This document provides an overview of the visual pathway from the eye to the primary visual cortex. It describes the key structures and cell types involved including the retina, optic nerve, optic chiasm, optic tract, lateral geniculate nucleus, optic radiations, and striate cortex. The retina contains rods and cones that convert light signals to neural signals relayed by the optic nerve. The optic chiasm allows for decussation of fibers so that the left visual field is processed in the right hemisphere and vice versa. The lateral geniculate nucleus acts as a relay station and contains magnocellular, parvocellular, and koniocellular cells before projections reach the primary visual cortex via the optic radiations

1. Visual pathway Presenter: Dr.NIKHIL PANPALIA
GUIDE: Dr. K.R.NAIK

3. INTRODUCTION
• Visual processing poses an enormous
computational challenge for the brain, which
has evolved highly organized and efficient
neural systems to meet these demands.
• In primates, approximately 55% of the cortex
is specialized for visual processing (compared
to 3% for auditory processing and 11% for
somatosensory processing) (Felleman and
Van Essen, 1991).

4. • These structures include
the eye, optic nerves,
chiasm, tracts, lateral
geniculate nucleus (LGN)
of the thalamus,
radiations, striate cortex,
and extrastriate
association cortices.

5. EYE
• The corneal epithelium and stroma are transparent to permit
passage of light without distortion (Maurice, 1970).
• The ciliary muscles dynamically adjust the shape of the lens in
order to focus light optimally from varying distances upon the
retina (accommodation). The total amount of light reaching
the retina is controlled by regulation of the pupil aperture.
• Ultimately, the visual image becomes projected upside-down
and backwards on to the retina (Fishman, 1973).

6. RETINA
• When light reaches the retina, its energy is
converted by retinal photoreceptors into an
electrochemical signal that is then relayed by
neurons.
• To arrive at the photoreceptors, light must
first pass through transparent inner layers of
the neurosensory retina, comprised of the
nerve fiber layer, ganglion cells, amacrine
cells, and bipolar cells .

7. Top, high-resolution
optical coherence
tomography.
Middle, histological
section.
Bottom, schematic
depiction of retinal
layers.

8. FUNCTION OF EACH LAYER OF RETINA
• RETINAL PIGMENT EPITHELIAL LAYER
The RPE provides structural and metabolic
support for the photoreceptors, primarily
through the vital function of vitamin A
metabolism (Wald, 1933).

9. VITAMIN A METABOLISM TAKES PLACE

10. • Photoreceptors maintain the ability always to
produce a signal by ensuring a constant, buffered
supply of 11-cis-retinal.
• The spontaneous transformation of all-trans-
retinal back to 11-cis-retinal occurs over a very
slow half-life (of several minutes), so that the
store of 11-cis-retinal is always being replenished
and is available to transduce incoming light
signals.

11. • Humans possess four
photoreceptor types: three
cones and the rods.
• Under most conditions, our
vision is mediated by cones,
which operate over an
enormous range of intensities.
• Each type of cone
photoreceptor has a unique,
optimal response to specific
wavelengths of light – short
(blue), middle (green), or long
(red).

12. • Rods, on the other hand, are saturated at natural light
intensities and are incapable of discriminating colors; their
greater sensitivity to light renders them effective for night
vision (scotopic vision).
• The functional specializations of cones and rods arise from
variations in the structure of opsin, since the opsin
molecule tunes the light wavelengths at which the retinal
chromophore (11-cis-retinal) will alter its conformation and
initiate the biochemical response to light.
• Despite their functional differences, cones and rods utilize
the same 11-cis-retinal chromophore.

13. DISTRIBUTION OF RODS AND CONES
• The distribution of cones and
rods across the retina is highly
skewed and directly reflects
the specialized functions of the
fovea and retinal periphery
(Osterberg, 1935).
• The macula is located
temporal to the optic nerve
and is approximately 5.5 mm
in diameter.

