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Anatomy of Extraocular Muscles • There are six true extraocular muscles responsible for
and Neural Control of Eye movements of the globe
• In addition there is one further ‘orbital’ muscle, the
Movements levator palpebrae superioris,
• The true extraocular muscles comprise
– four rectus muscles, which arise from the tendinous
ring at the apex of the orbit and insert into the sclera
about 4–8 mm behind the limbus
– two oblique muscles (superior and inferior), whose
tendons approach the globe from in front and insert
into the posterior aspect of the sclera

Gross Structure – Tendon fibers enter superficial sclera and quickly

merge with it
• Superior and lateral recti have posterior ends which are – Cessation of thick elastic fibers mark junction of
U-shaped tendon with sclera
• Inferior and medial recti have linear and dentate – Occasional slips leave main tendons to attach farther
osseous attachments back
• Scleral insertions: – These recurrent slips maybe missed at squint surgery
– By tendons whose fibers are parallel to long axis of
muscle
– Consist of collagen supported by thick elastic fibers
– Resemble scleral fibers – but differ in size
– Imparts glistening silky appearance to tendon

• Extraocular muscle is the most vascular in the body, next

Difference between EOM and Somatic Muscles to myocardium
• Similar to branchial muscles – Most vascularized region is the orbital aspect
• Fibers are small, narrower • They require and receive more O2
• The epimysium or muscle sheath of extraocular muscle is • In normal extraocular muscle there often appear to be
generally very thin by comparison with other muscles histopathological or ultrastructural changes normally
associated with myopathy
• The fibres are not tightly packed but are separated by
unusually large amounts of connective tissue (perimysium) 1. Mild mononuclear cellular infiltrate
rich in reticulin and elastic fibres 2. Large number of centrally placed nuclei
• Ie; they are not fasciculated with dense connective tissue 3. Disorganization of the sarcolemma, whorled fibers
• The muscle fibres are rounded or oval in shape 4. Disruption of the Z lines, vacuoles within myofibrils
• Small fibres (5–15μm) around the periphery of the muscle 5. Mitochondrial clumping
and larger fibres (10–40μm) in the centre – division as 6. Variability of shape and size of fiber
orbital and global zones 7. Higher proportion of smaller fibers

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• Extremely high density of nerves -1:3 to 1:5 – ie; smaller

motor units
• Allows precise control of ocular movements
• Nerve innervating muscle is disproportionately large to
muscle size
• Extraocular muscle contains large numbers of specialized
sensory or proprioreceptive endings
• Large muscle spindles up to 1 mm long (nuclear bag
fibres, nuclear chain fibres and annular nerve terminals)
• Golgi tendon organs - generally found within the tendons
of extraocular muscles in greater numbers than in
skeletal muscle
• EOM contain both slow and fast fibers

Orbital and Global Zones • Orbital and

global zones
• At birth fiber size is uniform
are
• Later form an outer shell of small fibers (orbital zone) distinctly
with a core of larger fibers (global zone) separate
• Orbital fibers (outer facing) – 5-15µm from each
• Global fibers (inner facing) – 10-40µm other
• Different subtypes of muscle fibers present within zones sometimes
by an
• Orbital layer of superior oblique completely encircle its
internal
global layer
perimysium
• In recti : Orbital zone deficient on internal surface
– Global layer exposed to fat around optic nerve –
“hilum”

• Recti are strap-like

General Features
– Maximum width at their global insertion of SR, IR, MR
– Maximum width 5mm behind insertion in LR • Each fiber consist of a sarcolemma surrounding a
• Muscle fibers extend end-to-end, however, orbital fibers granular sarcoplasm
end before muscle becomes tendinous • Inside has many myofibrils which lie in paralell
• Therefore, global fibers are longer than orbital fibers • Fiber multinucleated
• Only global tonic fibers run full length of muscle belly • Has striations
• Maximizes possible change in length of muscle in • Mitochondria are more numerous than skeletal muscle
contraction – cf sk. Muscle • 2 types of fibers
• Shorter fibers uncommon – ie; less myomyous junctions – Large diameter – fibrillenstrukter
• Size of fiber varies along muscle length – Smaller diameter – felderstrukter
• However, orbital and global fiber size similar at ends of
each muscle

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Fibrillenstrukter Felderstrukter
• Large diameter • Slow or “tonic” in action
• Rapid twitch fibers • Ill-defined myofibrillar arrangements
• Have regular distribution of myofibrils • Little sarcoplasm
• Abundant sarcoplasm • Chiefly aerobic respiratory metabolism
• Innervation by single “en-plaque” endings (motor end • Innervated by diffuse “en-grappe” endings
plates) • Multiply innervated
• Resemble somatic striated fibers elsewhere
• Rich in lipid droplets

• Have a perimysium of collagen, elastic fibers, vessels,

Connective tissue and blood supply nerves – surround fascicles
• Vessels and nerves enter each muscle belly at hilum • Extend between individual fibers as endomysium
• Blood supply of rectus muscle greater than myocardium • Continuous with epimysium – surrounds entire muscle
– due to richness of capillary network in orbital layer • Epimysium thin near osseus attachements, but well
• Capillaries are of closed type – show bidirectional developed near globe
transport • EOM have unusual amount of elastic fibers – may
• Blood supply needed for large number of singly contribute to graded contraction
innervated fast-twitch fibers in orbital layer – which have • Main factors contributing to graded contractions
high aerobic metabolism – Profuse innervation
• Fibers in orbital layer are arranged in discrete fascicles – Small size of motor unit
– less evident in global layer
– Thus very high twitch frequency before tetanus
• Abundant elastic facilitates delicate ocular movements ensures
• Conversely – disadvantagous in scar formation

• EOM have resident population of immunocompetent Nerve supply

cells – Each rectus muscle receives its motor supply from
– Macrophages nerve entering its global aspect
– Less amount of HLA-DR+ve T cells – Near junction of middle and posterior thirds
• B cells are absent – Trochlear nerve
• These cells are important in orbital immune disorders – • Enters orbital surface of superior oblique
eg; endocrine ophthalmopathy • In posterior 1/3 (anterior part)
• Majority are CD8+ T cells – in sk.muscle CD4+ cells – To inferior oblique
predominate
• From inferior division of oculomotor nerve
• Macrophages more numerous in medial and inferior
• Enter at middle of its posterior border
recti
– After entering muscle belly, each nerve divides and
send branches to front and back of muscle

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• The afferent fibres from extraocular muscles

– transmitted initially for part of their course in the
respective cranial nerve innervating the muscle
(either III, IV or VI)
– leave these nerves and join the ophthalmic division
of the trigeminal, either in the cavernous sinus or in
the brainstem Ultrastructural features of EOM
– Their cell bodies are situated in the mesencephalic
nucleus of trigeminal
– some muscle afferents to Purkinje cells in the
cerebellum - important role in positional sense and
control of ocular movements (both saccadic and
tracking)

• The sarcolemmal- associated protein dystrophin is

Contractile mechanism of EOM absent from extraocular muscle in the condition of
Duchenne muscular dystrophy but, unlike in skeletal
• Muscle fibre is elongated, polygonal in cross section,
muscle, no EOM degeneration results
fusiform in shape
• The cytoplasm (or sarcoplasm) shows several
• Each multinucleate fibre contains many ovoid
specializations, the most obvious being cylindrical
peripherally located nuclei, with adjacent Golgi bodies.
myofibrils composed of contractile protein and
• The characteristic transverse cross-bandings are the occupying 85-90% of the fibre's volume
basis of the term 'striated muscle‘
• Hundreds or thousands of myofibrils may be present in a
• The plasma membrane or sarcolemma is bilamellar single fibre
• Outside this is a layer of delicate reticular connective • The intermyofibrillar sarcoplasm contains, in addition to
tissue. nuclei, other organelles and membranous systems
• Satellite cells, at the interface of sarcolemma and basal including the T-system, sarcoplasmic reticulum,
lamina, may be capable of myoblastic differentiation mitochondria, Golgi apparatus, glycogen granules and
lipid bodies

• Myofibrils • An isotropic (I) band

• The myofibrils are polygonal in cross-section – contains only thin filaments and the dense Z-disc to
• Extend in parallel bundles along the full length of the which they are attached
fibre • Anisotropic (A) band
• Composed of linearly arranged myofilaments, which form – Contains the full extent of the thick filaments plus
the fibre's repeating unit, the sarcomere some thin filaments
• The gap containing thick filaments alone exhibits the
electron-lucent H (Henson) stripe divided by the M
• Myofilaments
(Mittlescheibe) line
• Chief elements of the sarcomere,
• Each sarcomere has:
• Thick (myosin) myofilaments is found interdigitating and – ½ I band + A band + ½ I band
overlapping with a series of thin (actin) filaments
• Actin filaments attached to Z-disc
• Give rise to banding pattern

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• Thick filaments (twice diameter of actin) contain myosin

– a golf-club shaped protein with tail and head
• Head has two active sites – actin binding site and
myosin ATPase binding site
• Thin filaments are actin – a fibrous protein forming
double-helix with tropomyosin running in its grooves
• Tropomyosin has 3 attachment sites
1. T - actin and other component binding
2. C- calcium binding and initiate contraction
3. I - inhibitory site shield interaction with myosin
• Therefore each thick filament is surrounded by six thin
filaments

• Sarcotubular system • During contraction

– Muscle fibrils are surrounded by vesicles and tubules – Spread of excitation via T-tubules
– Made of T-tubules and sarcoplasmic reticulum – Release of calcium from terminal cisterns
– T-tubules continuous with sarcolemma – Bind to troponin C – conformational change in actin
– Enter around fibril at A-I junction – Expose myosin-binding site of actin
– T-tubule + 2 cisterns of sarcoplasmic reticulum is – Activate myosin ATPase - hydrolyzes ATP
termed a triad – Cause sliding of thin filaments across thick filaments
– Cisterns store calcium – Power-stroke mechanism – latch-bridging
– There are 2 triads in each sarcomere – A-band does not change length
– Function of sarcotubular system is to transmit impulse – I band and H zone shorten
rapidly from cell membrane to all fibrils – Sarcomere shorten
– Myofibril shorten
– Active pumping of Ca terminates twitch

