Eye movements - Anatomy, Physiology, Clinical Applications

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Information about Eye movements - Anatomy, Physiology, Clinical Applications
Health & Medicine

Published on February 19, 2014

Author: drrahulkumarsingh

Source: slideshare.net


Presentation deals with the Anatomy and Physiology of Eye Movements. A brief discussion of the Applied Clinical Aspects is also mentioned.

Eye Movements Anatomy, Physiology and Clinical Implications


Eye movements Outline for the session To 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.

Why do the eyes move? Eye movements bring the image onto the fovea. Receptors for vision located on back of eyeball, on the retina. Visual axis

Why do the eyes move? Concentration of receptors providing high resolution (clear image) = fovea. More cortical area devoted to foveal region, so need to have image focused here.


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 Innervation of right l. r. (Firing rate in sp/s) –Sum to a non-linear increasing function that matches passive muscle properties When the eyes move, you need still more force - activity is proportional to position and velocity (stay tuned) Far left Midline Eye position Far right



Five types of eye movements Each eye movement: 1) serves a unique function and 2) has properties particularly suited to that function Five types: Gaze shifting 1) Saccades 2) Vergence 3) Smooth pursuit Gaze holding 4) Vestibular ocular reflex 5) Optokinetic reflex (OKR)


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 ms Right Target position Eye position Left Time

Saccades Saccade are fast (peak velocity 500o/sec), but peak velocity varies with saccade amplitude. Peak velocity (deg/s) Saccade amplitude ranges from miniature eye movements (0.1o) to movements ~45o amplitude from the straight ahead position. Saccade amplitude (deg)

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 5 ms Action potential

Neural control of saccades The saccade signal of motor neurons has the form of a pulsestep. Eye position Eye velocity Spikes/sec Height of the step determines the amplitude of the saccade Height of the pulse determines the speed of the saccade. Pulse Step Spikes

Neural control of saccades The saccade signal of motor neurons has the form of a pulsestep. Eye position Eye velocity Spikes/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. Pulse Step Spikes

Neural control of saccades The saccade signal of motor neurons has the form of a pulse-step. Eye position Eye velocity Spikes/sec The duration of the pulse determines the duration of the saccade. Pulse Step Spikes

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]

Neural control of saccades The direction of saccades is dictated by premotor neurons in two gaze centres in the reticular formation. 1) The horizontal gaze centre is in the paramedian pontine reticular formation (PPRF) next to the abducens nucleus.

Neural control of saccades 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 oculomotor nucleus.

Major Pathways for Saccadic Eye Movements

Major Connections of the Superior Colliculus Striate cortex (V1) SC Retina Superficial Layers Intermediate and Deep Layers Extrastriate cortex (e.g. V4, MT) Parietal cortex (e.g. LIP) Frontal Eye Field Dorsal lateral geniculate nucleus (dLGN) Inferior Pulvinar Brainstem Saccade generator Medio-dorsal thalamus

Visual and Motor Related Properties of Cells in the Superior Colliculus SC Superficial Layers: Visual Receptive Fields, Some enhanced Visual Responses, but no Presaccadic (motor) bursts; ‘visual’ cells Intermediate: Visual Receptive Fields and Presaccadic Bursts before saccades to ‘movement field’; ‘visuomotor cells’, ‘visually-triggered motor cells’ Deep Layers No visual RFs, just movement fields, Presaccadic burst gets earlier as you go deeper

Tuning of SC burst neuron to direction and amplitude of saccades Sparks and Mays, 1980

Enhancement of Superior Colliculus Visual Responses and the Need to Dissociate Behavioral Components Passive fixation Saccade to RF target Saccade to Control target

Movement field’ of Superior Colliculus neuron ‘

Map of Stimulation Evoked Saccades Rostral Caudal amplitude elevation

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 Target movement Amplitude If a target starts to move 1) a pursuit movement is generated after a short delay or latency (~100 ms) 2) a saccade is often used to catch up to the target 3) finally if the pursuit is perfect, your eye tracks the moving object 3 2 100 ms 1 Eye movement Catch-up saccade Time

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: Oculomotor nucleus Trochlear nucleus Pontine nucleus Abducens nucleus Medial longitudinal fasciculus Vestibulocerebellum Vestibular nucleus and PPRF


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

Vergence eye movements 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.

Vergence eye movements 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

Vergence eye movements Either blur or retina disparity will generate vergence. Latency for vergence movements is ~160 ms. Maximum velocity is 20o/sec.


Vestibuloocular 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.

Vestibular ocular reflex 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).

Vestibular ocular reflex 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).

Vestibular ocular reflex Three semicircular canals at right angles to each other. They each contain fluid (endolymph) and a transducer (cupula).

Vestibular ocular reflex 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) at 1) vestibular nucleus 2) abducens nucleus 3) lateral rectus muscle Vestibular nucleus Oculomotor nucleus Abducens nucleus

Vestibular ocular reflex pathway The medial rectus muscle is activated by BOTH the abducens nucleus and oculomotor nucleus. Head turning LR Medial longitudinal fasciculus M R Oculomotor nucleus Abducens nucleus

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: 20 Slow eye movements 25 30 Rapid eye movements Different development times suggest different neural systems. 35 Eyelid movements H T R I B 15 weeks

Summary …



Measuring Eye Movements/Position Scleral search coil scleral coil Infrared Eye Tracking magnetic field (2 axes) Temporal resolution: analog Spatial resolution: <0.1 deg. Temporal resolution: video frame rate, <500 Hz Spatial resolution: <0.25 deg.


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

• Mention must also be made of microsaccadic flutter, a rare micro saccadic oscillation (0.10.5°) 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 (21SJmin) 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. gaze 2nd deg: both on center and lat. side of beat 3rd deg: on center, and both lateral gazes. • Video Periph Gaze

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

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

Nystagmus: 2 types 1) Jerk nystagmus 500 ms 2) Pendular nystagmus

Pendular nystagmus congenital yes no Binocular Visual loss Evaluate for Visual loss yes Congenital Sensory nystagmus Treat and evaluate etiology of visual loss no Congenital Motor nystagmus yes Binocular Visual loss no MRI Structural lesion No structural lesion Other etiologies

Monocular or Asymmetric Oscillations Age? child adult Spasmus nutans no yes MRI normal Spasmus nutans abnormal R |o Cerebral lesion Monocular visual loss yes W-up ophthalmology MRI no Monocular pendular Monocular downbeat INO Sup. oblique myokymia

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

• Interconnections hard wired with extreme precision, predominantly controlled by the premotor neural integrators in the pons and midbrain, 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.

Further Reading…

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