Eye Movements and Vestibular

Question 1

What tract is critical for maintaining muscle tone?

Answer 1

[lateral vestibulospinal tract, and it’s extensor dominant]

Question 2

What is the ‘near’ response triad?

Answer 2

[eyes converge (disjunctive movement), pupil constricts (increases depth of field), lens thickens (increases refraction for close vision)]

Question 3

What is the PPRF?

Answer 3

[paramedian pontine reticular formation, aka horizontal gaze center]

Question 4

If you lost a pretectal nucleus on one side, what would happen to your pupillary reflex?

Answer 4

[probably nothing, …each pretectum receives from both eyes, each pretectum projects to both nu of Edinger-Westphal]

Question 5

What is the nu of Edinger-Westphal?

Answer 5

[This is the pre-ganglionic parasympathetic (GVE) component responsible for pupillary constriction and lens accommodation (thickening) located in the oculomotor complex (III). Axons leave with III and reach the ipsilateral ciliary ganglion (post-ganglionic parasympathetic) just behind the eyeball]

Question 6

What are the direct and consensual components of the light reflex?

Answer 6

[ when you shine the light into one eye, constriction of the pupil of that eye is considered the ‘direct’ response, constriction of the pupil of the other eye is the ‘consensual’ response]

Question 7

What’s the Argyll-Robertson pupil?

Answer 7

[a pupil that exhibits the accommodative response, but not the pupil (light) response. Associated with advanced syphilis, and autopsy reveals bilateral atrophy of pretectum… therefore pupillary constriction in accommodation does not depend on pretectum to get to the nu Edinger-Westphalt]

Question 8

Which is the only eye movement we make in which the eyes do not work as a ‘yoked pair’?

Answer 8

[vergence movements (e.g., accommodative response)]

Question 9

What is nystagmus?

Answer 9

[rhythmic movement of the eyes, usually a vestibular (peripheral) issue; 2nd most common is cerebellar damage, rarely does it involve 1 eye; for clinical reference, the horizontal nystagmus is the most common and exhibits a slow phase and fast phase. The slow phase is true vestibular signals, whereas the fast phase is a saccade. By (strange!) convention, the nystagmus is referenced to the fast phase]

Question 10

Name the 5 types of eye movements we make?

Answer 10

[vestibular ocular reflex, optokinetic reflex, pursuit, saccades, vergence]

Question 11

What is the purpose of the vestibular ocular reflex?

Answer 11

[when we move our head, the vestibular system triggers an eye movement equal and opposite of the head movement to maintain gaze; that way, we maintain gaze on the same target despite the head movement. We can do VOR in the dark, but calibration of system depends on vision and cerebellum (flocculonodular lobe)]

Question 12

What is the purpose of the optokinetic reflex?

Answer 12

[when the head translates through space, we cannot look at the same thing without generating an eye movement to counteract the spatial translation. This discrepancy is referred to as ‘retinal slip’. Optokinetic eye movements are basically, VOR with vision, keeping the eye locked on target as the head moves through space. An interesting difference between VOR and OKR for all you math fans… VOR keys on head acceleration signals, OKR on head velocity signals]

Question 13

What is the ‘special’ nucleus associated with the optokinetic reflex?

Answer 13

[nucleus of optic tract]

Question 14

What are pursuit eye movements?

Answer 14

[relatively slow movements we make to track moving objects… up to ~60 deg/sec. Pursuit system depends on activity in the anterior superior colliculus, which is active during pursuit, and during fixation (which is considered part of pursuit ( Yeah, I don’t know why either)]

Question 15

Why does state trooper Jane tell you to watch her finger as he sweeps it back and forth?

Answer 15

[she thinks you’ve been drinking, and is testing your pursuit eye movement system which is very sensitive to alcohol]

Question 16

What are saccades?

Answer 16

[the fast (up to 900 deg/sec) eye movements we make about 3 times/sec to bring the fovea onto different parts of our visual scene for detailed inspection]

Question 17

Which brain structures are considered selectively critical for saccades?

Answer 17

[frontal eye fields, superior colliculus; course, let’s not forget we also need cranial nerves III, IV and VI, the MLF, PPRF and RiMLF]

Question 18

What’s an ‘anti-saccade’?

Answer 18

[saccades made under testing conditions in which the subject is instructed to look away from a newly presented target in the visual field. For the record, it’s not easy to execute… takes a little practice. People with frontal lobe damage are horrible at it].

Question 19

What are the frontal eye fields?

Answer 19

[a specialized region of the superior frontal gyrus, BA 8, whose activity drives contraversive conjugate eye movements; mediates eye movements on command: e.g., ‘look left’]

Question 20

What is the ‘primate plan’?

Answer 20

[Specialization of the retina to have a fovea and high visual acuity and a large surround area without high acuity but sensitive to movement and contours. This ‘fovea’ is then coupled with a high-precision oculomotor plant that can place the fovea onto any target within oculomotor range with pinpoint accuracy]

Question 21

What are the PPRF and RiMLF?

Answer 21

[paramedian pontine reticular formation, rostral interstitial nucleus of the medial longitudinal fasciculus. PPRF is the ‘horizontal gaze center’ adjacent to the abducens nu: the left PPRF executes leftward gaze shifts, the right PPRF executes rightward gaze shifts]

Question 22

In the brainstem, how is a left conjugate eye movement made?

Answer 22

[Signals must reach the left PPRF which then triggers signals to engage abducens on that side, engage medial rectus on the right, and relax the abducens on the right and medial rectus on the left. Important! The signals going to the right medial rectus cross immediately (at the level of the pons nucleus and ascend the right MLF]

Question 23

What are the consequences of loss of right abducens nerve?

