visual pathway and lesions in the visual pathway and their visual field defect

1. By Dr. Henok Samuel (R1)
Moderator: Dr.Tiliksew Teshome ( Associate Professor, Consultant
Ophthalmologist and Vitreoretinal surgeon)
PHYSIOLOGY OF THE VISUAL PATHWAY
& CEREBRAL INTEGRATION

2. Contents
 Introduction
 Recap on anatomy of visual pathway
 Axonal conduction
 Role of myelin in axonal conduction
 Axonal transport
 Optic nerve injury and regeneration
 Retinotopic Organization and visual field defect
 Summary
 References
2

3. Introduction
 The role of the central visual pathways is to process and integrate visual
information that travels to the brain by means of the optic nerves.
 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)
3

4. Introduction
 When light reaches the retina, its energy is converted by retinal photoreceptors
into an electrochemical signal that is then relayed by neurons.
4

5. Retina Ganglion cells
 RGC axons begin at the RGC bodies in the
inner layer of the retina.
 The RGCs receive input from bipolar cells and
amacrine cells, and their axons form nerve
fiber layer.
5

6. Retina Ganglion cells
 10 types of RGC found
(two of them are well studied)
 Eighty percent of ganglion cells are Midget cells, 10% are Parasol cells, and 10%
are other types.

6

7. Retina Ganglion cells
7
 LARGE PARASOL RGC
- Project to the magnocellular / M cell system in LGN.
-for low spatial resolution, fast temporal resolution, stereopsis, contrast
sensitivity.
- high receptive field & more for peripheral vision.
 SMALL MIDGET RGC
-Project to the parvocellular / p cell system in LGN.
-for high spatial resolution but has low contrast sensitivity
-many in number & more for macular vision
 “K” (koniocellular) pathway
- more recently identified, small bistratified ganglion cells

8. Retina Ganglion cells
 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.
 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.
8

9. Cont…
 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.
9

10. Optic Nerve Head
 The ganglion cell axons form the optic nerve after they
leave the eye. And The optic disc or optic nerve head is
the point of exit for ganglion cell axons leaving the eye.
 There are no rods or cones overlying the optic disc, it
corresponds to a small physiological blind spot in each
eye.
 The optic disc in a normal human eye carries from 1 to 1.2
million neurons from the eye towards the brain
10

11. 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).
 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.
11

12. Optic nerve
 Intraocular
 Intraorbital
 Intracanalicular
 Intracranial
12

13. Retinotopic Organization of Optic Nerve
• 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. 13

14. Optic Chiasm
 Is the site of decussation for axons from
the optic nerve.
 It lies in the subarachnoid space of the
suprasellar cistern surrounded by
meningeal sheaths and cerebrospinal
fluid
 10 mm above the pituitary, which rests in
the sella turcica within the sphenoid bone
 The chiasm lies within the circle of Willis. 14

15. Relations with neighboring structures
15

16. Relations with neighboring structures
• The exact location of the chiasm with respect to the sella is variable.
•
16

17. Arrangement of Nerve fibres in Optic chiasm
 The lower (inferior) fibers (subserving the
superior visual field) traverse the chiasma
low and anteriorly - are first to cross.
 The upper nasal fibers traverse the chiasma
high and posteriorly.
 macular fibers tend to cross decussate in the
posterior most part of chiasm which is
related to supraoptic recess.
17

18. 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 .
18

19. Retinotopy of optic tract
 Macular fibers (crossed & uncrossed)
occupy dorsolateral aspect of optic
tract.
 Upper peripheral fibers (crossed &
uncrossed) medially situated
 Lower peripheral fibers laterally
situated
19

20. Lateral Geniculate Body
(LGB)
 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
 Primary termination of OT fibers
 Each LGN receives input from the
contralateral visual field.
20

21. 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
21

22. Lateral Geniculate Body
 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
22

23. Retinotopic arrangement of LGB
• 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
23

24. Geniculocalcarine Tract (optic radiations)
 Axons of LGN neurons travel to primary visual cortex
(Area 17) via the geniculocalcarine tract located in the
retrolenticular and sublenticular portions of the
internal capsule.
 Axons from upper visual fields take a looping course
into the temporal lobe on the way to visual cortex.
(=Meyer’s loop)
 Axons from lower visual fields take a more direct route
to visual cortex.
 Macular fibers are in an intermediate location in the
optic radiation
24

