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Eye Movements

Anatomy, Physiology and Clinical Implications

Introduction

Eye movements

Outline for the sessionTo understand and describe

The extraocular muscles and neural circuitry involved in moving the eyes.

The different types of eye movements: their purpose, neural structure, and how they differ.

Eye movements

Think of this function not as vision, but as an effector system required to move the eyes, therefore a legitimate area of motor control research.

This relatively simple motor system can be compared to other muscular systems, and the stimulus can be defined precisely.

Eye movements involve rotation of the eyes in the socket.

Why ???

Why do the eyes move?

We need our eyes to increase the visual range that can be covered.


Eye movements bring the image onto the fovea.Receptors for vision located on back of eyeball, on the retina.

Visualaxis


Concentration of receptors providing high resolution (clear image) = fovea.

More cortical area devoted to foveal region, so need to have image focused here.

How…

The III, IV & VI

MLF (medial longitudinal fasciculus)

• Internuclear connection• Nonvestibular pathways

(among CN nuclei)– VI-contralateral III– III-VII, VII-V, V-XII, XII-VII

• Vestibular pathways:– Eye– Ear– Neck– Limb extensors

p389

Conjugate Eye Movements• Yoking mechanism• Via MLF

E.g. CN VI contralat. CN III

Extraocular Muscles: three complimentary pairs

Muscle properties• More complex than somatomotor muscle

fibers–5 distinct fiber types (vs 2 - fast & slow)•Unclear why–More proprioceptors (?)•but proprioception is (too) slow–Much higher innervation ratio (nerve endings/fiber)

• Built for speed, not for comfort–8 ms twitch time (2-3 times faster than fast somatomotor fibers)

Muscle innervation (oculomotor nerves)

• At rest, firing rate of an individual nerve is linear with eye position

• Different nerves have different slopes and offsets

–Sum to a non-linear increasing function that matches passive muscle properties

MidlineFar left Farright

Eye position

Innervationof right l. r.(Firing ratein sp/s)

When the eyes move, you need still more force - activity is proportional to position and velocity (stay tuned)

Innervation…

Types….

Five types of eye movements

Each eye movement:1) serves a unique function and2) has properties particularly suited to that function

Five types:

Gaze shifting1) Saccades2) Vergence3) Smooth pursuit

Gaze holding4) Vestibular ocular reflex5) Optokinetic reflex (OKR)

Saccades…

Saccades

Rapid rotation of the eyes that bring images onto the fovea.Saccades are made spontaneously in response to a sudden appearing object, or to scan a scene or to read.Thus, saccades can be either voluntary or reflexive.

Saccades

Saccades allow us to scan the visual field on parts of the scene that convey the most significant information.

We make about 3 saccades a second, and > 150,000 saccadic eye movements a day.

Saccades

The trigger for a saccade is position error, the difference where your looking and where you want to look.So when the target isn’t centred on the fovea, a saccade brings the eyes onto the target.

200 msTarget position

Eye position

Time

Right

Left

Saccades

Saccade amplitude ranges from miniature eye movements (0.1o) to movements ~45o amplitude from the straight ahead position.

Saccade amplitude (deg)

Pea

k ve

loci

ty (d

eg/s

)Saccade are fast (peak velocity 500o/sec), but peak velocity varies with saccade amplitude.

Neural control of saccades

The discharge frequency of extraocular motor neurons is directly proportional to the position and velocity of the eye.

Saccade onset

Horizontal eye position

Abducens motor neuron

Action potential


The saccade signal of motor neurons has the form of a pulse-step.

Eye position

Spikes

Eye velocity

Pulse

Step

Spi

kes/

sec

Height of the step determines the amplitude of the saccadeHeight of the pulse determines the speed of the saccade.



Eye position

Spikes

Eye velocity

Pulse

Step

Spi

kes/

sec

The pulse is the phasic signal that commands the eyes to move.The step is the tonic signal that commands the eyes to hold in an eccentric position.



Eye position

Spikes

Eye velocity

Pulse

Step

Spi

kes/

sec

The duration of the pulse determines the duration of the saccade.

Saccadic Eye Movements(‘saccades’)

Subtypes often referred to:

1. Volitional (‘purposive’) -predictive, anticipatory

-memory-guided-antisaccades

2. Reflexive

3. Express saccades

4. Spontaneous

5. Quick phase of nystagmus

Velocity, Duration and the ‘Main Sequence’

Visually Guided Saccades

Deviations from main sequence:

-saccades in complete darkness

-saccades to auditory stimuli

-saccades to remembered targets

-saccades made in the opposite direction (antisaccades)

[abducens, trochlear, om nucleus]

[cerebellum, brainstem]

[pprf, mrf]

[dorsal raphe]


1) The horizontal gaze centre is in the paramedian pontine reticular formation (PPRF) next to the abducens nucleus.

