APPENDIX TO OCULAR MOTOR SYSTEMS AND CONTROL
This section is included for those who wish to use further "clinical cases" to test their knowledge of ocular motor functions.
| Example A1 |
Symptoms. A patient visits his primary care physician at the urging of his wife. She noticed that his left eye lid was drooping slightly and that his face appeared flushed. She was concerned he might have suffered a stroke. On examination, it was noted that his left pupil was much smaller than his right (Figure 8.A.1), but responded directly and consensually to light. Physical examination determines that touch, vibration, position and pain sensations are normal over the entire the body and face. There are no other motor symptoms.
Figure 8.A1 |
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You observe that the patient exhibits
- no loss of cutaneous sensation in the face area
- no loss of ocular motility
- miosis (pupil constriction)
- pseudoptosis (mild eye lid droop)
- flushing of the left side of the face
You conclude that his left eye's functional loss is
- not sensory
- an autonomic motor dysfunction
Pathway(s) affected: You conclude that structures in the following motor pathway have been affected is
- the sympathetic innervation of the face
Side & Level of Damage: As these symptoms
- involve only motor function
- involve sympathetic innervation
- do not involve other diencephalic or brain stem functions
- involve only one eye
- involve loss of pupil dilation
you conclude that the damage
- involves axons of the superior cervical ganglion
- is in a branch of the sympathetic nerve innervating the face
- is on the left side (i.e., the symptoms are ipsilesional)
Sympathetic Innervation of the Eye. Horner's syndrome is a constellation of symptoms that includes miosis, pseudoptosis and enopthalmosis (sunken eyeball). It is characteristic of damage to the sympathetic innervation of the face provided by the superior cervical ganglion. This syndrome also occurs when the hypothalamic output to the sympathetic preganglionic neurons in the lateral horn at T1 to T3 is interrupted or when the T1 to T3 anterior roots are damaged.
| Example A2 |
Symptoms. A 35 year-old female complains that she has double vision when she attempts to look to the right. When looking straight ahead, both her eyes assume normal positions (Figure 8.A.2). She is able to look up and down and to the left with both eyes. However, she cannot adduct her left eye (i.e., move it to the right). Both her eyes converge when a visual target is brought close to her eyes. Her vision and pupillary reflexes are normal in both eyes. She has normal sensation on her face and body and no other motor symptoms.
You observe that the patient's eyes
- assume the normal position when looking straight ahead
- have full mobility when looking up and down and to her left
- cannot move together toward the right (i.e., the left eye moves to mid position).
- do converge during accommodation
You conclude that her functional loss
- is not sensory
- does not present with a strabismus when the eyes are at rest position
- involves the left eye only when attempting a lateral gaze to the right
- is not lateral gaze paralysis because the left eye can be abducted when looking left
- is not paralysis of the left medial rectus because the left eye can be adducted during convergence and does not exhibit lateral strabismus at rest.
Side & Level of Damage: As her symptoms
- do not involve lower motor neurons or muscles (i.e., the left eye can adduct during convergence)
- involve upper motor neurons (i.e., conjugate lateral eye movements)
you conclude that the damage involves the
- medial longitudinal fasciculus (i.e., the abducens nucleus is not involved)
- left side (i.e., the symptoms are ipsilesional for the left eye)
Neural imaging tests indicate demyelination of the medial longitudinal fasciculus on the left side.
Damage to the medial longitudinal fasciculus. The medial longitudinal fasciculus (MLF) is a fiber tract that contains, in part, axons of the vestibular nuclei and of the contralateral abducens interneurons. Lesions in the MLF results in an abnormality of conjugate horizontal eye movements called an internuclear ophthalmoplegia. The medial rectus ipsilateral to the damaged MLF does not function during a lateral gaze in a contralesional direction. With the eyes at rest, both eyes are directed forward in the “normal” position. If the damage is unilateral, both eyes can be moved in an ipsilesional direction during an attempted lateral gaze (i.e., towards the left if the left medial longitudinal fasciculus is damaged). In contrast, the ipsilesional eye (i.e., the left eye ipsilateral to the severed left tract) cannot be moved beyond the midline during an attempted contralesional (right) lateral gaze.
Recall the left MLF carries the axons of the right abducens interneurons to the left oculomotor neurons, which control the medial rectus of the left eye (Figure 8.A.3). Also recall that contraction of the medial rectus of the left eye directs the left eye nasally (i.e., contralaterally to the right).
Both eyes are adducted on convergence as the axons from the supraoculomotor area to the oculomotor neurons controlling the medial rectus muscles of the two eyes are not affected by MLF lesions.
| Table II Classification of Eye Movement & Their Neural Control Structures |
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| Eye Movement | Function | Afferent Input* & Motor Control Structures |
| Vestibulo-ocular | Initiated by vestibular mechanisms during head movement | Vestibular Receptors & Vestibular 1° Afferent Neurons*
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| Vergence | Adjusts for different viewing distances | Visual System* including Visual Association Cortex
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| Smooth Pursuit | Follows (watches) a moving visual target | Visual System* including Visual Association Cortex “Temporal” Eye Field
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| Saccade | Directs eyes toward visual target | Visual System* including Visual Association Cortex Frontal Eye Field
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| KEY: VII - Abducens Interneurosn; VIm - Abducens Motor Neurons; III - Occulomotor Motor Neurons; IV - Trochlear Motor Neurons | ||
Horizontal Movements: Medial Vestibular Nucleus*
Lateral Rectus of One Eye
[1] Note that each oculomotor nerve controls the extraocular muscles of its ipsilateral eye, i.e., the right nerve controls the superior and inferior oblique and superior and inferior rectus of the right eye.
[2] For the curious, the vertical gaze center is located in the rostral interstitial nucleus of the medial longitudinal fasciculus and, according to some, also in the interstitial nucleus of Cajal.
[3] This is all you need to know about the role of the basal ganglion for ocular motor tasks.
[4] No need to memorize this.
[5]<See footnotes 3 and 4 above.
[6] Recall the posterior parietal cortex is part of the dorsal visual stream that determines the "where" of the visual scene (i.e., the location and movement of the visual target).
[7]Please note this is in disagreement with Nolte, pg. 521, Figure 21-15, which identifies the extrastriate cortex as the course o the cortical neurons controlling smooth pursuit.
[8]Recall from the lectures on the visual system that these cortical areas, MST and MT, are part of the visual sensory circuit involved with detecting the "where" of a visual stimulus.
[9]For the curious, the DLPN axons end in the flocculus, paraflocculus & vermis of the cerebellum.
[10] the paramedian pontine reticular formation and abducens interneurons coordinate the activities of antagonistic muscles involved in horizontal eye movements during saccades.
