The document discusses the control of gaze and eye movements through six neuronal control systems that keep the fovea on target. These include systems for saccadic, pursuit, and vergence eye movements, as well as vestibulo-ocular and optokinetic movements. It describes the neural pathways and brain structures involved in generating different types of eye movements like saccades, smooth pursuit, and vestibular-ocular reflexes. It also discusses how lesions in different parts of the brain can affect eye movement control and coordination.

1. THE CONTROL OF GAZE

2. • Organization of oculomotor system
• How visual information guides eye
movements ?

3. • We see best with fovea and when we want to
examine a object , we have to move the fovea to it.
• Gaze system performs this function through two
systems :
Oculomotor system
Head movement system

4. • Also gaze system prevents the image of object from
moving on retina.
Stabilizing the fovea when head moves require
information about head motion and this is given by
visual system and vestibular system

5. SIX NEURONAL CONTROL SYSTEMS KEEP THE FOVEA
ON THE TARGET
• Five systems have same effector pathway i.e through
oculomotor neurons in the brainstem
• Three keep fovea on target :
Saccadic eye movements
Pursuit eye movements
Vergence eye movements

6. • Two stabilize eyes during head movements :
Vestibulo-ocular movements
Optokinetic movements
VOM hold images still on retina during brief head
movements (driven by vestibular system)
OKM does the same during sustained head movements
• Sixth system is the ‘fixation system’ – holds eye
during intent gaze .
This requires suppression of eye movements.

7. EYE IS MOVED BY SIX MUSCLES
• Eye movements rotate the eye in
orbit – in 3 axes horizontal,
vertical and torsional.
1. Abduction – rotates eye away
from nose
2. Adduction – towards nose
3. Elevation – vertically up
4. Depression – vertically down
5. Intorsion – top of cornea towards
nose
6. Extorsion – top of cornea away
from nose

9. • Torsion movements maintain perceptual stability of
vertical lines. If defective, vertical line perceived as
tilt.
• Six EOM form 3 complementary pairs :
4 recti and 2 obliques.

10. • EOM are controlled by three cranial nerves
3rd N nucleus – supr. colliculus
4th N nucleus – inf. colliculus
6th N nucleus – at pons near floor of 4th ventricle

13. • 6th N lesion : loss of abduction beyond midline
and diplopia occurs on looking to direction of
paralyzed LR
• 4th N lesion : deficit in extrorsion & depression.
Skew deviation and torsional defects.
Pts. keep their heads tilted toward the normal
side to minimize diplopia.
• 3rd N lesion : down and out eye . With ptosis and
mydriasis

14. SACCADES
• Saccades (“jerks”) are quick refixation movements
They place the object, that have been registered on
peripheral retina, on fovea.
Also they are useful to inspect a complex scene like
painting (here short refixations take place to perceive fine
details)

15. • Saccades are highly stereotyped. They are extremely
fast occurs within fraction of sec ,at speeds upto 900
deg/sec.
We can change amplitude and direction of
saccades but not velocity

16. TYPES OF SACCADES
1. Reflexive S : externally triggered by sudden appearance
of target on retina (visually guided) or sudden noise in
surroundings (auditory guided).
2. Intentional S : Internally triggered with a goal.
visually guided – goal to catch target on periphery.
predictive – target expected at a specific location.
memory guided – toward remembered target /direction.

17. 3. Antisaccades : are made in direction opposite to a
suddenly appearing lateral visual target.
4. Spontaneous S : internally triggered without any goal
(ex: as during speech).
MECHANICAL PROPERTIES OF SACCADES
• Two elements – Pulse (velocity command)
Step (position command)
During saccades, as eye velocity
goes up from 0-900 deg/sec – firing rate of neurons
increase rapidly i.e PULSE OF ACTIVITY .
This is to drive the eyes quickly, overcoming the viscous
drag of eye in orbit.

