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Physiology of the

Khorrami Ph.D.
Retinofugal projections
• Retinogeniculostriate pathway
• Extra retinogeniculostriate pathway
– Retinotectal(superior colliculus) to:
• R.F. in arousal response
• LGN . . . Cortex
– Pretectal
– Pregeniculate nucleus…pontine
– Accessory optic nucleus….inferior
olive N….climbing fiber…
– SCN…circadian rhythm/ melanopsin in
Retinal projections
LGN & projections to cortex
Anatomy of visual pathway
Visual pathway
Central processing
• Orientation selective neurons, by edge
• What pathway: parvocellular, fine, color
and dept
– From P-type cells
– Slowly adapt
– V1,V2,V4 & IT
– IT(inferotemporal) cortex; visual long term
• Stimulated in epilepsy
• Where pathway: magnocellular: motion,
– Rapidly adapt
– V1,V2,V3, V5(medial temporal)
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
ØVestibulo-ocular eye movements
ØOpto-kinetic eye movements
• No movement in head
ØSaccadic eye movements (vertical or
ØSmooth pursuit eye movements
ØVergence 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

E xtra o cu la r N e rve s a n d N u cle i

O cu lo m o to r n e rve ( C N III) d ivid e s

in 2 : su p e rio r d ivisio n g o e s to th e
su p e rio r re ctu s a n d le va to r
p a lp e b ra e su p e rio ris ( e ye lid
e le va tio n ); in fe rio r d ivisio n g o e s to
m e d ia lre ctu s, in fe rio r re ctu s, a n d
in fe rio r o b liq u e .
A lso ca rrie s p re g a n g lio n ic p a ra -
sym p a th e tics to th e p u p illa ry
co n tricto r m u scle s a n d cilia ry
m u scle s o f le n s

Tro ch le a r ( C N IV ) in n e rva te s th e
su p e rio r o b liq u e m u scle
A b d u ce n s ( C N V I) in n e rva te s th e la te ra lre ctu s
cu lo m o to r n u cle u s co n sists o f se ve ra lsu b n u cle ia n d is lo ca te d a t
le ve lo f su p e rio r co llicu lu s a n d re d n u cle u s.
in g e r-W e stp h a ln u cle u s is site o f p a ra sym p a th e tic p re g a n g lio n ic n e u ro n
n ila te ra lle sio n s o f th e o cu lo m o to r n u cle u s a ffe ct th e ip sila te ra la n d
co n tra la te ra le ye sin ce so m e a xo n s cro ss in b ra in ste m b e fo re n e rve exit
Tro ch le a r n u cle u s in ca u d a lm id b ra in a t le ve lo f in fe rio r co llicu lu s
Tro ch le a r n e rve s a re th e o n ly cra n ia ln e rve s to exit d o rsa lsu rfa ce o f
b ra in ste m . T h e y cro ss a fte r exitin g .
d u ce n s n u cle ilie o n flo o r o f 4 th ventricle at level of mid-to-lower
ons travel ventrally to exit at the pontomedullary junction.
Diplopia (double vision)
ossible causes:
ØMechanical problems such as orbital fracture with muscle entrapment
ØExtraocular muscle disorder such as from thyroid disease or myositis
ØNeuromuscular junction disorder such as myasthenia gravis
ØDamage to CN III, IV, or VI, their nuclei or connecting pathways

n 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
Color perception
• R h o d o p sin o n ch ro m o so m e 3
• B lu e ( trita n ) o n ch ro m o so m e 7
• R e d ( p ro ta n ) a n d g re e n ( d e u ta n ) o n
ch ro m o so m e X
• Pro ta n o m a ly: p o o r re d -g re e n , d im m e r re d
• D e u tra n o m a ly: p o o r re d g re e n , n o rm a lre d
• Pro ta n o p sia
• D e u tra n o p sia

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
LF lesions interrupt input to medial rectus so the eye ipsilateral to
lesion does not fully adduct on attempted horizontal gaze; there is
often nystagmus in the contralateral eye.
his syndrome is called internuclear ophthalmoplegia (INO)
Common causes of INO:
multiple sclerosis
pontine infarct
tumors near MLF
rainstem Circuits for Vertical Eye Movements
ertical eye movements mediated by superior and inferior rectus and
superior and inferior oblique muscles.
enters controlling vertical eye movement located in rostral midbrain
reticular formation and pretectal area.
Ventral region mediates downgaze.
Dorsal region mediates upgaze.
ocked-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
rinaud’s Syndrome
ludes a group of eye abnormalities caused by compression of the dorsal
midbrain and pretectal area:
pairment of upgaze
rge, irregular pupils that do not react to light but may react to
yelid abnormalities ranging from bilateral lid retraction to ptosis
mpaired convergence

t common cause is pineal tumor and hydrocephalus.