The direction of saccades is dictated by premotor neurons in two gaze centres in the reticular formation.


2) The vertical gaze center is in the rostral interstitial nucleus of the medial longitudinal fasciculus (rostral iMLF) in the mesencephalic reticular formation near the oculo-motor nucleus.

Major Pathways for Saccadic Eye Movements

Superficial Layers

Intermediate andDeep Layers

Retina

Major Connections of the Superior Colliculus

Striate cortex (V1) Extrastriate cortex (e.g. V4, MT)

Parietal cortex (e.g. LIP)

Frontal Eye Field

Inferior PulvinarBrainstem Saccade generator

Dorsal lateral geniculate nucleus (dLGN)

Medio-dorsal thalamus

SC

Visual and Motor Related Properties of Cells in the Superior Colliculus

Superficial Layers:

Intermediate:

Deep Layers

SC

Visual Receptive Fields,Some enhanced Visual Responses, butno Presaccadic (motor) bursts; ‘visual’cells

Visual Receptive Fields and PresaccadicBursts before saccades to ‘movement field’;‘visuomotor cells’, ‘visually-triggered motor cells’

No visual RFs, just movement fields,Presaccadic burst gets earlier as you go deeper

Sparks and Mays, 1980

Tuning of SC burst neuron to direction and amplitude of saccades

Enhancement of Superior Colliculus Visual Responses and the Need to Dissociate Behavioral Components

Passive fixation

Saccade toRF target

Saccade toControl target

‘Movement field’ of Superior Colliculus neuron

Map of Stimulation Evoked Saccades

amplitude

elevation

Rostral

Caudal

Major Pathways for Saccadic Eye Movements

Lateral Intraparietal Area (LIP): visual, saccade-related and mnemonic responses

Incidence of ‘light-sensitive’, ‘saccade-coincident’ and ‘memory’ activity in LIP

Pursuit …

Smooth pursuit

Saccades involve fixating on a point then jumping to the next object of interest.Smooth pursuit involved keeping a visible moving target on the fovea.Although voluntary, smooth pursuit requires a stimulus to track; they cannot be executed in the absence of some environmental stimulus. The trigger for a smooth pursuit movement is a velocity difference between the eyes and the target.

Smooth pursuit

The pursuit system needs to compute the speed of the moving stimulus to produce the proper eye velocity. Fast moving stimuli (30o/s) cannot be tracked with precision, and they usually elicit a saccade.

Smooth pursuit

If a target starts to move1) a pursuit movement is generated after a short delay or latency (~100 ms)2) a saccade is often used to catch up to the target3) finally if the pursuit is perfect, your eye tracks the moving object

Target movement

Eye movement

100 msCatch-upsaccade

Time

Am

plitu

de1

2

3

Smooth pursuit

How well do pursuit movements match the movement of the object being tracked?Slow targets are matched perfectly; less than 0.33 mm retinal slip/sec.Target moving at higher speeds – large retinal slips.Retinal slip is the distance between the image of the target on the retina and the fovea.

Smooth pursuit vs. Saccade

Smooth pursuit isn’t ballistic, like saccades, and instead moves smoothly.

Agonists and antagonists are activated simultaneously – in saccades, only muscle agonists are used.

So smooth pursuit movements are produced by creating small differences in the tensions of the opposing ocular muscles.

Neural control of smooth pursuit

The sequence of structures that are used to generate pursuit eye movement:

Striate Cortex

MT & MST

Pontine nuclei

Cerebellum

Brainstem

Neural control of smooth pursuit

The brainstem structures that are used to generate pursuit eye movement:

Abducens nucleus

Oculo-motor

nucleus

Medial longitudinal fasciculus

Vestibulo-cerebellum

Trochlear nucleus

Pontine nucleus

Vestibular nucleus and PPRF

The FEF

Microstimulation of the Frontal Eye Field

Continuum of Visual and Motor Responses in the FEF

Stimulation-Evoked Smooth Pursuit Movements

Gaze-holding eye movements

Gaze holding eye movements include the vestibular ocular reflex and the optokinetic reflex. Their purpose is to keep the image of the whole scene still on the entire retina when the head moves (or the scene moves).

Vergence…

Vergence eye movements

Vergence eye movements aligns the fovea of each eye with targets located at different distances from the observer.


They are just disconjugate movements, i.e., eyes move in opposite directions, producing a convergence or divergence of each eye’s visual field to focus an object that is near or far.


Convergence is one of the three reflexive responses elicited by a near target.

The other two include accommodation of the lens, which brings the object into focus, and pupil constriction, which increases the depth of field and sharpen the retinal image.

Accommodation


Either blur or retina disparity will generate vergence.