14. • Within the macula is the fovea (diameter 1.5 mm) and
the foveola (0.35 mm). The fovea has up to 200 000
cones/mm2 (nearly 15-fold higher than in the
peripheral retina) so that it can provide excellent visual
acuity (Hirsch and Curcio, 1989).
• Progressively eccentric locations have much lower
concentrations of rods, and thus have decreasing
sensitivity.
• Rods are virtually absent in the fovea; rather, they are
the dominant photoreceptor in the periphery

16. © Stephen E. Palmer, 2002
Distribution of Rods and Cones
.
0
150,000
100,000
50,000
0
20 40 60 8020406080
Visual Angle (degrees from fovea)
Rods
Cones Cones
Rods
Fovea
Blind
Spot
#Receptors/mm2
Night Sky: why are there more stars off-center?

17. INNER NUCLEAR LAYER
• It consists of amacrine cells, horizontal cells
and bipolar cells which connect rods and
cones with Retinal ganglion cell layer.

18. Retinal Ganglion cell
• The excitatory “on” and “off” inputs to a
ganglion cell are arranged to form an
antagonistic center-surround receptive field
(Kuffler, 1953) .
• The action potential firing rate of an “on-
center” ganglion cell is highest when a light
stimulus is in the center of the receptive field,
with surrounding darkness.

19. • In contrast, the firing rate of “off-center” ganglion cells is
highest when a light stimulus is in the peripheral receptive
field, but not its center.
• With uniform illumination throughout a ganglion cell
receptive field, the summated center and surround
responses essentially cancel each other.
• However, when differential illumination (i.e., an edge of
light) occurs within the receptive field, the imbalance
between center and surround inputs allows the ganglion
cell to signal the local change in light intensity.

21. • There are three main types of ganglion cell,
each with specialized functions in the
detection of visual inputs
• Eighty percent of ganglion cells are midget
cells, 10% are parasol cells, and 10% are other
types.
• The different types of ganglion cells comprise
separate pathways that are named for their
targets in the LGN.

22. • Midget cells form the “P” (parvocellular)
pathway and parasol cells form the “M”
(magnocellular) pathway (Polyak, 1941;
Kaplan and Shapley, 1986; Hendry and
Yoshioka, 1994).
• In addition, small bistratified ganglion cells are
the most likely source of a more recently
identified “K” (koniocellular) pathway (Hendry
and Yoshioka, 1994).

23. • Midget ganglion cells have cone-opponent
receptive fields, allowing spectral selectivity
along the red–green or blue–yellow axes.
• These structural arrangements afford midget
ganglion cells the properties of an extremely
small receptive field, with specialization for
high spatial acuity, color vision, and fine
stereopsis (Livingstone and Hubel, 1988).

24. • At any given retinal eccentricity, parasol cells have a larger
receptive field and lower spatial resolution than midget
cells due to their broad dendritic arborization (Croner and
Kaplan, 1995).
• Parasol ganglion cells have spatially opponent center-
surround organization, allowing edge detection, but they
lack spectrally opponent organization; in essence, these
cells are color-blind.
• The anatomical features of parasol cells underlie their
specialization for low spatial resolution, motion detection,
and coarse stereopsis (Livingstone and Hubel, 1988).

26. • Foveal ganglion cells send axons
directly to the temporal aspect of
the optic disc in the papillomacular
bundle.
• The remaining temporal ganglion
cell nerve axons are arranged on
either side of the horizontal raphe
and form arcuate bundles that
course above and below the fovea,
and finally enter the superior and
inferior portions of the optic nerve.
• Finally, axons originating nasal to
the disc enter the nasal portion of
the optic nerve.

31. Optic disc

32. • The optic disc or optic nerve head is the point of exit
for ganglion cell axons leaving the eye. Because there are
no rods or conesoverlying the optic disc, it corresponds to a
small physiological blind spot in each eye.
• The ganglion cell axons form the optic nerve after they
leave the eye.
• The optic disc represents the beginning of the optic nerve
and is the point where the axons of retinal ganglion cells
come together.
• The optic disc is also the entry point for the major blood
vessels that supply the retina. The optic disc in a normal
human eye carries from 1 to 1.2 million neurons from the
eye towards the brain

33. Papilledema
Papilledema (or papilloedema) is optic disc swelling that is caused by
increased intracranial pressure. The swelling is usually bilateral and can occur over a
period of hours to weeks.