Sensory apparatus of EOM Muscle Spindles

• Sensory fibres from EOM pass in the third, fourth and • Stretch receptors for proprioceptive mechanism in
sixth cranial nerves, with cell bodies in the trigeminal control of eye movements
ganglion/ mesencephalic nucleus of TG • Each spindle is built around 3-10 small intrafusal fibers
• Second-order neurons pass to tectum and tegmentum attached in series with extrafusal fibers
and project to ventrobasal nucleus of thalamus • Differences with sk.muscle spindles
• Innervate – More delicate and smaller
1. Muscle spindles – Spindles have thinner capsules
2. Golgi tendon organs – Do not have nuclear bag region
3. Palisade endings – Distributed in proximal and distal third of muscle
4. Spiral nerve endings (away from central third which has motor end plates)
• Similar number to skeletal muscle – 22-71/muscle

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• Afferents from muscle spindles • Function of spindles

– 1st order neuron – in trigeminal ganglion 1. Cerebellum mediated proprioceptive loop providing
– 2nd order neuron – in main & spinal nucleus of size and end point of saccade to cerebellum
trigeminal 2. Reflex or subconscious control of muscular
– Then project to contractions
1. Ventrobasal nucleus of thalamus 3. Role in fixation nystagmus
2. Cerebellum 4. Dampen and correct overshoot of ocular movements
3. Superior colliculus
• Spindles do NOT mediate awareness of position – eye
position is not appreciated consciously in absence of
visual cues

• Gamma efferents in EOM

Golgi tendon organs
• Innervate spindle
• Regulate sensitivity of spindle afferents to either static or • Organ completely embedded in tendon
dynamic phases of stretch
• Rarely observed
• Active during contraction of muscle mass maintaining
• Innervate by one or more myelinated nerves
sensitivity in spindle

Spiral nerve endings

• In middle third of EOM – wrap around extrafusal fibers
• Innervated by myelinated nerves
• Protective role preventing overstretch similar to Golgi
tendon organs

Temperature sensitive receptors

Palisade endings
– Near arterioles

• Myotendinous cylinders
• Probably principle sensory apparatus in EOM Receptors for oculocardiac and
• Consist of encapsulated nerve endings lying at the oculorespiratory reflexes
myotendinous junction which interdigitate with
– Exact nature unknown
longitudinal fibers of global multiply innervated fibers
– Afferents carried via trigeminal nerve to
• Found in significant amounts in EOM
mesencephalic nucleus
• Most in horizontal recti
– These afferents can be blocked by local nerve block
during ocular surgery

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Types of skeletal muscle fibers

• Skeletal muscles have been classified depending on
speed of contraction and fatigue resistance
1. Slow twitch, fatigue resistant (type I)
2. Fast twitch, fatigue resistant (type IIA)
Classification of EOM 3. Fast twitch, fatigueable (type IIB)
4. Fast twitch, intermediate (type IIC)

• However, EOM are unique in both cellular

organization and constituent muscle fiber types from
skeletal muscles

Classifications of EOM
• Current classification by Spencer and Porter
• Uses following features
– Location – orbital/global
– Colour – red/intermediate/white
– Innervation – singly/multiply
1. OSIF – Orbital singly innervated fibers
2. OMIF – Orbital multiply innervated fibers
3. GRSIF – Global red singly innervated fibers
4. GISIF – Global intermediate singly innervated fibers
5. GPSIF – Global pale singly innervated fibers
6. GMIF – Global multiply innervated fibers

OSIF – Orbital singly innervated fibers OMIF – Orbital multiply innervated fibers
• Small • 20% of orbital zone
• Make up 80% of orbital layer • Resemble amphibian tonic fibers – slow twitch
• Probably account for most of sustained force generated • Moderate oxidative activity
by muscle • Sparse membranous systems, irregular myofibrils –
• Abundant mitochondria in clusters – for significant felderstruktur
demands in visual acuity • Have embryonic/neonatal myosin + other isoforms
• Abundant and well formed sarcoplasmic reticulum, T- • Multiply innervated
tubules, oxidative enzymes, regular myofibrils • Faster twitch in center, slow contractions at ends
• Various myosin isoforms along length of fiber
• Singly innervated by elaborate motor end plates
• Similar to sk.muscle type II fibers

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GRSIF – Global red singly innervated fibers GISIF – Global intermediate singly innervated
fibers
• A fast twitch type
• Makes 25% of global layer
• Makes 30% of global zone
• Fast twitch fiber
• Resembles Orbital singly innervated fibers
• Moderate levels of oxidative and aerobic enzymes
• Highly oxidant and glycolytic – Fatigue resistant
• Numerous small mitochondria
• High mitochondrial content
• Myofibril size and sarcoplasmic reticulum intermediate
• No variations of myosin isoforms
between other two types
• Resemble type IIB sk.muscle fibers

GPSIF – Global pale singly innervated

GMIF – Global multiply innervated fibers
fibers
• 30% of global layer • Slow fiber – resemble amphibian tonic
• Fast twitch type • 10% of global layer
• Resemble type IIB sk.muscle fiber • Weak oxidative properties
• Modest level of oxidative enzymes • Strong acid-stable ATPase
• High anearobic capacity • Large myofibrils, sparse membranous systems,
• Mitochondria small and few occasional mitochondria – felderstruktur
• Large motor end-plates • Multiply innervated with numerous en-grappe endings
• Fiber diameter increases from types 3-5 • However, hosmogenous staining unlike OMIF
• All show well-developed sarcoplasmic reticulum, T-
tubules (less so in GPSIF)

Features 1-OSIF 2-OMIF 3-GRSIF 4-GISIF 5-GPSIF 6-GMIF

Location Orbital Orbital Global Global Global Global Arrangement of fibers in orbital layer
Percentage 80% 20% 30% 25% 30% 10%
• This layer contains 2 types of small fibers which are rich
Trichrome Coarse Fine Coarse Granular Granular Granular in mitochondria and contain lipid vacuoles
staining
Mito Numerous Modera High Numerous Few Very few
• OSIF – have a moderately good amount of sarcoplasmic
in clusters te -medium reticulum
ATPase High Slow High Moderate Moderate Slow • Concerned with prolonged stamina-oriented and less
activity
fatigued contractions
Contractio Twitch Mixed Twitch Twitch Twitch Sustained
n mode • Muscle fibers are mostly parallel – but few myomyous
Contractio Fast Slow Fast Fast Fast Slow junctions present
n speed graded
Fatigue Very high Variable High Intermedi Low High
• Motor end plates confined to a large band in middle
resistance ate third of muscle
Recruitme 1st 3rd 2nd 5th 6th 4th
nt order

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• Many orbital zone fibers contain embryonic/neonatal

mysosins Arrangement of fibers in global layer
• Postnatal maturity of EOM parallels maturation of retinal
circuitry and establishment of interocular alignment • Contains one type of multiply innervated fibers and 3 types of
singly innervated fibers
• Development of eye movements parallels acquisition of
fatigue resistance • Singly innervated fibers – vary in size, mitochondrial supply,
sarcoplasmic reticulum
• GPSIF fibers are large, pale, relatively mitochondria free and
rich in sarcoplasmic reticulum
• They occupy core area – these are very fast but rapidly
fatigued
• GMIF cause sustained slow graded contractions – have high
fatigue resistance
• Large motor end plates found along entire length
• Myomyous junctions present – exhibit cholinesterase activity

• Majority of global zone EOM contain myosin specific to

EOM
Twitch fibers
• ATPase properties corresponding to family of fast • EOM are fastest contracting muscles in body
myosins
• Twitch fibers innervated by en-plaque endings
• Vertebrate EOM myosin is distinct from skeletal muscle
• Nerve supply small number of muscle fibers
myosin
• Are motor end plates rich in ACh esterase
• GMIF are similar to skeletal muscle type I fibers
• Distributed over middle third of muscle
• LPS – not divided into orbital and global zones and
innervated entirely by en-plaque endings
• Characteristic response to neural stimulation – twitch –
summation produces tetanus
• Due to release of ACh from nerve ending – cross
synaptic cleft – create EPP

• Two ACh isoforms present in twitch fibers

• Some multiply innervated fibers retain embryonic Tonic Fibers
isoform
• The advanced and sometimes exclusive involvement of • Resemble skeletal muscle type I fibers
EOM in myasthenia gravis has been attributed to • Multinucleated
differences in the acetylcholine receptor types • Mitochondrial plentiful in orbital fibers but sparse in
expressed in extraocular versus skeletal muscle global fibers
• It is not clear how this influences the pathogenesis-; of • Are felderstruktur
myasthenia since the antibodies preferentially bind to • Innervated by multiple en-grappe endings
the neuromuscular junctions of multiply and singly
innervated fibre. • At intervals, small swellings overlie muscle nuclei – stain
for ACh esterase
• En-grappe endings concentrated on distal third of
muscle belly

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• Many en-grappe ends occur on a single tonic fiber Other morphological and pharmacological
• En-grappe endings are smaller and lighter staining than features of EOM
end plates
• Extraocular muscle shows signs of ageing from early adult life
• However, total junctional area offered by it is greater
• Also, although mean fibre width of all fibre types is
• Axons supply them are smaller than twitch fibers maintained with age, the variance increases
• Stimulation produce a slowly graded contraction • The action of the muscle relaxant succinylcholine is different
• Do not exhibit propagated action potential – there is • In skeletal muscle, it is a depolarizing blocker of
passive electrotonic spread of depolarization from neuromuscular transmission
multiple sites across the fiber surface • In extraocular muscle it selectively activates the multiply
innervated fibres, certainly in global zone, possibly the orbital
• En-grape potentials are smaller than end plate potentials zone
• Due to smaller junctional area and lesser quantity of • This causes ocular alignment during general anaesthesia
neurotransmitter released approximating the primary position and has been interpreted
to indicate a role for multiply innervated fibres in achieving
• RMP of tonic fiber is lower than twitch fibers ocular alignment.

