Basics of Eye Movement Flashcards

Question

Describe the meaning of boxes, circles, and arrows in eye movement cybernetic box diagrams.

Answer 1

**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

Answer 2

**“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**

Answer 3

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)

Answer 4

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

Answer 5

The advantage of feedback control is **accuracy**

Answer 6

The advantage of feedforward control is a **QUICK response -** Less thinking is involved

Answer 7

**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

Answer 8

“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**

Answer 9

“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

Answer 10

**ALL eye movements** follow Sherrington’s Law, regardless of type “when an agonist contracts, its antagonist relaxes” **reciprocal action**

Answer 11

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

Answer 12

**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

Answer 13

**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

Answer 14

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

Answer 15

**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

Answer 16

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

Answer 17

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**

Answer 18

Eyes would be able to Do Dextroversion On levoversion - LEFT eye would not Abduct Right to the left side as normal

Answer 19

**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**

Answer 20

**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

Answer 21

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**

Answer 22

• **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 r**eceiving EQUAL amounts of innervatio**n

Answer 23

Accommodation is the adjustment of ocular focus for the sake of **optimal visual acuity** and **contrast**

Answer 24

Vergence is the adjustment of ocular alignment for the sake of **stereoscopic acuity** o **Convergence:** inward turning (positive) o **Divergence**: outward turning (negative)

Answer 25

**Retinotopic**: innervations **stimulated by specific retinal image characteristics** (ex: blur and absolute disparity) **Spatiotopic:** **innervations stimulated by perceived distance** -- voluntary at a conscious level

Answer 26

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**

Answer 27

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)

Answer 28

**A retinotopic process** → process driven by **characteristics of the retinal image alone**/ **stimulated by retinal image blur** BA innervation is proportional to blur

Answer 29

**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**

Answer 30

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)

Answer 31

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

Answer 32

BA is poor in people with **macular disease or amblyopia** The gain of BA is low when you have poor vision

Answer 33

Proximal accommodation innervation (PA) is stimulated by **perceived nearness (not blur), so it is “spatiotopic”**

Answer 34

The primary role of PA is to **initiate large changes of accommodation** (and vergence)

Answer 35

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

Answer 36

Slitlamp evaluation

Answer 37

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

Answer 38

**Automatically generated steady innervation** that is NOT stimulated directly by vision (always there) **Purpose:** to r**educe the workload** on positive blur accommodation, and thereby **improving near visual acuity**

Answer 39

* **Static tonicity** – a baseline innervation * **Tonic adaptation** – adjusting to sustained demand

Answer 40

**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

Answer 41

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

Answer 42

Slight Lead

Answer 43

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

Answer 44

The eyes a**ccommodate EQUALLY** accommodation is cyclopean o The ciliary muscles receive the same cyclopean innervation from the **EW nuclei** o Accommodative innervation c**annot differ between the eyes in a healthy person, even if the ocular stimuli differ**

Answer 45

**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

Answer 46

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 ## Footnote **Sustained accommodation** innervation **maintains or slowly changes accommodation**

Answer 47

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

Answer 48

This innervation is generated by accommodative “**burst cells” in the brainstem** **Konio Cells** in Brainstem

Answer 49

**Blur accommodation** innervation dominates normal sustained accommodation when r**etinal 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

Answer 50

**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

Answer 51

Normal lags and leads create the sustained retinotopic blur that **stimulate sustained blur accommodation innervation**

Answer 52

**Longitudinal chromatic aberration between L, M, and S cones** Accommodation adjusts itself to eliminate **red or green fringe**s 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

Answer 53

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

Answer 54

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**

Answer 55

**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

Answer 56

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**

Answer 57

**Crossed disparity stimulates convergence** • Total convergence response is the sum of convergence innervations **Uncrossed disparity stimulates divergence**

Answer 58

Proximal vergence innervation (PC) is **stimulated by perceived nearness it is spatiotopic** o Same precept that drives proximal accommodation

Answer 59

The primary role of PC is to **initiate LARGE changes of vergence** o Stronger transient effect o Weaker sustained effect

Answer 60

**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

Answer 61

BIO, and Slitlamp

Answer 62

o **Initiate LARGE changes in vergence** o To s**upplement other fatigue**d vergence innervations

Answer 63

o Diplopia – this is retinotopic behavior:--- observing the retinal image characteristic o Strained feeling about the eyes o Pure volition

Answer 64

To discourage voluntary effort: o “**look at the letters; make no special effort to see them”**

