Basics of Eye Movement Flashcards
Describe the motion of the eye when it is rotating and when it is translating.
• Rotation
o Eye turns around center of rotation (cr)
o Visually significant (keep foveal fixation)
• Translation
o Not visually significant / Tiny side to side movements not expected to be seen
Define the optic axis, the visual axis, the pupillary axis, and the line of sight
Optical Axis
• Straight line that connects the centers of curvature of the refracting surfaces of the eye and extends to the posterior pole DOES NOT represent where eye is looking
Visual Axis
- Line that runs from the fixation target (F) 1st nodal point 2nd nodal point fovea • Close to LOS and FA
LOS
- Gaze Direction and rotation are defined by LOS
- LOS is used in clinic
- LOS= the line from the fixation target to the center of the entrance pupil
o Entrance pupil= IMAGE of pupil seen when looking at patients’ eye
o Continues as ‘foveal chief ray’ from exit pupil to the fovea
Define primary, secondary, and tertiary positions of gaze.
Primary Position of Gaze (PPG)
- Eye is in the PPG when the LOS is perpendicular to the plane of the face
- Agonist and antagonist EOM innervations are approximately in balance in the PPG
Secondary Position of Gaze
- Gaze position directly above, below, left, or right of the PPG. Vertical mer stays vertical
Tertiary Position of Gaze
Gaze position which is neither primary or secondary Vertical meridian does NOT remain vertical, and instead tips
Define angle lambda.
o Where fovea is with respect to posterior pole is #1 determinant of angle lambda!
A normal angle lambda ≈ +11 PD (0.5mm nasal)
Angle lambda is the angle between the LOS and the pupillary axis
The genesis of the normal nasal corneal reflex in angle lambda tests:
o Temporal displacement of the fovea from the posterior pole
o LOS exits the cornea nasally from the optic axis
o The optic and pupillary axes are turned outward during fixation
o The cornea acts as an outward-turned convex mirror, displacing the corneal reflex relatively nasally from
the center of the entrance pupil
Identify the usual cause of an abnormal angle lambda
Monocular vision:
Eccentric fixation/viewing is the MOST common disorder of angle lambda uses off foveal location for fixation
Binocular vision (Hirschberg test):
Strabismus - Any difference between angle lumdas of eyes signifying that only 1 eye is fixating
List three advantages of using eye movement recording technologies to measure
eye movements, compared to standard clinical assessments such as the
Hirschberg test.
Advantages of accurate objective methods:
- Some are more accurate than standard clinical tests
- We can assess movement dynamics
- We can assess eye movement with minimal interference with vision
Select which eye movement recording technology is most accurate – EOG,
infrared reflection, video tracking, or search coil.
Search Coil
• Most difficult to use
• Costliest technology
• Most obtrusive
o Must put large hard lens on the eye with corneal anesthesia
o Can only be worn for 20 minutes
• By far the most accurate of all methods
• The search coil is best method for measuring
torsion
List the four types of versional eye movements in the horizontal, vertical, and
torsional planes
Versional Movement
- Horizontal dextroversion, Levoversion
- Vertical hyperversion, hypoversion
- Torsional dextrotorsion, levotorsion
List the two types of vergence eye movements in the horizontal, vertical, and
torsional planes.
Horizontal- convergence, divergence
Vertical - hypervergence, hypovergence
Torsional -encyclovergence, Excyclovergence
List the three synonyms that name equal movements of the eyes.
If the eyes move equally, the movement is called
Conjugate
Conjunctive
Versional
List the three synonyms that name unequal movements of the eyes.
If the eyes move differently, the movement is called
Dysjugate
Disjunctive
Vergence
Identify the purpose of each of the following eye movements:
- saccades
- pursuits
- vergence jumps
- vergence tracking
- vestibular
- optokinetic.
Saccades
- Voluntary movement - to put new images on the foveas by shifting gaze direction o Innervation: conjugate
Smooth Pursuit
- Voluntary movement - to MAINTAIN foveal fixation of moving objects by smoothly changing gaze direction o Innervation: conjugate
Vergence Jumps
- Change gaze direction in depth
- Place new images on the foveas by shifting fixation distance looking near to far or vice
- Innervation: dysjugate eyes rotate in opposite directions
Vergence Tracking
- Change gaze direction in depth
- Purpose: to maintain fixation on objects moving in depth by smoothly changing gaze distance, images on foveas
- Innervation: dysjugate
Vestibular
- Maintain image contrast in peripheral vision along with foveal vision Reflexive system
- Purpose: to maintain a steady retinal image when the HEAD moves
- Innervation: conjugate
Optokinetic
- Maintain image contrast in peripheral vision along with foveal vision
- Purpose: to maintain a steady retinal image when the VISUAL ENVIRONMENT moves
- Innervation: conjugate
Define oculomotor “kinematics”.
Kinematics is the study of how the eye rotates in the orbit
Select the type of visual perception (visual acuity, contrast perception, color
vision, stereopsis) most affected by a failure of cyclovergence.
Proper torsion is a binocular vision concern…
o Torsional misalignment can disrupt fusion and stereopsis even if bifoveal vision is attained
Define the “torsional posture” of the eye.
“torsional posture”
is the orientation of the vertical meridian of the eye relative to objective
vertical
Define “false torsion”.
A change of torsional posture caused by a combo of horizontal and vertical rotations is called
“false torsion”
State Donder’s Law.
Donder’s Law:
“the torsional posture of the eye at any position of gaze is the same, regardless of how the eye got there”
Distinguish between
Fick’s,
Helmholtz’
Listing’s
theoretical ocular rotation axis systems.
Fick - proposed a system in which horizontal rotation precedes vertical rotation axis: NO False Tortion
Helmholtz - proposed a rotation system in which vertical rotation precedes horizontal rotationMUCH
false torsion
Listing’s Law: “The torsional posture of the eye in tertiary gaze will be the same as if the eye rotated from the PPG about a single axis in Listing’s plane, that axis being perpendicular to the direction of the target”
o Listing’s Plane: a vertical plane passing through the center of rotation and approximately parallel to the face
State Listing’s Law.
Listing’s Law: “The torsional posture of the eye in tertiary gaze will be the same as if the eye rotated from the PPG about a single axis in Listing’s plane, that axis being perpendicular to the direction of the target”
Listing’s Plane: a vertical plane passing through the center of rotation and approximately parallel to the face
Listing’s law predicts a small amount of false torsion less than Helmholtz’ axes and more than Fick’s axes
List the two types of eye movement in which the eyes do not strictly follow
Listing’s Law
- There is more extorsion during CONVERGENCE than Listing’s law predicts, especially in down gaze Optimizes where eyes fall based on corresponding points to improve binocularity
- There is LESS false torsion during VISTIBULO OCULAR REFLEX than Listing’s law predicts
• Optimizes where eyes fall based on corresponding points to improve binocularity
Distinguish between “covert” and “overt” attention.
o Covert Attention: attending to something you are not directly looking at
o Overt attention: attentional target that you move your eyes to
• Overt attention for motion is “spatial”
Distinguish between reflexive (“bottom-up”) and voluntary (“top-down”) attention.
Control of Overt attention:
“top-down” Voluntary
• Driven by higher order processing in the brain occurs most of the time
o “bottom-up” (reflexive)
• Not consciously attending to something
• Ex: response to a startling event/loud sound in your environment
• Driven by lower order processing in the brain
Describe how the role of attention differs between
reflex attention eye movements,
psychooptic reflex eye movements,
voluntary eye movements,
pure reflex eye movements.
Pure Reflex Movement
- NO attention involved
- Pupilary light Reflex, Vestibolo ocular reflex(total dark)
Reflex Attention Movement
- Patient is aware of movement AFTER it happens
- Controlled by reflex attention shifts
- Refex to a loud noise
Psychooptic Reflex Movement
- Voluntary overt attention to target will not respond to covert attention
- NO conscious intent needed to initiate the eye movement occurs reflexively
- Reflex accomodation , fusional vergence
Voluntary eye Movements
- movement initiation are voluntarily controlled
- Aware of movement
- Voluntary Saccade
Describe the role of attention in each of the six types of eye movements
Saccades - Voluntary, put images on the fovea buy shifting gaze direction
Smooth persuits - Attention Maintain foveal fixation while targets move
Vergence Jumps - Attention Change gaze direction in depth, images on foveas by shifting fixation dist, near to far
Vergence Tracking - Attention Smooth movement vith image staying on fovea, Change gaze direction in depth
Vistibulocular reflex - NO Attention Maintain a steady retinal image when HEAD moves, Maintain image contrast in peripheral and foveal vision
Optokinetic - Attention Maintain steady retinal image when the visual environment moves
Describe the meaning of boxes, circles, and arrows in eye movement cybernetic box diagrams.
Boxes - Neural or muscular Mechanisms
Circles - represent arithmetic operations
• These are usually assumed to be addition or subtraction neural summation or inhibition
Arrows - represent signals going from one part of the system to the other
- Signals are quantifiable events in a system
Distinguish between “feedback” and “feedforward” oculomotor control.
“feedback control”
When a movement system checks the accuracy of its response and makes corrections.
“feedforward control”
When an eye movement system generates responses without checking for accuracy
o There is NO “feedback loop”
o There is NO “error” in feedforwardcontrol
• The advantage of feedforward control is a QUICK response
Describe the role of “error” in feedback control.
Feedback control systems are driven by “error”
- The signal that says “you should make a correction”
- want stimulus to equal response
- o Error=stimulus - response (gain 1.0)
Give an example of an eye movement that uses feedback control and an eye movement that uses feedforward control.
Feedback control:
It is NORMAL to have a tiny amount of error in fusional vergence → you need a little retinal disparity to stimulate fusional vergence
Feedforward Control
Vestibulo-ocular reflex you move your head and you get innervation to move your eyes almost instantly
Identify the principal advantage of feedback control in eye movement
The advantage of feedback control is accuracy
Identify the principal advantage of feedforward control in eye movement.
The advantage of feedforward control is a
QUICK response - Less thinking is involved
Define the term “gain” as it relates to eye movement.
Gain refers to mechanism performance (ex. Fusional vergence gain= fusional vergence innervation/retinal disparity)
How efficient/sensitive the neural mechanism is when doing its job
Saccades + Vergence Jumps
Gain= initial response magnitude/ stimulus
Sustained Vergences + Accommodation
Gain= sustained response magnitude/stimulus
All Smooth Movements
Gain= response velocity/stimulus velocity
List the gain value which represents “perfect” oculomotor control.
“Gain” = ratio of response/ stimulus stimuli and responses are measured in the same units
o A gain of 1.0 is ideal, but is rarely achieved
Identify an example of an agonist/antagonist extraocular muscle pair.
“when an agonist contracts, its antagonist relaxes” reciprocal action
Agonist: muscle that pulls the eye in the intended direction Antagonist: muscle pulling oppositely from the agonist
in temporal gaze, agonist=LR, antagonist=MR
State Sherrington’s Law
ALL eye movements follow Sherrington’s Law, regardless of type “when an agonist contracts, its antagonist relaxes” reciprocal action
Describe how the high resting firing rate of extraocular muscle fibers supports
Sherrington’s Law.
Amount of energy produced by the agonist as it increases force = a reduction of energy from the antagonist
o The EOM muscle fibers have a high “resting” firing rate in the PPG
o As agonist innervation goes up one unit, the antagonist drops one unit
o Linear reciprocity helps ensure precise gaze innervation during slow movements and steady fixation
Identify an oculomotor condition in which Sherrington’s Law appears to fail.
Extreme gaze
Retraction of the globe during strong convergence
All-or-none reciprocity during high speed saccades
Agonist is turned on the full amount for the amount of eye turn Much more force than what you would need to hold the eye at the target to overcome inertia
Antagonist is turned off completely during the saccades no residual innervation
o This would slow down the agonist, brain turns it off
Define yoked extraocular muscles
EQUAL innervation yoked muscles in each eye receive equal innervation
o Yoked agonists pull each eye in the “same” direction
o Yoked antagonists receive equally reduced innervation
Describe how extraocular muscle yoking is different in conjugate and dysjugate eye movements.
