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Neuroscience and NeuroAnatomy > 38 - NeuroScience - Occulomotor System > Flashcards

38 - NeuroScience - Occulomotor System Flashcards

1
Q

What are the differences between an eye and a camera?

A 
Camera = Still, Eye = Moving
Camera = 2D Image, Eye = 3D Image
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2
Q

Eye Muscle Anatomy

A 
3 Pairs of Muscles
Meridians:
Horizontal
Vertical
Vertical Twisty
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3
Q

Types and Functions of Eye Movements

A

Stabilization
Depth
Foveation

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4
Q

Brainstem Circuits

A

X

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5
Q

Subcortical Circuits

A

X

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6
Q

Cortical Control

A

X

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7
Q

Pair of muscles that moves the eye along the horizontal meridian (towards nose or away from nose)

A 
Lateral Rectus (Abducts)
Medial Rectus (Adducts)
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8
Q

Pair of muscles that moves the eye along the vertical meridian (up or down)

A 
Superior Rectus (Elevation)
Inferior Rectus (Depression)
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9
Q

Pair of muscles that moves the eye along the vertical meridian while twisting

A 
Superior Oblique (Depression & Intorsion)
Inferior Oblique (Elevation & Extorsion)
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10
Q

Intorsion

A

Top rotates towards the nose (Superior Oblique)

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11
Q

Extorsion

A

Top rotates towards the ear (Inferior Oblique)

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12
Q

Main Function - Stabilization

A

Stabilizes the visual world against large changes (moving head or moving world)
Primitive reflexes
Don’t require a fovea

Vestibulo-Ocular Reflex (VOR)
Optokinetic Nystagmus (OKN)
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13
Q

Main Function - Depth

A

Allow us to bring both eyes to focus at an appropriate distance

Vergence (slow)

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14
Q

Main Function - Foveation

A

Specific to animals that have a fovea
Place the fovea on selected items of interest

Saccades (rapid rotations of the eyeball)
Smooth pursuit (slow)
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15
Q

Vestibulo-Ocular Reflex (VOR)

A

Follow large, full-field motion caused by HEAD MOVEMENTS (no visual input)

Quick
Habituates
Relatively little voluntary control
Mostly Mediated by subcortical pathways

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16
Q

Optokinetic Nystagmus (OKN)

A

Follow large, full-field motion caused by EXTERNAL MOTION (visual input)

Quick
Does not habituate
Relatively little voluntary control
Mostly mediated by subcortical pathways

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17
Q

Phases of Nystagmus (both VOR & OKN)

A

Quick Phase
Slow Phase

See-Saw Pattern, resets when it reaches the limit in the orbit

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18
Q

VOR - Why does nystagmus in response to simple rotation of the head (no visual component) slowly habituate?

A

Vestibular signal is fairly transient

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19
Q

OKN - When visual components are added, does nystagmus habituate?

A

No!!

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20
Q

Vergence

A

Allows two eyes to simultaneously point at a single object.

Align eyes so that the single image hits the Foveal Region of each eye

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21
Q

Converging

A

Eyes rotate inward

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22
Q

Retinal Disparity

A

Difference between the displacements from the fovea that a single object exerts on each eye. Allows us to determine depth.

Encoded first in Primary Visual Cortex, used to compute distance relative to the center of gaze

Small range of disparities can be told apart. Anything outside of that small range (close to the object of focus) is actually seen in double. This double vision is filtered out of our perception.

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23
Q

Strabismus

A

Ocular misalignment

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24
Q

Types of Strabismus

A

Hypotropia
Hypertropia
Exotropia
Esotropia

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25
Q

Hypotropia

A

Eye Turns Down

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26
Q

Hypertropia

A

Eye Turns Up

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27
Q

Exotropia

A

Eye Turns Out

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28
Q

Esotropia

A

Eye Turns In

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29
Q

Effects of Strabismus

A

Images from each eye do not fuse with each other!!!!

Brain suppresses visual input from one of the eyes.

Monocular vision.

Some folks can alternate dominance of each eye. More commonly, one eye is favored.

