VISUAL PATHWAY AND

PUPILLARY PATHWAY

SENNY CHAPAGAIN
1ST YEAR
TIO
OVERVIEW:
Conducts signals from retina to occipital lobe
Each half of either eye mapped to contralateral cerebral
hemisphere
Light on photoreceptors stimulates ganglion cells
Ganglion cell axons converge to the optic nerve
Partial decussation at optic chiasma
Optic tract conducts information from chiasma to Lateral
Geniculate Body(LGB)
Fibres from LGB curve around the lateral ventricle as optic
radiations and reach the primary and secondary visual
cortices
 The Visual Pathway
Pathway extends from the ‘retina’ to the
‘visual cortex’ of the brain.
• Precise retinotopic organization
• Deficits due to lesions of the
RETINA
pathway give valuable localizing
information.

ON
OC

OT

LGN
OPTIC
RADIATIONS

ON = Optic Nerve
OC = Optic Chiasm
OT = Optic Tract
LGN = Lateral Geniculate Nucleus of Thalamus

VISUAL
CORTEX
Beginning of the Pathway
Pg. 2

4
Ganglion cells axons form the optic nerve

Bipolar cells

Cells
Rods and Cones
(Receptors)
of the
Retina

5
OPTIC NERVE
Intraocular portion (1 mm )
Intraorbital portion ( 24-30 mm)
Intracanalicular portion (6-9 mm)
Intracranial portion ( 10 mm )
ARRANGEMENT OF NERVE FIBRE IN THE
OPTIC DISC

Central fibres insert in the centre

of the disc

Peripheral fibres insert in the

periphery of the disc
ARRANGEMENT OF NERVE FIBRE IN THE
OPTIC NERVE JUST BEHIND THE EYEBALL
Distributed like retina
Upper and lower temporal
fibres on the temporal half of
the of the optic nerve
Separated from each other by
the area occupied by the
papilomacular bundle
Upper and lower nasal fibres
on the nasal side
ARRANGEMENT OF NERVE FIBRE IN THE OPTIC
NERVE NEAR THE CHIASMA

Macular fibres –centrally

placed
OPTIC CHIASMA:
A flattened band in the anterior
wall of the third ventricle
Lies between the two thalami
and projects into the chiasmatic
cistern
Overlies the sphenoid body
Anteriorly directed towards the
anterior clinoid process,
inclined at 45 o to the
horizontal
12 mm wide, 8mm long and
4mm thick
Relations of optic chiasma:
Anterior: Anterior
cerebral and anterior
communicating arteries
Lateral: Anterior
perforated substance and
Internal carotid artery
 Relations
Posterior: Tuber cinereum
and the mammillary body
Superior: Floor of the third
ventricle and the olfactory
tract
Inferior: Hypophysis,
cavernous sinus
Locational variance:

17% 79% 4%
FIBRE ORIENTATION:
 CLINICAL CORRELATION:
Lower nasal fibres traverse the
chiasma low and anteriorly
(vulnerable-expanding intrasellar
lesions like pitutary adenoma.)
 CLINICAL CORRELATION
As the upper nasal fibres traverse
high and posteriorly so affected in
craniopharyngioma
Lesions producing the chiasmal syndrome:
Tumours of the pituitary
Craniopharyngioma
Suprasellar meningioma
Chiasmal Glioma
Suprasellar aneurysms
Third ventricular dilatation
Chronic chiasmal arachnoiditis
TO SUM UP…
 Bitemporal hemianopia-nasal retinal fibres
including the nasal half of the macula cross,
temporal fibres remain uncrossed(MID
CHIASMA)

 Central bitemporal hemianopia- macular crossing

fibres pass in the posterior part of chiasma and
related to the supraoptic recess (POSTERIOR
CHIASMA)

 Junctional scotoma - central scotoma of the one

eye with superotemporal quadrantic defect of the
other eye
(ANTERIOR CHIASMA)
• Upper temporal quadrantic defects- lower nasal
fibres crossing low and anteriorly
• Lower temporal quadrantic defects- upper nasal
fibres travelling high and posteriorly
OPTIC TRACT:
5.1 mm long cylindrical band,
travelling posterolaterally
from angle of chiasma, between
tuber cinereum and anterior
perforated substance
Runs above and parallel to the
posterior cerebral artery
Crosses the occulomotor nerve,
uncus, corticospinal tract, globus
pallidus, internal capsule and the
hippocampus
Forms the medial and the lateral
roots, the latter spreading over the
Fibre projection from Optic tract
The fibres coming from the
retinal ganglion cells projects
to four subcortical regions in
the brain:
1) LGN
2) Superior Colliculus
3) Hypothalamus
( supraoptic pathway)
4) Pretectum
 NERVE FIBRE ORIENTATION IN OPTIC
TRACT
Each optic tract contains
ipsilateral temporal &
contralateral nasal fibres from
optic nerves.

Nerve fibres rotates 90º so that

superior fibers – dorsomedially
& inferior – ventrolaterally .