Some muscles are yoked for CONJUGATE movement
- RLR and LMR are yoked rightward agonists
- RMR and LLR yoked rightward antagonists
- Similar for vertical motion
Muscles are yoked differently for DYSJUGATE movement
- RMR and LMR are yoked NEAR agonists
- RLR and LLR are yoked NEAR antagonists
- Brain has separate neural controls for dysjugate innervation same convergence or divergence signal os sent to both eyes
Define Hering’s law
EQUAL innervation yoked muscles in each eye receive equal innervation
o Yoked agonists pull each eye in the “same” direction
o Yoked antagonists receive equally reduced innervation
Select the extraocular muscles that are yoked for conjugate motion and those that are yoked for dysjugate motion.
Some muscles are yoked for CONJUGATE movement
- RLR and LMR are yoked rightward agonists
- RMR and LLR yoked rightward antagonists
- RSR and LSR / RIR and LIR
Muscles are yoked differently for DYSJUGATE movement
- RMR and LMR are yoked NEAR agonists
- RLR and LLR are yoked NEAR antagonists
Select the part of Herings law (conjugate or dysjugate) that serves as the basis for testing extraocular muscle paralysis.
Hering’s Law is the basis of testing EOM paralysis due to oculomotor nerve damage
We apply a conjugate stimulus – equal movement of the eyes is expected
Paralysis prevents equal muscle response even when conjugate innervation is equal
o Unequal movement is easy to detect → unequal movement indicates PARALYSIS
Describe how the eyes will move in a “versions” test of oculomotor paralysis if the patient has a left lateral rectus paralysis
Eyes would be able to Do Dextroversion
On levoversion - LEFT eye would not Abduct Right to the left side as normal
Identify, in an eye movement recording, the difference between saccades and pursuit,
Eyes have same pattern of motion BOTH Saccades and Persuits
• Eyes fixate on a word together then jump together to the next word→ patterns identical between the two eyes
SACCADES - Changes of position are very rapid → takes almost no time to go the next position
PERSUITS - Slow steady change
Identify, in an eye movement recording, the difference between conjugate and
dysjugate movement.
Usually put right eye above left eye (based on convention)
Y axis → eye position (motion convention)
o Rightward motion of eyes = upward shift in the graph
o Leftward motion of the eyes = downward shift in the graph
DYSJUGATE
o Right eye turns relatively leftward
o Left eye turns relatively rightward
o SLOWER than saccade
o Movement in the two eyes are EQUAL but OPPOSITE
CONJUGATE
Saccade, Both eyes make a fast movement in the same direction, Or slow
.Read, in an eye movement recording, the amount and direction of eye movement.
Usually put right eye above left eye (based on convention)
Y axis → eye position (motion convention)
o Rightward motion of eyes = upward shift in the graph
o Leftward motion of the eyes = downward shift in the graph
Straight line - FAST Saccade
Curved line PERSUIT
An observer makes a slow and smooth eye movement from far to near along the line of sight of his left eye. The left eye remains stationary as the right eye adducts. Explain, on the basis of Hering’s law, how equal conjugate and dysjugate innervations sent to each eye can cause this unequal eye movement behavior.
• Can only occur is you SUM conjugate/dysjugate innervation
o Lateral gaze signal pushes eyes to the left (smooth pursuit innervation) → the conjugate signal
o At the same time, the approaching near target stimulates convergence → the dysjugate signal
• When you sum up conjugate/dysjugate innervation you get UNEQUAL movements even though EQUAL innervation is present
o In the eye that did rotate, the conjugate/dysjugate signals are in the SAME direction and cause eye movement in that direction
o In the eye that did not rotate, the conjugate/dysjugate signals pull the eye in opposite directions and cancel each other out
o Causes UNEQUAL physical rotation between the eyes even though the eyes are receiving EQUAL amounts of innervation
Describe the primary purpose of accommodation.
Accommodation is the adjustment of ocular focus for the sake of optimal visual acuity and contrast
Describe the purpose of vergence eye movements.
Vergence is the adjustment of ocular alignment for the sake of stereoscopic acuity
o Convergence: inward turning (positive)
o Divergence: outward turning (negative)
Distinguish between retinotopic and spatiotopic stimuli
Retinotopic:
innervations stimulated by specific retinal image characteristics (ex: blur and absolute disparity)
Spatiotopic:
innervations stimulated by perceived distance – voluntary at a conscious level
Select the type of oculomotor control (feedforward or feedback) used by
accommodation and convergence.
Both use continuous feedback control
*no feed forward* need the best precision, and the movements are slow anyways so more time can be taken for feedback
Calculate the value of the accommodative stimulus for a target 33cm from the spectacle plane, when viewed through a -2.00D add by an uncorrected 1.00D myope.
AS=1/d–S
Sis(+)or(-)
o Fixation target distance (d) from the spectacle plane
o Lenses (S) added to the far refractive correction
Patient is emmetropic or corrected to emmetropia (correct first so you know that their problems are not related to RE)
Consider a patient with the following uncorrected refractive error: OD +1.00 sph,
OS +2.00 sph, who is viewing a target at 50cm. Calculate the effective
accommodative stimulus if the eyes are (1) equidominant and (2) if the right eye
were amblyopic.
Define “blur accommodation” (reflex accommodation).
A retinotopic process → process driven by characteristics of the retinal image alone/ stimulated by retinal image blur
BA innervation is proportional to blur
Describe qualitatively how target spatial frequency and retinal eccentricity affect blur accommodation gain.
BA is dominated by FOVEAL Vision
BA is poor in people with macular disease or amblyopia
The gain of BA is low when you have poor vision
Hard to see blur when your macula isn’t working properly or when accommodative targets are
off-fovea
Peripheral vision is NOT good at seeing blur therefore the sensitivity of BA DECREASES
Identify the type of attentional control used by blur accommodation
Initiated by psychooptic reflex attention
Observers are aware of attending their fixation target, but are usually not aware of the associated accommodation to keep the target clear continuously why BA is also known as “reflex accommodation” (no associated effort)
You can stop your BA to a target by choosing not to look at the target (overt attention mechanism)
Explain how blur can stimulate normal blur accommodation when steadily accommodating to a near target even though normals don’t usually see blur in that situation.
Sensitive BA prevents blurred vision
o BA induces an accommodative change you don’t consciously see blur
o Your acc system may leave 0.25D (lag) because this is the minimum amount of defocus
normals need to activate their blur accommodation → this sustained lag drives your near accommodative response without you perceiving it because 0.25D is below your subjective depth of focus
List a common clinical disorder in which the patient has weak blur
accommodation.
BA is poor in people with macular disease or amblyopia
The gain of BA is low when you have poor vision
Define the stimulus to proximal accommodation.
Proximal accommodation innervation (PA) is stimulated by perceived nearness (not blur), so it is “spatiotopic”
Identify the special role of proximal innervation in the accommodative system.
The primary role of PA is to initiate large changes of accommodation (and vergence)
Define instrument myopia.
The nearness stimulus is much STRONGER than the optical accommodative stimulus, causing blur
• Strong magnification stimulates nearness percept
• Optical accommodative stimulus is typically ZERO
o Ex: Any microscope Perceive that the patient’s eye in the slit lamp is very close which causes you to reflexively accommodate
Identify optometric tests that are sometimes disturbed by instrument myopia in
both patients and examiners.
Slitlamp evaluation
List the two main roles of voluntary accommodation in normal vision
o To initiate LARGE changes of focus similar to PA
o To supplement other accommodative innervations when they are fatigued
• Not good at sustaining → more of a short-term strategy
Define tonic accommodation
Automatically generated steady innervation that is NOT stimulated directly by vision (always there)
Purpose: to reduce the workload on positive blur accommodation, and thereby improving near visual acuity
Distinguish between “static tonicity” and “tonic adaptation” in accommodation.
- Static tonicity – a baseline innervation
- Tonic adaptation – adjusting to sustained demand
Define the “tonic resting state of accommodation”.
Mean TA in population = 1D (1 meter away)
o Normal range of TA ≈ 0.5-1.5
o This is why it is a bad idea to over fog a patient during refraction eye will go into tonic accommodation
intermediate distance the eye focuses at ( zero accommodative
innervation to relax at infinity) – this is the distance where your eye focuses with no stimulus
Methods for removing accommodative stimuli:
• Darkness (“dark focus”; “night myopia”) – can happen while driving
o Can give spectacles with extra (-) to compensate for night myopia
• Ganzfeld luminance “empty field myopia”)
• Pinhole aperture with monocular occlusion at distance
o
Describe the three different stimulus conditions used to measure the tonic
accommodation resting state
Methods for removing accommodative stimuli:
• Darkness (“dark focus”; “night myopia”) – can happen while driving
o Can give spectacles with extra (-) to compensate for night myopia
- Ganzfeld luminance “empty field myopia”)
- Pinhole aperture with monocular occlusion at distance
Select the posture of normal emmetropic accommodation (slight lead, slight lag,
or in-focus) with respect to a far target.
Slight Lead
Select the type of reflex accommodation innervation – positive, negative, or none
– that is active during normal emmetropic far vision.
Negative
Describe the visual conditions which induce the adaptation of tonic
accommodation.
Very slow, requiring several minutes to adapt to each new change of demand (not done instantly to
carefully adjust to the distance of demand)
Accommodative adaptation is the adjustment of TA innervation in response to a prolonged change of
other accommodative innervations
Define “consensual accommodation”.
The eyes accommodate EQUALLY accommodation is cyclopean
o The ciliary muscles receive the same cyclopean innervation from the EW nuclei
o Accommodative innervation cannot differ between the eyes in a healthy person, even if the ocular stimuli differ
Define “step accommodation”.
Transient accommodation innervation initiates “step” changes of accommodation
o Step response = a shift of response from one level to another (ex. far to near)
• Transient = shift from one distance to another
• Sustained = staying on target
o Sustained innervation completes step responses
Differentiate the roles of transient and sustained innervation in accommodation.
Transient accommodation is a large burst of innervation that moves the ciliary muscle ‘quickly’ o This innervation is generated by accommodative “burst cells” in the brainstem
Sustained accommodation innervation maintains or slowly changes accommodation
List the latency and duration of the transient phase of the average normal step accommodative response.
Compared to all other eye movements, step accommodation is slow
o 1070 msec response time:
• 370 msec latency
o Involves slower brainstem neurons (konio cells slow responders)
• 700 msec average movement time (duration of accommodative change)
o 10D/sec peak velocity
List the innervations that drive the transient accommodative response.
This innervation is generated by accommodative “burst cells” in the brainstem
Konio Cells in Brainstem
List the sustained accommodation innervation that is directly controlled by
feedback in the accommodative system.
Blur accommodation innervation dominates normal sustained accommodation when retinal image defocus < 1D
o Other innervations such as Tonic Accomodation
o Neural integrator cells create persistent innervation
• Cells that generate sustained innervation have a property that they can produce innervation in a steady low (transient neurons cannot do anything in sustained manner, only bursts)
o This persistence can last up to ten seconds after accommodative stimulation is removed
Distinguish between accommodative “lead” and accommodative “lag”.
Lag = sustained underaccommodation
- The retinal image is focused BEHIND the retina
- Lag blur is similar to hyperopic blur
Lead = sustained overaccommodation
- The retinal image is focused in FRONT of the retina
- Lead blur is similar to myopic blur
Describe the role of accommodative lead and lag in the control of reflex
accommodation.
Lag and lead are behaviors of sustained accommodation does NOT apply to transient accommodation
Normal lags and leads create the sustained retinotopic blur that stimulate sustained blur accommodation innervation
Describe the two processes that indicate to reflex accommodation whether a
retinal image blur comes from a lead or lag of accommodation.
