Physiology of the eye

Khorrami Ph.D.
http://khorrami1962.spaces.live.com
khorrami4@yahoo.com
Perimetry
 Retinofugal projections
• Retinogeniculostriate pathway
• Extra retinogeniculostriate pathway
– Retinotectal(superior colliculus) to:
• R.F. in arousal response
• LGN . . . Cortex
– Pretectal
– Pregeniculate nucleus…pontine nucleus…mossy
fiber….vestibulocerebellum
– Accessory optic nucleus….inferior olive
N….climbing fiber…vestibulocerebellum
– SCN…circadian rhythm/ melanopsin in a type of
ganglion cells
Retinal projections
LGN & projections to cortex
Anatomy of visual pathway
Visual pathway
 Central processing
• Orientation selective neurons, by edge detecting
• What pathway: parvocellular, fine, color and dept
– From P-type cells
– Slowly adapt
– V1,V2,V4 & IT
– IT(inferotemporal) cortex; visual long term memory
• Stimulated in epilepsy
• Where pathway: magnocellular: motion, position
– Rapidly adapt
– V1,V2,V3, V5(medial temporal)
– Finally to medial temporal, medial superior temporal &
posterior parietal(Brodman5&7 )
 Striate cortex
• M channel
– Analysis of object motion
• P-interblob channel
– Analysis of object shape
• Blob channel
– Analysis of object color
– If defect . . . . Color blindness

• Layer VI . . . . To LGN for feedback

• Layer V . . . . To superior colliculus for visual reflex
• Layer II & III . . . . Between cortex
 Eye movements
• With head movements
Vestibulo-ocular eye movements
Opto-kinetic eye movements
• No movement in head
Saccadic eye movements (vertical or horizontal)
Smooth pursuit eye movements
Vergence eye movements
 Eye movements
• Superior muscles receive innervations from opposite side
• PPRP in horizontal movements
– Receive from: sup.col., Vest.N., cerebellum, frontal eye field, MLF,
perihypoglossal N.( in gaze holding)
– Ipsilateral LR & contralateral MR
– Left side lesion….cannot follow the object in left
• riMLF in vertical movements
• Vermis of cerebellum in generation of REM
• Superior colliculus
 Extraocular Nerves and Nuclei

Oculomotor nerve (CN III) divides

in 2: superior division goes to the
superior rectus and levator
palpebrae superioris (eyelid
elevation); inferior division goes to
medial rectus, inferior rectus, and
inferior oblique.
Also carries preganglionic para-
sympathetics to the pupillary
contrictor muscles and ciliary
muscles of lens

Trochlear (CN IV) innervates the

superior oblique muscle
Abducens (CN VI) innervates the lateral rectus
Oculomotor nucleus consists of several subnuclei and is located at
level of superior colliculus and red nucleus.
Edinger-Westphal nucleus is site of parasympathetic preganglionic neurons.
Unilateral lesions of the oculomotor nucleus affect the ipsilateral and
contralateral eye since some axons cross in brainstem before nerve exits.
Trochlear nucleus in caudal midbrain at level of inferior colliculus
Trochlear nerves are the only cranial nerves to exit dorsal surface of
brainstem. They cross after exiting.
Abducens nuclei lie on floor of 4th ventricle at level of mid-to-lower pons.
Axons travel ventrally to exit at the pontomedullary junction.
Diplopia (double vision)
Possible causes:
Mechanical problems such as orbital fracture with muscle entrapment
Extraocular muscle disorder such as from thyroid disease or myositis
Neuromuscular junction disorder such as myasthenia gravis
Damage to CN III, IV, or VI, their nuclei or connecting pathways

In young children where visual pathways are still developing, congenital

eye muscle weakness can produce strabismus that over time causes
suppression of one image resulting in amblyopia (decreased vision in
one eye). Early correction is critical for proper function of both eyes.
 Color perception
• Rhodopsin on chromosome 3
• Blue(tritan) on chromosome 7
• Red(protan) and green(deutan) on chromosome X
• Protanomaly: poor red-green, dimmer red
• Deutranomaly: poor red green, normal red
• Protanopsia
• Deutranopsia
Brainstem Circuits for
Horizontal Eye Movements
Brainstem Pathways for Control of
Controlled by lateral rectus (CN VI) Horizontal Eye Movements
and medial rectus (CN III).
MLF interconnects nuclei of III, IV, VI
and vestibular nuclei.
This interconnection makes conjugate
eye movements possible.
Nucleus VI acts as horizontal gaze
center by controlling movement of
both eyes by projecting to the
ipsilateral lateral rectus and the
contralateral III nucleus.
Pontine tegmentum near nucleus VI
has the paramedian pontine reticular
formation that projects to nucleus VI
to activate lateral gaze.
 Brainstem Lesions Affecting Horizontal Gaze