Macular fibres - dorsolateral

orientation.
 CONTD…
Larger diameter, faster-
conducting axons predominate
superficially, under the pia.
These fibers correspond to the
magnocellular layers in the
lateral geniculate nuclei.

 The parvocellular axons

dominate the center of the
optic tract, with fibers from the
opposite eye running in the
deepest, dorsal regions. The
ipsilateral parvocellular fibers
sit slightly ventrally
LESIONS OF THE OPTIC TRACT
Anterior optic tract lesion
produces an incongruous
homonymous hemianopia ,
decreased visual acuity, afferent
pupil defect (Wernicke’s
hemianopic pupil), and atrophy of
the optic disc with characteristic
bow-tie atrophy in the
contralateral eye.

A complete homonymous
hemianopia results from a lesion of
the posterior optic tract .
LATERAL GENICULATE NUCLEUS :
• Located in posterior thalamus below and lateral to
pulvinar nuclei and above ambient cistern. Medially
lies internal capsule
• Peaked mushroom shaped
 Layers and cells arrangement:

Major cell layers:-

Parvocellular (3,4,5,6 ) 6

Magnocellular (1 ,2 ) 5

Magnocellular layer 3
 Achromatic vision
2
 Low fine detail vision
1
 Fast motion vision
Parvocellular layer
 Chromatic vision
 High fine detail vision
 Slow motion vision
Retinotopic map representation in LGN:

6
5
4
3
2
1

Contralateral:1,4&6
Ipsilateral:2,3&5
NERVE FIBER ORIENTATION IN LGB
Macular fibers occupy posterior two-
thirds of LGB.

Upper retinal fibers occupy medial

half of anterior one third.

Lower retinal fibers occupy lateral

half of anterior one-third.
LESION OF LATERAL GENICULATE BODY
Visual field defect in lesions of
LGB is extremely rare.
Incongruous homonymous
hemianopia
No pupillary change
Relatively congruous
homonymous horizontal
sectoranopia.
OPTIC RADIATION
Connects the nerve fibers from LGB
to visual cortex in occipital lobe via
geniculocalcarine pathway.

Pass forward laterally through area of

wernicke as optic peduncle, anterior
to lateral ventricle and traversing the
retroloenticular part of internal
capsule behind the sensory fibers
and medial to auditory tract.
Spread out fanwise to form
medullary optic lamina
NERVE FIBRE ORIENTATION IN OPTIC
RADIATION
Axons carrying information
about the superior visual field
sweep around the lateral horn of
the ventricle under the temporal
lobe (Meyer’s loop).
Those carrying information
about the inferior visual field
travel under the cortex of the
parietal lobe.
 The macular fibers course
laterally and occupy central
position in the optic radiation.
OPTIC RADIATION LESIONS:
Temporal lobe lesions – mid
peripheral and peripheral
contralateral homonymous superior
quadrantanopia
Parietal lobe lesions- contralateral
homonymous inferior
quadrantanopia
Common causes:
a. Tumours
b. Stroke
c. Stroke and middle cerebral artery
lesions
 VISUAL CORTEX
Located on the medial aspect of the
occipital lobe in and near the
calcarine fissure.
Thinnest portion of cerebral cortex.
Area - 20-45 sq cm.
Occupies 3-5% of brain
Heavily weighted to central activity
i.e within central 10 degree of visual
field.
PARTS
Primary visual cortex
Also known as visuosensory
area/striate cortex/V1 /
Broadman area 17

Secondary visual
cortex
Includes peristriate area 18(V2)
and parastriate area 19(V3)
V1 (Striate Cortex)
PROJECTION OF NERVE FIBRES IN VISUAL
CORTEX
 Fibers of the optic radiation
terminate in the fourth layer of the
6 layers in the primary visual
cortex.
There is point to point projection
of the retina in the visual cortex in
such a way that the right visual
cortex is concerned with
perception of
objects situated to the left half.
PROJECTION OF NERVE FIBRES IN VISUAL
CORTEX (contd..)
Macular fibres –posteriorly in
visual cortex at occipital tip
Peripheral retina –anterior
to macular fibres.
LESIONS OF VISUAL CORTEX
Common causes:
Posterior cerebral
artery occlusion
Blunt injury to
occiput
 The Visual Pathway

RETINA

ON = Optic Nerve
OC = Optic Chiasm
ON
OC OT = Optic Tract
LGN = Lateral Geniculate Nucleus of Thalamus
OT

LGN
OPTIC
RADIATIONS

VISUAL
CORTEX
 1
2
4
3 5
6

8
7
BLOOD SUPPLY OF VISUAL PATHWAY
PUPILLARY
PATHWAY
 ANATOMY OF PUPIL
Aperture in the centre of iris
Shape - circular
Circularly arranged constrictor
muscles (Sphincter pupillae)
Supplied by parasympathetic nervous system
Radially arranged dilator muscles
(Dilator pupillae)
Supplied by sympathetic nervous system
Normal Pupil
 3-4 mm