Answer 23

[the right eye does not abduct, loss of conjugate gaze control with diplopia. Patient will maintain orbital position to minimize diplopia]

Question 24

What are the consequences of loss of right abducens nucleus?

Answer 24

[rightward gaze shifts are abolished. The right eye will not abduct because the right abducens nu is out. The left eye will not adduct because internuclear signals from the abducens and adjacent PPRF are out. Therefore the signal to adduct the left medial rectus never occurs.

Question 25

What is the difference between ‘right-way’ and ‘wrong-way’ eyes?

Answer 25

[‘Right-way’ eyes refer to fact that following damage involving the frontal eye fields (FEF), gaze is ‘stuck’ looking toward the side of cortical damage. Why… Because the purpose of the FEF was to drive conjugate eye movements away from that side of cortex. With one side gone, commands pushing contralateral gaze shifts cannot be countered, and the eyes move towards the side of damage. This is a transient effect…. Seemingly resolving in a week. However, we now know that there is a permanent effect. The person can no longer gaze away from the side of cortical of damage on command (e.g., look right, following left cortex damage). In ‘wrong-way’ eyes, the patient looks away (conjugate) from the side of pontine damage involving both fascicles of VI on that side + loss of the abducens and PPRF on that side. Thus, following pontine damage on the left, the eyes deviate to the right…only rightward horizontal gaze shifts can be made.]

Question 26

What happens if the right oculomotor nerve is cut?

Answer 26

[oculomotor palsy. Severe ptosis of right eye (loss of levator palpabrae), mydriasis (dilation of pupil with loss of parasympathetic, aka, ‘blown pupil’), eye is ‘down and out’… consequence of loss of superior, inferior, medial recti and inferior oblique, and now powered only by superior oblique and lateral rectus). Referred to a ‘diagonal diplopia’. Patient will cock head up and leftward to minimize diplopia (double vision)]

Question 27

What happens if the right trochlear nerve is cut?

Answer 27

[the patient will appear with the head down and cocked left to minimize a vertical diplopia. The superior oblique intorts and depresses the eyeball]

Question 28

What happens if the right abducens nerve is cut?

Answer 28

[The right eye no longer abducts, inducing a strabismus and diplopia that is maximal upon attempted rightward gaze]

Question 29

What happen when the right abducens nucleus is lost?

Answer 29

[rightward gaze shifts (by the eyes) cease. Driving the eyes to the right requires the right abducens nucleus and right PPRF (and there’s never been one without the other), as well as an intact left MLF and left oculomotor complex]

Question 30

What are the consequences of loss of left MLF regarding left/right gaze?

Answer 30

[The left MLF is critical for rightward gaze shifts. A rightward gaze shift requires a right abducens/PPRF, a left MLF and oculomotor complex. With the left MLF out, the patient will make the rightward shift with the right eye, but cannot adduct the left eye because the message to adduct would be carried by the left MLF. Whereas the right eye should be fine, it shows a horizontal nystagmus that no one can explain, but makes diagnosis easy! The clinical syndrome is referred to as internuclear ophthalmoplegia].

Question 31

What is the 1 and ½ syndrome?

Answer 31

[loss of MLF and abducens/PPRF on one side. For a left MLF/abducens/PPRF loss, rightward gaze would be impaired because of loss of left MLF, and the right eye would show a nystagmus. Leftward gaze would be impaired, nothing would happen. The left PPRF/abducens is lost (no abduction on left, no message sent to right oculomotor even if right MLF is intact]

Question 32

Name some disorders associated with impairment of vertical gaze?

Answer 32

[pineal tumor (aka, Parinaud’s syndrome), trouble looking up; progressive supranuclear palsy, trouble looking down]

Question 33

Which neurons seem to be very active during both fixation and smooth pursuit?

Answer 33

[anterior (rostral) portion of the superior colliculus]

Question 34

What is the role of the medial longitudinal fasciculus (MLF) in eye movements?

Answer 34

[it’s the great coordinator between the horizontal and vertical gaze centers, the 3 cranial nerve nuclei associated with the extraocular muscles, and vestibular nuclei involved in mediating the vestibulocular reflex]

Question 35

What is motion sickness?

Answer 35

[nausea, vertigo associated with mismatched signals (usually) between vision, vestibular systems, e.g., seasickness: below deck, everything looks stable, but vestibular system says things are swaying (puts out a rhythmic output to muscles that then affect proprioceptors as well)]

Question 36

What is the ‘sense of equilibrium’?

Answer 36

[sense of position in space. Dependent on cues from proprioceptive, vestibular, and visual input; all 3 should align, usually 2 of 3 is good enough]

Question 37

What is vertigo?

Answer 37

[sense of spinning]

Question 38

Do the vestibulospinal tracts preferentially target flexors or extensors?

Answer 38

[extensors]

Question 39

Identify the major targets of the vestibular nuclei?

Answer 39

[contralateral vestibular nuclei, cerebellum, spinal cord (medial and lateral vestibulospinal tracts), oculomotor nuclei (via medial longitudinal fasciculus)]

Question 40

What is the VOR?

Answer 40

[Vestibulocular reflex, a conjugate eye movement we make to be equal and opposite of a head movement to maintain gaze when the head moves. Does not require vision (except for calibration, which is done by circuits in the cerebellum)]

Question 41

What is balance?

Answer 41

[ability to distribute weight evenly to remain upright and stable]