35. Optic nerve
• Each optic nerve is comprised of
approximately 1.2 million retinal ganglion cell
axons (in constrast to the acoustic nerve, for
example, which has only 31 000 axons)
(Bruesch and Arey, 1942).
• The intraocular segment of the optic nerve
head (the optic disc) is typically located 3–4
mm nasal to the fovea and is 1 mm thick.

36. • The optic nerve travels posteriorly through the lamina
cribrosa to exit the back of the globe, where it abruptly
increases in diameter from 3 to 4 mm.
• In order to accommodate the rotations of the globe,
the length of the intraorbital segment of the optic
nerve is typically between 25 and 30 mm in length, at
least 5 mm longer than the distance from the globe to
the orbital apex (Glaser and Sadun, 1990).
• Upon passing through the lamina cribrosa, the optic
nerve becomes invested with meninges and also
becomes myelinated.

37. • Upon exiting the orbit, the optic nerve enters
the optic canal, within the lesser wing of the
sphenoid bone, for approximately 6 mm.
• The intracanalicular optic nerve rises at a 45
angle and then exits the optic canal, where it
continues in its intracranial portion for
approximately 17 mm before reaching the
chiasma.

38. • In the proximal third of the optic nerve the
positions of ganglion cell axons are rearranged.
• Macular ganglion cell axons which initially lie
temporally move to the nerve’s center.
• Peripheral temporal fibers become positioned
temporally, both superior and inferior to the
macular fibers.
• Finally, nasal fibers remain in the nasal portion of
the optic nerve.

39. RETINA
TEMPORAL NASAL
Srf
irf
saf
iaf
39

40. 40
• Peripheral fibers 
deep in Retina
superficially in optic
nerve
• Fibers close to optic
nerve head
superficial in retina
central in optic nerve
OPTIC NERVE HEAD:

41. macula
Upper temporal
Lower temporal
Lower nasal
Upper nasal
41
In the Distal Region of optic nerve (just behind eye):

42. • In the Proximal Region of optic nerve(near
chiasma):
42

43. OPTIC CHIASMA
• The chiasm, which has a dumbbell shape when viewed
in coronal section, is the site of decussation for axons
from the optic nerve (Fig. 1.9).
• It lies in the subarachnoid space of the suprasellar
cistern, above the diaphragma sella and the pituitary
gland, inferior to the hypothalamus, and anterior to
the pituitary stalk (infundibulum).
• The chiasm is typically 10 mm above the pituitary,
which rests in the sella turcica within the sphenoid
bone

44. ANTERIORLY : Anterior
cerebral artery and
their communicating
artery
POSTERIORLY: Tuber
cinerium, Hypophyseal
stalk, Pituitary body,
mamillary body,
posterior perforated
substance
SUPERIORLY:3rd
ventricle
INFERIORLY: Pituitary
gland
LATERALLY:
Extracavernous part of
ICA & Anterior
perforated substance
44

46. OPTIC CHIASMA
46
Uncrossed temporal
fibers
Crossed Nasal fibers

47. 47
Anterior
Knee of
Von-wille
Brand
Posterior
Knee of
Von-wille
Brand

48. OPTIC TRACT:
* Flattened cylindrical band that
travel posteriolaterally from
angle of chiasma
* Between tuber cinereum and
anterior perforated substance
upto lateral geniculate body.
* Each tract contains
uncrossed temporal
fibres and crossed nasal fibres .
48

49. OPTIC TRACT:
• Macular fibers (crossed
& uncrossed) occupy
dorsolateral aspect of
optic tract
• Upper peripheral fibers
(crossed &
uncrossed)medially
situated
• Lower peripheral
fibers laterally
situated
49

50. Fibers from optic tract:
50
Superior
Colliculus
Pretectal
nucleus
Dorsal
Lateral
geniculate
nucleus

51. SUPERIOR COLLICULUS
• The superior colliculi play a critical role
in generating orienting eye and head
movements to sudden visual (and other
sensory) stimuli. They are located in the
dorsal midbrain within the tectal plate.
• The superior colliculi are structurally
and functionally organized into
superficial and deep layers.
• The superficial layers solely process
visual information, with direct retinal
inputs comprising a visuotopic map of
the contralateral field (Cynader and
Berman, 1972)
• The deep layers of the colliculi receive
multimodal sensory inputs and help
mediate saccadic eye movements
through their efferent connections to
ocular motor systems.