• The aminoacyl class of local anaesthetics (lidocaine, • Botulinum toxin act by blocking the calcium-dependent
release of acetylcholine at the neuromuscular junction
mepivacaine and bupivacaine) used in the region of the
orbit, are myotoxic and may cause extraocular muscle • The A serotype is used clinically to induce transient
palsies weakening of EOM
• On injection into muscle they induce release of calcium – in the management of squint
from intracellular stores and sarcolemmal disruption – transient relaxation of the levator muscle to protect
ocular surface
• Thus unanticipated ptosis or diplopia may follow ocular
surgery under local anaesthesia – relaxation of facial and other muscles recruited in
dystonic muscular disorders
• The toxicity appears to result from direct injection of the
affected muscles, and it appears that a severe response • Injection of botulinum toxin into skeletal muscle, including
occurs only in the global, pale singly innervated muscle orbicularis, causes a paralysis secondary to denervation
atrophy of the injected muscles
fibres.
• Recovery of skeletal muscle, including the levator, is due to
motor neuron sprouting and functional reinnervation
• However, in EOM there are permanent effects

• Upper tendon
The Four Recti
– Arises from body of sphenoid
• Four recti are attached posteriorly by a short tendinous – Serves part of medial and lateral recti and whole of
ring – the annulus tendineus communis superior rectus
• Is oval in cross-section and encloses optic foramen and • Superior and medial recti are attached more anteriorly
inferomedial end of SOF than others – due to slope of orbital roof
• Annulus thickened above and below by two strong • SR and MR also attached more closely to dural sheath
tendons of optic nerve – pain in (extreme) movements in
• Lower tendon retrobulbar neuritis
– Attached to lesser wing of sphenoid between optic • Average length of recti – 40 mm
foramen and SOF • Width of all EOM (recti +obliques) – 9 mm
– Sometimes marked by infraoptic tubercle • Length – SR>MR>LR>IR
– Serves part of medial and lateral recti and whole of
inferior rectus

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s Superior Rectus
• Origin:
– Upper part of annular tendon superolateral to optic
foramen and optic nerve sheath
– In angle where dura splits in canal
• Course:
– Below attachment of LPS – continuous with
attachments of medial and lateral recti
– Passes anterolaterally beneath LPS
– At 230 to globe AP axis

• Insertion
Relations
– Pierce Tenon
• Superior :
– Attached to sclera 7.7 mm from limbus
– LPS, frontal nerve – separate SR from roof
• Dimensions • Inferior :
– Length – 42 mm – Orbital fat separates ophthalmic artery, nasociliary
– Width – 9 mm artery and nerves
– Tendon length – 5.8 mm – Reflected tendon of SO – between SR and globe
– Arc of contact – 8.4 mm • Lateral:
• Nerve supply – Lacrimal nerve and artery – between SR and LR
– Superior division of oculomotor nerve – Lateral rectus
– Enter at junction of middle and posterior thirds • Medial
• Blood supply – Ophthalmic artery and nasociliary nerve – between
– Lateral muscular branch of ophthalmic artery SR above and MR and SO below

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• Actions
• Primary action : elevation Inferior Rectus
– Increases in abduction, nil in full adduction
• Shortest of recti
• Secondary action : adduction
• Origin
• Tertiary action : intorsion
– Attached below optic foramen by middle part of
• SR is the only elevator in full abduction (IO is ineffective)
lower common tendon
• Paralysis : abducted eye cannot be elevated
• Course:
– Pass anterolaterally along floor of orbit
– Angle 230
• Insertion:
– To sclera 6.5 mm from limbus
– Lower lid by fascial sheaths

• Dimensions: Relations
– Length – 40 mm • Superiorly:
– Width – 9 mm – Globe
– Tendon length – 5.5 mm – Separated by fat, optic nerve and inferior division of
– Arc of contact – 9 mm CN III

• Nerves • Inferiorly :
– Inferior division of oculomotor nerve – Inferior oblique – sheaths combine
– Enter global surface 15mm from posterior end – Separated from orbital plate of maxilla by fat
– However, close to orbital process of palatine bone
– Infraorbital vessels and nerves
• Blood supply:
• Lateral:
– Medial muscular branch of opthalmic artery
– Lateral rectus
– Nerve to inferior oblique between LR and IR

• Actions: Medial Rectus

• Primary action : Depression
– Increases in abduction, nil in full adduction • Largest EOM, stronger than LR
• Secondary action : adduction • Origin:
• Tertiary action : Extortion – increases in adduction – Widely attached medial and inferior to optic foramen by
• Depress lower eyelid both parts of common tendon and sheath of optic nerve
• Course:
– Thicker than other muscles
– Pass along medial wall of orbit
• Insertion:
– To sclera 5.5 mm from limbus in horizontal meridian
– Visibility of muscle insertion through conjunctiva allows
swelling to be detected in endocrine exophthalmos

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• Dimensions Relations
– Length : 40 mm • Superior:
– Width : 9 mm – Superior oblique
– Tendon length : 3.7 mm – Between 2 muscles is ophthalmic artery, ethmoidal
– Arc of contact : 6 mm artery, ethmoidal and infratrochlear nerves
• Nerves • Inferior
– Branch of inferior division of oculomotor nerve – Floor of orbit
– Enters global surface about 15mm from orbital • Medially
attachment
– Peripheral fat, orbital plate of ethmoid and ethmoid
• Blood supply sinuses
– Medial muscular branch of ophthalmic artery • Laterally
– Central orbital fat and optic nerve

• Actions Lateral Rectus

• Pure adductor in primary position
– If axis is elevated or depressed by other muscles, • Origin
medial and lateral recti no longer exert a turning – Attached to both parts of annular tendon where it
force purely around vertical axis crosses SOF
– They also exert slight elevator and depressor – Attachment is continuous
movements – Includes spina recti lateralis on GWoS
– These are small and influence uncertain – U-shaped and concave towards optic foramen
– Use made when displacing insertions of horizontal – Limbs of U forming upper and lower heads of muscle
recti for vertically incomitant squint
• Course:
– First adjoins lateral orbital wall separated by small
amount of fat
– Anteriorly : passes medially to pierce Tenon capsule

• Insertion: Relations
– Pierce sclera 6.9 mm from limbus • At apex of orbit : surround oculomotor foramen
– Insertion visible often through conjunctiva and Tenon – Structures passing are said to be passing between the
• Dimensions: 2 heads of lateral rectus
– Length – 48 mm (longest recti) 1. Superior division oculomotor nerve
2. Nasociliary nerve
– Tendon length – 8.8 mm
3. Sympathetic branch from ICA plexus
– Arc of contact – 15 mm
4. Inferior oculomotor nerve
• Nerves: 5. Ophthalmic veins
– Abducent nerve – enter global surface just posterior 6. Abducent nerve – pass below inf.div.of CN III to
to midpoint become lateral to
• Blood supply : – Above annulus – Lacrimal, frontal, trochlear nerves,
SOV, recurrent lacrimal artery
– Lacrimal branch
– Below annulus – Inf.oph.vein only
– Lateral muscular branch

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• Superior • Laterally
– Lacrimal artery and nerve – Posteriorly – periorbita
• Nerve along whole upper border of muscle, artery
only anterior 2/3 – Anteriorly – perimuscular fat
– Lacrimal gland anteriorly – Most anteriorly – lacrimal gland between bone
• Inferior
– Floor of orbit • Actions
– Tendon of inferior oblique – anteriorly – Abducts eye
• It passes below then medial to LR to attach to in horizontal plane
globe
• Medially
– Near apex – between ON and LR are abducent nerve,
ciliary ganglion, opthalmic artery
– Between LR and IR - nerve to inferior oblique

• Course:
Superior Oblique – Belly passes forwards between roof and medial wall
of orbit
• Is the longest and thinnest EOM
– Muscle becomes rounded tendon 10 mm posterior to
• Length due to deflected tendon + belly trochlear
• Belly is fusiform and more rounded than other EOM – Turns at an angle of 550 at trochlear
• Dimensions: – Pierce Tenon
– Arc of contact : 5 mm – Descends slightly inferior to superior rectus
– Length : 60 mm – Spreads out in a fan-shaped insertion in
– Tendon length : 20 mm posterosuperior quadrant of globe
• Origin: • Insertion is convex posterolaterally
– Superomedial to optic foramen by a narrow tendon – Insertion makes an angle of 450 with AP axis
partially overlapping LPS – Has highest length of tendon insertion – 11 mm

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• Cartilagenous Trochlea • Highly vascular tissue around trochlea thought to

permit repair of working elements
– Is 5.5 mm long, 4mm high, 4mm deep
• Movement of tendon in trochlea is telescopic – ie;
– Axis is anteroposterior
sliding of concentric tendinous bundles
– Medial groove faces ethmoidal wall
– Therefore only central tendinous bundles complete
– Tendon of SO is 1.5mm wide at trochlea full excursion
– Tendon surrounded by loose fibrovascular sheath –
most vascular than any EOM
• Brown Syndrome
– Separated from saddle by a bursa lined by flattened
– Dysgenesis/inflammation in trochlea causes
non-endothelial cells
restricted upgaze in adduction
– Trochlea is surrounded by thick fibrous sheath –
– FDT will demonstrate restriction to elevation in
attaches cartilage to fossa medially
adduction
– Tenon cyst or mass maybe palpable in superonasal
orbit

• Nerves • Actions
– Trochlear nerve enters muscle after dividing into • SO elevates back and hence depress front of eyeball
3-4 branches – Primary action : Intortion
– Enters muscle in orbital surface superiorly – near – Secondary action : Depression
lateral border – Tertiary action : Abduction
– In posterior half of its belly • Depression increases with adduction, becoming less in
progressive abduction
• Blood supply • It is only depressor in adduction
– Lateral (Superior) muscular branch of ophthalmic
artery

