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Flashcards in Eye movements Deck (46):

How does the oculomotor system provide an example of most of the principles of organization that apply to the motor systems overall?

The extraocular motor neurons are activated by interneurons that are driven reflexively by vestibular input, and that also serve as simple pattern generators.
*These pattern generators can also be activated by command centers in the brainstem and cortex.
*Finally, the oculomotor system is subject to modulation by the cerebellum and basal ganglia.


How do we know that our eyes are constantly making micro-adjustments to focus on an image?

if we experimentally cause an image to be stabilized on the retina, it disappears.


What are the micro-adjustments the eye makes during foveation called?

The eye moves in small jumps called “microsaccades” to refresh the visual image several times per second so that it is never stabilized.


What are the 4 eye movement categories?

1. Smooth pursuit: tracking (to keep an object on the fovea)
2. Saccades: rapid, ballistic (to bring an object onto the fovea)
3. Vestibular ocular reflex (VOR) and optokinetic nystagmus (OKN): a combination of pursuit and saccades.
4. Vergence: moving the fovea to an object closer (convergence) or farther away (divergence).


what area of the brain is involved with simple tracking?

Tracking movements that are initiated by a moving stimulus involve analysis of the visual scene by cells in visual association cortex.


Characterize a visually-evoked saccade.

Visually-evoked saccades are "ballistic" in character. That is, they are programmed to foveate a particular target, even if the target moves after the saccade was initiated.


Explain the physical parameters that must be met for a saccade to foveate moving target

*key here is understand complexity, which helps us understand the diagnostic utility of eye movements

*A very high frequency burst (as high as 1000 Hz) is needed for the initial acceleration, and then a carefully calculated steady rate is required to maintain the new eye position. (If the head also rotates, as is usually the case, then the saccade has to include later modification to compensate for head rotation.)


Why is the VOR an example of a conjugate contraction?

*the eyes move the same amount in the same direction.
*A rotation of the head is signaled by the semi-circular canals. The center of gaze is maintained by contraction of the appropriate set of extraocular muscles so that eyeball rotation precisely opposes head rotation. This contraction is called a conjugate contraction because the eyes move the same amount in the same direction. For example, if the head turns down, the eyeball rotates up as the superior recti contract (and inferior recti relax).


What is nystagmus? Is it always a sign of pathology?

*eye movement that describes slow tracking, fast saccade to a new focus point
*normal response to head turning and moving targets, but CAN be a sign of pathology
*This sawtooth movement of the eyes, slow ramp opposite to head rotation, fast saccade to center of eye position, is called nystagmus, with the direction of nystagmus defined by the direction of the rapid saccade,
*i.e., "right-beating nystagmus" in this example


how do you define the direction of a nystagmus?

the direction of nystagmus defined by the direction of the rapid saccade,
*i.e., "right-beating nystagmus" in this example


Use the accommodation reflex as an example to describe vergence movements

vergence - (eyes moving in opposite directions, e.g., when both eyes turn nasally)
*such as during the near reflex (the combination of changes our eyes undergo when we attempt to focus on a near object).
*Several things happen at once.
*Both medial recti contract, pulling the eyes nasally.
*The pupils constrict to increase the depth of field.
*The ciliary muscles contract, allowing the lens to become fatter and thus focus on a near object.
*All together, these actions are called the near or accommodation reflex.
*All the motor neurons and preganglionics are in the oculomotor nuclei. These are driven by visual input to association areas of the visual cortex.


What is the cellular driving mechanism of the accomodation reflex?

*All the motor neurons and preganglionics are in the oculomotor nuclei. These are driven by visual input to association areas of the visual cortex.


How is coordinate contraction of the two eye's muscles controlled (general)?

Coordinate contraction of the two eyes is accomplished by interneuronal pattern generators that reside in the vicinity of the oculomotor and abducens nuclei (for the most part).
*Most eye movements are highly stereotyped and so their motor programs are relatively hard-wired.


Where are the neurons located that control horizontal and vertical saccades?

The pattern generator for vertical saccades is near the oculomotor nuclei.
*The pattern generator for horizontal saccades is in the reticular formation near the abducens nucleus (the paramedian pontine reticular formation, abbreviated PPRF).
*This is easy to remember if you recall that most motor neurons for vertical eye movements are in the oculomotor nucleus and that horizontal movements involve the abducens nucleus.


What are the higher order structures important for saccades?

The two important control centers for saccades are the cortex and the superior colliculus. While the motor neurons and pattern generators for saccades are found in the midbrain and brainstem, these voluntary movements can be driven by the frontal lobes


What is the frontal eye field and what does it have to do with coordinated eye movements?

In particular there is a place called the frontal eye field, which lies just anterior to the head representation in motor cortex.
*The frontal eye field can activate saccades by two pathways,
*one direct to the reticular formation and
*one via the superior colliculus to the reticular formation.
*This is similar to the parallel pathways for locomotion.


Use a bee buzzing on the right extreme of your vision field to explain the coordination of the superior colliculus.

