly - defective red Colour
- Deutranomaly - defective green Colour
- Triatanopia – complete blindness for blue
- Protanopia - complete blindness for red
- Deutranopia - complete blindness for green
- Ishihara chart, edridge green lantern test, Holmgren wool
test

54. Colour Blindness
- Most common – red green - genetic disorder that occurs almost
exclusively in males
- color blindness almost never occurs in females because at least
one of the two X chromosomes almost always has a normal gene
for each type of cone.
- Because the male has only one X chromosome, a missing gene
can lead to color blindness
- Because the X chromosome in the male is always inherited from
the mother - color blindness is passed from mother to son, and
the mother is said to be a color blindness carrier

55. Light Adaptation
- If a person has been in bright light for hours,
large portions of the photochemicals in both the
rods and the cones will have been reduced to
retinal and opsins.
- much of the retinal of both the rods and the
cones will have been converted into vitamin A.
- Because of these two effects, the sensitivity of
the eye to light is correspondingly reduced. This
is called light adaptation

56. Dark Adaptation
- if a person remains in darkness for a long time,
the retinal and opsins in the rods and cones are
converted back into the light-sensitive
pigments.
- vitamin A is converted back into retinal to give
still more light-sensitive pigments,
- the final limit being determined by the amount
of opsins in the rods and cones to combine with
the retinal - This is called dark adaptation

57. Dark Adaptation
- the sensitivity of the retina is very low on first entering
the darkness, but within 1 minute, the sensitivity has
already increased 10-fold
- At the end of 20 minutes, the sensitivity has increased
about 6000-fold, and at the end of 40 minutes, about
25,000-fold
- all the chemical events of vision, including adaptation,
occur about four times as rapidly in cones as in rods
- Despite rapid adaptation, the cones cease adapting after
only a few minutes, while the slowly adapting rods
continue to adapt for many minutes and even hours

60. Light and Dark Adaptation
- change in pupillary size
- Entering dark – mydriasis
- Entering light – miosis
- Adaptation 30-fold within a fraction of a second
- Neural Adaptation

61. Visual Pathways
Retina
↓
Optic nerve
↓
Optic chiasm
↓
Optic tract
↓
LGB
↓
Optic Radiation
↓
Visual cortex

62. Visual Pathways
- (1) from the optic tracts to the suprachiasmatic
nucleus of the hypothalamus, to control circadian
rhythms that synchronize various physiologic
changes of the body with night and day;
- (2) into the pretectal nuclei in the midbrain, to
elicit reflex movements of the eyes to focus on
objects of importance and to activate the pupillary
light reflex;
- (3) into the superior colliculus, to control rapid
directional movements of the two eyes

64. Visual Pathways - LGB
- Layers II, III, and V receive signals from the lateral half-
temporal fibers of the ipsilateral retina,
- layers I, IV, and VI receive signals from the medial half-
nasal fibers of the retina of the opposite eye
- Layers I and II - magnocellular layers - large neurons –
input large type Y retinal ganglion cells - rapidly
conducting pathway - color blind, transmitting only black
and white information.
- Layers III through VI - parvocellular layers - large
numbers of small to medium sized neurons - type X
retinal ganglion cells that transmit color - moderate
velocity of conduction

70. Autonomic Control
- The parasympathetic preganglionic fibers arise in the
Edinger Westphal nucleus - the visceral nucleus portion
of the third cranial nerve - third nerve to the ciliary
ganglion - lies immediately behind the eye
- here, the preganglionic fibers synapse with
postganglionic parasympathetic neurons, which in turn
send fibers through ciliary nerves into the eyeball.
- These nerves excite
- (1) the ciliary muscle that controls focusing of the eye
lens
- (2) the sphincter of the iris that constricts the pupil

71. Autonomic Control
- The sympathetic innervation of the eye originates in
the intermediolateral horn cells of the first thoracic
segment of the spinal cord.
- Sympathetic fibers enter the sympathetic chain and
pass upward to the superior cervical ganglion, where
they synapse with postganglionic neurons.
- Postganglionic sympathetic fibers from these then
spread along the surfaces of the carotid artery and
successively smaller arteries until they reach the eye -
innervate the radial fibers of the iris

73. Autonomic Control
- Accommodation reflex
- Convergence, pupillary constriction, ant.
Surface of lens becomes more convex
- Pathway
- Light reflex
- Direct, Indirect (consensual)
- Constriction of pupil
- Pathway

74. Autonomic Control
- A pupil that fails to respond to light but does
respond to accommodation (an Argyll Robertson
pupil) — syphilis
- Horner’s syndrome –cervical sympathetic chain
- Miosis
- Ptosis
- Enopthalmos
- Anhydrosis
- Persistent vasodilation

75. Thank You…