Latency for vergence movements is ~160 ms.

Maximum velocity is 20o/sec.

VOR …

Vestibulo-ocular Reflex

• Contralateral CN VI n.• From CN VI n

– ipsi. CN III n

Vestibular ocular reflex

Vestibular ocular reflex (VOR) stabilizes the eyes relative to the external world, compensating for head movements, by rotating the eyes in opposite direction.


This permits the visual axis, or gaze, to remain on the newly foveated stimulus (but, visual stimulus is not required!)This reflex prevents visual images from slipping on the surface of the retina (retinal slip) as head position varies.The latency of the VOR is 14 ms.It can accurately follow head velocities up to 300o/s.Can be produce without a stimulus (not visual).


The VOR also acts during the coordinated eye-head movements (gaze shifts), compensating for the portion of the head movement that lags the more rapid displacements of the eye.

Vestibular ocular reflex sensors

Head movements are sensed by the labyrinth of the inner ear which acts as an accelerometer. Acceleration and deceleration are the triggering stimuli (not velocity, so unaffected by a constant rate).


Three semicircular canals at right angles to each other.

They each contain fluid (endolymph) and a transducer (cupula).


The fluid transmits the direction and force of acceleration or deceleration of the head via the cupula to the oculomotor system to drive the eyes.

Vestibular ocular reflex pathway

The horizontal VOR is a short tri-synaptic path (3-neuron arc) at1) vestibular nucleus2) abducens nucleus3) lateral rectus muscle

Abducens nucleusVestibular

nucleus

Oculomotor nucleus

Vestibular ocular reflex pathway

The medial rectus muscle is activated by BOTH the abducens nucleus and oculomotor nucleus.

M RLR

Abducens nucleus

Oculo-motor

nucleus

Medial longitudinal fasciculus

Head turning

Optokinetic reflex

Sometimes also called Optokinetic nystagmus.VOR doesn’t work well for slow, prolonged movements, so vision through the optokinetic reflex (OKR) assists the VOR.OKR is activated when the image of the world slips on a large portion of the retina and produces a sense of self motion.

Optokinetic reflex

Sometimes consider to be a combination of smooth pursuit (following the visual field) and a saccade to return the eyes back to center – see a rhythmic back and forth movement of the eyes.

Plasticity and Development

The VOR gain (eye amplitude/head amplitude) can change, for ex. with glasses.VOR adaptation are controlled by the cerebellum.

Prenatal development of eye movements:

15 weeks 20

Eyelidmovements

Slow eye movements

BIR

TH

3525 30

Rapid eye movements

Different development times suggest different neural systems.

Summary …

Abnormalities…

Measuring Eye Movements/Position

Scleral search coil Infrared Eye Tracking

Temporal resolution: analogSpatial resolution: <0.1 deg.

Temporal resolution: video frame rate, <500 HzSpatial resolution: <0.25 deg.

scleral coil

magnetic field(2 axes)

ENG & VNG

Data Collection

Nystagmus• Nystagmus is an involuntary, to-and-fro, repetitive,

rhythmic and generally conjugate eye movement. • Nystagmus may be pendular or jerky• • Pendular nystagmus is usually congenital • Congenital nystagmus is often horizontal, does not induce

oscillopsia, increases in amplitude during fixation and decreases during eyelid closure.

• •

• Jerk nystagmus is more common and of great variety.

• Downbeat nystagmus is especially suggestive of a cervicomedullary junction abnormality; may also be observed in cerebellar degeneration or lithium intoxication

• Convergence-retraction and retractorius nystagmus (fast eyeball retractions into the orbit) strongly suggests a tectal lesion

• some forms of nystagmus have little localizing value, such as upbeat nystagmus, periodic alternating nystagmus (the direction of nystagmus is alternately inverted) and circumduction nystagmus (rotator movement around the eyeball axis, sweeping a circle or an ellipse).

• Monocular nystagmus is most often seen in internuclear ophthalmoplegia

Non Nystagmic Disorders• Ocular flutter - consists of bursts (6-12 Hz) of

horizontal saccadic oscillations (2_5° amplitude), without intersaccadic interval

• Opsoclonus - saccades are the same as in ocular flutter, except that they are omnidirectional and frequently associated with axial myoclonus.

• •

• Flutter and opsoclonus may be congenital or, in childhood, reveal a neuroblastoma

• In adults, they may appear after several infectious diseases (salmonella, coxsackie), during brain stem encephalitis or malignant pathology (paraneoplastic syndrome).

• They may be induced by drugs (lithium, haloperidol) or by fluid balance and electrolyte abnormalities

• Mention must also be made of microsaccadic flutter, a rare micro saccadic oscillation (0.1-0.5°) causing blurred vision, but without any associated neurological disease.