• Origin
Inferior Oblique – Rounded tendon from small depression on orbital
plate of maxilla
• Only EOM not originating from orbital apex
– Little behind margin
• Shortest tendon of insertion
– Just lateral to orifice of NLD
– Some fibers from fascia covering lacrimal sac
• Dimensions:
• Course
– Length : 37 mm
– Inclined posterolaterally at an angle of 450 to AP axis
– Tendon length : 1 mm
– Parallel to tendon of SO
– Arc of contact : 17 mm
– Goes between inferior rectus and floor

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• Insertion • Angle of plane of action

– By a short tendon convex upwards – Is usually 450
– Near lateral rectus – However wide variations present
– To posterolateral quadrant of globe – Narrowing angle will reduce torsional action of
– Largely below horizontal meridian muscle and increase vertical action
– Some fibers attach directly to sclera – Widening angle – achieve reverse
– Nasal (posterior) attachment of muscle overlies – Extreme variations results in anomalous A and V
macula – 5mm from ONH patterns
– Temporal (anterior) end lie in
same AP line as lower end of LR
insertion

Relations • Nerves
• Superiorly: – Inferior division of oculomotor nerve
– Fat and inferior rectus – Enters muscle on global surface
• Inferiorly: – Near midpoint of posterior border
– Medially in contact with periosteum of orbital floor –
sometimes send fibrous extensions (arcuate • Blood supply
expansions) – Medial muscular branch of ophthalmic
– Laterally separated from periosteum by fat – Infraorbital artery
– Lateral rectus and Tenons – posteriorly as insertion
twists while inserting to globe

• Actions
• It elevates the visual axis because it depresses posterior Oculocardiac Reflex
aspect of globe
• Bradycardia, nausea and faintness on applying stretch
on EOM or pressure on globe or orbit
• Primary action : Extortion
• Reflex can be eliminated by systemic atropinization
• Secondary action : Elevation
and retrobulbar anasthesia
• Tertiary action : Abduction
• Afferent :
– Via spinal trigeminal nucleus
• It is only elevator in adduction
– Then to visceral nucleus of vagus
• Elevation increases in adduction, nil in abduction

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Ocular Movements and Ocular Movements

Neural Control • For all practical purposes, ocular movements can be regarded
as rotations about three primary axes:
– Vertical, horizontal, anteroposterior
• The globe is prevented from visually significant displacement
during contraction of EOM
– by resistance of the incompressible soft tissues which
surround it
– and stability in the orbit brought about by presence of
supportive connective tissue sheaths, bands, septa and
capsules
• Any rotation must alter the distance between the orbital and
ocular attachments of all its six muscles; some shorten and
some lengthen

• No extraocular muscle normally acts alone

• The muscles of each eye act in concert to produce a
specific eye movement; contraction of one muscle
(agonist), is accompanied by a graded relaxation of its
antagonist
• Thus, the six muscles attached to one globe may be
regarded as three pairs of muscles, each member of a
pair acting reciprocally as ipsilateral agonist or
antagonist in a particular eye movement:
– Medial and lateral rectus
– Superior and inferior rectus
– Superior and inferior oblique
• Excitation of one member of a pair is associated with
reciprocal inhibition of the other

• Yoke Muscles • The yoke muscle pairs are thus

• The pair of muscles which move the eyes in the same – Medial rectus and contralateral lateral rectus :
direction in conjugate gaze are referred to as 'yoke‘ horizontal versions
muscles – Superior rectus and contralateral inferior oblique :
• They behave as synergists dextro or levo elevation)
• These are designated ipsilateral and contralateral, – Inferior rectus and contralateral superior oblique :
according to context dextro- or levo depression
(e.g. left lateral rectus is the contralateral synergist of right
medial rectus)
• By the same token, the terms ipsilateral and contralateral
antagonist are also used

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• The medial and lateral recti are natural opponents, whose

reciprocal contractions and relaxations move the visual
axes in a horizontal plane
• But both oblique muscles can also act as abductors and
the superior and inferior recti as adductors
• Moreover, if both muscles in a pair contract to an equal
extent, their tendencies to elevate or depress the visual
axis and to intort or extort it are opposed and cancelled
out
• Thus, the medial, superior and inferior recti act as an
adductor group
• Their abductor opponents being the lateral rectus and
both oblique muscles

Types of Ocular Movements (1) Types of Ocular Movements (2)

• Rapid movement (1) Monocular movements/Ductions
– Voluntary and involuntary saccades 1. Adduction : inward movement along vertical axis
– Fast phases of vestibulocular and optokinetic reflexes 2. Abduction : outward movement along vertical axis
– REM sleep 3. Supraduction (sursumduction)
• Slow movements • Upward movement along horizontal axis
4. Infraduction (deosursumduction)
– Voluntary pursuit
• Downward movement along horizontal axis
– Vergence movements
5. Incycloduction (intorsion)
– Slow phases of vestibulocular and optokinetic reflexes
• Rotatory movement along AP axis where superior
pole of cornea (12 o’clock position) moves medially
6. Excycloduction (extorsion)
• 12 o’clock moves laterally

(2) Binocular movements Classification of Versions

1. Versions / Conjugate movements
– Synchronous/simultaneous symmetric movements 1. According to direction of movement
of both eyes in the same direction • Dextroversion : both eyes rotate to right ( R-LR, L-MR)
– Maybe voluntary or involuntary • Levoversion : both eyes rotate to left (L-LR, R-MR)
– Involuntary are semi-reflex – occuring in response to • Supraversion/sursumversion: both eyes rotate straight
optical, auditory or other stimuli upwards (bilateral SR and IO)
• Infraversion/deosursumversion : both eyes rotate
2. Vergences / Disjugate movements straight downwards (bilateral IR and SO)
– Are disjugate, synchronous and symmetric • Dextroelevation : both eyes rotate up and to right (R-SR,
movements of the two eyes in opposite direction L-IO)
– Are tonic movements – much slower than versions • Dextrodepression : both eyes rotate up and to left (L-SR,
– Voluntary or optomotor reflex R-IO)

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• Levoelevation: both eyes rotate up and to left (L-SR, R- 2. According to specific features irrespective of
IO) direction
• Levodepression : both eyes rotate down and to left (L- 1. Saccades
IR, R-SO) – Are rapid conjugate eye movements performed to
• Dextrocycloversion : rotational movement around AP bring the image of an object quickly on the fovea
axis in which superior poles of both corneas tilt towards – Voluntary/involuntary
right (simultaneous contraction of R-IR+IO and L-SR+SO)
– Stimuli maybe optical, auditory, or other
• Levocycloversion : rotational movement around AP axis
– Eg: command random movement
in which superior poles of both corneas tilt towards left
(simultaneous contraction of L-IR+IO and R-SR+SO) • Voluntary refixation saccades
• Sensory evoked saccades (visual, auditory)
• Microsaccades
• Rapid pursuit
• REM, OKN, VOR fast phases

• Characteristics of saccades
2. Smooth pursuit / following movements
1. Purpose of saccade is to place the image on the fovea
– Made when tracking an object
and to keep it there as long as it attracts attention
– Function is to match eye velocity with target velocity
2. There is fast phase and tonic phase
– Eg: watching a bird fly
3. Alertness is required to produce saccade
– Helps to keep image of a moving object on fovea
4. Although visual world sweeps rapidly across retina –
constantly
there is no sense of blurring – saccadic omission
• Characteristics of smooth pursuit movements
5. Proceed according to preprogrammed velocity –
however, not ballastic : guided by extraretinal 1. Images moving away from fovea constitute the
information during their flight (adler pg232) strongest stimuli for pursuit movements
6. However, they are not guided by visual feedback 2. Latency 125 ms
7. Once initiated they cannot be stopped or modified 3. Velocity upto 300/sec to 400/sec
8. Long delay of 200 ms from stimulus to execution 4. Beyond this velocity – eyes tend to fall behind and
catch-up is via a small saccade (catch-up saccade)
9. Velocity 1000/sec to 7000/sec

5. Pursuit system has very limited ability to follow targets 3. Stabilization movements
moving back and forth – beyond 2Hz it breaks down – These movements stabilize gaze relative to external
6. Only one image can be tracked at a time world
7. Effectiveness of pursuit depends on degree of – VOR / doll’s eye reflex
alertness – Optokinetic nystagmus
8. Usually pursuits are performed to track an image of a
real object in space 4. Fixating movements
9. However, can be used to track an after-image on retina – These movements maintain foveal gaze lock by
– from an object in space or bright light means of rapid micromovements – flicks
10. Few people are able to track hallucinated targets, – And slow micromovements – drifts
suppressing the saccade system
– “physiological nystagmus”
11. Maybe voluntary (tracking moving object) or
involuntary (when repetitive visual pattern is displayed
continuously)

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Convergence
Classification of Vergences
• Convergence is disjugate movement in which both eyes
• There are 3 types of vergences rotate inward so that the lines of sight intersect infront
1. Convergence of the eyes
– Simultaneous and synchronous inward rotation of • Allows bifoveal single vision to be maintained at any
both eyes due to co-contraction of two medial recti fixation distance
2. Divergence • Convergence remains same throughout life – does not
– Simultaneous and synchronous outward rotation of deteriorate with increasing age such as with
both eyes due to co-contraction of two lateral recti accommodation
3. Vertical vergence • Power of convergence can be increased by exercises
– Are disjugate vertical movements of eyes

• Angle of convergence Horizontal Vergence

– Is the angle that is formed between primary lines of
sight during convergence • Described by 3 different measurement units
– Depends on fixation distance 1. Degrees
– Is smaller with increasing distance of fixation 2. Prism diopters (PD) = 100x tan angle in degrees
– Is smaller with reducing interpupillary distance 3. Meter angle (MA) = reciprocacl of distance in meters
• Near point of convergence measured from center of rotation of globe
– Is the point in space at which foveal lines of sight PD = MA x IPD in cm
intersect when maximal convergence is exerted
– Is the closest point at which an object can be seen
singly
– Is always closer than near point of accommodation

