38 - NeuroScience - Occulomotor System Flashcards
What are the differences between an eye and a camera?
Camera = Still, Eye = Moving Camera = 2D Image, Eye = 3D Image
Eye Muscle Anatomy
3 Pairs of Muscles Meridians: Horizontal Vertical Vertical Twisty
Types and Functions of Eye Movements
Stabilization
Depth
Foveation
Brainstem Circuits
X
Subcortical Circuits
X
Cortical Control
X
Pair of muscles that moves the eye along the horizontal meridian (towards nose or away from nose)
Lateral Rectus (Abducts) Medial Rectus (Adducts)
Pair of muscles that moves the eye along the vertical meridian (up or down)
Superior Rectus (Elevation) Inferior Rectus (Depression)
Pair of muscles that moves the eye along the vertical meridian while twisting
Superior Oblique (Depression & Intorsion) Inferior Oblique (Elevation & Extorsion)
Intorsion
Top rotates towards the nose (Superior Oblique)
Extorsion
Top rotates towards the ear (Inferior Oblique)
Main Function - Stabilization
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)
Main Function - Depth
Allow us to bring both eyes to focus at an appropriate distance
Vergence (slow)
Main Function - Foveation
Specific to animals that have a fovea
Place the fovea on selected items of interest
Saccades (rapid rotations of the eyeball) Smooth pursuit (slow)
Vestibulo-Ocular Reflex (VOR)
Follow large, full-field motion caused by HEAD MOVEMENTS (no visual input)
Quick
Habituates
Relatively little voluntary control
Mostly Mediated by subcortical pathways
Optokinetic Nystagmus (OKN)
Follow large, full-field motion caused by EXTERNAL MOTION (visual input)
Quick
Does not habituate
Relatively little voluntary control
Mostly mediated by subcortical pathways
Phases of Nystagmus (both VOR & OKN)
Quick Phase
Slow Phase
See-Saw Pattern, resets when it reaches the limit in the orbit
VOR - Why does nystagmus in response to simple rotation of the head (no visual component) slowly habituate?
Vestibular signal is fairly transient
OKN - When visual components are added, does nystagmus habituate?
No!!
Vergence
Allows two eyes to simultaneously point at a single object.
Align eyes so that the single image hits the Foveal Region of each eye
Converging
Eyes rotate inward
Retinal Disparity
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.
Strabismus
Ocular misalignment
Types of Strabismus
Hypotropia
Hypertropia
Exotropia
Esotropia
Hypotropia
Eye Turns Down
Hypertropia
Eye Turns Up
Exotropia
Eye Turns Out
Esotropia
Eye Turns In
Effects of Strabismus
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
Amblyopia
No depth perception
Strabismic or Refractive
2 - 3% of the population
Deficits: Driving Walking Manual Dexterity Reading Visual Function
Refractive Ambylopia
Two eyes have very different refractive errors, and one eye becomes suppressed
Traditional Theory on Amblyopia
“Critical Period”
Depth perception can only be learnt if there is normal visual input EARLY in life (6 - 12 months of age)
More Modern Theory on Amblyopia
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
Saccades
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)
Position Errors
The distance of the target from the current center of gaze
Smooth Pursuit
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
Velocity Errors
The velocity of a target relative to the retina
Sometimes called “retinal slip”
Stabilization Pathways
Vestibular/Full Field Rapid Reflexive Don't require much cognitive control Mostly subcortical pathways
Depth and Foveation Pathways
Small Stimuli
Requires selection (which target am I focusing on?)
Engages cortical areas like whoa
Lowest Level Pathway
Brainstem/Oculomotor Circuitry
Through cranial nerves
Directly drives ocular muscles
Middle Level Pathway
Basal Ganglia
Caudate
Substantia Nigra
Superior Colliculus
Projects down and drives the Brainstem nuclei
Highest Level Pathway
Cortical areas in the parietal and frontal lobe
Principles of Ocular Engineering
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
Inter-Ocular Coordination
Brainstem/Oculomotor Pathway
Neurons innervating EOM live in Nuclei III IV & VI in the brainstem, send axons through cranial nerves
Horizontal Conjugate Version (looking left or right with BOTH eyes) - Pathway
Ipsilateral Abducens Nucleus (Lateral Rectus)
Contralateral Oculomotor Nucleus (Medial Rectus)
Medial Longitudinal Fasciculus connects the two
Medial Longitudinal Fasciculus
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
Internuclear Ophthalmoplegia
Failure of horizontal conjugate version (fast or slow)
Position & Velocity Signals
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
Saccade “Burst” Velocity - Pathway
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)
Omnipause Neurons
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
Slow Eye Velocity - Pathway
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)
Signals of eye position
Specify stationary position in the orbit
Nucleus Prepositus Hypoglossi
Projects bilaterally to Medial Vestibular Nucleus & Abducens Nucleus
Calibration
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
Cerebellar Degeneration - Effects on Calibration
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)
Saccadic Adaptation
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
Cognitive Control
“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.
Visuomotor transformations when selection is made
SNpr typically inhibits Superior Colliculus
When a saccade is needed, Caudate Nucleus inhibits SNpr for a “pause,” disinhibiting Superior Colliculus
Frontal Eye Field
Projects to Caudate Nucleus
Projects to Superior Colliculus
Directly projects to brainstem
Closely related to final eye movement
Parietal Eye Field
Posterior Parietal Cortex
Projects to Caudate Nucleus
Projects to Superior Colliculus
Supplementary Eye Field
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
Frontal Eye Field Visual Neuron
Visual Neurons - Majority of Neurons in the FEF
Visual Neurons respond to the appearance of a salient object within its receptive field
Attentional Enhancement
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.
Frontal Eye Field Movement Neuron
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.
Some neurons do both.
They are prevalent in both FEF and PEF
Where are Movement Neurons found?
Exclusively in the FEF
Parietal Eye Field’s Goal
Selecting targets from the visual world.
Frontal Eye Field’s Role
Make the final decision about whether or not to move to that target.
Parietal Eye Field damage leads to
Parietal Neglect
Impaired attentional selection in visual space
Parietal Neglect
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.
Frontal Eye Field Damage
Impairs attentional selection
Impairs voluntary saccades
Combined Collicular & FEF lesions (in monkeys)
No saccades what so ever
Frontal lesions
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.
The Antisaccade Task
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
Supranuclear Control of Pursuit
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
Deficits in Smooth Pursuit - Origins
Cerebellar Disease Brainstem Disease Parietotemporal Lesions Frontal Lesions Clinical diseases with an attentional deficit (Alzheimer's or any frontal dementia, schizophrenia)