Answer 65

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”**

Answer 66

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**

Answer 67

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**

Answer 68

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**

Answer 69

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”**

Answer 70

**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

Answer 71

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

Answer 72

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**

Answer 73

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**

Answer 74

horizontal vergence innervations ; stereoscopic **sustained** disparity vergence : **small retinal disparity** **transient** disparity vergence : **large retinal disparity** **proximal** vergence : d**epth perception** voluntary vergence: arge magnitudes of diplopia

Answer 75

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

Answer 76

Transient vergence innervation **initiates step changes of vergenc**e *o Looking far, then suddenly changing to reading distance* o Transient vergence is a s**trong burst of innervation that moves the EOMs quickly, but does not sustain convergence** once the eyes reach destination the transient innervation goes away

Answer 77

• **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

Answer 78

Sustained v**ergence innervation MAINTAINS vergence** after a vergence step, and can SLOWLY change vergence Sustained vergence is controlled by the **retinotopic innervation “fine DV”**

Answer 79

* Vergence **resting state** → determined by **tonic vergence** * **Proximal**= small contribution, but helps you get closer to near point * **Accommodative vergenc**e is an **important** contributor to sustained near convergence response - s**ends info to the convergence system** * **Fine disparity vergence** controls the remainder of the convergence response at near → means that some fixation disparity is present

Answer 80

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*

Answer 81

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

Answer 82

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

Answer 83

Sustained vergence persistence causes **the SLOW decay of vergence observed when an occluder is** applied in a **cover test**

Answer 84

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 vergenc**e normal property of vergence control system o FD causes stimulation of the foveal retinal disparities this stimulates fusional vergence

Answer 85

**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 s**ubtends an UNCROSSED disparity stimulates negative fusional vergence (NFV) and turns the eyes out to the target • Negative fine sustained DV is stimulated**

Answer 86

The “near triad” synkinesis: 1. **Accommodation** 2. **horizontal vergence** 3. **pupil constriction**

Answer 87

The AC/A ratio is the **ratio of accommodative vergence (AC)** generated by **each unit of accommodation (A)**

Answer 88

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

Answer 89

More Accurate : **Calculated AC/A** = there are c**ombined 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)

Answer 90

**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

Answer 91

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

Answer 92

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

Answer 93

**Average = 1/12 in young adults** o 1D for every 12Δ of change in convergence

Answer 94

The **CA/C ratio is highly age-dependen**t, 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

Answer 95

**Accommodation and vergence mutually innervate each other** without dual interaction the 2 systems do NOT work together Dual interaction r**educes 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

Answer 96

Near tonic adaptation ## Footnote DECREASES blur accommodation innervation NO CHANGE accommodative lag DECREASES fusional vergence innervation DECREASES fixation disparity.

Answer 97

Increase the amount of Crossed fixation Disparity and stimmulate convergence

Answer 98

**Minus Stimulates ACC responce and produces Positive fusional** vergence Move the posture to Over convergence / stimulate Neg fixation disparity

Answer 99

**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

Answer 100

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

Answer 101

**• 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**

Answer 102

• Voluntarily select static or moving stimuli for **spatiotopic vergence jumps**

Answer 103

* **Generates pulse (transient) and step (sustained) for jumps which are sent to SOA** * A**djusts vergence gain for best alignment of the eyes** * **Mediates vergence adaptation** * Cerebellum assembles the signals that move the eyes according to Hering’s law

Answer 104

• Convergence vs. divergence cells o **Burst cells:** (“transient burst neurons”) fire briskly during t**he transient phase of accommodation and vergence** – not action during sustained accommodation & vergence o **Tonic cells**: relates closely to s**ustained 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

Answer 105

• SOA cells project to the **EWN and 3rd & 6th nerve Nuclea**

Answer 106

Vertical TV is usually zero (ortho)

Answer 107

Normal values: **+/-3Δ from ortho for smooth vergence** o Range of adaptation is less than horizontal

Answer 108

**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

Answer 109

Convergence Insufficiency (CI) • Synopsis – **weak convergence to near** o Differential Dx: pseudoCIs also have AI • Pathophysiology: Receded NPC – l**ow total vergence innervation Low AC/A ratio**, which causes: ## Footnote 1. **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** 1. Relatively large near accommodative lag from -CA 2. 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

Answer 110

Most saccades are led by a voluntary shift of **overt attention**

Answer 111

1. **Voluntary saccades** 2. **Reflex saccades** 3. **Spontaneous micro saccades** during fixation • NOT driven by stimuli or attention!! 4. **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**

Answer 112

Reflex and voluntary latencies: **200 msec +/- 50 msec** o Express latency: **100 msec latency**

Answer 113

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 f**ixation 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