Types of Convergence Maddox classification of vergence

• Reflex convergence
• Voluntary Convergence – Is convergence of visual axes not under voluntary
– Is the amount of convergence of visual axis that can control
be produced at will – Has four components
– Is separate from reflex convergence involved in 1. Tonic convergence
normal visual activities
2. Fusional convergence
– Not everyone is capable of doing or learning this
3. Accommodative convergence
– Large proportion of normal subjects can do
4. Proximal convergence
– Mediated through FEF
– Voluntary divergence is extremely rare

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• Tonic convergence • Fusional convergence

– Due to some inherent innervation tone to EOM when – Also known as positive fusional convergence
patient is awake – results anatomical position at rest
(which is 5 degrees diverged) – Convergence produced to ensure similar retinal
– Is the sum of excitatory and inhibitory influences images are projected to corresponding retinal areas
from different sources such as cortical and subcortical – Occurs without a change in refractive status of eye
centers, vestibular organs, head and neck muscles – Initiated by bitemporal retinal disparity
– Is important in determining position of person’s eyes – Is the responsiveness to disparate stimuli lying
– With tonic convergence, the eyes will be more outside Pannum’s fusional area
convergent than before but from an absolute point of
view – it will still be divergent – Not a voluntary process – an optomotor reflex
– Tonic convergence is most prominent in childhood – Important for achieving BSV
and decreases with age – It maybe convergent, divergent or vertical vergence
– Emotional level may affect tosnic convergence – Amplitude is 18D for far, 35D for near
– Abolished with deep general anaesthesia – Amplitude can be improved with orthoptic exercises

• Latency of fusional convergence is 1 sec • Clinical value:

• Centers : – Fusional vergence produce corrective eye movements
– Primary visual cortex to maintain proper alignment
– 3 types of cells present – In exophoria, fusional convergence is activated to
– Near cells, far cells, zero cells control the exophoria
– Respond to absence of presence of retinal dispariy – If this fails – by fatigue or illness, phoria manifests
(exotropia)
– Amplitude of fusional vergence can be improved by
• Measurement of fusional convergence
orthoptic exercises – sp. in convergence insufficiency
– Accommodation abolished with convex lenses exophoria
– Base out prisms or major synoptophore – Fusional divergence likewise helps to control
– Stronger for near esophoria

Testing of convergence • Fusional convergence is measured by placing a base-out

• Convergence is tested with an accommodative target that prism in front of 1 eye while the patient fixates on a
has enough detail to require an effort to see it clearly (a target, either near or at a distance
penlight or finger is not adequate) • The prism strength is increased until diplopia occurs (ie,
• Fusional and accommodative convergences are until fusion is broken)
simultaneously evaluated by determining the near point • The strength of the prism at which diplopia occurs is the
of convergence (NPC) convergence amplitude
• The patient fixates on a small accommodative target that • Divergence amplitudes are measured in a similar manner
is slowly brought toward the nose. with base- in prisms
• The NPC is the distance at which fusion is not maintained • Normal convergence amplitudes are 25 prism diopters
and a divergent movement occurs. (Δ) for distance fixation and 35Δ for near fixation (AAO)
• A normal NPC is approximately 3–5 cm from the nose

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• Accommodative converge • AC/A ratio

– Is the component of convergence that occurs when a – Is the quantitative relationship between
nerve impulse to accommodate discharges to the accommodation convergence and accommodation
eyes – Relationship is linear
– Stimulus for accommodation is retinal blur than – It is relatively stable throughout life
retinal disparity – Accommodative convergence is measured in prism
– Is part of the synkinetic near reflex with miosis and diopters
accommodation – Accommodation measured in lens diopters
– Normal AC/A ratio is about 3-5 prism diopters per
lens diopter of accommodation
– Majority of myopes have high AC/A ratio
– Hypermetropes have low AC/A ratio compared with
emmetropes

• Clinical significance
• However, there is no correlation between degree of
1. High AC/A ratio can be a cause of esotropia
refractive error and magnitude of AC/A
– Correction with glasses here has to relieve accommodation
• AC/A ratio is normal even in presbyopia by use of bifocal glasses
• Indicates that it is the stimulus for accommodation that – The angle of squint is larger for near than for far
evokes convergence rather than the actual amount of 2. Low AC/A ratio can be a cause of exophoria for near – ie;
accommodation convergence insufficiency
• IPD must also be considered in determination of AC/A 3. Parasympathethomimetics lower AC/A ratio as they induce
pharmacological constriction of the pupil
ratio – convergence required for an individual with wide
– There is pharmacological (peripheral) accommodation
IPD is greater than for a patient with narrow IPD looking without any central involvement
at same fixation distance – Therefore convergence is not stimulated
• Abnormalites of AC/A ratio can cause squints – high AC/A – Basis for penalizing technique in treatment of esotropia
ratio in accommodative esotropia using miotics
• A low AC/A ratio my cause a divergent squint – exotropia • They may also elevate AC/A ratio by weakening ciliary
when looking at near object muscles and inducing more accommodative effort

• Measurement of AC/A ratio • Proximal convergence

1. Prism/cover method done for distance and near – Induced by proximity of object of regard or
2. Lens gradient method awareness of proximity of a near object
– The lens gradient method entails performing the prism and – Initiated by psychological factors – occurs when a
alternate cover test to measure the ocular deviation with
distance fixation subject believes he is looking at a near object although
– The test is repeated with a –2.00 D lens placed in front of actually he is not
each eye – Eg: using haploscope
– The change in the ocular deviation after lens placement (in
prism diopters) is divided by 2 to determine the AC/A ratio – There is a linear relationship between proximal
– A normal AC/A ratio is 3–5 Δ/D convergence and changes in fixation distance –
3. Heterophoria method similar to accommodative convergence
– Determines the AC/A ratio by the following formula: – For each diopter change in fixation distance, an
– AC/A = pupillary distance (in centimeters) + (deviation near approximate change of 1.5 prism diopters occurs in
– deviation distance)/3.
proximal convergence
4. Amplitude method

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• Fusional divergence
Divergence
– Also called negative fusional convergence
• Refers to disjugate symmetrical and simultaneous – Is the divergence produced to ensure that similar retinal
outward rotation of two eyes from a given position images are projected onto corresponding retinal points
• Unknown whether voluntary divergence exists of two eyes
• Clinically, only significant form of divergence is fusional – Occurs without change in refractive status of eye
divergence – Initiated by binasal retinal disparity
– Is a kind of optomotor reflex – similar to fusional
convergence
– Paralysis of fusional divergence differentiated from
bilateral 6th nerve palsy by the fact that at a given
distance, the deviation is comitant and that the distance
between the double images remains the same irrespective
of position of object as it moves laterally in a circle

• Normal range : 4-6 D for far, 8-12 D for near

• End point of amplitude
Vertical Vergence
1. Endpoint for amplitude of fusional divergence for • Refers to disjugate vertical movements of two eyes in
distance opposite direction – one eye should rotate upwards,
– Beyond maximal limit of fusional divergence, one downwards
diplopia occurs • However, classified as positive vertical vergence if right
2. Endpoint for amplitude of fusional divergence for eye moves up relative to left eye
near
• Negative vertical vergence if left eye moves up
– In near vision, eyes are accommodated and also
converged • Occur in a bid to correct vertical heterophoria
– Therefore, when measuring, the accommodative • These are also reflexly controlled and stimulated by
convergence is relaxed to prevent retinal disparity retinal image disparity (are involuntary)
– But along with relaxing accommodative • Amplitude much smaller than horizontal vergences
convergence, accommodation also relaxes leading • Average amplitude : 3-8 D
to blurring of vision

Cyclovergence • Average values

1. Incyclovergence : 6-10 degrees
• Is the disjugate torsional movement in which vertical
2. Excyclovergence : 4-8 degrees
meridians of the two eyes move in opposite directions
to each other • Thus, these movements are:
• Incyclovergence : upper pole of cornea (12 o’clock) in – Slow
each eye tilts towards nose – Of low amplitude
• Excyclovergence : upper pole of cornea tilt away from – There significance in compensating for a manifest
nose cyclodeviation not clear
• Cyclovergences are also involuntary movements • Because cyclofusion occurs predominantly on a
stimulated by retinal image disparity due to cyclophoria sensory basis
• Thus occur to compensate for cyclophoria
• Amplitude expressed in degrees

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• Lesions in PPRF or rostral reticular formation lead to loss

Centers involved in Ocular movements
of horizontal or vertical conjugate movements
• Horizontal movements : in pons – PPRF • Lesions of certain afferent pathways impair generation of
• Vertical movements : in medulla – riMLF, INC nystagmus
• Cortical regions • Mesencephalic lesions impair vergence movements
– Occipital cortex, frontal eye field, parietal cortex • Lesions of co-ordinating structures such as cerebellum
• Cerebellum impair velocity and precision of eye movements
• Vestibular apparatus • All eye movements occur against viscous drag of orbital
tissues – including muscles and elastic restoring forces of
• Superior colliculi
orbital structures
• Perihypoglossal nuclei
• The EOM are among the fastest and most fatigue
• Medial longitudinal fasciculus resistant of mammalian muscles
• Its isometric contraction rate is twice as fast as limb
muscle

• Different types of motor units are regarded as final

common pathway for all forms of eye movements
• All types of fibers participate in every type of movement
– whether conjugate of disjugate
• In a saccade:
– OSIF and GRSIF are recruited first – well in off direction
of muscle
– Then multiply innervated units – probably near
primary position
– Then very fast but fatigable muscle fibers well into the
on-direction of the muscle
• EOM show significant degree of activity even when the
eye is directed well into off direction – this sustained
activity eliminates slack and allow eye movement system
to operate in the linear region of lengh-tension curve