25.  Superior colliculus
 Pretectum
 Pulvinar
 Hypothalamic nuclei
 AOS
25
Extra geniculate targets of the retinal projections

26. Superior Colliculus
26
 Approximately 10 percent of all retinal ganglion cells project to the SC.
 Cells in SC have ill-defined "On" "Off" regions, therefore will respond to most
visual stimulus regardless of shape, color, or orientation.
 SC cells seem most interested in location of visual stimulus, not identity of visual
stimulus, therefore, SC has often been referred to as the "where" system, rather
than the "what" system.
 SC appears to have important role in directing ballistic eye movements toward a
visual stimulus in the periphery
 Most of the fibers projecting to SC are from the M type of RGC, therefore,
messages often get to SC more quickly than to LGN.

27. 27
 A group of small midbrain nuclei, is
just rostral to the SC.
 Involved with the control of the
pupillary light reflex by means of a
projection to the Edinger–Westphal
nucleus of the oculomotor complex.
The pretectal complex

28.  The pulvinar is the largest nuclear mass in the primate thalamus and receives a
projection from the small-caliber fibers from the optic nerve and the SC.
 It projects to several visual cortical areas, including V1, and extrastriate,
parietal areas.
 Pathway that can bypass the LGN to get to V1 and may play a role in
processing form vision.
 Integrates neural signals associated with eye, hand and arm movements and
may receive signals associated with saccadic eye movements.
28
Pulvinar nucleus of the thalamus

29.  The suprachiasmatic nucleus receives a sparse projection from fibers that leave
the dorsal surface of the optic chiasma and has been implicated in the
synchronization of circadian rhythms.
 The paraventricular and supraoptic nuclei are likely also involved with the
regulation of the light–dark cycle for neuroendocrine functions
 The AOS plays an important role in optokinetic nystagmus (OKN) in which slow
compensatory and pursuit type eye movements alternate with fast saccadic-type
eye movements in response to viewing prolonged large field motion
29
Other targets RGC

30. Primary Visual Cortex (Area 17)
 Located on either side of & within the
calcarine fissure.
 Upper fields project to the lingual gyrus.
 Lower fields project to the cuneus.
 Macular representation is most caudal in
Area 17.
 Peripheral field representation is in the
rostral 2/3rds of Area 17.
 Lesions of Area 17 result in blindness in
the contralateral visual field.
30

31. Cont…
• Dorsal stream – Occipito-parietal stream spatial, Motion perception – action-
“where” or “how to”
• Ventral stream – Occipito-temporal stream object perception – identification –
“what” stream
31

32. Cont…
32

33. Cont…
33

34. Cont…
34

35. Visual Cortex
•
35
What/Where Pathways
Evidence from Neuropsychology
Visual agnosia:
Inability to identify objects and/or people
Caused by damage to inferior (lower) temporal lobe
Disruption of the “what” pathway
Visual neglect:
Inability to see objects in the left visual field
Caused by damage to right parietal lobe
Disruption of the “where” pathway

36. Deficits in Motion Perception:
Akinetopsia
•
36
Deficits in Color Perception -
Achromatopsia

37. Visual Cortex
 Like RGCs and cells of LGN, cells of the PVC have
receptive fields which monitor a restricted zone in
the retina.
 Cortical magnification: the disproportionally large
amount of cortical tissue dedicated to processing
the foveal retina compared to the peripheral
retina.
 Number of RGCs connected to photoreceptors in
fovea vs. RGCs connected to photoreceptors in
periphery. Remember degree of convergence?
37

38. 38
 Orientation specificity: cells in PVC
differentially respond to stimuli of
varying orientations.
 Simple cells: Well defined excitatory
region; location important.
 Complex cells: less well defined
excitatory region; location less
important.
 Hyper-complex: length of contour
important Oblique effect
Visual Cortex

39. 39
Direction specificity: cells in PVC also differentially respond to movement in
different directions. Simple cells: slower movement. Complex cells: faster
movement
Visual Cortex

40. • Binocular cells: Two receptive fields, one for each eye. Stronger response to one eye
(ocular dominance).
• Cells give a most vigorous response when a stimulus of the same size, shape, and
orientation is located in a particular position in 3-d space across the two retinae.
• Cells are important for the visual system's use of the depth cue called retinal disparity.
40
Visual Cortex

