Ocular Motor Control (Section 3, Chapter 8) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy - The University of Texas Medical School at Houston

8.1 Introduction

Normal visual perception requires the proper functioning of ocular motor systems that control the position and movement of the eyes to focus the image of the object-of-interest (i.e., the visual target) on corresponding areas of the retinas of the two eyes. For example, in addition to producing adjustments in pupil size and lens refraction, accommodation involves the convergence of the two eyes to direct onto the foveae the images of near objects. Eye movements are also controlled to direct the eyes towards a visual target and to follow the movements of the visual target. Such eye movements are controlled by gaze systems. They coordinate the movement of the two eyes to ensure that the images on the two retinas fall on corresponding areas of the binocular field. When this fails, diplopia (double vision) results.

8.2 Extraocular Muscles and their Innervation

The extraocular muscles execute eye movements and are innervated by three cranial nerves. The muscles are attached to the sclera of the eye at one end and are anchored to the bony orbit of the eye at their opposite ends. Contraction of the muscles produce movement of the eyes within the orbit. The cranial lower motor neurons innervate these muscles and thereby control their contractions.

Figure 8.1
The extraocular muscles of the right eye and their actions. Antagonistic actions pull the eye in opposite directions whereas synergistic actions pull the eye in the same direction.

A. The Extraocular Muscles

For each eye, six muscles work together to control eye position and movement. Two extraocular muscles, the medial rectus and lateral rectus, work together to control horizontal eye movements (Figure 8.1, left).

Contraction of the medial rectus pulls the eye towards the nose (adduction or medial movement).
Contraction of the lateral rectus pulls the eye away from the nose (abduction or lateral movement).

The actions of these two muscles are antagonistic: one muscle must relax while the other contracts to execute horizontal eye movements. Four other extraocular muscles working together control vertical eye movements and eye rotation around the mid-orbital axis (Figure 8.1, right). Contraction of the

superior rectus produces
- eye elevation
- minor movements: medial rotation and adduction
superior oblique produces
- eye depression
- other movements: medial rotation and abduction
inferior rectus produces
- eye depression
- minor movements: lateral rotation and adduction
inferior oblique produces
- eye elevation
- other movements: lateral rotation and abduction

To direct the eye upward or downward, two muscles contract synergistically as the two antagonist muscles relax. For example, to elevate the eye while looking straight ahead, the superior rectus and inferior oblique contract together as the inferior rectus and superior oblique relax. The superior rectus and inferior oblique muscles working together pull the eye upward without rotating the eye. To depress the eye while looking straight ahead, the inferior rectus and superior oblique contract together as the superior rectus and inferior oblique relax. The inferior rectus and superior oblique working together pull the eye downward without rotating the eye.

B. Extraocular Muscle Efferents

Three cranial motor nuclei provide efferent control of the extraocular muscles. Activation of the motor neurons produces contraction of the innervated muscle.

The abducens nucleus
- sends its axons in the abducens (VI cranial) nerve
- controls the lateral rectus of the ipsilateral eye.
The trochlear nucleus
- sends its axons in the trochlear (IV cranial) nerve
- controls the superior oblique of the contralateral eye.
The oculomotor complex contains nuclei that
- send axons in the oculomotor (III cranial) nerve
- control
  - the superior levator in the eyelid of both eyes
  - extraocular muscles, which include the
    - medial rectus of the ipsilateral eye,
    - inferior oblique of the ipsilateral eye
    - inferior rectus of the ipsilateral eye
    - superior rectus of the contralateral eye¹.

C. Upper Motor Neuron Control

Figure 8.2
The axons of the abducens interneurons decussate and travel in the medial longitudinal fasciculus to the contralateral oculomotor nucleus to excite the motor neurons controlling the medial rectus of the eye contralateral to the abducens nucleus.

The motor neurons controlling synergist and antagonist muscles must coordinate their activities to produce the desired eye movements. Within the abducens nucleus are abducens interneurons, which send their axons into the contralateral medial longitudinal fasciculus (MLF). They ascend in the MLF to end on oculomotor neurons controlling the medial rectus (Figure 8.2). The abducens interneurons coordinate the activity of the ipsilateral lateral rectus with that of the contralateral medial rectus. For example, excitation of the motor neurons in the left abducens nucleus will result in contraction of the left lateral rectus and abduction of the left eye (i.e., movement of the left eye towards the left). Excitation of the interneurons in the left abducens nucleus will excite neurons in the right oculomotor nucleus that innervate the right medial rectus. Contraction of the right medial results in adduction of the right eye (i.e., movement of the right eye towards the left). Consequently, both the right and left eyes will be directed towards the left when the left abducens nucleus is excited.