The activation by the superior colliculus is interesting because there is not only a retinotopic map (direct input from the retina) but also an auditory spatial map and a somatotopic map, all superimposed on a motor map for the movement resulting from the saccade.
*For example, a bee buzzes off to your right. You hear it and also see it with your peripheral vision.
*Neurons in the superior colliculus that deal with that part of space will be activated by both visual and auditory input, and neurons in deeper layers of the colliculus will fire a burst to cause a saccade, bringing your foveas to that point in space.


Using lesions in the superior colliculus and the frontal eye field, explain the interplay between these two areas in saccades

If the frontal eye field is damaged, there is a temporary loss of the ability to generate saccades.
*If the superior colliculus is damaged, saccades are less accurate and occur less often but still happen.
*If both the frontal eye field and the superior colliculus are damaged, there is permanent loss of the ability to make saccades
*can result in blind sight reflex where blind person's eyes foveate on a flash in a dark room without a percieved stimulus (retinal input to superior colliculus directly drives saccadic eye movement)


If the eyes saccade to the left, what hemisphere's frontal eye field was stimulated?

Horizontal saccades are driven contralaterally, that is, a saccade to the left is driven by activity in the right frontal eye field.
*This makes functional sense because the movement brings the fovea to an area that was being analyzed by that side of the brain (the right brain for movement of the eyes to the left).


There are all sorts of brain areas that control saccades either with downward modulation or reflexively. what are they and what are they abbreviated as?

Saccades can be reflexively directed from the parietal eye field (PEF)
*or voluntarily generated by the Frontal Eye Field (FEF).
*These activate the Brainstem Gaze Center (BGC) directly or indirectly through the superior colliculus (SC).
*Higher centers provide planning, inhibition and coordination (dorsolateral prefrontal cortex, DLPC, and supplementary eye fields, SEF)


How are the basal ganglia involved in saccades?

The basal ganglia are also involved: substantia nigra (pars reticulata, SNPR) inhibits SC (superior colliculus). Caudate nucleus (CN) inhibits SNPR.
*thus, striatum will activate a downstream target through disinhibtion


Describe the process of the VOR

Rightward head rotation is signaled by horizontal canals,
*leftward eye rotation is produced by excitation of motor neurons to the left lateral rectus in left abducens nucleus, and excitation of right medial rectus by motor neurons in right oculomotor nucleus.
*(There is also inhibition of antagonistic muscles - left medial rectus and right lateral rectus, to maintain coordination)


The MLF is mostly taught in our course as the connections between abducens and oculomotor nuclei. But is that all it does?

*the MLF actually extends as far caudally as the caudal medulla where it carries vestibulospinal axons.
*One way to remember this is to consider the fact that you need to coordinate neck movements with eye movements if you want to maintain your gaze on a fixed point and thus, much more information is being processed than we are discussing here.)


Describe the vestibular input in the VOR

As the head rotates to the right, fluid in the horizontal semi-circular canal lags behind, resulting in deflection of the cupula in both horizontal canals.
*In the right horizontal canal the deflection results in depolarization of the hair cells, in the left horizontal canal the hair cells are hyperpolarized
*(opposite effects always occur in two paired canals).
*Excitation on the right is transmitted to right vestibular nuclei.
*Cells in the vestibular nuclei project by way of the medial longitudinal fasciculus (MLF) to excite left lateral rectus motor neurons in the abducens nucleus


In the VOR of the head rotating to the right, What about excitation of the right medial rectus motor neurons?

Since the desired end result is to have left lateral rectus and right medial rectus contracting in synchrony, there must be some mechanism to ensure such coordination.
*This is achieved by having co-activation of abducens motor neurons and internuclear interneurons (about equal numbers of these in the abducens nucleus)
*whose axons cross over and ascend in the medial longitudinal fasciculus to excite right medial rectus motor neurons.
*Any stimuli that excite abducens motor neurons always also excite these internuclear neurons, thus ensuring co-activation of lateral rectus and contralateral medial rectus.
*The internuclear neurons serve as "pattern generators" for conjugate horizontal gaze


Damage to the MLF from a central brainstem lesion will disrupt the VOR. how?

The axons from these interneurons (between abducens and oculomotor) cross the midline at the level of the abducens nucleus and thus, damage to the MLF on the right side between VI and III damages axons coming from the left abducens nucleus.


If the right vestibular system is activated in a head rotation to the right what is going on in the left vestibular system?

remember the discussion of the reciprocal inhibitory connections
*On the left side the hair cells are "inhibited" by rightward head rotation and so opposite synaptic effects must occur compared to those on the right. Thus coordinated leftward eye movement is maintained


That pattern generators for downward and upward VOR (gaze reflex) is more simple than horizontal. But where are these neurons located?

The interneurons that constitute the pattern generator for upward gaze are located near the superior colliculi and posterior commissure and cells are distributed bilaterally.
*Timing signals for downward gaze come from deeper in the midbrain, near the dorsomedial edge of the red nucleus, and again are bilaterally distributed.


Can you clinically determine if a patient has lost VOR in certain extraocular muscles but that the muscles themselves are fine?

It is possible to determine that the medial rectus muscle and motor neurons are normal even though the muscle does not function properly during horizontal gaze.
*For example, the medial rectus may be unable to participate in horizontal gaze saccades or pursuit and yet the eyes work normally in vergence movements where both medial recti contract.


