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Ocular Motility > Final Material > Flashcards

Final Material Flashcards

1
Q

Pursuit latency for a fast vs slow target motion

A

Generally, the slower the pursuit, the longer the latency.

Fast target motion= 100ms latency.
Slow target motion= 125 ms latency.

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2
Q

What are the two summing locations in pursuits

A
  1. Retina compared target motion vs eye motion.

2. Other sums retinal velocity error with info that you get out of eye velocity positive feedback loop.

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3
Q

What factors are accounted for within the afferent pathways? Their outputs are combined and integrated before we get to the efferent pathway.

A

RAE- retinal acceleration
RVE- Retinal velocity
RPE- retinal positional errors

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4
Q

As the target gets faster, the eye matches it- up to a point. At what deg/sec can the eye not keep up anymore?

A

The eye can keep up with an object trailing at 80 deg/sec with approx 1.0 gain. Any faster, and the eye cannot keep up. You would need some saccades to get back on the target.

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5
Q

Why is gaze orientation so important?

A

Our brain must be capable of visualization and target predictability (sophisticated cortical development) in order to properly track pursuits. Important that the brain can SIMULATE.

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6
Q

2 frames of reference

A

Egocentric and allocentric. Transition occurs around 18 months of age.

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7
Q

Pursuit sys is slow. Can only travel up to __ deg/sec. Saccade sys is fast. Can travel up to ___ deg/sec

A

100
800

Prob bc the pursuit sys involves complex pathways and is more neurologically complicated than a saccade. Natures way around this slowness is prediction.

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8
Q

Best way to track a baseball

A

Track ball over the 1st part of the trajectory w smooth pursuit eye movements. Make a saccadic eye movement to a predicated point ahead of the ball, continue to follow it with peripheral vision. At the end of the balls flight, resume smooth pursuit tracking w the balls image on the fovea.

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9
Q

Movement across retina stimulates

A

Pursuits and OKN

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10
Q

VOR compensates for:

OKN compensates for:

A

VOR: Brief, transient head movements
OKN: Compensates for prolonged, sustained movements. Low frequency.

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11
Q

VOR responds to

A

Acceleration (angular velocity).

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12
Q

As acceleration becomes constant, VOR ____

A

Declines and OKN sys takes over.

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13
Q

What is OKAN

A

when rotation is complete, we should get a nystagmus in the opposite direction. Helps to cancel out this post rotational nystagmus that we naturally have.

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14
Q

OKAN is activated by

A

Rotational acceleration and velocity. It discharges after input as stopped. Tells EOMs “I want you to put in a compensatory action in the opposite direction to counteract what we should expect to happen based on physics”

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15
Q

Otoliths

A

calcium particles that sit on top of the gelatin in the macula of the saccule. When head is level, otoliths stay in place.

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16
Q

VOR latency

A

15 ms. Shortest latency for eye movement.

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17
Q

TVOR (Translational)

A

When head tilts, you get a gravitational force on the otoliths in a particular direction relative to the amt of head tilt.

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18
Q

Displacement needs to be ___ degrees for VOR to kick in

A

10-20 degrees

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19
Q

VOR stats
Peak head velocity to maintain VOR:
Peak head acceleration to trigger VOR:

A

100-250 deg/sec

1000-2500 deg/sec

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20
Q

Signal pathway from otoliths to eyes

A

Otoliths travels via CN 8 to the Vestibular nucleus –> CN 6 –> CN 3 –> eyes

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21
Q

VOR gain of less than one means

A

Eye movement is less than head movement.

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22
Q

Why does decreased frequency result in decreased VOR gain?

A

Bc VOR turns off at low freq and OKN turns on.

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23
Q

At close distances, VOR gain _____

A

Increases.

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24
Q

How does VOR affect myopes in glasses

A

As if pt is wearing BO prism. Myopes need LESS gain for a given head movement bc the prism contributes to decrease eye movement amount.

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25
Q

How does VOR affect hyperopes in glasses?