Longitudinal chromatic aberration between L, M, and S cones
Accommodation adjusts itself to eliminate red or green fringes on yellow images
o o
The retinal image looks like a circle with a yellow circle and red fringe green is more in focus in front of the retina, red is more out of focus and diffuse behind the retina
The area where the two wavelengths overlap is yellow represents UNDERACCOMMODATION
• there are specialized ganglion cells that sense this image
o Sometimes the image can look yellow with a green border/fringe→ this represents OVERACCOMMODATION
• There are specialized ganglion cells that sense this image
Identify, on a graph of accommodative response versus stimulus, the parts of the function that quantify accommodative amplitude, gain, accommodative resting distance, and lag.
o At large stimulus values, the function flattens out reached the accommodative amplitude limit
o At the bottom end, your accommodation cannot go absolutely to zero (tonic accommodation)
• Need some myopic blur on the retina to stimulate negative reflex accommodation
• Key parameters:
o 1/1 line – normal standard
o mid slope
o lag conveys the accommodative gain Most likely less than 1.0
separation between the slope line and the 1:1 line dependent on accommodative demand
o zero lag point the eye is exactly in focus here (no need for accommodative innervation) • relates to the accommodative resting point of the eye
o far limit
o near limit
Calculate the convergence stimulus for a target 17.3cm from the spectacle plane when viewed by a patient with a 60mm PD wearing 3∆ base-out prism.
CS=PD/d+Δ
o PD = the far interocular distance (in cm)
o d, in meters, is measured to the interocular baseline
It is assumed that the distance from the spectacle plane to the interocular baseline is 2.7 cm • We usually ignore the 2.7 constant if d ≥ 33 cm
o Base-out Δ is (+) because it increases the stimulus to convergence o Base-in Δ is (-) because it decreases the stimulus to convergence o Examples: (assume PD=6)
d = 0.173m, Δ = 3Δ BI; CS = 30 + 3 = (6/.2) + 3 = 33
Identify the type of attention the visual system uses to control disparity vergence
(no attention, pure reflex, psychooptic reflex, or voluntary).
Psychooptic reflex attention initiates DV
o Similar to reflex accommodation if the retinal disparities are within limits of the visual system, it will automatically align your eyes reflexively
List the value of the average threshold retinal disparity of disparity vergence.
2’-20’ Fine DV
10’ - 10deg
Threshold of fine DV ≈ 2’ (very small)
• Fine DV weakens for disparities > 20’
• Critically important in sustaining convergence keeps you a straight eyed person
Coarse Disparity Vergence
• Controlled by coarse disparity neurons in visual cortex
• Threshold disparity ≈ 10’
o Need at least 10’ in depth from where you are looking to stimulate coarse disparity
• Response weakens for disparities > 6Δ
o Very large retinal disparities will just produce diplopia (exceeds the range of fusional vergence)
o Operating range: 10’-6Δ
List the types of vergence innervation stimulated by crossed and uncrossed retinal disparities, respectively.
Crossed disparity stimulates convergence
• Total convergence response is the sum of convergence innervations
Uncrossed disparity stimulates divergence
Define the stimulus to proximal vergence innervation
Proximal vergence innervation (PC) is stimulated by perceived nearness it is spatiotopic
o Same precept that drives proximal accommodation
Describe the special role played by proximal innervation in convergence
The primary role of PC is to initiate LARGE changes of vergence
o Stronger transient effect
o Weaker sustained effect
Define instrument convergence.
instrument convergence”
o Instruments where the nearness stimulus is much STRONGER than the optical convergence stimulus
• Ex: slit lamp, binocular indirect, etc.
o Overconvergence with UNCROSSED DIPLOPIA
List two clinical instruments prone to cause instrument convergence.
BIO, and Slitlamp
List the two main roles of voluntary vergence in normal vision.
o Initiate LARGE changes in vergence
o To supplement other fatigued vergence innervations
List two nonspatiotopic stimuli to voluntary convergence.
o Diplopia – this is retinotopic behavior:— observing the retinal image characteristic
o Strained feeling about the eyes
o Pure volition
List patient instructions that would minimize a patient’s voluntary innervation during tests of convergence
To discourage voluntary effort:
o “look at the letters; make no special effort to see them”
List patient instructions that would maximize a patient’s voluntary innervation
during tests of convergence.
To elicit voluntary effort:
o “keep the letters clear and single.”
o “imagine looking at your nose and feeling the strained sensation around your eyes”
List three disadvantages of using voluntary innervation instead of fusional
vergence innervation for sustained convergence.
Patients who use voluntary effort continuously:
• See targets go in and out of focus and alignment
o If controlling vergence to prevent diplopia, they think that they have good single vision and eventually stop paying attention once attention is lost the patient will have diplopia again
• Experience asthenopia
• Cannot concentrate on their reading
List the purpose of training voluntary convergence during vision training.
This training is done when fusional vergence is very weak and needs temporary voluntary help
The ultimate goal of VT is to move the patient beyond the need for voluntary effort
Define the anatomical position of rest.
Anatomical position of rest = vergence posture in the absence of all EOM innervation determined by passive mechanical forces on orbit
o Not seen in clinical setting unless patient under anesthesia
Define the physiological position of rest.
Physiological position of “rest” – the vergence posture when…
- o Binocularity is dissociated
- o Accommodation is “active” in far vision
- o Otherwise known as the “far phoria”
Define the tonic vergence resting distance
Mean tonic vergence, TV = 3Δ eso (roughly 2 meters)
Eliminate all visual stimuli for accommodation/vergence eye will go into tonic vergence resting state
TV determines the CR when accommodation and vergence stimuli are eliminated by way of:
o Darkness (“dark vergence”) – no stimuli in the dark
o Ganzfield luminance
o Pinhole apertures or nonaccommodative target, dissociation and far fixation
List the necessary stimulus conditions to measure the tonic vergence resting
distance.
TV determines the CR when accommodation and vergence stimuli are eliminated by way of:
o Darkness (“dark vergence”) – no stimuli in the dark
o Ganzfield luminance
o Pinhole apertures or nonaccommodative target, dissociation and far fixation
Takes time for eye to return to phoria posture or to TV state
Describe the stimulus to tonic vergence adaptation.
Tonic Vergence (TV) is an automatic steady vergence innervation which is not stimulated by vision (it is always present there is always minimal tonicity in your extraocular muscles
o Static tonicity
o Tonic adaptation
o Neither static TV or TV adaptation are synkinetic with accommodation
Select the time needed for a normal observer to fully adapt tonic vergence from far vision to near vision (i.e., milliseconds, seconds, minutes, hours, or days).
o If the brain finds that it needs to supply a lot of vergence for a long time, it adapts and adds more
tonicity for sustained near vision (
• TV adaptation slowly changes TV throughout the day
• It takes many minutes of time to adapt TV significantly
.Match these horizontal vergence innervations: sustained disparity vergence,
transient disparity vergence, proximal vergence, and voluntary vergence, to their
appropriate stimuli (small retinal disparity, large retinal disparity, stereoscopic
depth perception, and large magnitudes of diplopia)
horizontal vergence innervations ; stereoscopic
sustained disparity vergence : small retinal disparity
transient disparity vergence : large retinal disparity
proximal vergence : depth perception
voluntary vergence: arge magnitudes of diplopia
List the average latency and duration of the normal step vergence response to near
Latency - 150 msec (milliseconds)
• This is the time between when your stimulus is
introduced and when the eye movement start
Duration - 500 msec
• Duration increases with magnitude
Define the role of transient innervation in vergence
Transient vergence innervation initiates step changes of vergence
o Looking far, then suddenly changing to reading distance
o Transient vergence is a strong burst of innervation that moves the EOMs quickly, but does not sustain convergence once the eyes reach destination the transient innervation goes away
List the vergence innervations that support the transient vergence response.
Looking for infinity to near
•
Proximal vergence innervation plays the biggest role
Spatiotopic voluntary innervation can also play a role depends on how strong proximal innervation is
Stronger proximal innervation= less voluntary innervation needed
These two innervations will get you close to the near target sustained innervation mechanisms will take over after
Define the role of sustained innervation in vergence.
Sustained vergence innervation MAINTAINS vergence after a vergence step, and can SLOWLY change vergence
Sustained vergence is controlled by the retinotopic innervation “fine DV”
List the vergence innervations that maintain the sustained vergence response.
- Vergence resting state → determined by tonic vergence
- Proximal= small contribution, but helps you get closer to near point
- Accommodative vergence is an important contributor to sustained near convergence response - sends info to the convergence system
- Fine disparity vergence controls the remainder of the convergence response at near → means that some fixation disparity is present
List the average gain of normal sustained vergence.
The average gain of sustained vergence ≈ 0.99
o Size of retinal disparity needed to stimulate vergence = 1% of total convergence innervation
o Convergence is extremely PRECISE/ACCURATE and tolerates very little retinal error
• Why is vergence so precise?
o You need very precise vergence to keep images on/near the horopter (where the best stereo is) o Tolerance for single vision only is more relaxed than for stereo
.Normal sustained vergence gain is much higher than normal sustained
accommodation gain. What is thought to be the reason for this difference?
Why is vergence so precise?
o You need very precise vergence to keep images on/near the horopter (where the best stereo is) o Tolerance for single vision only is more relaxed than for stereo
Describe the role the vergence neural integrator performs in normal vergence.
Sustained vergence innervation is maintained by “vergence neural integrator” cells
o These cells maintain innervation even in the ABSENCE of a stimulus
o In vergence, neural integrator persistence can last longer than ten seconds
o Sustained vergence persistence causes the SLOW decay of vergence observed when an occluder is
applied in a cover test
Describe how the vergence neural integrator reveals itself in clinical tests.
Sustained vergence persistence causes the SLOW decay of vergence observed when an occluder is applied in a cover test
Define fixation disparity.
Fixation disparity (FD) is a small misalignment of the eyes which does NOT disrupt foveal fusion
o Centers of the foveas do not point exactly at the target
o FD is a property of SUSTAINED disparity vergence normal property of vergence control system o FD causes stimulation of the foveal retinal disparities this stimulates fusional vergence
Compare and contrast eso and exo fixation disparity from crossed and uncrossed retinal disparity
• Its normal to have a little bit of exo disparity in your vision Analogous to accommodative lead and lag
• Exo FD as you are looking closer misalignment is small and within Panum’s Area so no diplopia
Underconvergence (normal) EXO
• The fixation target subtends a CROSSED foveal disparity
• Positive fine sustained DV is stimulated by the fixation target
• Causes targets to fall on temporal retinas (but not exactly on corresponding points) Creates crossed retinal disparity which is a stimulus for fusional convergence
Overconvergence (abnormal)ESO
• Lines of sight cross at a point closer than the target any eso FD is abnormal
• The fixation target subtends an UNCROSSED disparity stimulates negative fusional vergence (NFV) and turns the eyes out to the target
• Negative fine sustained DV is stimulated
List the oculomotor responses involved in the “near triad”
The “near triad” synkinesis:
- Accommodation
- horizontal vergence
- pupil constriction
Define “AC/A ratio”
The AC/A ratio is the ratio of accommodative vergence (AC) generated by each unit of accommodation (A)
Distinguish between the “stimulus AC/A ratio” and the “response AC/A ratio” test
methods.
Response AC/A = measured vergence change/measured accommodation change
Stimulus AC/A = measured vergence change/accommodative stimulus change
The response AC/A is usually HIGHER than the stimulus AC/A o Accommodation usually changes less than its stimulus
Population stimulus AC/A values:
o Average AC/A = 4/1 (response AC/A ≈ 5)
Normal range = 3/1 to 6/1
• Patients will have comfortable vision with good fusion and stereo
List which AC/A ratio test method is more accurate and which is easier to run.