Answer 114

* Fast phase of vestibular nystagmus * Fast phase of optokinetic nystagmus

Answer 115

Voluntary and reflex saccades are stimulated by target direction “error”

Answer 116

Oculocentric error= nonzero oculocentric target direction • Threshold error=15 minarc Monocular cue

Answer 117

**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

Answer 118

• 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**

Answer 119

Egocentric error=egocentric direction-registered gaze **• Threshold error= 3° gaze error**

Answer 120

Threshold error=15 minarc

Answer 121

“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

Answer 122

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**

Answer 123

o Corrective saccades are additional attempts to fovea the initial saccade image when the **initial saccade is inaccurate**

Answer 124

Neural Gain= **saccade INNERVATION**/ error

Answer 125

Response Gain= s**accade MOVEMENT**/error

Answer 126

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

Answer 127

Once started cant be stopped

Answer 128

A trajectory is the path of the line of sign through 3D space

Answer 129

**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

Answer 130

Pulse innervation determines saccade VELOCITY Pulse overcomes orbital resistance to move the eye **overecome inertia**

Answer 131

The fastest saccade **≈ 700 ̊/sec** ~ 10x faster than the fastest convergence movement **Average movement duration~50ms** (1/20 of a second)

Answer 132

Larger saccades take longer. **Average movement duration~50ms**

Answer 133

**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**

Answer 134

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

Answer 135

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

Answer 136

**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

Answer 137

``` 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

Answer 138

* Parietal Eye Fields (PEF): start REFLEX saccades * Frontal Eye Fields (FEF): initiates VOLUNTARY saccades & PREDICTIVE saccades

Answer 139

**“antisaccade test”** ## Footnote * 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

Answer 140

**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

Answer 141

**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

Answer 142

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 s**patial maps into horizontal, vertical and torsional vectors** for the appropriate saccade muscle groups • Converts spatial map eccentricity to s**accadic 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 don**e • 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

Answer 143

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

Answer 144

**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

Answer 145

**Voluntary attention** chooses the pursuit target o However, pursuit movement cannot occur purely by volition o Pursuit is a **psychooptic reflex** not reflexive

Answer 146

Continuous f**eedback control**

Answer 147

**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)**

Answer 148

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

Answer 149

In pursuit, the target’s velocity is predictable

Answer 150

**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**

Answer 151

**Fixation target retinal eccentricity** **Fatigue,** and **old age** all **REDUCE** pursuit gain

Answer 152

**• 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** v**ector of target velocit**y sends to cerebellum • Nucleus reticularis tegmentum ponti (**NRTP):** **calculate**s the **VERTICAL vecto**r 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 (n**ucleus 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

Answer 153

Reduced pursuit gain is revealed by **“catch-up saccades” which replace** the **defective pursuit**, and are often visible by direct observation

Answer 154

**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**

Answer 155

• **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

Answer 156

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

Answer 157

**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

Answer 158

1. Rotational VOR 2. Ttransitional VOR 3. Saccades 4. Smooth persuit 5. Accomodation 6. Vergence

Answer 159

Rotational: ## Footnote **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 t**oward the ampull**a causes **excitation** • Flow away cause inhibition

Answer 160

**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 A**natomical 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

Answer 161

**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**

Answer 162

**Anterior Canal** • Stimulated by head nod with chin **DOWN innervate elevation agonists** **Posterior Canal** • Stimulated by head nod with chin U**P** 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 posterio**r *stimulated* and vice versa Vertical effects cancel out _Dextrotorsion agonists innervated_

Answer 163

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

Answer 164

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

Answer 165

***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***

Answer 166

Continuous **feed forward control** o brain does not have feedback processing but instead finetunes its gain to ensure accuracy **VOR needs to be efficient**

Answer 167

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”**

Answer 168

VOR gain can be quickly changed when needed o **Convergence induces HIGHER gain** o Voluntary gaze change turns off the VOR o V**OR gain needs to be higher during NEAR fixation** than distance fixation

Answer 169

A natural VOR adaptation stimulus is the **increased orbital friction caused by the effects of aging**

Answer 170

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

Answer 171

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**

Answer 172

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

Answer 173

Saccade and Persuit

Answer 174

**Head Velocity Cells** **Eye Velocity Cells** **Eye Position Cells** **Vestibular Pause Cells**

Answer 175

**Head Velocity Cells** These cells receive 8th nerve afferents They **convert the acceleration signal from the ear to a velocity signa**l 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**

Answer 176

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

Answer 177

**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 * 1. Oscillatory rotation for VOR 2. Prolonged one-way rotation for nystagmus * 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**

Answer 178

**Bilateral labyrinthine disease & Nystagmus** ## Footnote * 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** T**he VOR is also reduced** Continuous **oscillopsia and vertigo are experienced**

Answer 179