Interconnections between the trochlear nucleus and oculomotor nuclear complex coordinate their activity to allow the upward and downward movement of the eyes. These interconnecting axons appear to travel along with the fibers of the tectospinal tract (that is, they do not travel in the medial longitudinal fasciculus).

8.3 Gaze Stabilization: Eye Movements that Counter-Act Head Movement

There are two functional classes of eye movements (Table I): those that stabilize the eye when the head moves or appears to move (gaze stabilization) and those that keep the image of a visual target focused on the fovea (a.k.a., foveation) when the visual target changes or moves (gaze shifting). Two gaze stabilization systems operate during head movement: the vestibulo-ocular and the optokinetic systems. Vestibulo-ocular and optokinetic movements are conjugate movements in which both eyes move in the same direction.

Table I Classification of Eye Movements
Eye Movement Type	Function
Vestibulo-ocular	Gaze Stabilization
Vestibulo-ocular	Initiated by vestibular mechanisms during brief/rapid head movement
Optokinetic (vestigial in humans)	Initiate by visual mechanisms during slow head movement
Vergence	Gaze Shifting
Vergence	Adjusts for different viewing distance
Smooth Pursuit	Follows moving visual target
Saccade	Directs eyes toward visual target

A. The Vestibulo-ocular Reflexes

Vestibulo-ocular reflexes produce eye movements that compensate for head movements detected by the vestibular system. You have learned in earlier chapters how the vestibular system detects head movements and initiates the vestibulo-ocular responses.

B. Optokinetic Nystagmus

Optokinetic nystagmus is elicited

by slow head movements undetected by the vestibular system,
by moving objects that produce the illusion of head movement (e.g., alternating bands of light and dark lines rotated around the viewer's head)
as corrections for small spontaneous eye movements

Notice that optokinetic nystagmus is a visual-ocular response - driven by visual stimuli moving across the visual field. Vestibular nystagmus is a vestibulo-ocular response - driven by a vestibular stimulus (i.e., accelerating head movement). In humans, the smooth pursuit system predominates in producing eye movements that track moving visual targets. As the optokinetic system is vestigial in humans, it will not be covered in this lecture.

8.4 Gaze Shifting: Eye Movements to Focus the Image on the Fovea

Three gaze shifting systems function during foveation: smooth pursuit, which directs the eyes to follow a moving visual target; saccade, which directs the eyes toward a visual target; and vergence, which alters the angle between the two eyes to adjust for changes in distance from the visual target. We have covered the neural control of convergence during accommodation in the previous lecture.

A. Voluntary Saccades

Voluntary or guided saccades are eye movements initiated to bring an object-of-interest into view or initiated under direction (e.g., to the command “eyes left”). Saccades consist of short, rapid, jerky (ballistic) movements of predetermined trajectory that direct the eyes toward some visual target.

The Voluntary Saccades Circuit

The neurons in the frontal eye field (Figure 8.3)

are involved in initiating voluntary saccades that locate and focus on a particular object-of-interest.
are located posteriorly in the middle frontal gyrus.
compute the direction and amplitude of the saccade.
send their axons in the internal capsule, crus cerebri and corticotectal tract to the midbrain where they decussate and end in the superior colliculus.

The superior colliculus neurons

also receive afferent input from the
- retina, via the brachium of the superior colliculus
- inferior colliculus (auditory)
- parietal (visual association) area
based on afferent information, correct and send control signals for the amplitude and direction of the saccades to the vertical and horizontal gaze centers
send their axons to the gaze centers within the tectospinal tract (i.e., not in the medial longitudinal fasciculus)

The vertical gaze center

is located in the midbrain reticular formation²
has direct control over the lower motor neurons in the oculomotor and trochlear nuclei

Figure 8.3
The voluntary saccades circuit. The frontal eye field generates the command signals that initiate eye movement in a contralateral direction (i.e., to the right in this figure). The signal is sent to the superior colliculus and caudate nucleus. The superior colliculus, in turn, sends control signals to the gaze centers in the midbrain and pons reticular formation. The posterior parietal cortex, part of the dorsal visual stream, determines whether the visual target has been achieved and sends corrective signals to the frontal eye field and superior colliculus when the visual target has not come into view. The basal ganglion structures, the caudate and substantia nigra, help regulate the action of the superior colliculus.