52. PRETECTAL NUCLEAS
• A portion of the fibers in the optic tract subserve the
pupillary light reflex and synapse at the pretectal nuclei
in the midbrain.
• There is consensual innervation to both pretectal
nuclei, and each pretectal nucleus has dual
connections to each Edinger–Westphal nucleus.
• The Edinger–Westphal nuclei give rise to
parasympathetic efferent fibers which travel with the
oculomotor nerve and regulate pupillary size via
pupillary constrictors.

54. LATERAL GENICULATE BODY:
Elevation produced by
lateral geniculate
nucleus in which
most optic tract
fibers end
Axons of ganglion cells
of retina synapse
with dendrites of
LGB cells
3rd order neurons
begins
54

55. LATERAL GENICULATE BODY
Dorsal nucleus
Ventral nucleus (rudimentary)
6 laminae( alternating grey & white
matter)
Axons from the ipsilateral eye –
2, 3, 5
Axons from the contralateral eye - 1, 4,6
55

56. Lateral Geniculate Body:
56
• Large magnocellular neurons (M
cells) - 1 and 2 layer-Y ganglion
cells
perception of movement, gross
depth, and small differences in
brightness
• Small parvocellular neurons (P
cells)- 3,4,5,6 layer- X ganglion
cells
Colour perception, texture shape &
fine depth
• Koniocellular cells(K cells or
interlaminar cells)
Short-wavelength "blue" cones

57. LATERAL GENICULATE BODY:
57
Macular fibres - posterior
2/3 of LGB
Upper retinal fibres - medial
half of anterior 1/3 of LGB
Lower retinal fibres - lateral
half of anterior 1/3 of LGB

58. • The LGN is a critical relay station with dynamic control upon
the amount and nature of information that is transmitted
to visual cortex (Guillery and Sherman, 2002).
• In addition to retinal afferents, which may comprise only
5–10% of the synapses in the LGN (Van Horn et al., 2000),
the LGN also receives extensive modulating connections
from the thalamic reticular nucleus and layer 6 of the visual
cortex.
• The LGN thus provides a bottleneck to information flow,
filtering visual information for relevance to the present
behavioral state.

59. OPTIC RADIATIONS:
Geniculocalcarine pathway extend
from lateral geniculate body 
visual cortex
MEYERS LOOP(inferior retinal
fibers)-pass through temporal
lobe looping around inferior horn
of lateral ventricle
BARUMS LOOP(superior retinal
fibers)- directed posteriorly
through parietal lobe, occipital
lobe,internal capsule and relay
on visual cortex
59

60. OPTIC RADIATION:
60
Inferior
retinalower
part of optic
radiation
superior retina
upper part of
optic radiation

61. Visual Cortex:
Striate cortex Extrastriate cortex
61
•

62. VISUAL CORTEX(CORTICAL RETINA):
62
•Impulse from
corresponding 2 points
of retina meet
•Right visual
cortexreceive impulse
left half of visual field
•Left visual
cortexreceive impulse
from right half visual
field
MACULA posteriorly
PERIPHERAL RETINA anteriorly
UPPER RETINA above calcarine sulcus
LOWER RETINA below the calcarine sulcus

63. TWO STREAM HYPOTHESIS:
63
• Ventral
Ventral
Pathway(parvocellular)
temporal lobe
Dorsal
Pathway(magnocellular)
 parietal lobe
Recognistion &
indentification
Spatial
location
Visual
agnosia
Visual
neglec
t
Parvocellular
“what”
pathway
Magnocellular
“where”
pathway