A

AS if pt is wearing BI prism. Hyperopes need more gain for a given head movement (around 2.5% per D)

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26
Q

Neuro pathway for VOR and head translation

A

Neurological pathways from otoliths. Synapse with vestibular nucleus and CN 6.

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27
Q

Neuro pathway for VOR and head tilt

A

Neurological pathway from semi circular canals. Synapse with vestibular nucleus and CN 3. Travels through medial longitudinal fasciculous. Get counter eye roll from head tilt.

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28
Q

Where are VOR centers in the brain?

A

In sides (near inner ear) and back of head. Semicircular canals, cerebellum- flocculus and vestibular nuclei are all close.

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29
Q

ISC Impulse. What is it and what can it test?

A

Very expensive technology for testing eye movements
Can test for:
VOR
BPPV (benign paroxysmal postural vertigo)
Vestibular disorders
Nystagmus
Gaze positions
Skew Deviations (specific type of vertical stimulus)

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30
Q

VOR bilateral vs unilateral loss

A

Bilateral loss: gain of less than 1 OU. Lots of catch up saccades must be made to keep up. Symmetric. Bilateral loss results in fewer symptoms.

Unilateral loss: Gains are different for each eye. Asymmetric. Pt will be very symptomatic.

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31
Q

What is BPPV (Benign paroxysmal postural vertigo)

A

Disorder caused by problems in the inner ear. Caused by loose calcium otolith crystals that breaks out of the gel matrix and gets stuck in the semicircular canal. Crystal in canal will push against the cupola and hair cells within the base of the canal. Gives false information about the location of the head= positional vertigo.

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32
Q

Epley Maneuver

A

Helps dr determine what cancel the loose otolith is in. Helps get the crystal back into the saccule/utricle where they belong.

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33
Q

What is OKN and what induces it?

A

it is an involuntary jerk nystagmus that is indued by motion of the visual field. Peripheral retina driven- not by fovea. Clarity of vision is not important for a good OKN response.

34
Q

OKN neurology pathway

A

Peripheral retina stimulated. Some info from 1 side of field will go directly to the NOT (nucleus of ophthalmic tract). Info from other field will travel to the visual cortex for higher motor processing and then to NOT so all the info can be integrated together

35
Q

What is the main neural integrator for OKN

A

NOT- nucleus of ophthalmic tract.

36
Q

Will a deep central scotoma affect OKN gain?

A

Not really. Peripheral retina dominates OKN system. Therefore, OKN is not very affected by blur.

37
Q

OKN latency

A

140ms.

38
Q

OKN drum. The direction that the slow phase is moving relates to the direction of the stripes how?

A

The slow phase ought to be moving in the direction that the stripes are moving.

39
Q

Gain for “stare” OKN (no attention)

Gain for “look” OKN (with attention)

A

0.8
closer to 1.0

Best gain is for velocities less than 20 deg/sec. Too fast and it will all be a blur.

40
Q

When checking infants monocular movements, what should you expect when moving an object from side to side in front of their face

A

Temporal to nasal movements: Smooth eye movement

Nasal to temporal movements: Jerky eye movement.

41
Q

When do temporal to nasal vs nasal to temporal eye movements in an infant equalize?

A

They should equalize between 3-6 months. If children do not equalize, they have a high tendency to become strabismic.

42
Q

Functional ambylopia

A

Not caused by pathology. Presents similar to neurological disease. Will want to rule out neurological disease before sending patient to VT.

43
Q

Unilateral Peripheral (acute) vestibular disorder

A

Transient imbalance that will get better over time.
Spontaneous nystagmus
Slow phase of nystagmus will go towards the lesion. Greater in the dark.

44
Q

Bilateral peripheral (acute) vestibular disorder

A

Results in oscillopsia. Decreased vision= inadequate compensation from VOR. Vertigo

45
Q

Central vestibular disorder

A

Lots of problems. Refer out for MRI to look for brain stem lesion. Signs will be dependent on location of injury. Nystagmus, head tilt, skew deviation, perceived tilt of world.

46
Q

Congenital nystagmus

A

Asymmetric VOR and OKN. Reduced gain- makes sense bc visual experience isn’t normal.

