8. Ocular Motor Control
Part 3 of 5

Valentin Dragoi, Ph.D.
.

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.  

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. 

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.

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. 

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. 

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.

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. 

• 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.

Back | Table of Contents | Home Page | Index of Terms | Next

Contact the author(s) at nba_course@uth.tmc.edu
© 2003-present, All Rights Reserved
The University of Texas Health Science Center at Houston
Created through the Multimedia Scriptorium in Academic Technology