Frontal Eye Fields (FEF) • Afferents

1. Thalamus
• Is the frontal ocular motor area 2. Superior temporal cortex
• Brodmann area 8, with parts of 6 and 9 3. Peristriate cortex
• Occupies posterior part of middle frontal gyrus 4. Parietal cortex (area 7) : where visual and eye-
(prearcuate gyrus) movement related neurons have been identified
• Efferents
• Stimulation results in
1. Contralateral FEF
1. contralateral conjugate deviation of eyes
2. Ipsilateral cortical areas concerned with visual
2. Head movements perception (parietal cortex – area 7, peristriate area
3. Pupillary dilatation – area 19)
• Mediates both voluntary and reflex ocular movements 3. Descending fibers travel in anterior limb of internal
capsule and divide into ventral and dorsal tracts in
• Occipital association and thalamic efferents (dorsomedial
upper part of midbrain
nucleus) reach this area

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• Dorsal tract • FEF encodes neural activity topographically (similar to

– Synapse in thalamic nuclei and pulvinar superior colliculus)
– Goes to pretectal nuclei and deep superior colliculus • Activity at different sites relates to saccades of different
• Ventral tract size and direction
– Descends in cerebral peduncle • Purely vertical saccades are elicited by simultaneous
– Some fibers to subthalamic nucleus and deep stimulation of corresponding sites of both FEF
superior colliculus • FEF maybe concerned in maintaining visual attention,
– Majority to PPRF directing eyes to objects of interest while other images
• Third prefrontal bundle are ignored
– Arise at diencephalic-mesencephalic junction and • Human frontal lobe lesions cause transient loss of
rostral red nucleus contralateral saccades
– Project unilaterally to riMLF and INC
– Bilaterally to nucleus of Darkschewitsch and upper
part of oculomotor nucleus

• Occipital cortex maybe concerned with fixation reflex

Striate Cortex (area 17)
– Bringing onto the fovea the image of an object which
• Is the primary cortical reception area for visual has gained interest in periphery of retina
information and has many connections • Stimulation of visual areas 17 and 18 causes conjugate
• Afferents deviation contralaterally (and various directions)
1. Pontine reticular formation • Accommodation elicited by stimulation of area 18
2. Pulvinar of thalamus • Parieto-occipital lesions affect ipsilateral smooth pursuit
• Efferents
1. Pretectal
2. Superior colliculus
3. Posterior thalamus

• Neurons in primate inferior parietal lobes are active

Parietal Cortex before and during certain ocular movements
• Area 7 of parietal lobe is related to attention to visual • Fixation neurons fire during fixation or smooth pursuit
targets • Tracking neurons fire during pursuit only
• Afferents • Saccadic neurons fire before and during visually evoked
– Cingulate gyrus, basal forebrain saccades – not in spontaneous saccades
– Pretectum and superior colliculus via thalamus • Activity related to volition
– Frontal eye field and peristriate cortex • Associated with maintaining or shifting attention
• Efferents • Conjugate deviation occurs by stimulating angular gyrus
– Pretectum and superior colliculus – in posterior end of middle temporal lobe
– Periaqueductal gray matter • Biparietal lesions may produce ocular apraxia
– Ipsilateral and contralateral parietal lobes

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Subcortical Regions Cerebellum

• There are connections between FEF and basal ganglia • Major co-ordinator of movements of skeletal muscles
• Between superior colliculus and substantia nigra including EOM
• Comprises of older archeocerebellum – flocculonodular lobe
• Patients with extrapyramidal diseases frequently show
saccadic abnormalities • Palaeocerebellum (spinocerebellum) – anterior lobe
excluding lingula, but including pyramid and uvula of middle
• Pulvinar receives afferents from visual cortex and lobe
superior colliculus
• Neocerebellum – middle lobe including vermis
• Stimulation of thalamus induces saccades • Mossy fibers carry main afferent input from olive,
• Lesions impair saccadic accuracy and ability to match spinocerebellar, pontocerebellar and vestibulocerebellar
ocular target with position pathways
• Climbing fibers carry input from pontine nuclei, inferior
olive, medial reticular formation – has 1:1 ratio to Purkinje
cells

• Basic anatomy of cerebellum (10% of brain) • Midline structures : lingula, culmen, declive, folium,
tuber, pyramid, tonsil
• Lies in infratentorial compartment in posterior cranial
fossa – in concavity of occipital bone • Tonsil – inferior aspect – in tonsillar herniation
• Posterior to midbrain – connected by 3 peduncles (sup – • Nodule – lies on roof of 4th ventricle
midbrain, middle – pons, inferior – medulla) • Nodule connected to flocculus by slender band of white
• Has two hemispheres united by midline vermis matter
• In between – cavity of 4th ventricle • Cortex grey matter, deep white matter
• Vermis lies on superior medullary velum • Deep nuclei – largest and most lateral – dentate
• Has fine slit like sulci and in between folia • Globose, emboliform, fastigial
• Divided by horizontal fissure – no functional significance • Purkinje cells – largest cell
– Divides it into superior and inferior halves • Development : from metencephalic part of
rhombencephalic vesicle
• Primary fissure – small anterior lobe, larger
posterior/middle lobe • Oldest part to develop is archaecerebellum

• Superior peduncle – efferents from dentate nucleus to

red nucleus, thalamus, cortex. Afferents from anterior Flocculonodular Lobe/ Vestibulocerebellum
spinocerebellar and tectocerebellar
• All receive direct input from vestibular nuclei
• Middle – afferents from pontine nuclei of opposite side
• Include flocculi, nodules, ventral uvula and paraflocculi
• Inferior – from vestibular nuclei, post.spinocerebellar,
olivocerebellar, cuneocerebellar • Afferents
• Arteries – superior cerebellar and PICA and AICA – From inferior olivary nucleus (climbing fibers)
• Anastomose on surface – perforating branches are end – Reticular formation (mossy fibers)
arteries – Vestibular and perihypoglossal nuclei
• PICA syndrome – lateral medullary/Wallenburg • Efferents : reciprocal connections to vestibular nuclei
• PICA is largest and most tortuous branch of vertebral art. and nuclei prepositi hypoglossi
• Venous drainage – nearest venous sinus • Visual information reaches flocculus via connections
• Straight and transverse sinus – superiorly involving retina, contralateral pretectum, inferior olivary
• Inferior petrosal, sigmoid, occipital sinuses - inferiorly nucleus

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• Nucleus of optic tract and floccular neurons encode Vermis

information about direction and velocity of ocular
targets • Concerned with saccadic control
• Vestibulocerebellum modules smooth pursuit and • Afferents
vestibulocular refelx – Vestibular nuclei
• It is concerned with adjustments matching head and eye – Pontine nuclei – receive afferents from superior
movements with target movements colliculus, LGB, striate cortex
• Dorsal lesion results loss of coordination of ocular – Cervical and ocular proprioceptive afferents
movements with overshoot of saccades • Efferents
– Indirectly to oculomotor nuclei via vestibular
connections
• Purkinje cells in vermis discharge 25ms before a saccade

Cerebellar Hemispheres Vestibular Apparatus

• From hemispheres reach ocular motor nuclei via • Provides information used in synthesis of eye
brachium conjunctivum directly or via nucleus reticularis movements and adjustment of trunk and limb posture
tegmenti pontis with respect to head movements
• This nucleus is just anterior to PPRF • VOR prevents image slip during eye movements
• Has reciprocal connections with ocular motor neurons • Membranous labyrinth in temporal bone contains
• Stimulation of hemispheres produce both saccades or cristae of semicircular canals and maculae of utricle and
smooth pursuit saccule
• Has hair cells with stereocilia
• Longest cilium – kinocilium
• Deflection of stereocilia towards kinocilium stimulates
cells, deflection inhibits it
• Inside is endolymph

• Semicircular canals
– Stereocilia of cristae embedded in gelatinous cupula
– One in each ampulla of 3 canals
– Flow of endolymph towards ampulla in horizontal
canals is excitatory
– Flow of endolymph away from ampulla in anterior
and posterior canals are excitatory
– An excitatory stimulus from one side is reinforced by
contralateral inhibitory stimulus
• Each canal induces ocular movements approximately in
its own plane – Floren’s law
• It influences the yoke pair of EOM which are prime
movers in that plane, regardless of initial position of eye

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• Utricle and Saccule

– Maculae of these respond to linear acceleration –
particularly gravity
– Lie in planes at right angles
– Hair cells have processes embedded in gelatinous
matrix containing CaCO3 crystals – otoconia
• Vestibular nerves
– Ends perforate lamina cribrosa of ear to reach
vestibular ganglion at lateral end of internal auditory
meatus
– Form vestibular nerve – pass to CP angle inferior to
facial and posterior to cochlear nerves in IAM
– Project mainly to vestibular nuclei and
floccularnodular lobe

• Vestibular nuclei Vestibular connections

– 4 nuclei – superior, medial, lateral, inferior • Mossy fibers of vestibular nerve project directly to
flocculus, nodulus, ventral uvula and paraflocculus
– Clustered under floor of 4th ventricle
1. Purkinje cells of flocculus project
– Complex reaches caudally into pons
– Directly to ipsilateral vestibular nuclei, perihypoglossal
• Efferents
nuclei, and deep cerebellar nuclei
– To MLF – distributed to ocular motor and brainstem
– Indirectly via fastigial nucleus bilaterally
nuclei
2. Vestibulothalamic connections
– From inferior vestibular nucleus to
vestibulocerebellum and vermis 3. Parietal connections
– Vestibulospinal efferents from lateral vestibular • Vestibulocerebellar lesions have little effect on VOR and
nucleus maintenance of eye position
• Flocculectomy cause post-saccadic drift
• Ablation of vermis + fastigial nucleus cause saccadic
overshoot

Perihypoglossal Nuclei
• Lie medial to the vestibular nucleus
• Involved in neural integration of vertical and horizontal
eye movements
• Most prominent is nucleus prepositus hypoglossi
• It extend from rostral pole of hypoglossal nucleus to
almost to abducent nucleus
• Caudally, it continues to nucleus intercalatus – between
hypoglossal nucleus and dorsal vagal nucleus
• Another member is – sublingual nucleus
• It lies ventral to rostral hypoglossal pole – near its
radicular fibers

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• Afferents Medial Longitudinal Fasciculus