47
Q

Nystagmus is defined by which two properties?

A

Waveform: pendular or jerk
Direction: Vertical or horizontal

48
Q

Pendular waveform

A

Smooth back and forth motion. Velocity is similar in both directions. Amp can vary depending on drift degree.

49
Q

Three types of jerk waveform nystagmus

A

Jerk, gazeholding/latent manifest and vestibular

50
Q

Congenital Jerk waveform

A

Slow phase and quick re-fixating phase. Velocity of the slow drift increases as you get further away from primary gaze and then eyes jerk back to primary gaze.

51
Q

Gaze holding/latent manifest jerk waveform

A

Attempt to hold eyes in extreme gaze. They will drift away from position pt was attempting to hold. Velocity towards end of drift will slow down and then jerk will take it back to the eccentric position.

52
Q

Vestibular jerk waveform

A

Steady velocity within a given slow phase. Could get faster as they tilt their head in a particular direction, but velocity will remain constant during slow phase.

53
Q

Pendular Nystagmus
Amp
Frequency
Peak velocity

A

Amp: 0.5-10 degrees
frequency: 2-8 hz
Velocity: up to 100 deg/sec

54
Q

Two types of pendular nystagmus

A
  • pendular is usually associated with detectable ocular anomaly
    1. Congenital. usually horizontal. Associated with albinism (under developed eyes)
    2. Acquired. Often has vertical and torsional. More variability in waveform. Could be due to Myelin disease (MS), central brainstem stroke, or monocular vision loss (OD 20/20, OS 20/200)
55
Q

Is Jerk nystagmus usually associated with an ocular anomaly?

A

No. Jerk is usually idiopathic. Pendular is usually associated with detectable ocular anomaly such as Albinism, MS, ON neuropathy, or aniridia.

56
Q

Pendular nystagmus is commonly associated with which ocular anomalies?

A
  1. MS (acquired)
  2. Albinism (congenital) - underdeveloped eyes Infant will search due to foveal hypoplasia.
  3. Congenital cataract
  4. ON atrophy
  5. Aniridia
57
Q

Congenital Jerk Nystagmus

  1. Usually arises when?
  2. Amplitude
  3. Frequency
  4. Slow phase velocity gets up to ___ deg/sec
  5. Horizontal or vertical motion?
  6. What reduces and what worsens it?
  7. VA?
  8. How to treat
A
  1. Usually arises during 1st year. Relatively benign. Not likely to get a whole lot worse.
  2. 0.2-5 degree amp (tighter range than pendulum)
  3. 1-5 hz (tighter range than pendulum)
  4. 100 deg/sec
  5. Horizontal and conjugate
  6. Reduced with convergence. Worsens with intentional fixation.
  7. 20/20 VA
  8. Treat with prism (yoked or BO), surgery, VT, biofeedback, CLs
58
Q

Two types of congenital jerk nystagmus

A
  1. Latent. Typically not seen binocularly. May see if you occlude 1 eye. May get worse.
  2. Manifest. Will see pendular or jerk movements with both eyes open.

Overall, when 1 eye is covered, usually gets worse. Drifts towards occluded eye, with refutation towards viewing eye.

59
Q

Gaze holding Jerk Nystagmus

A

Normal! Ex: physiological end point. Elasticity pulls eye back to primary gaze. Nystagmus jerks it back to try to maintain gaze.

Similar to congenital except that velocity decreases during slow phase (unlike congenital). Opposite waveforms.

Can be seen in: Drug use, cerebellar disorder, vestibular disorder, MS.

60
Q

Vestibular jerk nystagmus. 2 types

A

central: Usually vertical and bad. Refer to neuro.
Peripheral: usually horizontal. BPPV, inner ear infection. Usually involves some history. May need epley.

61
Q

Characteristics of vestibular jerk nystagmus

A

Constant-velocity slow phase
Amp, freq, and velocity overall vary (velocity does not vary WITHIN the slow phase).
Made worse by head position change.