18. • Once eye reaches new position, it is held steady
by EOM. The difference between initial and final
discharge levels is called STEP.
• Height of step determine AMPLITUDE of saccades
• Height of pulse – VELOCITY of saccades.
• Duration of pulse – DURATION of saccades.
PULSE - STEP command

19. • During saccadic production, higher centers of brain
make sensory maps of visual environment. By
comparing actual position of orbit to desired
position, higher centers calculate the pulse-step to
be generated.
• SACCADIC OMISSION
During saccades, vision sweeps across retina
in high velocity and visual blur is prevented by
saccadic omission.
?? Central inhibitory mechanisms

20. • SACCADIC OMISSION
During saccades, vision sweeps across
retina in high velocity and visual blur is
prevented by saccadic omission.
?? Central inhibitory mechanisms

21. • Occulomotor signals describe velocity and
position of eyes at a given time.
How are these parameters determined?
Higher centers only specify the desired
change in eye position.
Interneurons in brainstem reticular formation
transform these signals into necessary velocity
and position via ocular cranial N.
Horizontal component – PPRF & rostral medulla
Vertical component – Mesencephalic reticular formation

22. HORIZONTAL SACCADES ARE GENERATED IN PPRF
•Neurons giving rise to pulse
component – BURST NEURONS
a) Medium lead BN : direct
excitatory connections to 6th N
b) Long lead BN : receive input
from higher centers and drive
medium lead BN
c) Inhibitory BN : suppress
contralateral 6th N . These are
excited by medium lead BN

23. OMNIPAUSE CELLS :
• situated in DRN on midline – below
and behind 6th N nucleus.
•GABAergic ; inhibit all burst neurons
in pons and midbrain.
•They fire continuously except at the
time of saccade production.
•So, unwanted saccades are avoided.
Useful in visual fixation.

25. Mechanism of saccades
production

27. Horizontal Leftward
Voluntary Saccade (“Look
to the left”)
1. R Frontal Eye Field
2. R saccade center
3. L horiz. gaze center
4. L 6th nucleus (L eye out)
5. R MLF
6. R 3rd nucleus (R eye in)
R L
Saccade
Center
Horiz.
Gaze
Center
(PPRF)
3 - RMR
6 - LLR
R MLF
FEF
Base Artwork & Animations David E. Newman-Toker, MD

28. Neural integrator
•For fixation of gaze
If 6th N receive information from only burst
neurons, then eyes drift back to original
position after the saccade because there
would be no new position signal to hold
eye in new place.
This is done by ‘neural integrator’.
1. Cerebellar flocculus
2. MVN - NPH (bil.)
These are TONIC neurons . Here
velocity coded information
converted to position coded.

29. MLF (medial longitudinal fasciculus)
•Burst signals and tonic signals as
supplying LR , also has to supply
contralateral MR. This occurs
through MLF.

31. VERTICAL SACCADES
• Burst and tonic neurons
for vertical saccades lie in
riMLF (rostral interstitial
MLF) in midbrain.
• Vertical saccades require
activity of both sides and
communication between
them traverse through
posterior comissure.

32. • Main structures are INC, riMLF and 3rd N subnuclei.
• Voluntary vertical eye movements are initiated by both
FEF simultaneously.
• riMLF serves as generator of vertical saccades.
• INC act tonically to hold eccentric vertical gaze.
They connect with their contralateral nuclei via PC.
• Projections from upgaze pass through PC before
descending to 3rd N nuclei, while those of down gaze
pass directly – thus accounting for frequent upgaze
palsies.

33. SACCADES ARE CONTROLLED BY CEREBRAL CORTEX
•PPRF and midbrain circuits provide
motor signals to drive EOM. But
the decision of when and where to
make a saccade is made in cerebral
cortex.
1. Cerebral cortex controls
saccadic system mainly through
superior colliculus ( SC )
2. Higher cortical centers
3. Basal ganglia
4. cerebellum

34. COLLICULAR SYSTEM
• SC is the major ‘visuo-motor integrator’.
• Two functional regions are present :
Superficial layer.
Intermediate and deep layers.
 Superficial layer – receive input from retina and striate
cortex about the entire contralateral hemifield.
 Intermediate and deep layers – mainly movement related
activity . Receive visual information from occipital and
parietal cortex ; motor information from frontal eye field.
Direct efferents to PPRF.