MLF lesions interrupt input to medial rectus so the eye ipsilateral to the
lesion does not fully adduct on attempted horizontal gaze; there is also
often nystagmus in the contralateral eye.
This syndrome is called internuclear ophthalmoplegia (INO)

Common causes of INO:

multiple sclerosis
pontine infarct
tumors near MLF
Brainstem Circuits for Vertical Eye Movements
Vertical eye movements mediated by superior and inferior rectus and
superior and inferior oblique muscles.
Centers controlling vertical eye movement located in rostral midbrain
reticular formation and pretectal area.
Ventral region mediates downgaze.
Dorsal region mediates upgaze.
Locked-in syndrome caused by large pontine infarct/hemorrhage often
damages corticospinal tracts bilaterally and nucleus VI, thereby
eliminating body movement and horizontal eye movement; patient can
then communicate only via vertical eye movements.
Brainstem Circuits for Vergence Eye Movements
Convergence is produced by medial recti muscles and divergence by
lateral recti muscles.
Exact location of brainstem vergence centers not known, but neurons in
midbrain reticular formation appear to be involved.
Visual cortex and parietal cortex involved as part of the accommodation
response.
Parinaud’s Syndrome
Includes a group of eye abnormalities caused by compression of the dorsal
midbrain and pretectal area:
1. Impairment of upgaze
2. Large, irregular pupils that do not react to light but may react to
accommodation
3. Eyelid abnormalities ranging from bilateral lid retraction to ptosis
4. Impaired convergence

Most common cause is pineal tumor and hydrocephalus.

Hydrocephalus can cause dilation of the suprapineal recess of the 3rd
ventricle which pushes downward on the tectum.
Hydrocephalus in children can produce the bilateral “setting-sun sign”
in which the eyes are deviated inward due to CN VI palsy and
downward due to Parinaud’s Syndrome.
Forebrain Control of Eye Movements
Multiple paths descend from forebrain and affect eye movements.
These paths project either directly to brainstem nuclei involved with eye
movements or relay via the superior colliculus.
Frontal eye fields appear to be in area 6.
FEF generates saccades in the contralateral direction via connections to
contralateral PPRF.
Parieto-occipital-temporal cortex functions in smooth pursuit eye
movements in ipsilateral direction via connections with the
vestibular nuclei, cerebellum,
and PPRF.
Inputs from visual cortex and
visual association cortex influence
FEF activity.
Basal ganglia also appear to play
a role in eye movements.
Visual cortices
Dorsal and ventral stream
Right-Way Eyes and Wrong-Way Eyes
Cerebral cortex lesions may impair eye movements in the contralateral
direction and so produce eyes directed toward the lesion side.
This gaze preference is typically accompanied by muscle weakness
contralateral to the lesion side so that eyes look away from the side of
paralysis. This is the typical “right-way eyes.”
Certain lesions/abnormalities can cause eyes to look toward the side of
paralysis, which is “wrong-way eyes.”
Causes of “wrong-way eyes”:
1. Cortical seizures can drive eyes in
contralateral direction by activating
FEFs, while causing weakness on
the contralateral side of body
controlled by seizing cortex.
2. Thalamic hemorrhage can disrupt
corticospinal paths of internal capsule
and also cause eyes to deviate toward
the side of weakness. This may be
accompanied by coma.
3. Pontine basis and tegmentum lesion which
damages corticospinal fibers can also
damage VI nucleus or PPRF causing
ipsilateral gaze weakness.
Cerebellar, Vestibular and Spinal Control of Voluntary and
Reflex Eye Movements

Two common reflex eye movements:

