3. • Primary Visual cortex ( Area 17)
• Visual Association area ( Area18 & 19)
• Frontal eye field
• Superior colliculli
• Pretectal nucleus
• Suprachiasmatic nucleus
4. • Frontal Eye field : ( Area 8)
• Located in frontal gyrus
• It controls saccadic eye movements
Convergence , divergence and near response is
influenced by activity in an area anterior to
the frontal eye fields .
5.
6. Superior colliculli :
These receives inputs from the optic tract fibers
and visual cortex and in turn projects to
various thalamic nuclei.
1. These help in coordinate simultaneous
bilateral eye movements.
2. Maintains head and eye position.
7. Pretectal nucleus :
Fibers from optic nerve tract project to the
pretectal nucleus and causes activation of the
Edinger- westphal nucleus.
This is involved in regulation of visual fixation.
8. Suprachiasmatic nucleus :
It is located just above optic chiasm.
It plays an important role in Biological clock
activity.
9. Quadrantanopia
• Quadrantanopia refers to an anopia affecting
a quarter of the field of vision.
• It can be associated with a lesion of an optic
radiation.
• Homonymous denotes a condition which
affects the same portion of the visual field of
each eye.
10. • A lesion affecting one side of the temporal lobe
may cause damage to the inferior optic
radiations which can lead to superior
quadrantanopia on the contralateral side of
both eyes
• If the superior optic radiations are lesioned, the
visual loss occurs on the inferior contralateral
side of both eyes and is referred to as an
inferior quadrantanopia.
11. • Binasal (either inferior or superior)
quadrantanopia affects either the upper or
lower inner visual quadrants closer to the nasal
cavity in both eyes.
• Bitemporal (either inferior or superior)
quadrantanopia affects either the upper or
lower outer visual quadrants in both eyes.
15. Visual acuity (VA) commonly refers to the clarity
of vision :
It is ability of eye to identify two closely placed
points as two distinct points.
Visual acuity is dependent on optical and neural
factors, i.e.,
(i) the sharpness of the retinal focus within
the eye,
(ii) the health and functioning of the retina,
16. A common cause of low visual acuity is
refractive error (ametropia)
or errors in how the light is refracted in the
eyeball.
17. Causes of refractive errors include aberrations in
the shape of the eyeball or the cornea, and
reduced flexibility of the lens.
These anomalies can mostly be corrected by
optical means (such as eyeglasses, contact
lenses, laser surgery, etc.).
18. Neural factors that limit acuity are located in the
retina or the brain
(or the pathway leading there).
19. Examples :
Detached retina
Macular degeneration
A mblyopia
In some cases, low visual acuity is caused
by brain damage, such as from traumatic brain
injury or stroke.
20. FACTORS AFFECTING VISUAL ACUITY :
1) Optical factors
2) Retinal factors
3) Stimulus factors ( Like size , distance , colour ,
shape , contrast , brightness of object )
Visual acuity is directly proportional to visual
angle.
21. Visual acuity is a measure of the spatial
resolution of the visual processing system.
22. VA, as it is sometimes referred to by optical
professionals, is tested by requiring the person
whose vision is being tested to identify so-called
optotypes :
stylized letters,
pediatric symbols
symbols for the illiterate
standardized letters
or other patterns – on a printed chart (or some
other means) from a set viewing distance.
23. Visual acuity is often measured according to the
size of letters viewed on a Snellen chart .
A reference value above which visual acuity is
considered normal is called 6/6 vision.
In the expression 6/x vision, the numerator (6) is
the distance in meters between the subject and
the chart and the denominator (x) the distance
at which a person with 6/6 acuity would discern
the same optotype.
26. • Color vision is possible due to photoreceptors in
the retina of the eye known as cones.
• These cones have light-sensitive pigments that
enable us to recognize color.
• Found in the macula (the central part of the retina),
each cone is sensitive to either red, green or blue
light (long, medium or short wavelengths).
27. Human eye does not respond to
electromagnetic radiation more than 750 nm
( Infrared rays ) and less than 400 nm
( Ultrtaviolet rays )
Some animals like bats can see infrared rays.
28. Color blindness, also known as color vision
deficiency, is the decreased ability to see
color or differences in color.
29. Trichromacy : Normal colour vision uses all three types
of light cones correctly and is known as trichromacy.
People with normal colour vision are known as
trichromats.
The different anomalous conditions are :
1. protanomaly, which is a reduced sensitivity to red
2 . deuteranomaly which is a reduced sensitivity to
green light and is the most common form of colour
blindness
3. tritanomaly which is a reduced sensitivity to blue
light and is extremely rare.