Relatively normal vision, but LACK OF DEPTH PERCEPTION

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30
Q

Amblyopia

A

No depth perception

Strabismic or Refractive
2 - 3% of the population

Deficits:
Driving
Walking
Manual Dexterity
Reading
Visual Function
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31
Q

Refractive Ambylopia

A

Two eyes have very different refractive errors, and one eye becomes suppressed

32
Q

Traditional Theory on Amblyopia

A

“Critical Period”

Depth perception can only be learnt if there is normal visual input EARLY in life (6 - 12 months of age)

33
Q

More Modern Theory on Amblyopia

A

Improvements can happen at any point, but just with LOTS of practice. This theory is undergoing a lot of research

Sue Barry gained depth perception at 48 yo
https://www.youtube.com/watch?v=XCCtphdXhq8

34
Q

Saccades

A

Rapidly moves the fovea to a new position

Target moves
Brief extreme burst of eye velocity
Eye snaps to a new position very rapidly
Referred to as a “step” in eye position

Relies on “position errors”
“Muscle Burst”
Vision is suppressed during saccade (no visual input for 10 - 50 ms)

35
Q

Position Errors

A

The distance of the target from the current center of gaze

36
Q

Smooth Pursuit

A

Matches eye velocity to target velocity

Target moves
Eye moves initially in the direction of the VELOCITY of the target, not necessarily the new position.
Kicks in earlier than the position system (Saccades).
When the position system has caught up, the eye tracks the target smoothly

Relies on “velocity errors”
Slow
Foveal vision is not suppressed

37
Q

Velocity Errors

A

The velocity of a target relative to the retina

Sometimes called “retinal slip”

38
Q

Stabilization Pathways

A 
Vestibular/Full Field
Rapid
Reflexive
Don't require much cognitive control
Mostly subcortical pathways
39
Q

Depth and Foveation Pathways

A

Small Stimuli
Requires selection (which target am I focusing on?)
Engages cortical areas like whoa

40
Q

Lowest Level Pathway

A

Brainstem/Oculomotor Circuitry
Through cranial nerves
Directly drives ocular muscles

41
Q

Middle Level Pathway

A

Basal Ganglia

Caudate
Substantia Nigra
Superior Colliculus

Projects down and drives the Brainstem nuclei

42
Q

Highest Level Pathway

A

Cortical areas in the parietal and frontal lobe

43
Q

Principles of Ocular Engineering

A

Inter-ocular coordination: Conjugate and disconjugate movements

Separate neural signals for:
High velocity (saccadic “burst”)
Low velocity (smooth pursuit, VOR, OKN, vergence)
Position

Calibration by the cerebellum

44
Q

Inter-Ocular Coordination

A

Brainstem/Oculomotor Pathway

Neurons innervating EOM live in Nuclei III IV & VI in the brainstem, send axons through cranial nerves

45
Q

Horizontal Conjugate Version (looking left or right with BOTH eyes) - Pathway

A

Ipsilateral Abducens Nucleus (Lateral Rectus)
Contralateral Oculomotor Nucleus (Medial Rectus)
Medial Longitudinal Fasciculus connects the two

46
Q

Medial Longitudinal Fasciculus

A

Coordinates ipsilateral Abducens nculeus to contralateral Oculomotor nucleus for horizontal conjugate version

Susceptible to stroke or MS, leading to Internuclear Ophthalmoplegia

Vergence is STILL INTACT

47
Q

Internuclear Ophthalmoplegia

A

Failure of horizontal conjugate version (fast or slow)

48
Q

Position & Velocity Signals

A

Intense bursts of nerve activity corresponding with saccade

Firing rate scales with saccade amplitude
Peak velocity of eye increases with the size of eye movement

Tonic firing maintained after the burst

Firing rate scales with position of the eye

49
Q

Saccade “Burst” Velocity - Pathway

A

Frontal Eye Field (SOME excitation) + Omnipause Neurons (STRONG inhibition)
Superior Colliculus
Paramedian Pontine Reticular Formation (“burst generator”)
Abducens Nucleus
Lateral Rectus & Contralateral Medial Rectus (Via MLF, then Occulomotor Nucleus)

50
Q

Omnipause Neurons

A

Housed in the Dorsal Raphe
Provide strong inhibition to the “burst neurons”
Active continuously when eye is still
Pause activity when the eye is in motion

It’s a STRONG brake within the brainstem on the saccadic system

51
Q

Slow Eye Velocity - Pathway

A

Semicircular Canals, Subcortical Input (OKM) & Cortical Input (speed)
Medial Vestibular Nuclei
Bilateral input to Abducens Nucleus
Lateral Rectus & Contralateral Medial Rectus (Via MLF, then Occulomotor Nucleus)

52
Q

Signals of eye position

A

Specify stationary position in the orbit

Nucleus Prepositus Hypoglossi
Projects bilaterally to Medial Vestibular Nucleus & Abducens Nucleus

53
Q

Calibration

A

Adjust neural signal to compensate for muscular weakness (greater neural signal necessary for same saccadic movement)

Adjust for curent position of the eye, elastic restoring forces in the orbit (greater signal required to move the eye to a more eccentric orbital position because of the elastic restoring force

Calibration provided by the Cerebellum

54
Q

Cerebellar Degeneration - Effects on Calibration

A

Eye movements are too small (if the eye is moving further deviated)

Eye movements are too large (if the eye is moving towards the center)

55
Q

Saccadic Adaptation

A

Tests how subjects compensate for visual errors.