35. • Rostral SC facilitates visual fixation and has
representation of fovea. Here neurons are
active during fixation. These stimulate
omnipause neurons and inhibit intermediate
layers.
Superficial
layers
Pulvinar &
thalamus
Cerebral
cortex
Intermediate
layers

36. HIGHER CORTICAL CENTRES
1. Parieto-collicular pathway :
reorienting gaze to novel visual
stimuli with shifting of visual
attention to new targets in
extrapersonal space.
2. FEF – collicular pathway:
self generated gaze changes –
i.e related to remembered ,
anticipated or learned behavior.
(voluntary saccades)

37. 3. Supplementary eye field:
role in planning saccades to visual / non
visual cues as a part of learned behavior .
(control of sequential eye movements).
4. DLPFC : saccades to remembered
location of targets.
5. Hippocampus : control temporal working
memory for memorizing chronological
order of sequence of saccades.

39. • FEF lesions : impair non visually guided
saccades. Also defect in generating voluntary
saccades (anticipatory/remembered)
• Parietal lesions : impair visually guided
saccades. Also increases saccade latency,
saccadic slowing present.
• FEF + SC lesions : inability to form saccades.

40. BASAL GANGLIA
•Substantia nigra pars compacta (SNpc) – sends
inhibitory projections to SC. This nigro-collicular
inhibition is tonic and spontaneously active . It is
inhibited only at the time of saccades . ( same as
omnipause cells controlling burst neurons)
•SNpc is under the inhibitory control of caudate
nucleus.

41. At the time of saccades,
Superior colliculus
SN pc
-
Caudate nucleus
-
Frontal eye feild
+

42. CEREBELLUM
• Vermis & Fastigous – maintain pulse (velocity)
size.
• Flocculus – maintain pulse – step match.

44. PURSUIT MOVEMENTS
• This system keeps the image of moving target
on fovea. It requires a moving stimulus in
order to calculate eye velocity. So, verbal or
imaginary stimuli cannot produce smooth
pursuit movements.
• These have a velocity upto 100 deg/sec, much
less than saccades.

45. SMOOTH PURSUIT MOVEMENTS INVOLVE
CORTEX, CEREBELLUM AND PONS
Oculomotor nuclei receive projections from PPRF
and MVN-NPH.
PPRF receive projections from vermis of
cerebellum.
MVN-NPH from flocculus of cerebellum.
Cerebellum receive signals from cortex via
DORSOLATERAL PONTINE NUCLEUS.

47. • Left motor system mediates smooth pursuit
movements to left , while rt. mediates to right.
• Pathway decusstes TWICE at pontocerebellar
level.
DLPN Cerebellum
VN
6th N
nucleus

48. CORTICAL INPUTS
1. MT – MST : medial temporal & medial supr. temporal
lobes.
MT neurons mainly describe the retinal image motion and
its position in space. i.e they provide sensory information
to guide pursuit movements. They calculate the velocity of
target.
(MT-MST homology in humans is
located in lateral occipital cortex
and angular gyrus of parietal lobe)

49. • Disruption here leads to loss of ability to respond to
targets in that hemifield and also decreased
amplitude & velocity of pursuit movements.
• Frontal eye field : ? Initiation of pursuit movements
• Pathways for pursuit movements are less well
defined. One probably originates from posterior
parietal cortex and adjucent temporo occipital
cortex.
Part of FEF have shown to participate in pursuit
movements, but of far less significance.

50. • Lesion anywhere in the above
path prevents from making
pursuit movements.
pt uses combination of defective
smooth pursuit movements +
small saccades.
• Cerebellum & brain stem
lesion – pt cannot pursuit
targets moving towards the
side of lesion.