The horizontal gaze center

is called the paramedian pontine reticular formation (PPRF)
has direct control over the abducens lower motor neurons and interneurons
- Recall that the abducens nucleus contains
  - lower motor neurons that send their axons in the ipsilateral abducens nerve to the lateral rectus muscle
  - interneurons that send their axons in the contralateral medial longitudinal fasciculus to the oculomotor neurons controlling the medial rectus

Nuclei of the basal ganglion

modulate the activity of the superior colliculus³
the caudate, receives excitatory input from the frontal eye field and sends inhibitory input to the substantia nigra⁴
the substantia nigra, provides an inhibitory input to the superior colliculus but is inhibited by the caudate nucleus.⁵

The superior colliculus can initiate and control saccades independent of input from the frontal eye field. However, the motor control signals initiated by the frontal eye field and the superior colliculus differ in function.

Normally the frontal eye field initiates voluntary and memory-guided saccades,
whereas the superior colliculus initiates reflex orienting saccades.

However, when the frontal eye field is damaged, the superior colliculus will compensate for the loss following a short period of dysfunction. For example, damage to the right frontal eye field produces a transient inability to look voluntarily to the left side.

Afferent Control of Voluntary Saccades

Because voluntary saccades are not, in general, initiated by visual stimuli, afferent visual control occurs only after the fact. That is, the visual system (i.e., the posterior parietal visual association cortex⁶ in Figure 8.3) is used to determine whether the saccade was successful in bringing the desired object into view. Consequently, the saccades consists of a series of short, fast eye movement, followed by a check by the visual system as to whether the desired visual target is in view, which may be followed by another series of brief eye movements to locate the visual target. The repeated sequence of brief, rapid eye movements and image check until the visual target is in view characterizes saccades.

B. Smooth Pursuit

Smooth pursuit (tracking) is an eye movement elicited by a moving visual target that the eyes follow voluntarily or under direction (e.g., the request to "watch the moving pen"). Pursuit movements are described to be voluntary, smooth, continuous, conjugate eye movements with velocity and trajectory determined by the moving visual target. By tracking the movement of the visual target, the eyes maintain a focused image of the target on the fovea. Notice that a visual stimulus (the moving visual target) is required to initiate this eye movement.

The Smooth Pursuit Circuit

Temporal eye field neurons in the non-human primate (parts of Brodmann's areas 39 or MST- medial superior temporal gyrus & 37 or MT- middle temporal gyrus.

are believed to be involved in the initiation and guidance of smooth pursuit eye movements⁷(Figure 8.4)
compute the direction and velocity of the moving visual target.⁸
correspond to neurons in superior temporal-inferior parietal areas in humans. That is, damage to the temporal-parietal areas in humans produce symptoms similar to those produced by damage to MT and MST in non-human primates.
send their axons to the dorsolateral pontine nucleus (DLPN).

Frontal eye field neurons, however,

appear to initiate the smooth pursuit - at the request of the temporal eye field neurons
also send their axons to the dorsolateral pontine nucleus

Dorsolateral pontine nucleus

computes the direction and speed of eye movement (pursuit) necessary to match the direction and velocity of the moving visual target
axons decussate and end in the contralateral cerebellum⁹

The cerebellum

sends its axons to the vestibular nuclei

The vestibular nuclei

send axons to the abducens, trochlear and oculomotor nuclei via the medial longitudinal fasciculus
control smooth pursuit eye movements - for the temporal eye field

Consequently, the vestibular nuclei help coordinate the activities of antagonist muscles involved in eye movements during smooth pursuit and vestibule-ocular reflexes.¹⁰

Note that there are two decussations (double crossings) involved in the horizontal smooth pursuit pathway (i.e., the DLPN axons and the axons of the vestibular nuclei providing excitatory input to the abducens nucleus). Consequently, the command signals generated by the MST and MT cortical neurons result in an execution of smooth pursuit eye movement in a direction ipsilateral to these cortical neurons. Normally, a command generated by the left MST and MT cortical neurons results in both eyes tracking the movement of an object moving to the left.