 Small in infants – Dilator muscle not well

developed

 Large in Adolescent – Sympathetic over action

 Small in old age – Fibrotic sphincter pupillae

 Small during sleep

▪ Sympathetic activity reduced
▪ Parasympathetic activity enhanced
 Pupillary Constriction
(Miosis) Pupillary Light Reflex
Right Afferent limb = Left
Optic Nerve
Direct Consensual
Reflex Reflex

Efferent limb = Oculomotor Nerve

Postganglionic
Preganglionic

Intercalated
Neurons /
Internuncial
Fibres to
both sides
 Near Reflex:
Two components:
Convergence Reflex
Accommodation Reflex
Triad of Synkinetic Near
Response:
Convergence
Accommodation of lens
Constriction of pupil
Parasympathetic Control of pupillary Size
Near Point Stimulus :
Retina Edinger Westphal Nucleus
Ciliary Ganglion III Nerve
(undetermined pathway)

Optic Nerve
Short ciliary Frontal Lobe (undetermined
nerve pathway)
Optic
Chiasma
sphincter
Pupillae Occipital Cortex
Optic Tract

Lateral Geniculate Optic Radiation

body
PUPILLARY DILATATION PATHWAY
Posterior Long ciliary nerve
hypothalamus
Dilator pupillae
Ciliary ganglion (No
synapse)
Brain Stem

Nasociliary nerve
Cranial Spinal Cord

Sympathetic plexus
Synapse at C8T1-2 (Around the Ophthalmic
artery)

Superior cervical Sympathetic plexus

ganglion synapse (Along Internal carotid artery)
 Other Pupillary Reflexes:
Darkness reflex
Abolition of light reflex- relaxation of the
sphincter pupillae
 Contraction of dilator pupillae
Psycho sensory reflex
Cortical reflex
Loud noise or pain causes pupillary dilatation
Lid closure reflex
Constriction of pupil with blinking
Dilatation of pupil with lid closure
Abnormal Pupillary
Reactions:
Afferent pupillary conduction defects

Efferent pupillary defects

Pupillary light near dissociation

Afferent Pupillary Conduction
Defects:
Total Afferent Pupillary Defect ( TAPD)
 Amaurotic Pupil
 Caused by complete optic nerve lesion

Relative Afferent Pupillary Defect (RAPD)

 Caused by incomplete optic nerve lesion or severe retinal disease

Wernicke’s Hemianopic Pupil

 caused by optic tract lesion
SWINGING FLASH LIGHT TEST
GRADING OF RAPD
1+ = initial constriction followed
by early release of the affected
pupil
2+ = no movements initially
followed by pupillary release
3+ = immediate pupillary
dilation
4+ = amaurotic eye (no light
perception)
Efferent Pupillary Defects:
Characterized by absence of both direct and
consensual light reflex on the affected side and
presence of both direct and consensual light
reflex on the normal side
on the affected side, near reflex is absent
pupil remains dilated and fixed

Common causes
Effect of drugs – e.g. Atropine
Internal ophthalmoplegia
Third cranial nerve palsy
Reflex abolished if afferent or efferent is damaged.

Right Left Right Left

Afferent
defect

Efferent
defect

Nolte 17-38
Pupillary Light-Near Dissociation:
Situation in which the pupillary near reaction is
present and the pupillary light reaction is absent

Causes
Argyll Robertson pupil
 seen in tertiary neurosyphilis
B/L old total retinal detachment or bilateral optic
atrophy
lesions in the midbrain
Diabetes, Alcoholism
Adie’s Tonic pupil
Anisocoria:
Importance
Many benign & life threatening etiologies

Detail history & careful physical exam to stratify the

etiology & determine whether the patient needs
imaging, urgent referral or routine follow up care
Causes of Anisocoria:
Physiological Anisocoria
approx. 20% of the population
always <1.0 mm difference
pupillary constriction normal to
light and during near vision
Equal in dim and bright light
Causes of Anisocoria:
Abnormally Constricted Pupil
U/L use of miotics, morphine
Iritis
Horner’s syndrome
Argyll Robertson pupil
Long-standing Adie’s pupil
Pontine haemorrhage
(Head injury)
Causes of Anisocoria :
Abnormally Dilated Pupil
U/ L use of mydriatics
Iris sphincter muscle damage (trauma)
Adie’s tonic pupil
Third cranial nerve palsy
Acute congestive glaucoma
Horner’s Syndrome:
 Oculosympathetic palsy
 May be congenital
 Critical signs:
 Anisocoria greater in dim light
 Mild ptosis
 Reverse ptosis
 Miotic pupil that reacts equally to light and near
 Dilatation lag
 Apparent enophthalmos
 Anhydrosis of the affected side of the face
 Heterochromia of the affected iris
REFERENCES:
Fundamentals and Principles Of Ophthalmology –
AAO
Neuro-Ophthalmology – AAO
Snell’s anatomy
Wolff’s Anatomy
Ophthalmology – M. Yanoff
Clinical ophthalmology – Kanski 7th edition
THANK YOU!!