More Accurate :
Calculated AC/A = there are combined blur and spatiotopic accommodative stimuli (ex. Proximal stimuli)
• Comparing far and near phorias based on the PD more phoria change =higher AC/A
• GREATER accommodative stimulation and innervation
• MORE accommodative vergence
• HIGHER stimulus AC/A
Easier:
Gradient AC/A = there is ONLY a blur stimulus to accommodation
• This is when you put a lens on the eye and measure the effect on the phoria
• Gives us a change of phoria caused by a change in blur patient’s accommodative change is not
going to be 1D even though you put +1D in front of their eye
o Measure the phoria change for the true response)
List the average normal stimulus AC/A ratio
List the range of normal stimulus AC/A ratios
Population stimulus AC/A values:
o Average AC/A = 4/1 (response AC/A ≈ 5)
o Normal range = 3/1 to 6/1
• Patients will have comfortable vision with good fusion and stereo
Describe how the response and stimulus AC/A ratios change with age.
Both AC/As rise rapidly in early presbyopia a lot of ciliary muscle demand generates a lot of accommodative innervation for only a little bit of accommodative response
The response AC/A rises modestly with age
The stimulus AC/A is unchanged by age, up to presbyopia
• Can’t measure AC/A in absolute presbyopes
Presbyopia
But all the accommodative efforts will generate synkinetically a lot of accommodative vergence Small amount of accommodation for A LOT of convergence
Define the CA/C ratio.
The CA/C ratio is the ratio of convergence accommodation (CA) per unit of convergence (C)
o ‘Convergence’ in this case means only fusional vergence
List the average CA/C ratio in young adults.
Average = 1/12 in young adults
o 1D for every 12Δ of change in convergence
Describe how the CA/C ratio changes with age.
The CA/C ratio is highly age-dependent, like the amplitude of accommodation
o It drops to near zero at age 40
The CA/C ratio is NOT often tested in clinical practice
Identify each of the components of the dual interaction diagram of
accommodation and vergence.
Accommodation and vergence mutually innervate each other without dual interaction the 2 systems do NOT work together
Dual interaction reduces innervation loads on BA and DV enables better vision
o Tonic and proximal would REDUCE the AR and CR loads, leaving less work for dual interaction
Describe, in terms of “increase”, “decrease”, or “no change”, how normal near
tonic adaptation affects blur accommodation innervation, accommodative lag, fusional vergence innervation, and fixation disparity.
Near tonic adaptation
DECREASES blur accommodation innervation
NO CHANGE accommodative lag
DECREASES fusional vergence innervation
DECREASES fixation disparity.
Select the posture of normal convergence with respect to a 6M fixation target
(small eso FD, small exo FD, or aligned).
Alligned
Select the posture of normal convergence with respect to a 40cm fixation target
(small eso FD, small exo FD, or aligned).
Small EXO
A normal observer has a slight exo fixation disparity in normal near vision.
Describe the effect of adding base-out prism before both eyes to the fixation disparity.
Increase the amount of Crossed fixation Disparity and stimmulate convergence
A normal observer has a slight exo fixation disparity in near vision. Describe the effect of adding minus sphere lenses before both eyes on the fixation disparity.
Minus Stimulates ACC responce and produces Positive fusional vergence
Move the posture to Over convergence / stimulate Neg fixation disparity
A patient’s reflex accommodation innervation is 2.5D and his AC/A ratio is 5/1. Calculate the amount of accommodative vergence innervation.
A patient’s total accommodation innervation is 3D. The tonic accommodation
innervation is zero. His disparity vergence innervation is 8∆ and the CA/C ratio is
1/10. Calculate the amount of blur accommodation innervation. (hint: the dual
interaction diagram can help you solve this problem)
List the components of the dual interaction model of accommodation and
vergence that are not included in the Maddox model of vergence.
ONLY RELEX ACC was recognised
o Tonic
o Accommodative
o Fusional
o Proximal
o Has no concepts for transient versus sustained innervations
o Tonic adaptation effects were NOT considered significant
o Convergence-induced accommodation was not in the Maddox model
o Multiple sources of accommodative innervation were not in the Maddox model
Describe the roles of the cerebral cortex in the control of accommodation and vergence.
Coarse disparity neurons calculate transient vergence stimuli
Fine disparity neurons calculate sustained vergence stimuli
o Coarse and fine disparity vergence neurons travel down from visual cortex to the brainstem -
o supraoptic area (this area has a lot to do with accommodation/convergence)
Perception of blur for voluntary vergence is processed here
Describe the role of parietal cortex in accommodation and vergence
• Computes perceived distance for spatiotopic responses
o For where you perceive things relative to your body, and for visually guided movements
• Switches reflex attention to targets
o Driven by loud sounds or rapid motions of large objects in peripheral vision
Generates proximal responses
Electrical stimulation initiates the near triad
Describe the role of frontal cortex in accommodation and vergence.
• Voluntarily select static or moving stimuli for spatiotopic vergence jumps
List the roles of the cerebellum in horizontal vergence control.
- Generates pulse (transient) and step (sustained) for jumps which are sent to SOA
- Adjusts vergence gain for best alignment of the eyes
- Mediates vergence adaptation
- Cerebellum assembles the signals that move the eyes according to Hering’s law
Describe the roles of the neural cells in the Supraoptic area of the brainstem in
accommodation and vergence.
• Cell activity is only correlated with accommodation & vergence
• Convergence vs. divergence cells
o Burst cells: (“transient burst neurons”)
fire briskly during the transient phase of accommodation and vergence – not action during sustained accommodation & vergence
o Tonic cells: relates closely to sustained accommodation & vergence
o Burst-tonic cells: adds up burst and tonic innervations
o More convergence cells than divergence
cells
• SOA cells project to the EWN and 3rd & 6th nerve
requires more energy
• SOA cells generate Hering’s law dysjugate
nuclei innervation
cyclopean eye
List the target nuclei receiving supraoptic innervation.
• SOA cells project to the EWN and 3rd & 6th nerve Nuclea
List the average value of the vertical vergence resting state (i.e., phoria).
Vertical TV is usually zero (ortho)
List the range of normal vertical vergence.
Normal values: +/-3Δ from ortho for smooth vergence
o Range of adaptation is less than horizontal
Compare and contrast the cybernetic control of vertical vergence to horizontal vergence
NO accommodative or proximal influence these are horizontal influences
o Vertical vergence is a product of vertical disparity
Vertical vergence is controlled by psychooptic reflex attention NO voluntary influence
List the accommodation and vergence mechanisms which malfunction, causing
“convergence insufficiency” and “convergence excess”.
Convergence Insufficiency (CI)
• Synopsis – weak convergence to near
o Differential Dx: pseudoCIs also have AI
• Pathophysiology:
Receded NPC – low total vergence innervation Low AC/A ratio, which causes:
- Weak transient and sustained accommodative vergence
• Must generate PFV at near for long periods of time and when breaks down it causes diplopia
High load on near + FV with high exo FD
Need a lot of crossed retinal disparity= a lot of PFV
2. Weak positive vergence adaptation mechanism (many CIs), which causes:
o Very slow or nonexistent vergence adaptation
o High sustained near load on positive FV with high exo FD Patients cannot maintain alignment at near
3. If TV adaptation is weak, it compounds the effects of a low AC/A on sustained near vision
4. Relative near accommodative lead from high +CA
Convergence Excess
Synopsis – excessive accommodative convergence innervation at near Pathophysiology:
o High AC/A ratio (>>6/1)
Excessive accommodative vergence at near due to high AC/A
Negative FV compensates for high accommodative vergence
Eso FD accompanies negative FV Negative fusional vergence at near is not normal
• Causes an accommodative lag
- Relatively large near accommodative lag from -CA
- Weak TA adaptation in many CEs can NOT adjust TA efficiently to near vision so tend to stay far away
- Causes high sustained load on +BA
Large accommodative lag
o Causes excessive accommodative vergence
High BA x high AC/A = excess accommodative vergence
Distinguish “overt” attention from “covert” attention.
Most saccades are led by a voluntary shift of overt attention
List the types of attention that initiate saccades.
- Voluntary saccades
- Reflex saccades
- Spontaneous micro saccades during fixation • NOT driven by stimuli or attention!!
- Saccade-Like movements
No attentional control
Attentional effect depends on the stimulus, like watching Saccade Stimuli
• Fast phase of vestibular nystagmus
• Fast phase of optokinetic nystagmus
List the average latency of saccades.
Reflex and voluntary latencies: 200 msec +/- 50 msec
o Express latency: 100 msec latency
Distinguish express, predictive, and voluntary saccades from each other.
Voluntary saccades
• Most saccades are led by a voluntary shift of overt attention
Types:
o Visual search
o Reading eye movements
o Scan pathes saccades complex eye movement mediated by brain remembrance of previous
o Movements during REM sleep
Express saccades
• The current fixation target is turned OFF when the new target is presented→ shortens saccade latency
• Usually when you shift attention it takes some time to disengage your attention from the original stimulus to the new
Predictive (anticipatory) saccades
• Attention and eye movement is voluntarily directed to a known location at or before target appearance make educated guess about when target will appear based on past experience
o Will find NO latency with this type of saccade if you can anticipate accurately
List two types of involuntary eye movement that contain periods of motion that
are as fast as saccades.
- Fast phase of vestibular nystagmus
- Fast phase of optokinetic nystagmus
Compare the role of saccades to the role of head movements in shifting gaze
direction.
Voluntary and reflex saccades are stimulated by target direction “error”
Define saccade stimulus in terms of oculocentric direction.
Oculocentric error= nonzero oculocentric target direction
• Threshold error=15 minarc
Monocular cue
Define saccade stimulus in terms of egocentric direction.
Egocentric error=egocentric direction-registered gaze
• Minimum error is 15 minarc
• Targets are not on the foveas eccentricity serves as an error signal
o When target visual egocentric direction ≠ egocentric gaze direction, you have a stimulus for a saccade
Select the type of saccade system error, oculocentric or egocentric, that initiates
saccades to unseen sounds
• Error computation for nonvisual targets:
o e.g. sounds, tactile targets, remembered targets
o Egocentric keeps spatial location for all of the senses
o Egocentric error=egocentric direction-registered gaze
• Threshold error= 3° gaze error
EGOCENTRIC
Identify the threshold error (in degrees) for stimulating saccades when there are
visual targets.
Egocentric error=egocentric direction-registered gaze
• Threshold error= 3° gaze error
.Identify the threshold error for stimulating saccades when there are no visual targets.
Threshold error=15 minarc
Distinguish “sampled-data” eye movement control from “continuous” eye movement control
“Sample data control” means that vision intermittently samples error to check whether the eye is off target
• Saccades are processed at a conscious level and is only done intermittently
Continious - Acc feedback system
Identify the type of control - feedback or feedforward - used in saccades.
Saccades are feedback controlled
o Saccades are repeated until the target image is on the fovea
o Usually one saccade is enough to foveate
o Corrective saccades are additional attempts to fovea the initial saccade image when the initial saccade is
inaccurate
Define “corrective saccade”.
o Corrective saccades are additional attempts to fovea the initial saccade image when the initial saccade is inaccurate
Define saccadic neural gain.
Neural Gain= saccade INNERVATION/ error
Define saccadic response gain.
Response Gain= saccade MOVEMENT/error
List two factors that cause a normally-sighted observer to make more frequent
corrective saccades.
Inaccuracy is usually LESS than 10% not as accurate as sustained convergence
UNDERSHOOTS occur for LARGE saccades and OVERSHOOTS for SMALL saccades
Fatigue and age reduce accuracy
Define “ballistic” eye movements.
Once started cant be stopped
Define “saccade trajectory”.