Figure 8.4
The smooth pursuit pathway. The temporal eye field sends signals to the dorsolateral pontine nuclei indicating the direction and velocity of movement of the visual target. The dorsolateral pontine nuclei determines the direction and velocity of eye movement necessary to tract the visual target and sends that information on to cranial nerve nuclei by way of the cerebellum and vestibular nuclei. That is, this pathway engages the vestibulo-ocular circuit to control smooth pursuit eye movements. The frontal eye field appears to initiate, but not direct, the eye movement "at the request" of the temporal eye field.

8.5 Clinical Signs of Damage to Ocular Motor Systems

Damage to the lower motor neurons that innervate an extraocular muscle results in a flaccid paralysis of the muscle, whereas damage to upper motor neurons produce deficits only in selective types of movements (e.g., smooth pursuit).

A. Lower Motor Neurons

Damage to an extraocular muscle’s motor neurons results in a paralysis of the muscle that is often manifested as a strabismus (a misalignment of the two eyes). At rest (while attempting to look straight ahead), the denervated eye is deviated from its normal position by the unopposed action of the muscle that is its antagonist. The strabismus may result in double vision (diplopia) because the image falling on the retina of each eye will be from non-corresponding areas in the binocular visual fields. When the patient closes one eye, the double image is replaced by a single image.

Damage to the oculomotor nerve. As we have already covered this topic in the previous lecture, a brief summary of the effect of oculomotor nerve lesion on eye movements will be presented.

All of the extraocular muscles, except the lateral rectus and superior oblique, will be denervated and paralyzed and the patient will be unable to elevate or adduct the eye ipsilateral to the oculomotor nerve damaged.
The innervation of the superior palpebrae muscle and the ciliary ganglion (postganglionic parasympathetic innervation of the iris sphincter and ciliary muscles) will also be lost. Consequently, there will be ptosis, dilated pupil and lateral strabismus in the denervated eye.

Figure 8.5
Observe the patient's response to the commands of the control buttons.
Symbols: The arrow indicates the direction of the eye movement. The plus symbol represents the position of the eye that has not deviated from mid position.

If the left oculomotor nerve is damaged,

at rest, the eye is deviated down and laterally (is depressed and abducted) - a lateral strabismus - because the lateral rectus is unopposed.
on an attempted gaze to the right, the left medial rectus will not contract to adduct the left eye (i.e., it will not move the eye toward the nose, medially).

Consequently, at rest and during an attempted right lateral gaze, the lateral strabismus will result in a diplopia. On attempting to adduct the eye (i.e., look right or during convergence), the left lateral rectus relaxes and the left eye deviates to the midline, but not past it.

Damage to the trochlear nerve. When the trochlear nerve is damaged, the symptoms are mild. The downward and lateral movement of the eye may be weakened and may cause diplopia when reading or descending stairs. A patient may present with his head tilted because the damaged eye is extorted (i.e., rotated with top of the eye tilted away from the nose) and slightly elevated because of the paralysis of the superior oblique muscle. Tilting the head away from the affected eye brings the visual axis of the partially paralyzed eye into alignment with the visual axis of the normal eye.

8.6 Clinical Example #1

Symptoms. A 65 year-old male presents with a medial strabismus of his left eye (Figure 8.6, Rest) and cannot move his left eye to the left (Figure 6, Left). His right eye has normal motility and his pupillary reflexes are normal. His vision is normal in both eyes. He has normal sensation on his face and body and no other motor symptoms.

Figure 8.6
Observe the patient's response to the commands of the control buttons. Symbols: The arrow indicates the direction of the eye movement. The plus symbol represents the eye that has not deviated from mid position.

You observe that the patient

has a left medial strabismus
has limited mobility in his left eye (i.e., it moves to the midpoint when he attempts to look to the left)
cannot fully abduct his left eye
can move his right eye in all directions.

You conclude that his functional loss

is not sensory
involves only one eye
may involve an extraocular muscle or its lower motor neurons

Side & Level of Damage: As his symptoms

does not involve brain stem functions
is restricted to a left medial strabismus

you conclude that the damage involves the

lateral rectus OR
abducens nerve
left side (i.e., the symptoms are ipsilesional)

Electrophysiological tests indicate that the left lateral rectus is responsive (i.e., normal). You conclude that the left abducens nerve has been damaged.