52. VESTIBULOCULAR MOVEMENTS
Normally images have to slide
over retina slowly, else things
blur. So, some corrective system
have to be present for eye in
humans (continues head
movements) .
Vestibular system drives the eye
with the same velocity, but in
opp direction of head.

53. Vestibular reflexes stabilize eyes and body when
the head moves
Body uses vestibular reflexes to compensate
for head movement and perception of motion in
space.
VOR – keep eyes still when head moves
VSR – enables musculoskeletal
system to compensate for head
movements.

54. Vestibular system is designed to answer :
which way is up?
where am I going?

55. VOR compensate for head movements
When head moves ,eyes are kept still by VOR.
While reading –
when we move head, we can still read.
when we move book, we cannot.
Visual processing is much slower and less efficient than
vestibular processing for image stabilization.
• Vestibular apparatus signals how fast head is rotating
• Oculomotor system uses this information to stabilize eyes
in order to keep image on retina.

56. • 3 types
rotational VOR – from SCC
translational VOR – for linear head movements
ocular counter rolling response – for head tilt in
vertical
• Ocular counter rolling response – when head tilts out
of its vertical position along the axis running from
occiput-nose, otoliths estimate deviation from vertical
and initiates the response.

58. • SCC of both ears are yoked in
such a way that, when head
rotates one canal increases
rate of firing and other slows.
So, excited vestibular N
deviates the eyes to opposite
side.

60. • Vertical VOR : excitatory impulse from VN cross
brainstem and ascend in MLF – synapse in 3, 4
cr. N where appropriate movements are
represented.
so, lesions of MLF cause INO and also impair
vertical VOR.

61. VSR : vestibulospinal reflex
how people know that they are falling?
One way is visual. Also because head moves ,
vestibular system gets activated.
(as vestibular system responds much faster than
visual, it provides early warning of fall to the spinal
cord and helps in maintenance of posture)

62. HEAD POSITION
• Labyrinth provides information about the static
position of head.(angular acceleration by SCC)
• This is done by utricle and saccule.
• Pathway :
Utricle and saccule project to the lateral VN . From
here ipsilateral connections (inhibitory) travel through
asc. tract of DEITER. Contralateral excitatory connections
travel through MLF.
Linear or translational movements of head (up-down while
running) are detected by otolith organs.

63. • Bilateral vestibular dysfunction
Stable gaze while sitting/standing, but
develop impaired vision or oscillopsia during
walking because of excessive motion of
images on the retina due to failure of VOR

64. OPTOKINETIC SYSTEM
1. Vestibular system and VOR keep the eyes still when
head moves – to stabilize image on retina.
When outside environment moves relative to steady
head position (ie steady vestibular system), OKS is useful.
2. VOR becomes fatigued in about 30 sec. so a different
system is required to maintain the eyes on target during
prolonged head motion in same direction.
3. SCC don't respond to very slow head movements.

65. • Optokinetic reflex requires full field stimulation. where as
in pursuit movements target has to be projected on
macula.
• OKS may induce a compelling sensation of self rotation –
‘circular vection’ (without vestibular stimulation)
• When optokinetic system is involved, nystagmus appears
physiologically. (OKN)

66. Optokinetic reflex
• Optokinetic nystagmus
• Neural pathway
convergent with VOR

67. Subcortical and cortical structures contribute to
optokinetic reflex
• Movement of images on retina or head
movement induces nystagmus and perception of
self motion.
This occurs because vision neurons project to VN.
Retinal neurons project to optic tract in the pretectum,
which projects to VN (which also receive vestibular afferents).
So, these can’t differentiate visual and vestibular signals.
They respond identically to head movement and
movement of images on retina.

68. • Other cortical structures involved are :
striate cortex, middle temporal area and medial
superior temporal area.
• Pt with lesion in these pathways have defective
OKN to visual stimuli moving towards the side
of lesion.