A trajectory is the path of the line of sign through 3D space
Contrast the roles of the “pulse” and “step” innervations in saccades
Pulse Innervation
o Strong but brief neural innervation that rapidly moves the eye, and determines saccade velocity “gets you there”
o Pulse innervation determines saccade VELOCITY Pulse overcomes orbital resistance to move the eye
Step Innervation
o A lesser but steady innervation which holds the eye in position after a saccade o Step innervation alone would move the eye slowly
• Too weak to move the eye rapidly
o Neurologically, step innervation is usually a fixed percentage of the pulse innervation
Identify the reason that the pulse innervation in a given saccade is stronger than
the step innervation in that same saccade.
Pulse innervation determines saccade VELOCITY Pulse overcomes orbital resistance to move the eye
overecome inertia
Identify the highest velocity attained by saccadic eye movements
The fastest saccade ≈ 700 ̊/sec ~ 10x faster than the fastest convergence movement
Average movement duration~50ms (1/20 of a second)
Describe how saccade duration relates to saccade size.
Larger saccades take longer.
Average movement duration~50ms
List a naturally occurring anatomical change in the normal oculomotor system
that demands saccadic gain adaptation in order to maintain accuracy.
Normal aging: more innervation may be needed to make the same eye movement because of changes in the orbital contents
o Older people do NOT have inaccurate saccades because they get older have the same accuracy if they are healthy, but have a longer latency
o There is more orbital resistance with age, but the brain adapts so that the saccadic gain is correct to maintain accuracy
List the consequences to the patient if their oculomotor system does not adapt its
saccadic gain to a new pair of glasses.
Rule of thumb for magnification: 1.5% magnification per diopter o Ex: a pair of 5D lenses, there is a change of gain by 7.5%
More PLUS: HIGHER gain needed
More MINUS: LOWER gain needed
Consequences of incorrect gain:
o Habitual need for corrective saccades
- slows reading and other visual tasks
- Eye strain
Explain how saccadic gain adaptation to new anisometropic spectacles “violates”
Hering’s law of equal innervation
Motor aniseikonia caused by anisometropic spectacles demands
DIFFERENT ocular rotations for what should be a “conjugate” stimulus → this is done by a saccade and a positive corrective fusional vergence movement
• Saccadic system can learn to do PARTIAL UNEQUAL GAIN ADAPTATION violates Hering’s law
.List the roles of the oculomotor neurons, in the following areas of the brain, in saccade generation:
cerebral cortex
Cortical role: select targets and process stimuli
Posterior parietal cortex (PPC): calculates egocentric direction
Parietal Eye Fields (PEF): start REFLEX saccades
Frontal Eye Fields (FEF): initiates VOLUNTARY saccades & PREDICTIVE saccades
o Remember: this is the area of the brain that also initiates vergence jumps • Areas closely related to FEF:
o Supplemental eye fields (SEF): initiates complex sequences of saccades such as scan paths
o Dorsolateral prefrontal cortex (DLPC): initiates memory-guided saccades
o The connections of SEF and DLPC to other brain areas are like the FEFs
.List the roles of the oculomotor neurons, in the following areas of the brain, in
saccade generation: superior colliculus,
Superior colliculus (SC) **calculates where your eyes are and where you want to go(cyclopean)** Role: controls **gaze trajectory of a saccade** o **SN, PEF, and FEF inputs** end up in the SC o Gaze trajectory = eye + head o *Right SC sees left VF, left SC sees right VF*
Superficial: sensory input
Intermediate: sensorimotor
• Involved in saccadic movements
Deep: motor outputs
• Not eye movements, more for body movements Superficial layer inputs:
o A direct retinal input to the SC shows “retinotopic” mapping in the superficial layer
o Visual cortex also projects to the superficial layer with matching retinotopic mapping
Inputs:
• FEF and PEF project to the build-up layer
o The build-up layer represents the part of the visual field where the target of interest is
o This is a crude selection of the part of your visual field that will be the destination of your saccade
• SN projects to the fixation zones
o Where the foveal neurons are
o When the fixation zone is turned off, the burst layer is allowed to be active
o Cellular types:
• Fixation cells: activate while fixating;
0°=central fovea
• Buildup cells: represent intended target location
• Burst cells: send gaze shift command to brainstem
o Burst layers remains on as long as eyes are moving
o When the eye moves to the destination, the activity moves to the fixation zone
Distinguish the roles of the frontal eye fields and parietal cortex in the control of saccades
- Parietal Eye Fields (PEF): start REFLEX saccades
- Frontal Eye Fields (FEF): initiates VOLUNTARY saccades & PREDICTIVE saccades
Describe the “antisaccade” task.
The SN pathway to the SC acts as an on-off switch in the interaction between PEF and FEF
• Parkinson’s damages the SN and its inhibitory control
“antisaccade test”
- Have patient fixate on your nose
- Hold up your left and right and simultaneously
- Tell patient to look at your left hand as soon as I wave my right hand (or vice versa)
- Pt needs to employ voluntary control the moving hand will cause a reflex saccade that patient must turn off
- Parkinson’s patient will look at the moving hand → reflexive saccade overpowers the voluntary saccade
Select the regions of the brainstem that generate the pulse and step innervation
for vertical saccades.
Excitatory Burst Neurons (EBN)
• Vertical & Torsional: rostral interstitial nucleus of the MLF (riMLF) o Outputs: to each N3, N4 and inC
• Neural Integrator Neurons (NIN)
Vertical & torsional NINs:
• Located in the interstitial nucleus of Cajal (inC)
• Output sent to N3 and N4
Select the regions of the brainstem that generate the pulse and step innervation
for horizontal saccades.
Excitatory Burst Neurons (EBN)
Horizontal: paramedian pontine reticular formation (PPRF)
o Outputs: ipsilaterally to PAB/N6 and NPH, and contralaterally to N3 (via PAB & MLF)
Inhibitory Burst Neurons (IBN)
• Horizontal: nucleus paragigantocellularis dorsalis (NPG)
Neural Integrator Neurons (NIN)
Horizontal NINs
Located in the medial vestibular nucleus & nucleus propositus hypoglossi (VN &NPH)
Output sent to the ipsilateral parabducens and N6
Briefly describe the roles of the following oculomotor neurons in the production of saccade innervation: long-lead burst neurons, excitatory burst neurons, pause
neurons, inhibitory burst neurons, and neural integrator neurons.
Long-lead burst neurons
• Separates gaze shift into eye and head portions decides if you need to move your head, and if so, how much it needs to move
• Partitions spatial maps into horizontal, vertical and torsional vectors for the appropriate saccade muscle groups
• Converts spatial map eccentricity to saccadic pulse magnitude/innervation
o origin of the “main sequence” behavior of saccades
Excitatory burst neurons
Role: generate saccadic PULSE for AGONISTS
• Activity profile of EOMs= activity profile of EBN where muscular force begins
• All EBN starts at once to have the max excitatory effect for EOMs
Pause neurons
Role: synchronizing the EBNs for high speed pulse generation
Does NOT directly initiate activity that goes to muscle >regular muscular energy shuts down the EBNs when the saccade is done
• Inhibitory neuron When it is turned on, the saccade is paused. When it is turned off, the saccade is allowed to happen
Inhibitory burst neurons
Role: inhibit antagonist EOMs and promotes saccade completion
Neural integrator neurons
Role: generating the saccadic step
• Helps generate steady fixation after the saccade is done
• Steps are smaller signals than pulse associated with it
o They receive input from the LLBNs or EBNs on the SAME SIDE
Identify, in eye movement recordings, a pulseless saccade, a glissadic
undershoot, a glissadic overshoot, and a multi-step saccade.
Define the stimulus to smooth pursuit eye movement.
The observer must perceive motion to generate smooth pursuit
Voluntary attention chooses the pursuit target
o However, pursuit movement cannot occur purely by volition
o Pursuit is a psychooptic
List the latency and the maximum velocity of smooth pursuit eye movements in the average normal observer.
Maximum velocity ≈ 70 ̊/sec 1/10 velocity of saccade
Latency = 100 msec
About half of a voluntary saccade
• Short latency because no need to shift attention in smooth pursuit already fixating on the target they want to pursue
• Latency is only in the oculomotor calculation, not in attention shifting
Select the type of attention that controls smooth pursuit movements
Voluntary attention chooses the pursuit target
o However, pursuit movement cannot occur purely by volition o Pursuit is a psychooptic reflex not reflexive
Select whether smooth pursuit is controlled continuously or by sampled-data.
Continuous feedback control
List the average gains of smooth pursuit for target motions which are
unpredictable and for those which are predictable
Gain ≈ 0.9 for brief pursuit, perhaps 1.0 if > 1sec duration
o When pursing, the eye is rotating at 90% of the velocity of the target (0.9 gain)
o The target will eventually be off the fovea, so you’d have to perform a saccadic eye movement to put it
back onto the fovea so you can pursue it again retinal image slip
Prediction:
• Creates zero-error pursuit, if motion is predictable (gain = 1.0)
Describe the two types of error signal that can drive smooth pursuit
1) Difference between perceived target velocity and eye’s rotational velocity (egocentric)
o Brain perceives motion of target compared to self possibly from auditory or proprioceptive stimuli
o Not very effective method used by brain
2) Retinal image slip (oculocentric)
o Target slides across fovea away from the center if target is moving faster than the eye is rotating
o Velocity of retinal movement is the stimulus for smooth pursuit to keep image on retina
Identify that property of smooth pursuit affected by prediction.
In pursuit, the target’s velocity is predictable
List the two properties of normal pursuit that can change pursuit gain.
New spectacles and old age change pursuit innervation demands for the same reasons as in saccade adaptation need to adjust pursuit gain as you AGE
List two factors in normals that reduce pursuit gain.
Fixation target retinal eccentricity
Fatigue,
and old age
all REDUCE pursuit gain
Describe the roles of areas MT, MST, FEF, DLPN, NRTP, the cerebellum, inC,
and NPH in the control of smooth pursuit eye movement.
• Afferent pathway: retina→LGN→visual cortex
- Midtemporal cortex (MT): calculates target retinal motion
- Midsuperior temporal cortex (MST) - Calculates target egocentric motion - respect to you
• Posterior parietal cortex (PPC): drives attention to a moving target by selecting the target in MT/MST
Projects to the FEF (it tells the FEF what target is been selected for pursuit)
• Frontal eye fields (FEF): predicts target motion
• Dorsolateral pontine nucleus (DLPN): calculates the HORIZONTAL vector of target velocity sends to cerebellum
• Nucleus reticularis tegmentum ponti (NRTP): calculates the VERTICAL vector of target velocity sends info to
cerebellum
• Cerebellum (CB):
o Computes INTENDED eye velocity Computes for both horizontal and vertical based on info from the DLPN and NRTP
o Adapts pursuit gain
o Direct computation pathway for pursuit no cerebellum=no pursuit
• VN (vestibular nucleus)/NPH (nucleus prepositus hypoglossi): converts intended HORIZONTAL eye velocity to
changing position innervation passed on to the oculomotor nuclei
• inC (interstitial nuclei of Cajal): converts intended VERTICAL eye velocity to changing position innervation
passed on to the oculomotor nuclei
Select the type of eye movement that typically replaces smooth pursuit when it fails
Reduced pursuit gain is revealed by “catch-up saccades” which replace the defective pursuit, and are often visible by direct observation
List two binocular anomalies known to reduce pursuit gain.
Amblyopia
Poor vision lowers motion sensitivity: low gain will see more catch-up saccades
Infantile (“congenital”) Esotropia
o Background information
• Onset in 1st 6 months
• Latent nystagmus - Only appears if the patient is monocular
Disease induced persuit anomalies
• Cerebellar disease and Alzheimer’s disease also reduce pursuit gain (you will see more catch-up saccades)
• Alcohol and barbiturates reduce pursuit gain
o Pursuits are used in road-side sobriety testing
Define, in a general sense, the stimulus for vestibular eye movement.
Vestibular-ocular reflex (VOR)
o Eye movement designed to maintain fixation and visual contrast during transient or oscillatory head movement
o Happen at almost every moment of the day
List the latencies of the rotational and translational VOR.