30. People with dichromatic colour vision have only
two types of cones which are able to perceive
colour .
People suffering from protanopia are unable to
perceive any ‘red’ light, those with deuteranopia
are unable to perceive ‘green’ light and those
with tritanopia are unable to perceive ‘blue’
light.
31.
32. • People with monochromatic vision can see no
colour at all and their world consists of
different shades of grey ranging from black to
white
33. • The most common form of color deficiency is red-
green. This does not mean that people with this
deficiency cannot see these colors at all. They simply
have a harder time differentiating between them,
which can depend on the darkness or lightness of the
colors.
Another form of color deficiency is blue-yellow. This is a
rarer and more severe form of color vision loss than
red-green, because people with blue-yellow deficiency
frequently have red-green blindness too.
In both cases, people with color vision deficiency often
see neutral or gray areas where a particular color
should appea
34. • Usually, color deficiency is an inherited condition
caused by a common X-linked recessive gene, which
is passed from a mother to her son. But disease or
injury that damages the optic nerve or retina can
also cause loss of color recognition.
Some diseases that can cause color deficits are:
• Diabetes , glaucoma , macular degeneration
• Alzheimer's disease
• Parkinson's disease , multiple sclerosis
• chronic alcoholism , leukemia
• sickle cell anemia , Other causes for color
35. Ishihara’s Test for Colour Deficiency:
There exist four different types of plates:
• Vanishing design: Only people with good color vision
can see the sign.
• Transformation design: Color blind people will see a
different sign than people with no color vision
handicap.
• Hidden digit design: Only colorblind people are able to
spot the sign. If you have perfect color vision, you
won’t be able to see it.
• Classification design: This is used to differentiate
between red- and green-blind persons.
36.
37. • Diplopia, commonly known as double vision,
is the simultaneous perception of two images
of a single object that may be displaced
horizontally, vertically, diagonally (i.e., both
vertically and horizontally), or rotationally in
relation to each other
38. • It is usually the result of impaired function of
the extraocular muscles (EOMs), where both
eyes are still functional but they cannot turn
to target the desired object.
39. • Problems with EOMs may be due to
mechanical problems, disorders of
the neuromuscular junction, disorders of
the cranial nerves (III, IV, and VI) that
stimulate the muscles, and occasionally
disorders involving the supranuclear
oculomotor pathways or ingestion of toxins
40. • Diplopia can be one of the first signs of
a systemic disease, particularly to a muscular
or neurological process, and it may disrupt a
person’s balance, movement, and/or reading
abilities.
41. • Monocular Diplopia
• Binocular Diplopia
• Temporary binocular diplopia can be caused
by alcohol intoxication or head injuries.
• Permanent binocular diplopia – neuropathies
43. • Rhodopsin is an extremely sensitive molecule.
• As long as the light is of low intensity, rods quickly regenerate
rhodopsin and the retina continues to respond to light stimuli.
• In high light intensity rhodopsin is bleached as quickly as
rhodopsin can be produced making some of the rods
nonfunctional.
• If this happens the cones take over. There is an automatic
adjustment of retinal sensitivity to the amount of light present.
• This automatic adjustment is not only explained by the breakdown
of photoreceptor pigments, other retinal neurons are involved
44. • Light adaptation
• This occurs when we move from the dark into bright
light.
• The bright light momentarily dazzles us and all we
see is white light because the sensitivity of the
receptors is set to dim light.
• Rods and cones are both stimulated and large
amounts of the photopigment are broken down
instantaneously, producing a flood of signals
resulting in the glare.
45. • Within about one minute the cones are
sufficiently excited by the bright light to take
over.
• Visual accuracy and colour vision continue to
improve over the next ten minutes.
• During light adaptation retinal sensitivity is lost.
46. • Dark adaptation
• Dark adaptation is essentially the reverse of light
adaptation.
• It occurs when going from a well light area to a dark
area. Initially blackness is seen because our cones cease
functioning in low intensity light.
• Also, all the rod pigments have been bleached out due to
the bright light and the rods are initially nonfunctional.
• Once in the dark, rhodopsin regenerates and the sensitivity
of the retina increases over time (this can take
approximately one hour). During these adaptation process
reflexive changes occur in the pupil size.
47. Short notes :
Visual Pathways & Lesion
Visual Reflexes
Refractive errors of eye
Physiology of Vision
Colour-blindness
Visual acuity