• It could be due to malfunction of the brain stem omnipause neurones

•

• Square wave jerks (SW]) consist of consecutive to-and-fro, horizontal saccades of small amplitude (O.S-3"), with a 200-ms inter saccadic interval.

• They usually increase during smooth pursuit and fixation. SW} are found in cerebellar pathology, degenerative diseases, particularly in PSP, and, rarely, in hemispheric diseases.

•

• Ocular bobbing - consists of an initial rapid downward eye movement, followed after a few milliseconds by a slow return to the initial position, with a frequency of 10-1 S per minute.

• It suggests a cerebellar or pontine lesion.

• Inverse ocular bobbing (or ocular dipping) consists of an initial low downward movement, followed by a rapid return to the baseline

• • Reverse ocular bobbing consists of a rapid upward eye

movement, followed by a slow return. These other forms of ocular bobbing have been described in widespread diseases (metabolic encephalopathy, bilateral hemispheric lesions).

•

• Ping-Pong gaze consists of alternating (2-1SJmin) large-amplitude (60-80°) horizontal slow eye movements, and is observed in comatose: patients suffering from bilateral mesodiencephalic lesions

• iSuperior oblique myokymia is a monocular vertico-rotatory fast eye movement, appearing spontaneously in midlife or rarely revealing a tumour, and may be reduced by carbamazepine

Peripheral Gaze Nystagmus:• strongest on gaze in

direction of beating• never vertical• declines quickly (within

days to a couple of weeks)

• Alexander's Law:1st degree Nystagmus: present only on lat. gaze2nd deg: both on center and lat. side of beat3rd deg: on center, and both lateral gazes.

• Video Periph Gaze

mms://ecclesvideo.med.utah.edu/NOVEL/Digre/2-15.wmv

Central Nervous System Lesions:

• Often bilateral beating• Can have vertical beating• declines slowly if at all

Some Central Gaze Nystagmi:

• Bilateral Horiz. Gaze (Brun's) Nystagmus:• Rebound Nystagmus:• Periodic Alternating Nystagmus:• Vertical Nystagmus:• Congenital Nystagmus:

What is Going on here?:Voluntary Nystagmus


Bilateral Horiz. Gaze (Brun's) Nystagmus:

• in large CPA tumors.• Gaze ipsi to lesion generates large slow nyst,

with exp. decay in slow phase.• Gaze contra to lesion generates small fast nyst,

in opposite direction of ipsi resp.

• Video Bruns

http://ecclesvideo.med.utah.edu/NOVEL/Digre/2-11_CD.wmv

Rebound Nystagmus:

• Cerebellar disease• movement-generated,

decays rapidly (10-20s)• Beats in direction of

movement• Video Rebound


Periodic Alternating Nystagmus:

• Medullary disease. Periodic Alternating Video• cyclic, 90 s one direction,• 10 s nothing or vertical, • then 90s in other direction, 10 s down time,• and back again.• present w/ eyes open or closed.• strongest in middle of phases>>visual impairment.


Vertical Nystagmus:

• Brainstem/Cerebellar or Inf. olivary disease• Can be generated by alcohol, drugs, too.• Upbeat Video• Downbeat Video



Congenital Nystagmus:• From fixed brain defect either genetic or

developmental in origin.• Pendular and/or jerk-type• Disorder of slow eye movement sub-

system.• Null points or periods.• Convergence inhibition• Congenital Video


Nystagmus: 2 types1) Jerk nystagmus

2) Pendular nystagmus

500 ms

Pendular nystagmus

congenital

yes no

Evaluate forVisual loss

BinocularVisual loss

yes no yes no

CongenitalSensory

nystagmus

CongenitalMotor

nystagmus

BinocularVisual loss

MRI

Structurallesion

No structurallesion

Other etiologiesTreat and evaluate

etiology ofvisual loss

Monocular or Asymmetric Oscillations

Age?

child adult

Spasmus nutans

yes no

MRI

normal abnormal

Spasmus nutans R |o Cerebral lesion

Monocular visual loss

yes no

W-upophthalmology

Monocular pendularMonocular downbeat

INOSup. oblique myokymia

MRI

To Summarize… • 5 distinct eye movements• Saccades• Smooth pursuit• VOR• OKN• Vergence

• Interconnections hard wired with extreme precision, predominantly controlled by the pre-motor neural integrators in the pons and mid-brain, ably assisted by vestibulo cerebellar inputs

• The precision, the need and the type is precisely analysed from the sensory input at PPC and FEP and associated areas and translated into meaningful triggers to the subserving neural integrator at brainstem.

• Distinct pathology at different points in the neuro axis can produce distinct and sometime varied ocular movement abnormalities

• Some of them are highly localizable and some are not.

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