Rotation VOR
The latency of the rotational VOR = 16 msec shortest of all eye movements
Translation VOR
Latency = 30 msec 2x slower than rotational VOR
Gain = 1.0
Sort the following eye movement list in the order of shortest latency to longest latency: translational VOR, rotational VOR, saccades, smooth pursuit, accommodation, and vergence.
- Rotational VOR
- Ttransitional VOR
- Saccades
- Smooth persuit
- Accomodation
- Vergence
Compare the rotational, translational, and counterrolling VORs in terms of the type of head movement that stimulates them, their gains, and the vestibular mechanisms that drive them.
Rotational:
Nodding (pitch) - VERTICAL eye rotation to compensate for head movement Gain = 1.0
Turn (yaw) - Causes HORIZONTAL eye rotation - Gain = 1.0
Tilt (roll) Causes TORSIONAL eye rotation Gain = 0.5
Endolymph flow direction causes augmentation or inhibition of the sustained rate for agonist or antagonist muscular effects respectively
Anterior & posterior canals: flow away from the ampulla causes excitation • Flow towards the ampulla causes inhibition
Lateral canal: flow toward the ampulla causes excitation • Flow away cause inhibition
Compare the rotational, translational, and counterrolling VORs in terms of the type of head movement that stimulates them, their gains, and the vestibular mechanisms that drive them.
The Translational VOR
• Stimulus= any head motion that is not rotational
o Heave (side-to-side) - moving the head for motion parallax
horizontal
o Bob (up and down)- when walking or running vertical
Probably the MOST COMMON head translation
o Surge (fore-and-aft) An uncommon VOR Horizontal
Anatomical basis – Otolith organs
o Utricles sense HORIZONTAL translations in any direction (heave, surge, and intermediate directions)
o Saccules sense VERTICAL translation (bob) and horizontal surge
Compare the rotational, translational, and counterrolling VORs in terms of the type of
head movement that stimulates them, their gains, and the vestibular mechanisms
that drive them.
The Counterrolling VOR
Stimulus= static head tilt (no motion)
o Ex. your head is tilted to one side, but you are not rotating your head This is the only VOR NOT stimulated by motion
o The semicircular canals are not involved
o Gravity stimulates the Utricular hair cells Very weak signal and doesn’t last too long Eye movement components:
WEAK cyclorotation opposite the head
Ex: If you tilt your head to the left, there is a small dextrotorsion that rotates the eyes to the right
Static torsional gain = 0.1 (a vestigial response)
High threshold
Unequal vertical rotation – depending on target nearness
The vertical movement components underpins the Bielchowsky head tilt test
Clinical test in which you passively roll the patient’s head and observe the counterroll of the eyes
Can pick up on SO paralysis
Match semicircular canal type (anterior, posterior, lateral) to the agonist innervation they generate (elevation, depression, horizontal).
Anterior Canal
• Stimulated by head nod with chin DOWN innervate elevation agonists
Posterior Canal
• Stimulated by head nod with chin UP innervate depression agonists
Lateral (horizontal) Canal
• Each lateral stimulated by head-turn to the SAME side
Each lateral is inhibited by head-turn to the OPPOSITE side
Innervation for “contraversional” agonists
NOT stimulated by head tilt
Right Tilt
Right anterior stimulated & left posterior inhibited and vice versa Vertical effects cancel out
Levotorsion agonists innervated
Left Tilt
Right anterior inhibited & left posterior stimulated and vice versa Vertical effects cancel out
Dextrotorsion agonists innervated
Describe how the three semicircular canals of the left vestibule are coupled with the three semicircular canals of the right vestibule for agonist / antagonist function.
The interconnected vestibular nuclei treat innervation from the 6 total canals as 3 excitation/inhibition pairs:
o Left and right laterals
o Left anterior and right posterior
o Right anterior and left posterior
Define Flouren’s Law.
Flouren’s law: _stimulation of a single semicircular canal generates movement in the plane of that cana_l
o The movement is a VOR for a brief stimulus, or nystagmus for prolonged stimulated
Describe the type of nystagmus, in terms of horizontal motion, vertical motion, and
torsional motion, that would be caused by a lesion of each semicircular canal when the patient is attempting to look straight ahead.
Damage in a single canal** causes an o**pposite direction of movement as stimulation,** but in the same
plane imbalance shows rotation in the canal
EX: damage to the right lateral semicircular canal would cause the left semicircular canal to **push the eyes to the right while the left canal is unopposed
Identify the type of control (feedforward or feedback) that drives the VOR
Continuous feed forward control
o brain does not have feedback processing but instead finetunes its gain to ensure accuracy VOR needs to be efficient
Describe the role of “velocity storage” neurons in vestibular eye movements.
The key to effective sustained vestibular nystagmus is innervation persistence (velocity storage)
o Semicircular canals drive vestibular nystagmus
• Vestibule output lasts ~6 seconds after the start of head rotation, because of endolymph inertia
• The vestibular nucleus (VN) extends “vestibular” innervation to 15 seconds by way of a neural process called
“velocity storage”
List two causes of rapid VOR gain change that are not gain adaptation.
VOR gain can be quickly changed when needed
o Convergence induces HIGHER gain
o Voluntary gaze change turns off the VOR
o VOR gain needs to be higher during NEAR fixation than distance fixation
Identify a natural cause of vestibular gain adaptation.
A natural VOR adaptation stimulus is the increased orbital friction caused by the effects of aging
Describe how spectacle-induced vestibular gain adaptation is similar to spectacle induced saccade adaptation, and how it is different.
New spectacle corrections demand VOR adaptation
o PLUS lenses INCREASE the motor error as in voluntary movements opposite for minus
o Unlike voluntary movements, there is NO VISUAL SENSORY ERROR in the VOR because the vestibules
don’t “see” optical space
More of a challenge for VOR adaptation compared to saccade and pursuit adaptation in the same glasses
o The VOR must then adapt to all of the increased motor error caused by spectacle magnification on its own!
Recall that voluntary movements adapt to the difference between the sensory and motor errors
o Patients may experience a little vertigo and even nausea until they adapt VOR gain to their new glasses
o Partial adaptation to anisometropic spectacles can also occur
Define VOR habituation.
Habituation is a REDUCTION of VOR gain that occurs over repeated vestibular stimulation in the DARK
o Eyes will make VOR movements even in the dark because it is not stimulated by visual input
o VOR is only a thing that can move eyes in a predictable way in the dark
The practical significance of habituation is that tests of VOR gain in the dark
.Describe a behavior that would stimulate normal vestibular nystagmus.
Vestibular nystagmus is a “jerk” nystagmus
There is a fast phase & a slow phase
Fast phase – a saccade-like “jerk” to a new direction of gaze
• Innervated by saccadic EBNs and IBNs
Slow phase – a slow rotation that stabilizes the retinal image
- Innervated by vestibular neurons – same as VOR
- The key to effective sustained vestibular nystagmus is innervation persistence (velocity storage)
o Semicircular canals drive vestibular nystagmus
List the two types of voluntary eye movement that have similar velocities as the slow and fast phases of normal vestibular nystagmus.
Saccade and Persuit
List the four types of vestibular nucleus cells.
Head Velocity Cells
Eye Velocity Cells
Eye Position Cells
Vestibular Pause Cells
List the roles of the four types of vestibular nucleus cells in controlling the VOR and
vestibular nystagmus.
Head Velocity Cells
These cells receive 8th nerve afferents
They convert the acceleration signal from the ear to a velocity signal tell the vestibular nucleus how fast the head is rotating in space
Eye Velocity Cells
Firing rate represents intended eye velocity
Eye velocity = head velocity x VOR gain
Calculates the needed velocity of the eyes to maintain fixation during head rotation
Eye Position Cells
These cells generate the changing innervation which will move the eye
Eye position = ∫ (eye velocity) dt
The velocity-to- position conversion happens in the MVN (medial vestibular nucleus) & NPH (nucleus propositus hypoglossi)
Vestibular Pause Cells
Receive info from the cortex and superior colliculus
Inhibit the VOR during voluntary gaze shifts
Identify the purpose of each connection of the vestibular nucleus with each of the following regions of the brain: neocortex, cerebellum, paramedian pontine reticular formation, and the oculomotor nuclei.
VN→ oculomotor nuclei: innervates the VOR
VN→ cerebellum→ VN: adjusts VOR gain
Cerebellum→ VN:)OKN sensory signal stimulates VN to generate nystagmus
VN→ PPRF: triggers nystagmus quick phases (triggers EBNs to generate the quick phase of nystagmus)
VN→ thalamus→ vestibular cortex: awareness of body orientation, posture, balance
PPC→ VN: VOR suppression during voluntary gaze shifts
There are also nonvisual connections (ex. spinal reflexes for balance)
o Typically a 3-5 neuron arc
Explain how to test for labyrinthine damage using the Barany and caloric tests
The Barany Test
- The patient sits in a rotating chair
- The patient’s head is positioned to isolate a pair of semicircular canals
- The patient is then rotated in darkness Use darkness so that vision doesn’t interfere with the vestibular nucleus
- Oscillatory rotation for VOR
2. Prolonged one-way rotation for nystagmus
- Oscillatory rotation for VOR
- Rotation can be accurately calibrated for Both rotation directions are tested quantitative analysis
- Objective eye movement recording is used
The Caloric Test
- The patient sits in a stationary chair
- Patient’s head is tipped back 60 degrees so that lateral canals are vertical
- Warm or cold water is inserted in one ear ears can be individually tested
- Endolymph convection currents stimulate the lateral canal
- “COWS” predicts the nystagmus direction “Cold opposite, warm same”
This test only assesses lateral canal function Cold and warm water don’t affect the vertical canals because they are too far away from the auditory meatus
Objective eye movement recording is usually used
Allows us to test each ear individually
List how eye movements and symptoms differ between patients having unilateral
labyrinthine damage and bilateral labyrinthine damage.
If vestibular, is the case peripheral or central?
o Ex: is it caused by an ear infection or brain disease?
- Peripheral is usually horizontal + torsional
- Fixation effort and a good fixation stimulus often suppress peripheral nystagmus
- central is often unidimensional and nystagnus not supperesed
o OKN can directly test vestibular nystagmus generation
If the vestibular nucleus is damaged, it won’t respond to OKN nystagmus motion signals
• If the nystagmus cause is peripheral, what is its direction?
o The nystagmus direction indicates which ear is defective
Bilateral labyrinthine disease & Nystagmus
- There is no nystagmus because there is no rotation sensing or vestibular tonus to affect the EOMs
- Loss of VOR
- Degraded visual acuity and oscillopsia occur when the head is in motion
Unilateral Labyrinthine Disease & Nystagmus
- Most unilateral cases affect all 3 canals on one side
- Horizontal nystagmus is present when the head is stationary because left/right tonicity is unbalanced
Fast phase is away from the damaged ear
The vertical movement effects of the anterior and posterior canals cancel out – NO vertical nystagmus
The VOR is also reduced
Continuous oscillopsia and vertigo are experienced
Describe how the oculomotor system attempts to compensate for the deleterious
effects of nystagmus caused by unilateral vestibular disease.
Benign paroxysmal positional vertigo
Benign paroxysmal positional vertigo
o A common cause of vestibular jerk nystagmus in older patients age-related degeneration
o Exceptional because it is caused by damage in a single semicircular canal (the posterior)
Differentiate passive OKN from active OKN in terms of the innervations for each.
Active OKN
- voluntary movement
- Slow phase = smooth pursuit
- Fast phase = saccade
Therefore, active OKN has pursuit and saccade dynamics
The pursuit responds to ALL SIZES of moving objects (Ex: a moving train or line of moving ants) Active OKN functions for a few seconds and then may be replaced by passive OKN for some stimuli
Passive OKN
Responds to LARGE moving objects or environmental motion
Watching a moving train
Watching scenery from a bus window
Many seconds of motion stimulation are needed to activate passive OKN
slow Passive OKN dominates the control of prolonged OKN
Passive OKN uses vestibular nystagmus neurons to create the nystagmus
Compare and contrast the stimuli for smooth pursuit versus OKN.
