This document discusses the anatomy and manifestations of lesions along the visual pathway, including the optic nerve, chiasm, optic tract, lateral geniculate bodies, optic radiations, and visual cortex. Key points covered include the structures of each component of the visual pathway and the visual field defects that result from lesions in different locations, such as optic neuropathies, chiasmal syndromes, and homonymous hemianopsias from retrochiasmal lesions. Specific conditions like cortical blindness, dyschromatopsia, alexia without agraphia, and palinopsia that can arise from lesions in different areas are also mentioned.

1. Anatomy and
Manifestations of Visual
Pathway Lesions
Raed Behbehani , MD, FRCSC

2. Visual Pathway

3. Visual Pathway

4. Visual pathways
 Prechiasmal: optic nerve-chism.
 Retrochiasmal: optic tract, the optic radiations,
and the occipital cortex.

5. Optic Neuropathy
 Unilateral.
 RAPD, dyschromatopsia.
 Central, cecocentral.
 Arcuate (superior, inferior).
 Altitudinal.
 Generalized decrease in sensitivity.

6. Optic Nerve
 Axoplasmic transport : clearance of expired
organelles, structural maintainance, and energy
requirements.
 Interruption of axoplasmic transport : ischemia,
compression, inflammation.
 Orthograde axonal transport : away from the cell
body LGN.
 Retrograde axonal transport : toward cell body.

7. ONH Blood Supply

8. RGC axons
http://www.city.ac.uk

9. Intra-orbital Optic Nerve
 Myelination (oligodendrocytes).
 20-30 mm Long.
 Axons: mylein and glial cell (metabolic support
at the nodes of Ranvier).

10. Intracranalicular Optic Nerve
 Within the two bases of the LWS.
 Medial wall of canal forms lateral wall of
sphenoid sinus (can be absent !).
 Within canal : meninges, ophthalmic artery and
sympathetic plexus.
 10 mm length.
 Tight space !
 Internal carotid artery.

11. Intracranial Optic Nerve
 Leaves the cranial end of the optic canal
(medially, backwards, upwards).
 4-15 m (depending on the position of chiasm).
 Upward 45 degree-angle.
 Anterior cerebral and anterior comunicating
artery lie superior.

12. Arcuate
Early Late

13. Altitudinal

14. Central

15. Chiasm

16. Chiasm
 Floor of the third ventricle.
 5-10 mm above the diphragma sella and the
hypophysis cerebri.
 12mm wide, 8mm A-P , 4 mm thick.
 Important relations: 3rd ventricle, hypothalmus,
pituitary stalk, sella, dorsum sellam anterior and
posterior clinoid processes, cavernous sinus.
 Nasal fibers cross ; temporal fibers do not
(53:47).
 Wilband’s knee.

17. Chiasm

18. Chiasmal syndrome
 Unilateral or Bilateral.
 Junctional scotoma.
 Bitemporal defect.
 Homonymous defects.
 Diplopia (III, IV, VI cranial nerves or hemi-field
slide phenomenon).

19. Causes of Chiasmal syndrome
 Pituitary adenoma
 Suprasellar meningiomas
 Supraclinoid internal carotid artery aneurysms
 Craniopharyngiomas
 Optic nerve gliomas
 Uncommon : Optic nerve or chiasmal neuritis
,Pachymeningitis , Trauma,Inflammatory (e.g.,
sarcoidosis)

20. Bitemporal defect

21. Junctional Scotoma (Anterior
chiasmal syndrome)

22. Traquair scotoma
 A monocular hemianopic visual field loss is
referred to as junctional scotoma of Traquair.

23. Posterior Chiasmal Syndrome
 90% of chiasmal fibers have macular origin
(superior and posterior portions of chiasm).

24. Chiasm

25. Band atrophy
From (Practical viewing of the optic disk)

26. Retrochiasmal Visual Pathway
Lesions
 Bilateral.
 Homonymous.
 Complete or incomplete.
 Congrous or incongrous.

27. Optic Tract Lesions
 Contralateral RAPD (may be an ipsilateral
afferent pupillary defect if a concomitant optic
neuropathy exists)
 A specific form of optic atrophy (band atrophy)
due to the involvement of nasal fibers (temporal
field) in the contralateral eye
 An incongruous homonymous hemianopsia.

28. Optic Tract
 Travel around the cerebral peduncles at dorsal
midbrain.
 Divides into lateral root LGN , and a smaller
medial root pretectal area (pupillary light
reflex)

29. Optic Tract

30. Optic tract lesions
Band Atrophy due to compression
Hoyt Wf,
Kommerell G. Der fundus oculi bei homonyermeinaopia.
of the left tract.
Klin Monatsblat Augenheilkd 1973; 162: 456-464)

31. Lateral Geniculate Bodies Lesions
 Part of the thalamus.
 Hilum, medial and lateral horn.
 Six laminae (layers 1-6), crossed fibers1,4,6 ,
uncrossed fibers 2,3,5.
medial
lateral

32. LGB
 Upper quadrant medial aspect of LGN,
Lower quadrant lateral aspect of LGN.
 Macular fibers central wedge of LGN.