69. VERGENCE SYSTEM
• In contrast to all other eye movements which are
conjugate , vergence system is disconjugate.

71. • They ensure that object of interest is on the
same place on both retinas, since objects
ordinarily occupy slightly different places on
two retinas.
• The visual system uses the slight differences of
retinal position, or retinal disparity, to create a
sense of depth. The vergence system uses this
disparity to drive these movements.

72. • Accommodation
• Accommodation and vergence are linked.
Blur is stimulus for accommodation. Whenever
accommodation occurs, eyes converge.
Retinal disparity induces vergence. Whenever
eyes converge accommodation also occurs.
• Near response = accommodation + vergence +
pupillary constriction.

73. Pathway :
Occipital cortex
Thalamus (decussation occurs)
Premotor vergence neurons(near response cells) lie in
midbrain, adjacent to occulomotor N.
Near response neurons are of – convergence and
divergence neurons.
These neurons project to MR and LR respectively.
(vergence movements involve fine coordination b/w 3rd
and 6th cranial nuclei – probably outside MLF)
cerebellar flocculus - ? role

74. FIXATION SYSTEM
• Vision is most accurate when
eyes are still. When we see an
object of interest, fixation
system prevents eyes from
moving.
• Neural integrator is
important in fixation
system.

75. Neural integrator
•For fixation of gaze
If 6th N receive information from only burst
neurons, then eyes drift back to original
position after the saccade because there
would be no new position signal to hold
eye in new place.
This is done by ‘neural integrator’.
1. Cerebellar flocculus
2. MVN - NPH (bil.)
These are TONIC neurons . Here
velocity coded information
converted to position coded.

76. ASSESSMENT OF
VISUAL MOTOR SYSTEM

77. Inspection
Evaluation of ocular alignment
Version test
Others to aid diagnosis of supranuclear disorders
Convergence test
Saccades’ and pursuits’ movements
Doll’s eye movement
OKN test
Caloric responses

78. Inspection
HEAD POSTURE:
1) Face turn- towards side of weakness
e.g. 6th CN palsy ,Duane’s
2) Head tilt- e.g. away from side of 6th CN palsy.
3) Chin up/down
e.g. bilateral 6th CN palsy

79. Ptosis - 3rd CN palsy
Primary position – manifest strabismus
Corneal reflexes – asymmetry indicates
deviation.
Pupils -anisocoria

80. EXTRA OCULAR MOVEMENTS
• Check versions ( both eyes) and ductions (one
eye) in all 9 positions of gaze
-ask patient to follow target ( pen-torch)
-ask patient to report any diplopia during test
look for any abnormality; under/overaction,
paresis/restriction .

83. SACCADES
Examine horizontal/vertical saccades
 ask patient to look rapidly between widely separated
targets
result: ---normal / slow
hypo/ hypermetric
 Useful in detecting internuclear ophthalmoplegia
 VELOCITY MAGNITUDE ACCURACY

84. Test arrangement for saccade testing.
Zinkernagel M S et al. Br J Ophthalmol 2009;93:1247-1250
©2009 by BMJ Publishing Group Ltd.

86. SMOOTH PURSUIT
• Smooth pursuit is tested by having the patient
slowly follow a moving target 1m a way.

87. CONVERGENCE
assess to - both accommodative and
non- accommodative target
normal / reduced
Hold a target in front of patient and
progressively bring it nearer , whilst observing for
convergence of the two eyes

88. OPTOKINETIC NYSTAGMUS
Examine OKN -horizontal / vertical
 slowly rotate an OKN drum in horizontal and vertical
direction
result : Normal / absent

90. CALORIC RESPONSE
• Caloric testing is dependent on endolymph
convection currents.
• Normal response (COWS)
Warm water in the right ear produces a right-
beating nystagmus
coldwater in the right ear produces a left-
beating nystagmus

91. DOLL’S EYE MOVEMENTS