41. 41
 Cell columns: in the PVC cells (s,
c, hc) are arranged in layers by
their preferred orientation.
 Cell hyper columns: the layers of
orientation specific cells are
arranged such that an orderly
incrementing of orientation
change exists across layers until a
complete cycle has been achieve.
Include both eyes.
 Layer 4: input layer, monocular
cells.
 Blobs: non-orientation specific
cells for color processing.
Visual Cortex

42. Axonal conduction
 Retinal ganglion cell electrophysiology and synaptic
transmission
 RGCs receive synaptic input from bipolar and amacrine cells,
which primarily use glutamate as the major excitatory
neurotransmitter.
 Axonal conduction
 Action potentials
RGC axons transmit information via action potentials, which are
all-or-nothing spikes of electrical activity. This is in contrast to
most intercellular communication within the retina, where graded
potentials are used to transmit information
42

43. 43
 Mechanism of axonal conduction
 AT REST(Non depolarization state)
 Negative voltage in the axon ( negative resting potential)
 Due to flow of K down its concentration gradient ( from inside to outside) which
create a leak current giving negative potential
 Leak current continue until concentration gradient becomes equal which forms
K equilibrium potential
 At rest flow of Na down its concentration gradient (from outside to inside)
occur giving Na equilibrium potential but its much more smaller than K flow

44. 44
 DEPOLARIZATION
 Occurs when voltage sensitive Na channels activated More Na enter the cell so
axon becomes positive (depolarized)
 REPOLARIZATION
 Its the return of membrane potential to resting state & its necessary for another
AP to be transmitted down the axon
 Due to closure of voltage gated Na channels & transient opening of voltage gated
K channels
 Mechanism of axonal conduction

45. Role of myelin in AP conduction
 It’s a multilaminated fatty structured produced by oligodendrocytes which
insulates each axon
 It increase the speed & efficacy of AP conduction by these mechanisms;
 DECREASE CAPACITANCE (ion needed to change voltage)
- less Na needed to depolarize axons
 INCREASE RESISTANCE (the resistance for ion leakage)
- less leakage of charge across the membrane
 The above two decrease amount of ion flux needed to change voltage across the
membrane
45

46.  Node of Ranvier
 Its myelin free space in the axon containing many Na channels
so AP jump from one node to the other speeding up AP conduction
 Such type of conduction is called salutatory conduction
46
Role of myelin in AP conduction

47. Axonal transport
 Axonal transport occurs in two directions, orthograde (away from the cell
body and towards the brain), and retrograde (towards the cell body and
away from the brain).
Orthograde Axonal Transport
 Transport away from the cell body &
toward the brain
 Has two types;
47

48. 1. Slow axonal transport; two classes
 Slower class ( 0.2 – 1 mm/day )
- for cytoskeletal proteins (tubulin & neuro filament)
 More rapid class (2 – 8 mm / day)
- for actin , myosin , enzymes
2. Fast axonal transport ( 90 – 350 mm/day)
- for neurotransmitters to axon terminal
- continue after transection of the cell body from the axon
48
Axonal transport…

49. Introduction
Retrograde Axonal Transport
 Transport toward the cell body and away from the brain
- Occur as half velocity of the fast axonal transport
- For neurotrophic molecules & growth factors which induce
transcription & translation of gens for axonal survival & growth.
•
49

50. Optic nerve injury
 Optic nerve injury from the various forms of optic neuropathy affect the RGC by
the following mechanisms;
1. Blockage of axonal transport
-build up of excess retrograde transported molecules
-lack of neurotrophic factors for cell survival
2. Demyelination
3. Excitotoxicity from excess glutamate
4. free radical formation
 If the pathology not treated the final common pathway is RGC death by apoptosis
50

51. Axon repair
 It’s a mechanism for protecting RGC & enhancing their survival
after an insult on the axons by the following ways;
 Remyelination
-using steroids & immune modulators in demyelinating diseases
 Neuroprotection
-Blocking excitotoxicity from glutamate
-Administer neurotrophic factors
-Inhibition of apoptosis at its various stages
51

52. Axonal regeneration
 No axonal regeneration after optic nerve injury but there is an
early sprouting called abortive regeneration which latter dies
 Mechanisms preventing axon regeneration
1. Glial associated inhibitory signal
- Active molecules from astrocyte & oligodendrocyte prevent
Regeneration( myelin & proteoglycan)
- Glial cells unable to secrete trophic signals after injury
•
52

53. Axonal regeneration…
2. Neuron intrinsic limitation
- Due to gradual increment of gens which limit axonal
growth & gradual decrement of gens important for
rapid growth
•
53