– From riMLF, INC representing visual input
– PPRF and flocculus • Is a group of myelinated fibers
– From vermis via fastigial nucleus • Extending from rostral midbrain to spinal cord
– All ocular motor nuclei • Situated close to the midline just anterior to the
cerebral aqueduct, 4th ventricle and central canal of cord
• Cause ipsilateral inhibition and contralateral excitation • In intimate relation with many motor and ocular nuclei,
of ocular motor neurons including ocular motor nuclei
• Represent an additional vestibulocerebello-ocular • Contain fibers from nuclei at various levels of brainstem
pathway for modulation of vertical and horizontal eye
movements

• Below abducent nucleus – most fibers are descending

• Above abducent nucleus – most fibers are ascending
• At its cranial end – it is connected to interstitial posterior
commisural and other nuclei lateral to 3rd ventricle
• In midbrain – it is ventral to central gray matter
• In pons – anterior to floor of 4th ventricle
• Connects oculomotor, trochlear and abducent nuclei
• Connects them to all 4 vestibular nuclei
• Extensive connections with cerebellum via these nuclei
• Provides an intersegmental integration of movements
associated with vision and hearing
• Also connects CN 7, CN 9 nuclei (in addition to II, III, IV, VI,
VIII) and spinal nerves at cervical level

• Descending fibers • Afferents

– Originate mainly in medial vestibular nucleus 1. From vestibular nuclei – to oculomotor nuclei
– Provides both crossed and uncrossed fibers – From superior vestibular nucleus ascend in
– To upper cervical motor neurons – provides inhibitory ipsilateral fasciculus to CN 4 and dorsal oculomotor
signals nucleus (for inferior rectus motor neurons)
– In labyrinthine regulation of head position – From lateral vestibular nucleus – to contralateral
– Also in reticular formation, INC, superior colliculus CN6, CN4 nuclei and parts of CN 3 nucleus
– From inferior vestibular nucleus – sparse
– Reciprocal fascicular connections represent axons of
internuclear neurons in oculomotor and abducent
nuclei
– Superior projections are contralateral – crossing at
level of abducent nucleus

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• There is a bilateral projection from oculomotor to

abducent nucleus
– Predominance of ascending projections
– As half of abducent neurons are internuclear
– But only 3% of CN3 neurons are internuclear
– Abducent internuclear neurons project mainly to
contralateral CN3 neurons for medial rectus and Generation of Eye Movements
inferior recti
2. From reticular formation – to cerebellum
– From internuclear oculomotor neurons and superior
colliculus
– Thence project to cerebellar vermis

Vestibulo-ocular Reflex
• VOR and OKN both systems combine and maintain
visual direction despite head movements
• Angular acceleration of even brief head movements
stimulates semicircular canals – visual system responds
accordingly to the moving visual world
• VOR generates
– A slow following response in opposite direction to
head movement
– And then a rapid phase in same direction (towards
approaching visual scene)

• Latency of VOR is very short – 14ms • Spontaneous discharge of vestibular apparatus is

• Velocity ranges from 3000 – 5000/sec for slow phase modulated in response to head movements – rotation,
• Rapid phase is saccadic tilting and tipping of head
• Otoliths in labyrinth generate ocular counter-rolling
• Mediated by two systems response to head tilt
1. A three-neuron reflex arc • Indirect excitator vestibular projection via MLF and
– Vestibular nerve lateral vestibular tract of Deiter
– Vestibular nuclei • Vestibular neurons project to:
– Oculomotor nuclei – Contralateral abducent nucleus
– Abducent motor neurons
2. A parallel polysyaptic accessory optic route involving – Internuclear neurons
– Reticular formation • These carry signal via MLF to ipsilateral medial
– Perihypoglossal nuclei rectus motor neurons
– Interstial nucleus of Cajal

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• For vertical eye movements

– Vestibular neurons project via MLF and possibly
superior brachium to oculomotor and trochlear
neurons
• Two additional vestibular neurons reinforce VOR
1. Type I vestibular neurons
• Excited by ipsilateral horizontal rotations and
inhibited by contralateral rotations
2. Type II vestibular neurons
• Show reverse response to type I
– An intervestibular commissure allows type I neurons
to activate contralateral type II neurons receiving
input from ipsilateral horizontal canal
• Similar reciprocal innervation exists for vertical
rotations

Generation of VOR
• Transducer:
– Opponent pairs of 3 semicircular canals
– Horizontal canals paired
– Anterior canal paired with contralateral posterior
canal
– Lie roughly in pull direction of 3 muscle planes
– Converts head rotation into neural code
• Excitatory impulses go to vestibular nuclei
• Occurs at subcortical level – not abolished in cortical
lesions
• Used to differentiate betwen supranuclear gaze palsies

• Horizontal VOR
– Vestibular nuclei stimulate contralateral abducent
nucleus
– Activate contralateral lateral rectus
– Also stimulate ipsilateral oculomotor MR subnucleus
via interneuron (MLF)
– Activate ipsilateral medial rectus
• Vertical VOR
– Similar innervation by vestibular nuclei to CN III and IV
nuclei

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• Role of cerebellum
The Optokinetic System
– Flocculus essential for adaptation of VOR to optical
distortions • Optokinetic response is evoked by rotation of visual fields
– Receives retinal slip and canal signals and provide a before the eyes
negative feedback signal • Consists of eye movement following the moving scene
– Error correction signal via Purkinje cells to floccular succeeded by a rapid saccade to opposite direction
target neurons (FTN) to make appropriate changes to • Response is to peripheral retinal stimulation
VOR • Visual afferents project to vestibular nuclei by several
routes facilitating integration of VOR and OKR
• Transient head rotation thus stimulates both VOR and
OKR
– VOR with a latency of 10ms occurs first
– Reinforced by OKR with latency of 70ms – indicate
retinobulbar response time

• During sustained rotation with the eyes open - vestibular • Thus, during combined vestibular and optokinetic
drive decreases as endolymph movement ceases stimulation - which occurs for instance during self rotation
• However, optokinetic system maintains a steady – As the vestibular drive declines
discharge from the vestibular nuclei to sustain – Optokinetic input persists
compensatory optokinetic nystagmus – Maintains a steady vestibular discharge and
• Optokinetic nystagmus is induced by moving full-field – Continues to generate compensatory eye movements
visual stimuli • Visual input from the retina reaches the vestibular nucleus
• Eyes reach stimulus velocity within 2 ms of stimulus the accessory optic path
onset, mainly via a smooth pursuit response • Includes pretectal nuclei such as :
• Response is then sustained by stored neural activity – Nucleus of the optic tract (NOT)
within vestibular nuclei – Reticular nucleus of the pontine tegmentum
– This velocity storage mechanism is responsible for – Medial pontine nuclei
optokinetic after-nystagmus which is evident in – Perihypoglossal nuclei
darkness – Vestibular commissure

Accessory Optic Pathway • Cortical contribution to OKN comes from

• Pathway involved in OKR consists of retinofugal projections – Middle temporal (MT)
to Nucleus of Optic Tract (NOT) & accessory optic systems – Medial superior temporal (MST)
• They are relayed to medial vestibular nucleus via nucleus – Posterior parietal (PP)
prepositus hypoglossi and medullary reticular formation – They respond to large moving visual stimuli with
• There is significant transcortical projections short latency
• Main function of this system is to correct for retinal slip of • MST project to accessory optic system and dorsolateral
images during self movement pontine nuclei of smooth pursuit pathway
• Outflow to vestibular systems assist in stabilizing eyes, • Neurons of NOT and dorsal terminal nucleus - encode
neck, trunk, and limbs during rotation speed of movement of images on retina during OKN
• Consist of 3 target nuclei in rostral midbrain – dorsal, • Lesions abolish the velocity storage components of
lateral and medial terminal nuclei OKN responsible for optokinetic after-discharge, but
• And 2 sets of retinofugal optic fibers – inferior and leave smooth pursuit intact
superior fasciculi

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• OKN in newborn – mediated entirely by accessory optic • Bilateral occipital lobectomy cause loss of smooth pursuit
system pathways component of OKN and induces nasotemporal
– Show nasotemporal asymmetry asymmetry – unilateral lesion do not
– Ie; more developed monocular response to targets • MT area damage : impair smooth pursuit and saccades
approaching from temporal side to targets in the contralateral hemifeild
– This immature response retained in amblyopes • MST lesions (Broadmann 19, 39) cause impaired smooth
pursuit towards side of lesion and impaired full field
– Normal symmetrical response achieved by 2 months
of age – with maturation of transcortical pathways • Unilateral parietal lobe lesions : cause asymmetry of
smooth pursuit and impairment of OKN with stimuli
moving towards side of lesion
• Bilateral occipital lobe lesions : cause lack of OKN –
depends also on amount of extrastriate involvement

Pathway for OKR - Adler Nucleus of Optic Tract

• Transducer • Cortical inputs – via MST (similar with smooth pursuit)
– Motion sensitive ganglion cells in retina – Project to ipsilateral NOT
– Respond exclusively to motion in certain directions – Binocular cortical cells receive projections from both
and orientations eyes
• Visual signals for OKR is received via 2 pathways – Code ipsilateral motion from the contralateral visual
1. Projections to striate cortex - V1 via LGB field at higher velocities than the subcortical system
2. Projections to midbrain via accessory optic tract • Subcortical inputs
• Nucleus of Optic Tract (NOT) – for horizontal – From the contralateral eye – ie; crossed
target to ipsilateral side – nasal to temporal – They have large receptive fields and respond to large
direction textured stimuli moving in specific directions
• Lateral and medial terminal nuclei (LTN, MTN) for
vertical motion

• Stimulation of the NOT causes conjugate movements of OKR in infantile esotropia

both eyes to the ipsilateral side • Until age of 3–4 months, the monocular subcortical projections
predominate because the cortical projection has not yet
• Each NOT projects signals developed
– Via the inferior olive to the vestibular nuclei • Therefore OKN in infancy is driven mainly by the crossed
subcortical input
– Possibly to the flocculus via the climbing fibers • Monocular stimulation only evokes OKN with temporal-to-nasal
motion but not with nasal-to-temporal motion
• After 3–4 months of development, the infant’s cortical projections
• Motor response for OKR from NOT via vestibular nuclei predominate and horizontal OKN responds to both monocular
is then similar to VOR temporal-ward and nasal-ward image motion
• The cortical projections to the NOT fail to develop in infantile
esotropia
• As target moves faster there is a lag phase and at velocities higher
than 1000/sec OKR cannot be elicited • As adults these patients exhibit the same asymmetric OKN
pattern as observed in immature infants
• This is responsible for a disorder known as latent nystagmus in
which a jerk nystagmus occurs when one eye is occluded with the
slow phase directed toward the side of the covered eye.