Damage to the abducens nerve. The lateral rectus will be denervated and paralyzed and the patient will be unable to abduct the eye. For example, if the left abducens nerve is damaged, the left eye will not abduct fully (move away from the nose, towards the left, laterally). While attempting to look straight ahead, the left eye will be deviated medially towards the nose (medial or nasal strabismus) due to the unopposed action of the medial rectus of the left eye. On attempting to gaze left, the left eye may deviate to the midpoint, but not past it, because the medial rectus of the left eye is relaxed. The patient may complain of double or blurred vision (diplopia) when looking towards the ipsilesional side (i.e., left) or when looking straight ahead.

B. Upper Motor Neurons

Damage of upper motor neurons does not result in a flaccid paralysis. However, the muscle will not be activated into the response normally controlled by the upper motor neuron (e.g., voluntary saccades controlled by the frontal eye field). However, the muscle will perform reflex responses (e.g., convergence during accommodation or nystagmus during head rotation) and responses controlled by other intact ocular motor circuits.

8.7 Clinical Example #2

Symptoms. A 65 year-old male presents with a left medial strabismus and cannot move both his eyes to the left (Figure 8.7). His vision and his pupillary reflexes are normal in both eyes. He has normal sensation on his face and body and no other motor symptoms.

Figure 8.7
Observe the patient's response to the commands of the control buttons. Symbols: The arrow indicates the direction of the eye movement. The plus symbol represents the position of the eye that has not deviated from mid position.

You observe that the patient

has a left medial strabismus
has limited mobility in his left eye (i.e., it moves to the midpoint when he attempts to look to the left)
cannot fully abduct his left eye
cannot move both eyes toward his left.

You conclude that his functional losses

are not sensory
involve both eyes
may involve upper and lower motor neurons

Side & Level of Damage: As his symptoms involves

a medial strabismus of the left eye
an inability to perform a lateral conjugate gaze to the left
brain stem functions

you conclude that the damage involves the

abducens motor neurons
abducens interneurons (failure of conjugate lateral gaze)
left side (i.e., the symptoms are ipsilesional for the left eye paralysis)

Neural imaging tests indicate a small infarct (i.e., a lacunar stroke) in the region of the left facial colliculus. You conclude that the damaged area includes the left abducens nucleus.

Damage to the abducens nucleus. The result is an abnormality of conjugate horizontal eye movements called lateral gaze paralysis. With the eyes at rest, there is a medial strabismus in the eye ipsilateral to the damage (indicating abducens motor neuron damage). During an attempted lateral gaze, both eyes cannot be moved beyond the midline in an ipsilesional direction (i.e., toward the damage side). As the left abducens interneurons send axons to the right oculomotor neurons innervating the medial rectus of the right eye (Figure 8.2), the failure to perform a lateral gaze to the left suggests an abducens nucleus lesion. An attempted lateral gaze in a contralesional direction (away from the damaged side) is successful. Note that as the lower motor neurons (i.e., the abducens motor neurons), as well as a motor control center (i.e., the abducens interneurons), are damaged, both reflex and voluntary eye movements in the horizontal plane are affected.

An example of the effect of damage to the medial longitudinal fasciculus is presented in the Appendix.

8.8 Clinical Example #3

Symptoms. A 65 year-old male was brought to the emergency room because he suddenly lost the ability to speak and could not move the right side of his body or face. He was described to be right handed and on antihypertensive medications. Examination revealed weakness in his right face, no movement in his right arm and weakness in his right leg with Babinski's sign. His speech was nonfluent. He could not move his eyes to the right when asked to "look right" (Figure 8.8). He was able to move his eyes in other directions. Sensation over the body and face was decreased on the right side. His vision and hearing appeared within the normal range.

Figure 8.8
Observe the patient's response to the commands of the control buttons. Notice at the "look straight" command, this patient exhibits a "left gaze preference" when the eyes are at rest. Symbols: The arrow indicates the direction of the eye movement. The plus symbol represents the position of the eye that has not deviated from mid position.

You observe that the patient's eyes

are directed to the left at rest (i.e., exhibits a left gaze preference)
have full mobility when looking up and down and to his left
cannot move together toward the right (i.e., both eyes stop at mid position).

You conclude that his functional loss

is not sensory
involves a right hemiplegia (i.e., he can't move his right body or face)
involves Broca's aphasia (i.e., his speech is non-fluent)
involves failure of both eyes to perform a lateral gaze to the right

Side & Level of Damage: As his symptoms

does not involve lower motor neurons or muscles
involve upper motor neurons (i.e., conjugate lateral eye movements)
involve cortical functions (i.e., hemiplegia and aphasia)

you conclude that the damage involves the

caudal frontal cortex including the frontal eye field
left side (i.e., the loss of right lateral gaze and the right hemiplegia and aphasia)

Neural imaging tests indicate infarction of branches of the medial cerebral artery supplying the lateral surface of the left frontal cortex.