64. LESIONS OF VISUAL PATHWAY
64

65. 1) LESIONS OF OPTIC NERVE :
Causes:
1. Optic atrophy
2. Indirect optic neuropathy
3. Acute optic neuritis
4. Traumatic avulsion of optic nerve.
Characterised by:
Complete blindness in affected eye with loss of both
direct on ipsilateral & consensual light reflex on
contralateral side.
Near reflex is preserved.
Eg. Right optic nerve
involvement
65

66. 2)CHIASMAL LESIONS:
66
Anterior
Chiasmal
lesions
Middle
Chiasmal
lesions
Posterior
Chiasmal
lesions

67. ANTERIOR CHIASMAL LESIONS:
67
• Affects the ipsilateral optic nerve fibers and
the contralateral inferonasal fibers
• Ipsilateral optic neuropathy manifested as a
central scotoma and a defect involving the
contralateral superotemporal fieldalso
known as a junctional scotoma
Abolition of direct light reflex on affected side
& consensual light reflex on contralateral side.
 Near reflex intact.

68. MIDDLE CHIASMAL LESIONS:
CENTRAL LESIONS OF CHIASMA (SAGITTAL)
Causes:
Suprasellar aneurysm
Tumors of pituitary gland
Craniopharyngioma
Suprasellar meningioma &
glioma of 3rd ventricle.
Third ventricular dilatation
due to obstructive hydrocephalus.
68

69. 69
 Characterised by:
Bitemporal hemianopia
Paralysis of pupillary
reflex(usually lead to partial
descending optic atrophy)

70. LATERAL CHIASMAL LESIONS :
Causes:
Distension of 3rd ventricle causing pressure on each side
of optic chiasma
Atheroma of carotids & posterior communicating artery.
70

71. 71
Characterised by :
Binasal hemianopia
Parallysis of pupillary reflex
(usually lead to partial descending optic atrophy)

72. POSTERIOR CHIASMAL SYNDROME
72
• macular fibers cross more posteriorly in the
chiasm
• paracentral bitemporal field loss
• Posterior lesions may also involve the optic
tract and cause a contralateral homonymous
hemianopia.

73. 3)LESIONS OF OPTIC TRACT :
Causes:
1. Syphilitic meningitis/ Gumm
2. Tuberculous meningitis
3. Tumors of optic thalamus
4. Aneurysm of posterior
cerebral arteries.
73

74. 74
Characterised by :
Incongruous homonymous hemianopia with C/L hemianopic
pupillary reaction( wernicke’s reaction)
These lesions usually lead to partial descending optic atrophy &
may be associated with C/L 3rd nerve paralysis(RAPD) &
ipsilateral hemiplegia
Wernickes pupil

75. 4)LESIONS OF LATERAL GENICULATE BODY :
Leads to homonymous hemianopia with sparing
of pupillary reflexes & may end in partial optic
atrophy.
75

76. 5)LESIONS OF OPTIC RADIATIONS :
Causes:
Vascular occlusion(Anterior choroidal artery,middle cerebral or
posterior cerebral artery)
Primary & secondary tumors
Trauma
Characterised by : No Optic Atrophy
Normal pupillary reactions
TOTAL OPTIC RADIATION
INVOLVEMENT
COMPLETE
HOMONYMOUS
HEMIANOPIA
( sometimes sparing
macula)
76

77. INFERIOR QUADRANTIC
HEMIANOPIA
Lesion of temporal lobe
(pie on sky)
SUPERIOR QUADRANTIC
HEMIANOPIA
77
Lesion of parietal lobe
(pie on floor)

78. 6)LESIONS OF VISUAL CORTEX :
Congruous
homonymous
hemianopia(sparing
macula)
Occlusion of posterior
cerebral artery
supplying anterior part
of occipital cortex
Congruous
homonymous macular
defect
Head injury/gun shot
injury leading to
lesions of tip of
occipital cortex
78
Normal pupillary reactions and no optic atrophy

82. REFERENCES
• Clinical neuro-ophthalmology  Thomas
duane and Edward jaegar
• Neuroanatomy Carpenter
• Neuroanatomy Snells

84. • Thank you