54. Retinotopic Organization & Visual field defect
Visual field
• It is tested monocularly, with the patient looking straight ahead at a fixation point.
•
54

55. Cont…
 Inversion and reversal of the field are caused by
the optical system of the eye
 The superior field is imaged on the inferior retina
 The inferior field on the superior retina;
 The nasal field is imaged on the temporal retina
 The temporal field on the nasal retina
55

56. Cont…
 The nasal part of the field for one eye is the
same as the temporal part of the field seen by
the other eye, with the exception of the far temporal
periphery, which is called the temporal crescent
 The temporal crescent is imaged on the nasal
retina of one eye but not on the temporal retina
of the other eye.
 Within each temporal field is an absolute scotoma,
the physiologic blind spot.
56

57. Retinal nerve fiber layer
 Papillomacular bundle Central /centrocecal/paracentral scotoma
 Temporal retinal fiber Arcuate visual field defects
 Nasal retinal fiber Temporal wedge shaped defects
 Nasal retinal + temporal fiber defect Altitudinal defect
 Disorder of rod Ring scotoma,
 Disorder of cones Central scotoma
57

58. Introduction
• The role of the central visual pathways is to process and integrate visual
information that travels to the brain by means of the optic nerves
58

59. LESIONS OF VISUAL PATHWAY
59

60.  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
- loss of both direct on ipsilateral &
consensual light reflex on contralateral
side.
60

61. Describe the visual field defect ?
•
61
Bitemporal Heteronymous Hemianopia
 Paralysis of pupillaryreflex (usually lead to partial descending optic
atrophy)
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 hydrocepha

62. Describe the visual field
defect ?
•
62
Junctional scotoma: lesion at junction of optic nerve
and chiasm
 ANTERIOR CHIASMAL
LESIONS:
• Ipsilateral optic neuropathy 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.

63. POSTERIOR CHIASMAL SYNDROME
 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.
63

64. Describe the visual field defect ?
•
64
POSTERIOR CHIASMAL SYNDROME
 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.

65. Describe the visual field defect ?
•
65
Left incongruous homonymous hemianopia
 Contralateral hemianopic pupillary reaction( wernicke’s
reaction)
LESIONS OF OPTIC TRACT :
Causes:
1. Syphilitic meningitis/ Gumm
2. Tuberculous meningitis
3. Tumors of optic thalamus
4. Aneurysm of posterior
cerebral arteries.

66. Describe the visual field defect ?
•
66
Left Homonymous Hemianopia

67. Describe the visual field defect ?
67
Left homonymous hemianopia with macular sparing

68. Describe the visual field defect ?
•
68
Right superior quadrantanopia >> temoporal lobe lesion
 LESIONS OF OPTIC RADIATIONS :
Causes:
• Vascular occlusion(Anterior
choroidal artery, middle cerebral
or posterior cerebral artery)
• Primary & secondary tumors
• Trauma
Characterized by : No Optic
Atrophy
Normal pupillary reactions

69. Describe the visual field defect ?
•
69
Left inferior quadrantanopia >> parietal lobe lesion
 LESIONS OF OPTIC RADIATIONS :
Causes:
• Vascular occlusion(Anterior
choroidal artery, middle cerebral or
posterior cerebral artery)
• Primary & secondary tumors
• Trauma
Characterized by : No Optic Atrophy
Normal pupillary reactions

70. Describe the visual field defect ?
•
70
Right homonymous hemianopia
Congruous
homonymous macular
defect
Head injury/gun shot
injury leading to
lesions of tip of
occipital cortex

71. Describe the visual field defect ?
•
71
Enlarged Blind Spot

72. Describe the visual field defect ?
•
72

73. Describe the visual field defect ?
•
(A) Posterior choridal artery occlusion leads to homonymous horizontal sectroanopia.
(B) Anterior choridal artery occlusion causes sector-sparing homonymous hemianopia

74. References
 Duanes clinical ophtalmology 2012
 Anatomy of the eye, R. Snell 2nd edition
 BCSC Fundamentals and principles of ophthalmology , AAO 2016-2017
 wolff’s anatomy of the eye and orbit, 8th edition
 ADELER’S physiology of the eye 11th edition
 Clinical Anatomy and physiology 3rd edition
 Clinical neuro-ophthalmology – Thomas duane and Edward jaegar
74

75. Thank You!