Aim for 21 degrees, and the computer tricks you by moving to 15 degrees.

You adapt by aiming for 15 degrees in the future.

Can’t do it with cerebellar degeneration

56
Q

Cognitive Control

A

“Scan Path” depends critically on what subjects are trying to do. Ask about riches, they look at the furniture. Ask about age, they look at the face. Duhhhhh

Eye precedes hand, leaves before hand is done.

57
Q

Visuomotor transformations when selection is made

A

SNpr typically inhibits Superior Colliculus

When a saccade is needed, Caudate Nucleus inhibits SNpr for a “pause,” disinhibiting Superior Colliculus

58
Q

Frontal Eye Field

A

Projects to Caudate Nucleus
Projects to Superior Colliculus
Directly projects to brainstem

Closely related to final eye movement

59
Q

Parietal Eye Field

A

Posterior Parietal Cortex

Projects to Caudate Nucleus
Projects to Superior Colliculus

60
Q

Supplementary Eye Field

A

Higher level structure
Poorly understood
Has to do with eye movements

Activity is more cognitive and task-dependent

May provide cognitive control to the Frontal Eye Field

61
Q

Frontal Eye Field Visual Neuron

A

Visual Neurons - Majority of Neurons in the FEF

Visual Neurons respond to the appearance of a salient object within its receptive field

62
Q

Attentional Enhancement

A

Visual Neuron firing is STRONGER if the subject is planning to make an eye movement to that stimulus. The subject is USING the visual stimulus to plan a movement, so there is a greater signal.

No temporal relationship to saccade. Visual Neuron firing is over by the time the eye moves.

No Visual Neuron firing in the dark, even in the presence of saccades.

63
Q

Frontal Eye Field Movement Neuron

A

Movement Neurons respond VERY weakly to the appearance of a salient object within its receptive field.

When the subject plans and executes an eye movement, the neuron gears up, then fires really hard to execute the saccade.

These neurons respond to a saccade in the dark.

64
Q

Some neurons do both.

A

They are prevalent in both FEF and PEF

65
Q

Where are Movement Neurons found?

A

Exclusively in the FEF

66
Q

Parietal Eye Field’s Goal

A

Selecting targets from the visual world.

67
Q

Frontal Eye Field’s Role

A

Make the final decision about whether or not to move to that target.

68
Q

Parietal Eye Field damage leads to

A

Parietal Neglect

Impaired attentional selection in visual space

69
Q

Parietal Neglect

A

Patients lose awareness of visual stimulae that are contralateral to the parietal lesion (often in a hemifield)

Not blindness. Completely unaware that there is something there.

70
Q

Frontal Eye Field Damage

A

Impairs attentional selection

Impairs voluntary saccades

71
Q

Combined Collicular & FEF lesions (in monkeys)

A

No saccades what so ever

72
Q

Frontal lesions

A

Can’t make antisaccades.
Can look AT something all right, following visual input.
Can’t look AWAY from something, executing a movement of the EOMs without visual guidance.

73
Q

The Antisaccade Task

A

Have patient stare straight ahead
Flash a stimulus on one side and tell the patient to look AWAY from it.
This voluntary ability is severely impaired with frontal damage

74
Q

Supranuclear Control of Pursuit

A

Velocity Errors (movements of small targets across the retina)

Striate Cortex
Projects to Middle Temporal (MT) and Middle Superior Temporal (MST), which contain movement-sensitive neurons.

Project to brainstem nuclei (Nucleus Reticularis Tegmenit Pontis)
Provide command for slow eye velocity

OR

Project to FEF (adjacent to representation of rapid saccadic eye movement) deep in the suclus. Important for INITIATING smooth pursuit

75
Q

Deficits in Smooth Pursuit - Origins

A 
Cerebellar Disease
Brainstem Disease
Parietotemporal Lesions
Frontal Lesions
Clinical diseases with an attentional deficit (Alzheimer's or any frontal dementia, schizophrenia)

Neuroscience and NeuroAnatomy (41 decks)

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