rocephalus can cause dilation of the suprapineal recess of the 3rd
ventricle which pushes downward on the tectum.
rocephalus 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.
orebrain Control of Eye Movements
ltiple paths descend from forebrain and affect eye movements.
ese paths project either directly to brainstem nuclei involved with
movements or relay via the superior colliculus.
ontal eye fields appear to be in area 6.
F generates saccades in the contralateral direction via connections to
contralateral PPRF.
rieto-occipital-temporal cortex functions in smooth pursuit eye
movements in ipsilateral direction via connections with the
vestibular nuclei, cerebellum,
and PPRF.
puts from visual cortex and
visual association cortex influence
FEF activity.
sal ganglia also appear to play
a role in eye movements.
Visual cortices
Dorsal and ventral stream
ig h t-W a y E ye s a n d W ro n g -W a y E ye s
e re b ra lco rtex le sio n s m a y im p a ir e ye m o ve m e n ts in th e co n tra la te ra l
d ire ctio n a n d so p ro d u ce e ye s d ire cte d to w a rd th e le sio n sid e .
h is g a ze p re fe re n ce is typ ica lly a cco m p a n ie d b y m u scle w e a kn e ss
co n tra la te ra lto th e le sio n sid e so th a t e ye s lo o k away from the side
paralysis. This is the typical “right-way eyes.”
ertain lesions/abnormalities can cause eyes to look toward the side of
paralysis, which is “wrong-way eyes.”
auses 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.
bellar, Vestibular and Spinal Control of Voluntary and
Reflex Eye Movements
common reflex eye movements:
okinetic 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
ons of frontal cortex disrupt fast phase of OKN while lesions of posterio
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
beating in contralateral direction.
Visual pathways
h e Pu p ils a n d O th e r O cu la r A u to n o m ic Pa th w a ys
p ils u n d e r b o th p a ra sym p a th e tic ( co n strictio n ) a n d sym p a th e tic ( d ila tio n
co n tro l.
g h t re flex : o p tic n e rve > o p tic tra ct> p re te cta la re a ; p re te cta ln e u ro n s>
ila te ra lE d in g e r-W e stp h a ln u cle i> cilia ry g a n g lio n > co n stricto r m u scle s
re ct re sp o n se a n d co n se n su a lre sp o n se .
ila te ra lp u p illa ry co n strictio n a lso o ccu rs via a slig h tly d iffe re n t p a th w a y
d u rin g th e a cco m m o d a tio n re sp o n se .
cco m m o d a tio n re sp o n se in clu d e s p u p illa ry co n strictio n , a cco m m o d a tio n
o f le n s cilia ry m u scle , a n d co n ve rg e n ce o f e ye s.
cco m m o d a tio n re q u ire s a ctiva tio n o f visu a lco rtex ( re co g n ize clo se r o b je
e n s is n o rm a lly u n d e r te n sio n fro m su sp e n so ry lig a m e n t.
ilia ry m u scle a cts a s sp h in cte r a n d w h e n co n tra cte d ca u se s su sp e n so ry
lig a m e n t to re la x p ro d u cin g a m o re ro u n d e d le n s fo r n e a r fo cu s.
m p a th e tic p a th w a y fo r p u p illa ry d ila tio n in vo lve s co n n e ctio n s fro m
yp o th a la m u s via la te ra lb ra in ste m to th o ra cic co rd T 1 -T 2 sym p a th e tic
re g a n g lio n ic n e u ro n s w h o se a xo n s g o to su p e rio r ce rvica lg a n g lio n .
e u ro n s o f S C G p ro je ct to p u p illa ry d ila to r m u scle s o f e ye .
m p a th e tic p a th a lso co n tro ls su p e rio r ta rsa lm u scle w h ich e le va te s th e
p p e r e ye lid , g ivin g a w id e -e ye d sta re .
m p a th e tic a xo n s tra ve lin g w ith th e se a lso in n e rva te sw e a t g la n d s o f fa c
n d n e ck ; w h e n d a m a g e d th is g ive s H o rn e r’ s syn d ro m e
Pupillary Abnormalities
C a u se s in clu d e p e rip h e ra lo r ce n tra lle sio n s, sym p a th e tic
p a ra sym p a th e tic le sio n s, o r d iso rd e rs o f iris m u scle o r
visu a l
p a th w a ys.
Pu p illa ry a b n o rm a litie s ca n b e b ila te ra lo r u n ila te ra l.
U n ila te ra la b n o rm a lity p ro d u ce s p u p ila sym m e try =
a n iso co ria

1. O cu lo m o to r Le sio n s
U n ila te ra ld ila te d p u p il ( w h e n la rg e = b lo w n
p u p il)
D e cre a se d o r a b se n t d ire ct a n d co n se n su a llig h t
re sp o n se

2 . H o rn e r’ s S yn d ro m e
D isru p tio n o f sym p a th e tic p a th s to e ye a n d fa ce
P to sis, m io sis ( co n strictio n ), a n d a n h yd ro sis
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
Classic example is Argyll Robertson pupil typically
associated with
neurosyphilis in which pupils are small and irregular
show light-near dissociation.
LND also seen in diabetic neuropathy and Parinaud’s
(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
• Common causes of ptosis:
 Horner’s syndrome
 oculomotor nerve palsy
 myasthenia gravis
 redundant skin folds that occur with aging
• 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

Electrode placement
IT: inferotemporal
PP: posterior parietal
ST: superior temporal
Visual location
Motion( middle temporal
Achromatopsia( occipito-
temporal gyrus)
Visual agnosia( posterior &
medial temporo-occipital
Visual neglect( inferior parietal
syndrome*( posterior parietal

Optic ataxia, ocular apraxia &

A: visual location

C: Achromatopsia

D: Visual agnosia

( post. & medial

E: Visual neglect (inf.

F: Balint-Holmes syd.

(post. Parietal)
Normal color vision