  • Fixation helps peripheral vestibular nystagmus (diff from congenital)
  • Fixation worsens central vestibular nystagmus.
62
Q

Spasmus Nutans

A

Rare condition with the clinical triad of nystagmus, head nodding, and torticollis (head turn)

Onset at age 3-15 months. Disappearance by 3-4 years. Subsides spontaneously.

Pendular, rapid nystagmus (8 hz), small amp, bilateral.

Asymmetric, horizontal.

Must rule out tumors

63
Q

Coloric testing

A

Warm or cold water in ear to induce nystagmus.

COWS. Cold opposite, Warm same. (with reference to the fast movement phase)

Ex: Cold water in right ear. Will slowly move to the right and make fast movement back to the left.

64
Q

Pendular nystagmus. Foveal fixation occurs when velocity is ____

A

Slowest.

65
Q

Jerk nystagmus. Foveal fixation is when after the saccade/fast movement?

A

Immediately.

66
Q

Are reading eye movements saccades or pursuits

A

Saccades.

67
Q

Perceptual span during reading eye movements

A

Amount of text processed during a fixation. English extends from 4 characters to the left of fixation over to 15 characters to the right of fixation. Successive areas of overlap allows for integration of info.

68
Q

Fixation duration during reading eye movements

A

Length of time the eye pauses/fixates. Approx 225 ms (saccadic latency is 200-250)

This is text dependent. ex: grammar, predictability, font, line length.

69
Q

Average college reader reads how may wmp and what is the wmp if skimming

A

College: 290-300
skimming: 400-500

70
Q

Top down process

A

Cognitive process that initiates with our thoughts. Thinking about what you already know and filling in the blanks.

71
Q

Two main types of dyslexia.

A
  1. Developmental/congenital.
    - Language deficit
    - Visual spatial
  2. Acquired dyslexia
72
Q

How do the magno and parvo systems play roles in reading

A

Half way through a fixation, we will get a sustained parvo response that will persist through the next saccade and half way through the next fixation. It will then tapper off and another fixation will start. There is clutter. Magno system works to suppress the area of overlap. This minimizes confusion and allows for better perception.

73
Q

Magnoceullar deficit theory and dyslexia AKA transient system deficit theory

A

Postulates that dyslexia is the result of the reduced masking/sensitivity in the magnocellular system. Thought that dyslexia is the failure to separate neural activity elicited during different fixations.

Fails to address the question of how we figure out where our next fixation should go. Also the magno system must be more than just an eraser.

74
Q

Preview System

A

More updated than the magnocelular deficit theory.

Where parafoveal field comes into play.

Preview system looks ahead and pre-processes spatial info about the size of words, where they begin and where they end. Allow for the oculomotor system to know how far to move the eyes for most efficient reading.

Parvo system looks 1/3 of the way in. Fixation point. Magno system looks at what is coming next. Pre process zone. We get an idea of what is coming next, how long the world is. Simulateanous. This is the attention window in action.

75
Q

Near parafovea is used for ?

Far parafovea is used for?

A
  1. Semantics. How a word relates to others. Context.

2. Used for motor planning. Where we will put our next saccade.

76
Q

Continuous sampling or not?

A

Nah. Our perception of the world is always a little behind the actual events that occur out in space.

77
Q

Percent of words you need to read in order to understand what you read.

A

9%

78
Q

Why can severe dyslexics see an eccentric target that a normal reader cannot see?

A

Normal reader has effective masking in place due to the magnocellular pathway. Normal readers are more aware of the overall shape and spacing peripherally in the pre processing zone and less worried about the detailed info of individual letters.

79
Q

Reading. Lots of fixations, regressions, and skipping around. What does this indicate??

Music reader. Lots of fixations, regressions, and skipping around. What does this indicate??

A

Poor reader

Good musician. Current visual input is ahead of action by 1-2 seconds. Typically jump well ahead and then work backwards towards where the action is.

80
Q

Regressions made by good musician vs regressions made by poor musicians

A

good: 50-57%
bad: 20-25%

Ocular Motility (8 decks)

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