33. LGB
1- Optic nerve
2- Optic chiasma
3- Optic tract
4- Lateral geniculate body
5- Optic radiation
6- Visual cortex
7-Superior colliculus of the
midbrain
8- Putamen
9- Long association bundle -
inferior occipitofrontal
fasciculus
10- Pulvinar of the thalamus
11-Calcarine fissure
12- Posteroinferior horn of
the lateral ventricle

34. Lateral Geniculate Nucleus
 Posterior thalamus.
 Mushroom-shaped structure (6 layers).
 Hilum, medial and lateral horn.
 Six laminae (layers 1-6), crossed fibers1,4,6 ,
uncrossed fibers 2,3,5.

35. Lateral Geniculate Nucleus

36. Lateral Geniculate Nucleus
 Upper quadrant medial aspect of LGN,
Lower quadrant lateral aspect of LGN.
 Macular fibers central wedge of LGN.
 Layers 1,2: magnocellular. (motion)
 Layers 3-6: Parvocellular. (color)

37. LGB lesions
 An incongruous wedge defect tending to point
toward fixation (spears to fixation)
 Usually complete or nearly complete field
homonymous defect.

38. LGB lesions

39. Optic radiations
 Nerve fibers bundles with cell bodies in the
LGN.
 Loop of Meyers (around temporal and inferior
horn of LV).
 Inferior fascicle.
 Superior fascicle.

40. Optic radiations
 Inferior fascicle anterior pole of temporal
lobe lower calcarine cortex.
 Superior fascicle parietal lobe upper
calacrine cortex.

41. Parietal lesions
 “Pie on the floor” homonynous defect.
 Associated neurologic signs and symptoms
(e.g., hemiplegia, hemisensory loss, visual, or
neglect) may be present .

42. Anterior temporal lobe
 “Pie on the sky” homonymous.
 Often incongrous.
 Seizures, hemiparesis, hemianesthesia.
 Contralateral neglect (Non-dominant).
 Aphasia (Dominant).

43. Optic radiation lesions

44. Occipital lobe lesions

45. Primary Visual Cortex
 Optic radiations terminate in layer 4 (lamina
granularis) .
 Layer 4 is divided into 3 layers (Line of
Gennari).
 P-cells  4C bets.
 M-cells  4C alpha.
 Macular fibers – terminate posterioly.
 Lateral fibes – termriate anteriorly.

46. Primary Visual Cortex ( V1)
 Upper bank and lower bank (Calcarine fissure).
 Inferior visual filed (upper bank) , Superior
visual field (lower bank).
 Macular projections represented by 50%-60% of
the area of the calcarine cortex.
 Occipital tip is for foveal vision.

47. Occipital cortex lesions
 Isolated (i.e., without other neurologic deficit)‫ز‬
 Congruous.
 Paracentral or peripheral.
 Complete or incomplete
 Macular involvement or macular sparing of the
central 5 degrees may occur (occipital pole
involvement).

48. Occipital cortex lesions

49. Visual cortex
-Anterior striate cortex
(8%-10%) is monocularly
innervated (temporal
crecsent of contralateral
eye).

50. Visual association areas

51. Visual Association Areas
 V2: input from V1.
 V3: sends info to basal ganglia and midbrain.
 V3a: perceive motion and direction.
 V4 : (lingual and fusiform gyrus) color.
 V5 : (medial temporal visual region) speed and
direction, origin of pursuit movemen.
 V6 : (parietal) represent “extra personal space”.

52. “What” Pathway
 Ventral stream (occipitotemporal) : object
recognition , color, shape, and pattern.
 Continuation of the parvocellular pathway.
 V1 V2V4 inferotemporal cortex
angular gyrus limbic structures.
 Alexeia, anomia, agnosia, amenesia.

53. “Where” Pathway
 Dorsal stream (occipitoparietal): Spatial
orientation ,visual guidance of movement.
 V1 V3 V5Parietal and superotemporal
cortex.
 Continuation of magnocellular pathway.
 Simultagnosia, optic ataxia, acquired oculomotor
apraxia, and hemispatial neglect.

54. Cortical blindness
 Due to bilateral occipital lobe lesions.
 Often misdiagnosed as functional vision loss.
 Stroke, severe blood loss, Eclampsia,
hypertension, angiography, CO poisoning,
cyclosporine.

55. Dyschromatopsia
 Bilateral occipital lobe lesions in the lingual or
fusiform gyri of the medial occipital lobe (medial
occipito-temporal lobe).
 Rarely no field defect.
 Unilateral involvement may cause
hemidyschromatopsia.

56. Alexia without Agraphia
 Loss of ability to read but can write.
 Left occipital lobe and splenium of corpus
callosum.

57. Palinopsia
 Persistant or recurrence of visual stimulus after
it has been removed.