The pursuit responds to ALL SIZES of moving objects (Ex: a moving train or line of moving ants)
Active OKN functions for a few seconds and then may be replaced by passive OKN for some stimuli
Compare the control mechanisms of passive OKN versus active OKN.
Therefore, active OKN has pursuit and saccade dynamics
The pursuit responds to ALL SIZES of moving objects
Responds to LARGE moving objects or environmental motion
Passive OKN dominates the control of prolonged OKN
Passive OKN uses vestibular nystagmus neurons to create the nystagmus
Describe how vestibular nystagmus and OKN interact with each other during whole body rotation.
OKN also helps stimulate nystagmus during prolonged head rotation
o Vestibular innervation controls EARLY nystagmus during head rotation, but then decays
Remember: Any vestibular response is stimulated by acceleration of your head
o Vestibular innervation decay leads to retinal image motion begins optokinetic nystagmus
o Retinal image motion stimulates active and then passive OKN, which sustains the rotational nystagmus
Control of Passive OKN
REFLEX behavior passive OKN happens automatically and cannot be voluntarily created o Retinal image motion causes the nystagmus
Continuous feedforward control
Slow phase gain = 0.8
o Reduces retinal image speed enough so you can see clearly
Identify those neural pathway components involved in smooth pursuit, OKN, and vestibular nystagmus.
MT & MST create motion perception signals information received from magnocellular cells
o Remember: MT represents retinal image motion while MST represents egocentric motion
MT & MST project to the Nucleus of the Optic Tract (NOT) & Accessory Optic System (AOS) on the SAME side
o NOT and AOS are specific for nystagmus
NOT & AOS also receive direct vestigial crossed inputs directly from the retinas
NOT & AOS project to the DLPN and NRTP
o Rightward motion processed by MT & MST projects to NOT &A OS on the right side of the brainstem and then projects to the DLPN & NRTP → cerebellum …same pathway as smooth pursuit
Prolonged stimulation of the vestibular nucleus creates velocity storage innervation
Velocity storage innervation drives the nystagmus
Define OKAN.
Passive OKN is tested by way of OKAN
o Lights are extinguished after prolonged viewing
o Smooth pursuit stops immediately, but not passive OKN
Identify the stimulus conditions that activate levotorsion, dextrotorsion, and excyclovergence
Dynamic head tilt:
conjugate rotational VOR tilting you head towards one shoulder or another Remember: Innervation of the vertical canals & utricles (gain of 0.5)
Static head tilt:
conjugate counterrolling VOR
Remember: when your head is stationary, the semicircular canals are nonfunctional The utricles bend hair cells due to gravity and can then sense the tilt
Near cyclovergence
Eyes EX cyclorotate when looking at near
Synkinetic with HORIZONTAL vergence
Feedforward control Brain doesn’t check accuracy for this
Fusional cyclovergence
Stimulated by torsional binocular disparities (inaccurate cyclorotation)
process: Psychooptic reflex attention control
Continuous feedback control
List the ranges of fixation in supraduction, infraduction, adduction, and abduction.
Range of fixation: KNOW THIS
- Supraduction: 42 ̊ age related decrease in ability to look up
- Infraduction: 51 ̊
- Adduction: 57 ̊
- Abduction: 54 ̊
Describe the process for stimulating “endpoint nystagmus” in normals.
A small normal nystagmus when the eyes are at a limit of gaze
Sustained innervation does not last forever due to weakening & the eye drifts back
The person then makes a saccade back to the target → causes nystagmus o Drift towards the PPG due to neural integrator leak
Distinguish between the three types of eye movement occurring during normal “steady fixation” with respect to their speed, magnitude, and interocular conjugacy.
Tremor
High frequency: 30-100 Hz
Low amplitude: <30’’
Binocularity uncoordinated
o Eyes going in independent directions so not occurring from cyclopean innervation
Probably caused by muscle fiber action potentials
NOT a registered eye movement
Slow Drift
- 5 minarc/sec drift rate
- 1-2 per second about one 20/20 Snellen letter per second 1-5 minarc magnitudes
Binocularity uncoordinated
o Likely caused by oculomotor nuclei innervation instability/muscular response instability
• Probably the cause of the autokinetic effect
o Look at a dim light in a totally dark room. After looking at it for a while, the light starts to drift around (illusory)
• NOT a registered eye movement
Microsaccades
5 minarc average magnitude tiny
Can be as large as 25 minarc
Binocularly coordinated
o Supranuclear innervation origin
o Probable purpose: to prevent fixation target fading
ARE registered eye movements neurons are sending corollary discharge signal to the cerebral cortex to tell it that your eyes moved
- A demonstration of microsaccades
- o View the black dot for ten seconds
- o Change your view to the white dot
- o An afterimage of the grid moves with your microsaccade
Identify the type of nystagmus expected in alcohol and barbiturate intoxication.
Gaze- Evoked Nystagmus
The slow phase decelerates away from the fixation target and toward the PPG
Fast phase moves the eye back to the target
o The eye cannot maintain sustained innervation after a saccade sustained neurons fail (inC, NPH)
• Caused by abnormal neural integrator leakage
Distinguish between the symptoms “oscillopsia” and “vertigo”.
Vertigo is an illusion of self-motion damage to VN is telling your body you are rotating in space because the net difference between the 2 ear signals
Oscillopsia is an illusion of environmental motion
Describe how age relates to oscillopsia in nystagmus patients.
Acquired nystagmus causes oscillopsia and vertigo congenital nystagmus does NOT
o Nystagmus eye movement is registered in perception if it develops early (congenital)
o These patients with congenital nystagmus still have poorer acuity, but no oscillopsia/vertigo patients with symptoms probably have disease
Several factors reduce the impact of nystagmus on visual acuity:
Null position
A direction or distance of gaze where the nystagmus is reduced to a minimum
If you see a severe nystagmus, have the patient look in different directions of gaze and find where the nystagmus is smallest
You could Rx BO prism to keep eyes always converged to promote stability
nystagmus may allow patient to see better
Head tilt improves some cases Slow-phase fixation
Define the null position of nystagmus.
Null position
A direction or distance of gaze where the nystagmus is reduced to a minimum
If you see a severe nystagmus, have the patient look in different directions of gaze and find where the nystagmus is smallest
You could Rx BO prism to keep eyes always converged to promote stability
nystagmus may allow patient to see better
Identify the impact of looking in the null position on a patient’s visual acuity and oscillopsia.
Nystagmus can reduce visual acuity due to retinal image motion
VA and Oscillopcia reduced in Null Position
Acquired nystagmus causes oscillopsia and vertigo congenital nystagmus does NOT
Define “slow phase fixation” in nystagmus, and how it affects the patient’s vision
.Given videos of patients’ eye movements and a description of what the patients were watching, identify the following eye movement abnormalities: oculomotor apraxia, gaze palsy, slow saccades, hypermetric saccades, hypometric saccades, internuclear ophthalmoplegia, macrosaccadic oscillation, pendular nystagmus, and jerk nystagmus.
internuclear ophthalmoplegia
macrosaccadic oscillation
ARE registered eye movements neurons are sending corollary discharge signal to the cerebral cortex to tell it that your eyes moved
Binocularly coordinated
- o Supranuclear innervation origin
- o Probable purpose: to prevent fixation target fading
pendular nystagmus
- Eye movement waveform Congenital
- EARLY visual loss impairs oculomotor stability
- The nystagmus is mostly HORIZONTAL
- Other examples: rod monochromatism, albinism,
- Acquired Caused by inherited degeneration or acquired disease
- Can be any combination of HORIZONTAL, VERTICAL and/or TORSIONAL movements
- Present in Pelizaeus- Merzbacher Disease
jerk nystagmus.
The slow phase accelerates AWAY from the fixation target
o Accurately fixate for some time and then drift away until a saccade is made to regain fixations
• Gets worse by any effort to fixate
o Best thing to do is gaze passively
Opsoclonus
Rapid and variable amplitude saccadic oscillations WITHOUT an intervening refractory period
- looks like fast pendular nystagmus
- o Eyes NEVER stop moving at saccadic speed followed by saccade continuously
- o EBNs are continuously stimulated
- Associated with encephalitis, toxicity, neoplasia, especially in neonates
- Probably caused by cerebellar fastigial nucleus damage in adults
List the percentages of total refractive power of the unaccommodated eye provided
by the cornea and the lens.
Cornea
o 75% of the eye’s focal power in far vision is from the cornea o Unchanging power
• Lens
o 25% of the eye’s refractive power in far vision o INCREASES power for near vision
Describe the roles of parasympathetic and sympathetic autonomic innervation on ciliary muscle function.
Parasympathetic Innervation
o Drives agonist ciliary muscle action for near accommodation
o All forms of accommodative innervation (e.g. blur, proximal, tonic) produce parasympathetic innervation
o Far accommodation is achieved by:
- Relaxation of parasympathetic innervation
- Elastic tissues pulling the CB backward:
- • Posterior zonule stretched in near accommodation
• Elastic tendon of the ciliary muscle stretched in accommodation
- near: activate parasympathetic innervation
- far: relax parasympathetic innervation
• Sympathetic Innervation
o There are NO β1 (agonist) receptors in CM
o Β2 receptors inhibit parasympathetic innervation
Acts on the same muscle fibers as the parasympathetic innervation
This sympathetic innervation changes very SLOWLY: 40 seconds not used dynamically to change accommodation
This innervation is thought to be an aid in restoring far accommodation
Identify which ciliary muscle fibers, longitudinal or circular, not only change lens
shape during near accommodation, but also move the lens forward.
Longitudional Fibers
Primary action: pull the back of the ciliary body towards the scleral spur
o Moves CB zonule attachment towards the lens
• Secondary action: opening the trabecular meshwork
Describe the relative contraction speeds of extraocular striated muscle, gut smooth muscle, and ciliary smooth muscle.
All CM fibers work together as a single functional unit
Ciliary muscle is smooth (nonstriated) muscle
Nevertheless, ciliary muscle resembles striated muscle in several respects:
o Most myofibrils are parallel - Provide unidirectional force
Unlike gut smooth muscle fibers which are omnidirectional
o A large number of mitochondria supports fatigue resistance
Identify the mechanical changes of ciliary muscle tension, posterior zonule tension, anterior zonule tension, lens capsule tension, anterior radius of curvature, posterior radius of curvature, and lens thickness when accommodating to near vision according to the “relaxed tension” theory of accommodation espoused by Young, Helmholtz, Gullstrand, and Fincham.
Events in accommodation to near:
o Ciliary muscle moves anteriorly and toward the lens equator (forward motion due to longitudinal fibers) o PPZ (pars plana zonules) & CM tendon are stretched
o AZ force is reduced
o Lens capsule force is reduced ”relaxed tension”
o Lens rounds out
- *Anterior** surface moves forward and becomes more curved
- *Posterior** surface moves slightly back (mostly blocked by vitreous) and becomes more curved
Lens thickens
Equatorial diameter is reduced (accommodated lens = smaller diameter & thicker)
• Events in restoring accommodation to far:
o Ciliary muscle force is reduced
o The ciliary body is pulled backwards by elastic forces: CM tendonPPZ fibers
o AZ tension is increased
o Increased capsule force flattens the lens
Identify the effects of normal aging on ciliary muscle tendon elasticity, anterior
zonule elasticity, unaccommodated lens diameter, lens capsule elasticity, and lens
substance plasticity
An old lens has the same diameter as a young unaccommodated lens o A presbyopic lens is thicker than its younger counterpart
The “lens paradox”: a thicker lens is associated with hyperopic refractive shift
The paradox is explained by the loss of graded indices of refraction Layers of the lens falls apart making a uniform index of refraction
o The lens is much less plastic in old age
Does not change shape during attempted accommodation – even when the zonules are slack This is the main cause of presbyopia
Cilliary Muscle changes:
- Tissue changes reduce CB motility
- Loss of CM tendon elasticity replaced by collagen
- Increase of inelastic collagenous tissue in CM
Describe the two theories on how the lens hardens in presbyopia.