**Benign paroxysmal positional vertigo** o A common cause of v**estibular jerk nystagmus in older patients ag**e-related degeneration o Exceptional because it is caused by **damage in a single semicircular canal (the posterior)**

Answer 180

**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 nystagmu**s

Answer 181

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**

Answer 182

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**

Answer 183

OKN also helps stimulate nystagmus during **prolonged head rotation** o **Vestibular innervation controls EARLY nystagmus** during head rotation, but then **decays** Remember: Any v**estibular 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

Answer 184

**REFLEX behavior passive OKN happens automatically** and cannot be voluntarily created o Retinal image motion causes the nystagmus Continuous f**eedforward control** **Slow phase gain = 0.8** o Reduces retinal image speed enough so you can see clearly

Answer 185

**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 vestigi**al 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

Answer 186

Passive OKN is tested by way of OKAN o Lights are extinguished **after prolonged viewing** o **Smooth pursuit stops immediately, but not passive OKN**

Answer 187

**Dynamic head tilt**: conjugate rotational **VOR tilting you head towards one shoulder or another** Remember: Innervation of the v**ertical 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

Answer 188

Range of fixation: KNOW THIS 1. Supraduction: 42 ̊ age related decrease in ability to look up 2. Infraduction: 51 ̊ 3. Adduction: 57 ̊ 4. Abduction: 54 ̊

Answer 189

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**

Answer 190

**Tremor** ## Footnote **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 P**robable 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

Answer 191

Gaze- Evoked Nystagmus ## Footnote 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

Answer 192

**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**

Answer 193

**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**

Answer 194

**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

Answer 195

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**

Answer 196

**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 o**f 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

Answer 197

**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 e**ncephalitis, toxicity, neoplasia, especially in neonates** * Probably caused by cerebellar fastigial nucleus damage in adults

Answer 198

**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

Answer 199

**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: ## Footnote * **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**

Answer 200

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

Answer 201

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 **omnidirectiona**l o A large number of **mitochondria** supports **fatigue resistance**

Answer 202

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 r**educed** 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 tendon**PPZ fibers o **AZ tension is increased** o Increased capsule force flattens the lens

Answer 203

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

Answer 204

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 **begin**s in the **nucleus** and **extends** outwards with age o *Evidence favors Gulstrand’s theory of hardening*

Answer 205

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

Answer 206

**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

Answer 207

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

Answer 208

Premise: a **muscle’s weakness** is most evident in i**ts “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

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**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**

Answer 210

**Collagen bands Elastin** **Smooth muscle**

Answer 211

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

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**Vertical rectus pulley heterotopy** causes **torsional noncomitancy** that stimulates oblique paralysis **Horizontal rectus pulley hetertopy** can induce change**s of horizontal pulling force during elevation or depression** *that can cause the A and V pattern*

Answer 213

**Fiber types and function:** White: **greatest force**, but f**atigue 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

Answer 214

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** ## Footnote **_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

Answer 215

**Rapid eye movement:** White & Intermediate **Steady fixation:** RED twitch & Tonic

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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

Answer 217

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 a**gonist directions**

Answer 218

Motor unit: a motor neuron and its associated muscle fibers o 1**0 muscle fibers/neuron** in EOMs **(50 fibers/1 neuron in skeletal muscle**)

Answer 219

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**

Answer 220

Myasthenia Gravis o **Autoimmune disease** that attacks **acetylcholine receptors** o **Poor eye position control** with micro diplopia ## Footnote 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 s**triated muscle protein** “**dystrophin” degenerates**, starting in early childhood The EOMs **substitute “utrophin” for decaying dystrophin**, which *_skeletal muscles CANNOT do_* Slow saccades

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* *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

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• **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

Answer 223

**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 innervation**Dilator • **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**

Answer 224

**gamma (konio) ganglion cells** (melanin-containing ganglion cells) sends iris control signals to the **pretectal nucleus**

Answer 225

• 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 p**roject to each EWN** • _Consequence: direct and consensual responses are EQUAL_

Answer 226

The Near-Reflex Afferent Pathway • **PEF and FEF cortical eye movement field**s send cyclopean near response signals to the **midbrain supraoptic areas** • **Supraoptic innervatio**n 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**

Answer 227

**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**

Answer 228

**Feedback control** regulates the pupil response to light Pupil gain = pupil-induced retinal illuminance reduction / retinal stimulus luminance increase

Answer 229

**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**

Answer 230

**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

Answer 231

**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

Basics of Eye Movement Flashcards

(265 cards)