Damage to the voluntary saccades circuit. Damage to the frontal cortical eye field and the midbrain (superior colliculus) effect voluntary and reflex saccades, particularly those in the horizontal plane. Immediately following unilateral damage of the frontal cortical eye field, there is an inability to voluntarily initiate a horizontal eye movement in a direction contralateral to (away from) the side of the lesion. That is, immediately following a right frontal lobe lesion, both eyes cannot be moved voluntarily to the left beyond the midline. However, both eyes will move to the left beyond the midline to vestibular stimulation. Both eyes can also be directed to the side ipsilateral to the lesion and may tend to deviate toward the lesion when the eyes are at rest. The deficits disappear with time if the damage is localized to the frontal cortical eye field and does not involve the superior colliculus.

8.9 Clinical Example #4

Symptoms. A 55 year-old male was brought to the emergency room. He was overweight and reportedly normally right-handed, a heavy smoker and drinker. He had lost consciousness during a game of basketball and when he awoke, appeared confused. When examined in the ER, he was conscious but followed no commands and could not repeat. He could mimic gestures and was able to voluntarily look to the left and right (Figure 8.9). His eyes followed a pen moving to his right with a smooth pursuit movement. However, his eye movements became jerky and ballistic at midpoint in the attempt to follow the pen as it moved to his left.

Figure 8.9
Observe the patient's response to the commands of the control buttons. Notice at the "look straight" command, the patient's eyes tend to wander when at rest. Also notice at the "look left" command, the patient's eyes tend to move in a jerky, step-like manner. Symbols: The arrow indicates the direction of the eye movement. The plus symbol represents the position of the eye that has not deviated from mid position.

You observe that the patient's eyes

tended to move about when at rest position
have full mobility when performing saccades
cannot smoothly track a visual target moving toward his left

You conclude that his functional loss

is not sensory
involves Wernieck's aphasia (i.e., impaired comprehension and inability to repeat)
involves failure of smooth pursuit to the left

Side & Level of Damage: As his symptoms

does not involve lower motor neurons or muscles
involve upper motor neurons (i.e., conjugate lateral eye movements)
involve cortical functions (i.e., aphasia)

you conclude that the damage involves the

temporal-parietal cortex including Wernieck’s area
left side (i.e., aphasia and no smooth pursuit to the left)

Neural imaging tests indicate infarction of branches of the left medial cerebral artery supplying the caudal superior temporal gyrus and inferior parietal gyrus.

Damage to the smooth pursuit circuit: Damage to the temporal eye field causes deficits in the ability to fixate on objects and to track them. Attempts to fixate on a target will be undermined by severe instability and wandering of the eyes. Tracking movements are jerky rather than smooth when attempting to follow an object moving in a direction toward (ipsilateral to) the side of the lesion. Note that the smooth pursuit circuit includes a double crossing and the temporal eye field controls ipsilateral eye movements (i.e., right cortex controls smooth pursuit to the right). When the temporal eye field is damaged, the two eyes may follow a visual target in an ipsilesional direction; but does so using the voluntary saccades circuit. That is, if the frontal cortical eye fields are intact, the eyes may be moved voluntarily (guided saccade) toward an object of interest ipsilateral to the impairment. However, in this case, the movements will be jerky unlike the eye movements in smooth pursuit. Tracking of visual targets contralateral to the lesion will be smooth.

8.10 Summary

This chapter reviews the ways in which voluntary eye movements are initiated by cerebral cortical activity and involve more ocular motor control structures than the simple ocular reflexes. The cortical areas initiate eye movements and work through brainstem ocular motor centers to produce a response, i.e., there are no direct connections between the cerebral cortex and the extraocular motor nuclei. The smooth pursuit system utilizes a pontine nucleus, the cerebellum, and the vestibulo-ocular reflex pathway to execute eye movements to tract visual targets. The voluntary saccades system is similar to other voluntary motor systems in engaging areas in the frontal cortex to initiate the response and in influencing the motor neurons indirectly through lower motor control structures (i.e., the vertical and horizontal gaze centers). The gaze centers function to coordinate and control the activity of motor neurons to insure that the extraocular muscles act synergistically to produce conjugate saccades.

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