Multifactorial theory
- Lens hardening biggest factor causing loss of accommodative power
- Capsule inflexibility
- Reduced ciliary body motility
- Probably closest theory to correct
Lens Hardening Theories
Donder’s theory – the lens hardens uniformly
Gulstrand’s theory – hardening begins in the nucleus and extends outwards with age
o Evidence favors Gulstrand’s theory of hardening
List the minimum amount of accommodation an accommodating intraocular lens
should generate in order to provide clear and comfortable near vision.
Any device should yield ≥5D amps of accommodation
o Half amp in reserve at 40 cm for comfort
o Amp of accom <5D yields prepresbyopia Sx in natural accommodation
Accomodating IOL’s
Single Lens Translations
o Tetraflex IOL and Crystalens IOL
o Lens more forward without shape change
Many nonmammalian vertebrates do this o Theoretical limit: 1.5D in man (not enough)
Dual Lens Translation o Synchrony IOL
o Galilean lens pair
o Front (+) lens moves forward
o Theoretical limit: 3D (not enough)
Alvarex Optical System
- o Turtle IOL
- o Two nonlinear lenses slide across each other to cause a net spherical focus change
- o Theoretical limit: 8D
List the primary, secondary, and tertiary actions of each of the six extraocular muscles, according to the classical interpretation of muscle mechanical action.
Distinguish a muscle’s “field of action” from its “primary action”.
Each muscle action is a vector of the line of action with respect to the center of rotation
A muscle’s actions are ordered by their relative amounts of vector force
- o Primary: strongest
- o Secondary: intermediate
- o Tertiary: weakest
• The relative strength of a muscle’s actions depends on the direction of gaze
Describe how the “field of action” concept is used to identify a paralyzed muscle.
Premise: a muscle’s weakness is most evident in its “field of action”: the direction of gaze where the muscle has only a horizontal or vertical primary agonist action (no secondary or tertiary actions)
o When you do the EOMs test, you are isolating each much as best as possible intentionally move the eyes into a direction of gaze where we will challenge the selected muscle without synergism help from other muscle
o Don’t look at torsional because too hard to see
Describe the locations of the rectus muscle fascia pulleys
Coronal section:
o The pulleys are thick collagen rings through which each muscle moves
o The pulleys are interconnected by collagen bands
o The pulleys are bands together comprise Tenon’s posterior capsule
o Elastin and smooth muscle in the nasal bands provide TENSION, keeping the ring/band structure taught
The pulley structure is halfway between the center of rotation and the posterior pole
Identify the three types of tissue found within extraocular muscle “fascia” pulleys
**Collagen bands
Elastin**
Smooth muscle
Define a “heterotopic” pulley.
EOM Pulley Pathophysiology
Pulley heterotopy
A pulley displaced from its proper position in the coronal place is heterotopic
o Inappropriate secondary and tertiary actions and strabismus
Identify the type of strabismus associated with horizontal rectus heterotopy.
Identify the type of strabismus associated with vertical rectus heterotopy.
Pulley anomalies tend to cause NONCOMITANT STRABISMUS
- *o Noncomitant strabismus:** the deviation changes with direction of gaze
- *o Comitant strabismus:** the deviation does NOT change with direction of gaze
Vertical rectus pulley heterotopy causes torsional noncomitancy that stimulates oblique paralysis
Horizontal rectus pulley hetertopy can induce changes of horizontal pulling force during elevation or depression
that can cause the A and V pattern
List the four types of extraocular muscle fiber.
Fiber types and function:
White: greatest force, but fatigue rapidly Important for saccadic velocity
Red twitch and tonic: provide lower but steady force More important for maintaining eye position + Control the pulleys
Intermediate: behavior between white and red types
Tonic: Important for steady eye position and pulleys
o ALL fiber types contribute to ALL types of eye movement
Identify which types of extraocular muscle fiber are associated with the global and
orbital layers of the extraocular muscles.
Global Layer
Singly innervated 3 types of twitch fibers
• Red: highly oxidative, fatigue resistant Holds pulleys in position
• White: minimally oxidative, fatigueable, very fast - saccadic pulse
• Intermediate
Multiply innervated tonic fibers
- Slower than twitch
- Smooth ongoing force No action potential
- Contain proprioceptive nerve endings
Orbital layer
Generating sustained force
Singly innervated red twitch fibers
Multiply innervated tonic fibers important for maintaining eye position and controlling pulleys
.Select the two types of EOM muscle fiber most important for rapid eye movement.
Select the two types of EOM muscle fiber most important for maintaining steady
fixation.
Rapid eye movement:
White & Intermediate
Steady fixation:
RED twitch & Tonic
.Differentiate the roles of the global and orbital layers of the extraocular muscles in ocular motility.
o Global layer inserts on the eye ROTATES the eye
o Orbital layer inserts on the pulley (does NOT attach to eye) do NOT directly rotate eye
.Define the “motor field” of an EOM twitch fiber
Motor Fields
• A “motor field” is the range of gaze positions linearly related to a motor unit’s innervation
• Motor field size ranges between 20 to 60 degrees
• Motor units have a range of thresholds:
o Low threshold neurons become active in antagonist directions
o High threshold neurons become active in agonist directions
Compare the ratio of muscle fibers to neuron in EOM muscle units to typical skeletal muscle units.
Motor unit: a motor neuron and its associated muscle fibers
o 10 muscle fibers/neuron in EOMs
(50 fibers/1 neuron in skeletal muscle)
Describe the presumed importance of proprioceptive fibers to the control of eye movement as opposed to registered gaze.
What the proprioceptors don’t do:
- o Adjust muscle force to varying loads
- o Register gaze direction
• What the proprioceptors might do:
- Long term oculomotor recalibration
- Feedback of saccade trajectory
.Explain how differences between extraocular muscle and skeletal muscle physiology make extraocular muscle relatively susceptible to the effects of some systemic muscle diseases like Myasthenia Gravis and relatively immune to the effects of the systemic muscle disease Duchenne’s Dystrophy.
Myasthenia Gravis
o Autoimmune disease that attacks acetylcholine receptors
o Poor eye position control with micro diplopia
WHY:
Unique embryonic-like acetylcholine receptors in tonic fibers are especially hard hit- more than twitch fibers
• This leads to loss of fine alignment control and pulley heterotopia High twitch firing rates (in saccadic pulse) are ill-sustained
Duchenne’s muscular dystrophy
Systemic muscle atrophy & X-linked recessive disease
The striated muscle protein “dystrophin” degenerates, starting in early childhood
The EOMs substitute “utrophin” for decaying dystrophin, which skeletal muscles CANNOT do
Slow saccades
Describe the behaviors of burst, burst-tonic, and tonic oculomotor nucleus neurons during saccadic eye movement.
- *Burs**t – most active in rapid movement
- *Tonic** – most active in steady gaze and slow movement
- Steady innervation and steady position*
- *Burst/tonic** – combination of burst and tonic activities
List the three ways in which the pupil can enhance vision.
• Controls retinal illumination
o MUCH FASTER than photoreceptor adaptation
• Constriction increases depth of focus in near response
o Assists accommodation Especially important in older people who are losing accommodative ability
• Constriction reduces peripheral aberrations for best acuity in photopic vision
Describe the roles of the sphincter and dilator in pupil function and their placement in the iris.
Parasympathetic Innervation sphincter
• Innervation is stimulus-contingent - light/nearness
• EWN pupil fibers are in the UPPER portion of the CN3 in the MIDBRAIN
• These pupil fibers then move to the MEDIAL side of CN3 in the CAVERNOUS SINUS
o Vascular anomalies in the Circle of Willis can affect the efferent pupillary fibers
• Pupil efferent synapse ciliary ganglion
o Out of the ciliary ganglion come short
posterior ciliary nerves→ innervate 20
sectors in the sphincter
Sympathetic innervationDilator
• Hypothalamic innervation (follows 1st preganglionic nerve) passes to the Ciliospinal center of Budge in cervical spinal cord
• 2nd preganglionic axons leave the spine, crossing over the lung apex to synapse on the superior cervical ganglion
o Damage here (due to lung infection, tumor, etc.) is the basis of HORNER’S SYNDROME→ ptosis, miosis, anhidrosis on side of lesion
• Postganglionic axons follow the carotid artery, ophthalmic nerve, and the long ciliary nerves to enter the eye and dilator
• Hypothalamus also sends INHIBITORY inputs to EWN
o Is necessary to inhibit the sphincter because the sphincter is STRONGER than the dilator
Identify the type of retinal ganglion cell - alpha, beta, or gamma - thought to be most important for pupil control.
gamma (konio) ganglion cells (melanin-containing ganglion cells) sends iris control signals to the pretectal nucleus
Describe the neural pathway which controls the pupillary light reflex.
• Both rods and cones serve vision and the pupil
• A subgroup of gamma (konio) ganglion cells (melanin-containing ganglion cells) sends iris control signals to the
pretectal nucleus
o Thin axons, small cell bodies, and long retinal circuits make for SLOW response
o Alpha and beta ganglion cells project to the LGN/cortex to serve vision
• Gamma cell axons partially decussate then symmetrically innervate each pretectal nucleus
• Pretectal cell axons bifurcate to symmetrically project to each EWN
• Consequence: direct and consensual responses are EQUAL
Describe the neuroanatomical pathway that controls the pupillary near response.
The Near-Reflex Afferent Pathway
• PEF and FEF cortical eye movement fields send cyclopean near response signals to the midbrain supraoptic areas
• Supraoptic innervation projects to the EWNs to activate both irises
• BOTTOM LINE ON AFFERENT PATHWAYS Any light or near stimulus, monocular or binocular, EQUALLY
innervates both irises!
o A sensory defect in EITHER EYE equally affects BOTH pupils
o Differential iris responses to the same stimulus must arise within the efferent pathways o For instance, anisocoria (unequal pupils) is an EFFERENT pupil anomaly
Identify the two oculomotor responses that usually accompany the pupillary near reflex
Lid Closure Response
• Neurologically equivalent to the near triad response (accommodation, convergence, miosis)
• Used on non-cooperative patients who won’t look at a near target
• Testing:
o Hold eyelids open with fingers
o Patient tries to close eyes
o Near response is triggered by the effort to close the eyes
Identify the type of control - feedback or feedforward - that drives the pupillary light reflex.
Feedback control regulates the pupil response to light
Pupil gain = pupil-induced retinal illuminance reduction / retinal stimulus luminance increase
.Identify the factor that causes the transient pupillary light reflex gain to be higher than the sustained pupillary light reflex gain.
Transient gain > sustained gain because of light adaptation → causes “pupillary escape”
Once illuminated, the pupil slowly starts to re-dilate even through the light stimulus is still present
Define “anisocoria”.
Define “hippus”.
Hippus → pupillary unrest
- o Random oscillations by autonomic noise
- o Higher rate in bright light
anisocoria (unequal pupil sizes)
- o 1/5 of pop has aniso >0.4mm
- o Size spontaneously varies
Diseased and pupil responce differ
Light Reflex and Gamma Ganglion Cells
• Gamma ganglion cells dominate the light reflex pupillary light reflex does not always respond to disease similarly to vision
- *o Leber’s optic neuropathy:**
- *Gamma cells minimally** affected while alpha and beta ganglion cells are severely damaged Light reflex is near normal despite severe visual impairment
o Retrobulbar optic neuritis
All ganglion cell types are damaged
Both vision and the pupil are impaired