1. Optokinetic nystagmus (OKN) – can be triggered in patient by moving a
thick ribbon with vertical stripes horizontally in front of the eyes.
Eyes alternate between smooth pursuit movements in the direction
of stripe movement and backup saccades in the opposite direction.
Sometimes called “train nystagmus” because it can be observed in
the eyes of train passengers as they view passing scenery while on
a moving train.
Slow phase (smooth pursuit) mediated by ipsilateral posterior cortex via
connections to vestibular nuclei and cerebellum projecting to the
PPRF and nucleus VI.
Fast phase (saccades) mediated by FEFs projecting to contralateral
PPRF
Lesions of frontal cortex disrupt fast phase of OKN while lesions of posterior
cortex disrupt smooth pursuit movements.
2. Vestibulo-Ocular Reflex (VOR) – stabilizes eyes on visual image
during head and body movements.
Vestibular nuclei inputs via MLF control extraocular nuclei.
Tested using oculocephalic maneuver or cold water calorics.
While prone head is rotated and eyes should move opposite
to direction of head turning.
Cold water irrigation of ear should produce nystagmus with eyes
beating in contralateral direction.
Visual pathways
The Pupils and Other Ocular Autonomic Pathways
Pupils under both parasympathetic (constriction) and sympathetic (dilation)
control.
Light reflex: optic nerve>optic tract>pretectal area; pretectal neurons>
bilateral Edinger-Westphal nuclei>ciliary ganglion>constrictor muscles
Direct response and consensual response.
Bilateral pupillary constriction also occurs via a slightly different pathway
during the accommodation response.
Accommodation response includes pupillary constriction, accommodation
of lens ciliary muscle, and convergence of eyes.
Accommodation requires activation of visual cortex (recognize closer object).
Lens is normally under tension from suspensory ligament.
Ciliary muscle acts as sphincter and when contracted causes suspensory
ligament to relax producing a more rounded lens for near focus.
Sympathetic pathway for pupillary dilation involves connections from
hypothalamus via lateral brainstem to thoracic cord T1-T2 sympathetic
preganglionic neurons whose axons go to superior cervical ganglion.
Neurons of SCG project to pupillary dilator muscles of eye.
Sympathetic path also controls superior tarsal muscle which elevates the
upper eyelid, giving a wide-eyed stare.
Sympathetic axons traveling with these also innervate sweat glands of face
and neck; when damaged this gives Horner’s syndrome
 Pupillary Abnormalities

Causes include peripheral or central lesions, sympathetic or

parasympathetic lesions, or disorders of iris muscle or visual
pathways.
Pupillary abnormalities can be bilateral or unilateral.
Unilateral abnormality produces pupil asymmetry = anisocoria

1. Oculomotor Lesions
Unilateral dilated pupil (when large = blown pupil)
Decreased or absent direct and consensual light response

2. Horner’s Syndrome
Disruption of sympathetic paths to eye and face
Ptosis, miosis (constriction), and anhydrosis
Impaired dilation response
Direct and consensual light response intact; following dilation
slowed
Locations for lesions causing Horner’s Syndrome:
Lateral brainstem, spinal cord, T1 & T2 roots, sympathetic chain,
carotid plexus, cavernous sinus, orbit.

3. Afferent Pupillary Defect (Marcus Gunn Pupil)

Direct light response in one eye is absent while the consensual response
in that eye is normal.
Caused by lesion in retina, optic nerve or eye.

4. Benign Anisocoria
In about 20% of general population there is a slight pupillary
asymmetry which can vary over time.

5. Pharmacological Miosis (constriction) and Mydriasis (dilation)

Opiates cause bilateral pinpoint pupils.
Barbiturates cause small pupils.
Anticholinergic agents like atropine or scopolamine cause dilation.
Anticholinesterase agents (sarin, nerve gas) cause constriction.
6. Light-Near Dissociation
Pupils constrict much less in response to light than to
accommodation.
Classic example is Argyll Robertson pupil typically associated with
neurosyphilis in which pupils are small and irregular and
show light-near dissociation.
LND also seen in diabetic neuropathy and Parinaud’s syndrome
(compression of dorsal midbrain).
 Ptosis (drooping eyelid)

• Eye opening involves levator palpebrae superior (CN III) and

Muller’s
• smooth muscle in upper eyelid (sympathetic control);
frontalis
• muscle of forehead (CN VII) also plays accessory role.
• Eyelid closure done by orbicularis oculi muscle (CN VII).
• Common causes of ptosis:
Horner’s syndrome
oculomotor nerve palsy
myasthenia gravis
redundant skin folds that occur with aging (pseudoptosis)
EOG
ERG
 ERG
• Holmgren (1865) found that a light stimulus
could cause a change in the electrical
potential of the amphibian eye
• Gotch (1903) 2 waves
• Einthoven and Jolly (1908) 3 waves
Electro-Oculo-Graphy
Electrode placement
IT: inferotemporal
PP: posterior parietal
ST: superior temporal
Visual location
Motion( middle temporal gyrus)
Achromatopsia( occipito-temporal gyrus)
Visual agnosia( posterior & medial temporo-
occipital cortex)
Visual neglect( inferior parietal lobe)
 Balint-Holmes syndrome*( posterior parietal
lobe)

•Optic ataxia, ocular apraxia & simultanagnosia

 Visual cortices
A: visual location
B:Motion
blindness(middle
temporal)
C: Achromatopsia
(occipito-temporal)
D: Visual agnosia ( post. &
medial temporo-occipital)
E: Visual neglect (inf.
parietal)
F: Balint-Holmes syd.(post.
Parietal)
Normal color vision
Protanopia
Deuteranopia
Tritanopia
Speech