MS patients commonly have problems with corrdinating horizontal gaze during traction. Why is this?

Due to its length, the MLF is especially vulnerable to interruption.
*MLF damage can disconnect the coordination of medial and lateral recti during horizontal gaze movements. This condition is called internuclear ophthalmoplegia (INO) and is common in patients with multiple sclerosis.


how can you test the presence/intactness of the nystagmus pattern generator?

The similarity in movement between vestibular and optokinetic nystagmus suggests that there is in some sense a "nystagmus pattern generator".
*This notion is supported by the fact that nystagmus can also be elicited by artificially causing movement of the fluid in semi-circular canals.
*This is usually accomplished by placing cold water in the ear canal and gives rise to a whirling sensation with accompanying eye movements.
*This is termed "caloric nystagmus".
*Here the nystagmic pattern of eye movements is independent of visual input, and elicited by a highly unusual pattern of vestibular input, yet is very similar in design to "normal" nystagmus.
*Thus it appears as though the pattern generator, once activated, produces coordinate extraocular muscle contractions independently of sensory input.


what are the learning objectives for this lecture?

Describe the four types of eye movements.

Know the difference between conjugate and vergence eye movements.

Describe saccade eye movements and how they are generated.

Describe the properties of smooth pursuit eye movements, how fast can they be, and why are they limited to relatively slow speeds.

Describe the control of the VOR for a person sitting on a chair that is rotated to the right (clockwise rotation if you look down on them from above).

Define internuclear ophthalmoplegia. Describe what you observe for the patient, how you can decide if the medial rectus motoneurons and/or nerve are intact, and what is the most likely structure that is affected.

Describe nystagmus. Give examples where nystagmus occurs normally and examples where it occurs abnormally.


Describe the Spontaneous position—cover/uncover test

*use an occluder to test if the eyes move upon occluding the other eye
*have patient look forward, neutral position no matter what
*cover one eye for a couple seconds and note any "other eye" movement
*take off the occluder and see if there is correction.


What are the eye movements you should know about to note?

Single Extra-ocular muscle functions

Horizontal conjugate movements

Vertical conjugate movements—upward vs. downward

Pursuit movements

Saccadic movements (voluntary and reflexive)

Vergence movements (convergence and divergence)

Oculovestibular and oculocephalic reflexes

Utilize passive head rotation

Utilize warm or cold water irrigation

Nystagmus—what’s normal, what’s not


What features of the pupils should you look for in patients?

Size, shape, position, and symmetry

Pupillary Light reflexes

Size and reactivity in room light vs. dark vs. bright

“Swinging flashlight” test to detect APD

Near vision reflexes (convergence, accommodation, constriction)


What are you looking for in funduscopy?

Cornea, lens, iris, vitreous

Optic disc—located about 15-20 degrees nasally from the fovea

Retina—leave the fovea and macular region until last

Vessels—optic vein venous pulsations

Green, red-free light on ophthalmoscope helps with exam of vessels


When testing visual fields, what are you doing?

Confrontation technique

Mapping of blind spot—need to know where it is


What is the confrontation technique in visual field testing?

*cover one eye and test all the peripheral vision of the uncovered eye
*then repeat that with the other eye
*the whole purpose is to define as precisely as possible the extent of the visual field loss


What are the given examples in class of pathological eye movements?

VI nerve palsy

III nerve palsy

Internuclear opthalmoplegia (INO)

Afferent Pupillary Defect (APD)


Down-beat nystagmus with Chiari malformation


Horner syndrome


describe the findings in VI nerve palsy

VI nerve palsy - abucens nerve in one eye isn't working.
*patient can follow an object in a coordinated fashion in one direction but not the other
*in the affected direction the eye will only go midline, not fully abducted


Describe the findings of III nerve palsy

*preserved ciliary reflex (pupillary restriction)
*abduction in affected eye is normal
*loss of supraduction, adduction and infraduction


Describe the findings of internuclear opthalmoplegia (INO)

*result of MLF lesion (MS in young people)
*during horizontal tracking movements one eye in one direction will lag behind teh other
*example of patient looking quickly right, reporting double vision, and you see the left eye lag behind the right


Describe the results of an afferent pupillary defect test

*the most sensitive method of clinically showing a unilateral optic nerve lesion
*on the affected side, the pupil dilates in response to light


you see downbeat nystagmus and you think...?

Chiari malformation, cerebellar herniation or problems


describe the syndrome of Opsoclonus-myoclonus ataxia

essentially the eyes make random coordinated movements that are not explained by foveation
*can't maintain focus but their eyes jerk away somewhere
*myoclonic movement of the eyes


You can see evidence of horner syndrome in the eyes how?

Horner syndrome in eyes - dilation lag. One pupil dilates faster than the other
*sympathetic problem
*Horner syndrome (Horner’s syndrome) results from an interruption of the sympathetic nerve supply to the eye and is characterized by the classic triad of miosis (ie, constricted pupil), partial ptosis, and loss of hemifacial sweating (ie, anhidrosis).

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