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Pathophysiology of Latent nystagmus in infantile Saccades

esotropia
• During monocular fixation, the stimulated retina • A saccade is a rapid eye movement changing fixation to
increases the activity of neurons in the contralateral a new object of interest
NOT via subcortical crossed projections • Also occur in fast phase of REM sleep
• Cause ipsilateral conjugate eye movements • Typical saccade
• But it is unable to innervate the ipsilateral NOT via the – Accelerates to a peak velocity about half-way
ineffective cortical-tectal projection through the movement
• The result is that both eyes’ positions are drawn to the – Gently decelerates
side of the stimulated NOT (i.e. the side of the covered – Then stops abruptly at a new eye position
eye) • A fixed relation exists between peak velocity (maximum
• The fixation error is corrected with a saccade and a 7000/sec) and amplitude of movement
repeated sequence is described as latent or occlusion • Saccadic reaction time is about 200ms
nystagmus

• A saccade is programmed based on retinal error : the

distance between retinal target image and fovea
Cortical Control of Saccades
• Within the time taken for visual signal to traverse retinal
1. Frontal eye fields
and central pathways and reach brainstem ocular motor
mechanisms (about 70ms) – the saccadic response can – Mediate voluntary control of contralateral saccades
be modified by visual information – FEF is active whether saccades occur or not
• Beyond this – response cannot be changed – Activity is related to visual attention
• Retinal blur is not appreciated during saccades – due to – Related activity in the FEF precedes saccades by 50 ms
elevation of visual threshold by approx. 0.5 log units
– Surface of the FEF has a coarse retinotopic
• 2 components of saccade :
organization
1. Rapid phase – a pulse of neural impulses overcome
orbital viscous drag to move eyes rapidly from one – Stimulation of a particular area causes a saccade to
point to another change eye position in a specific direction and
2. Tonic step phase – maintain new position against amplitude
orbital elastic restoring forces – These cells are active before saccades

• FEF cells in one hemisphere causes conjugate saccades to • Both SC and FEF can be ablated without abolishing
the contralateral side saccades. If both ablated – loss of saccades
• Vertical saccades - stimulation of both hemispheres • Superior colliculus
needed – Function to represent intended gaze direction
• Modalities that can stimulate movement fields – Has retinotopic mapping
– Vision – Stimulation of one colliculus cause conjugate saccade
– Audition to contralateral side
– Touch – Stimulation of both colliculi cause vertical saccades
• Efferents : Two main pathways – Modalities sensitive : visual, auditory and touch
– One projection is to the superior colliculus (SC) - (similar to FEF)
ipsilateral
– The other is to the pons – PPRF for horizontal saccades,
and midbrain - riMLF for vertical saccades –
contralateral pathway

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• Horizontal and vertical saccades are generated by

Pulse Component
groups of neurons located in the brainstem and
controlled by frontal system (for voluntary saccades) • Neural substrate for:
and collicular system (for involuntary saccades)
– Horizontal saccades : lies in the caudal pons
• Brainstem neurons form final premotor circuit
– Vertical saccades : lies in the rostral mid brain
• These neurons create saccades by a pulse – step
• Saccadic size is encoded in these premotor centres by
innervation system
the duration of firing
• Pulse is created by sudden firing of neurons to ocular
• The spatial information provided by topographical
muscles
sensory maps of the striate cortex, frontal eye field and
• After eyeball is moved into new position, to keep it in superior colliculus are converted into a temporal series
the same position sustained contraction of muscle is of impulses at these sites
required – the step component
• The CNS converts a visual signal about target position on
the retina into information about target location in space
using eye, head, and body position signals

• Burst Neurons: • Inhibitory 'burst' neurons lie just caudal to the abducent
nucleus in the rostral medulla
• There are excitatory and inhibitory ‘burst’ neurons
– Provide a reciprocal innervation
• The premotor command for the pulse of a horizontal
– Send inhibitory signals to the contralateral abducent
saccade arises in neurons in the PPRF nucleus
• PPRF project to the ipsilateral abducent nucleus • The premotor command for the pulse of a vertical
• They discharge shortly before and during the saccadic saccade arises in neurons in the riMLF at ventral
motor neuron pulse ('medium lead' burst neurons) midbrain-thalamic junction
• The firing rate is correlated with eye velocity • These neurons project to the ocular motor nuclei
concerned with vertical movement and to the interstitial
• Burst neurons also project to nucleus of Cajal (INC)
– Internuclear neurons in the abducent nucleus • Lesions in the prerubral fields cause vertical saccadic
– Whose axons pass to the contralateral medial rectus palsies
motor neurons • Lesions in the INC disturb visually guided but not
– To bring gaze to the same side vestibularly induced contralateral saccades

• Neurons in the more rostral PPRF fire several hundred Pause cells / Omnipause cells
milliseconds before horizontal and vertical saccades - • Are cells near the abducent nucleus in the middle raphe
'long lead' burst neurons’ complex
• Encodes saccadic direction • Tonically inhibit 'burst' cells between saccades
• They receive projections from the superior colliculus, • Their function is to suppress 'burst' cell activity during
frontal eye fields and nucleus cuneiformis (lateral to mid maintained fixation
brain reticular region)
• Their activity pauses just before and for the duration of
a saccade
– Permits the burst cells to discharge
– If such 'pause' cells are stimulated during saccades,
movement is aborted

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Step Component Paramedian Pontine Reticular Formation

(PPRF)
• New position at the end of a saccade is maintained by a
train of impulses arising from tonic neurons of the PPRF • Is the primary supranuclear center for horizontal eye
movements
• Which may be part of a neural integrator
• Lies in pons from level of trochlear to abducent nucleus
• Every position is specified by a unique pattern of activity
in the ocular motor neurons • Inputs:
– FEF
– Superior colliculi
• Pulse (slide) and step components are independently – Vestibular nuclei – for postural correction
under cerebellar control – Cerebellum – modulation
– Parahypoglossal nuclei – for gaze holding
– riMLF

• Types of cells
• Output:
• Adler : 4 types of cells present – burst, tonic, burst-tonic,
– Ipsilateral abducent nucleus
pause
– Interneurons to contralateral MR subnucleus – the
– Excitatory burst neurons
MLF
1. Medium-lead burst
– riMLF – for vertical gaze
– On direction
– Contralateral PPRF and vestibular nuclei – reduce
innervation to antagonist during saccade – Controls pulse component
2. Long-lead burst
– No direction sensitivity
– Discharge upto 200 ms before saccade
– Receive input from FEF and SC
– Drive medium lead burst cells
– Inhibitory burst neurons – to opposite abducent
nucleus – inhibit antagonist

• Pause cells /Omnipause neurons (OPN)

– Gate initiation of pulsation by constantly inhibiting
burst cells
– Located in nucleus of dorsal raphe below abducent
nucleus
– Same OPN inhibit saccades in all directions
– Stops discharge immediately before and during
saccade

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Rostral interstitial Medial Longitudinal

Fasciculus (riMLF)
• Inputs from
Anatomical
– FEF
scheme for
the synthesis – Superior colliculus
of signals for • Outputs to
horizontal eye
movements – Ipsilateral trochlear nucleus
– Both oculomotor nuclei

Disorders of Saccades
Integrators of Saccades
• Accuracy – dysmetria
• Horizontal saccades
– Can occur in cerebellar disorders
– Medial Vestibular Nuclei
– Too large amplitude – hypermetric
– Nucleus Prepositus Hypoglossi (NPH)
– Too small amplitude - hypometric
• Velocity – glissades
• Vertical saccades
– When pulse component is too small and saccade will
– Interstitial nucleus of Cajal (INC) slide – post-saccadic drift/glissade
• Inappropriate timing – intrusions
• Flocculus of cerebellum – Caused by cerebellar disorders and progressive
– integrate velocity signals to position signals supranuclear palsy

• The neural substrate for smooth pursuit movements is

Smooth Pursuit System uncertain
• Is separate from optokinetic slow phases • But signals related to pursuit movements have been
• Smooth pursuit maintains a target image on the fovea recorded from:
throughout a tracking movement 1. Accessory optic system
• Latency is 130 ms • Nucleus reticularis tegmenti pontis (NRTP)
2. Brainstem reticular formation
• Stimulus for smooth pursuit is movement of an image in
the region of the fovea • Dorsolateral pontine nucleus (DLPN)
• Lateral pontine nucleus (LPN)
– System is primarily sensitive to retinal slip velocity
3. Cerebellar flocculi
– (displacement of the target image from or towards
4. Occipitoparietal region and other cortical areas
the fovea)
• V5 (MT area)
– And adjusts eye velocity to match that of the target
• MST area – follow targets while head is moving
by negative feedback control
• Posterior parietal cortex
• Retinal image position may also be a factor

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• The medial superior temporal (MST) area is also involved

Cortical areas for smooth pursuit
in generating pursuit signals in response to moving stimuli
• Impulse for smooth pursuit originates in area V5 —the • The area appears to be supplied with information about
(MT) visual area in the rhesus monkey head movement (from MT) as well as eye movement
• Lies in superior temporal sulcus commands (efference copy)
• MT encodes speed and direction of visual stimuli in three – Thus generates pursuit movements to follow a target
dimensions relative to eye while the head is moving
• Receives input from : – Combine retinal and efference copy signals
– Primary visual system – both striate and extrastriate – Ipsilateral system
areas – Efferents to DLPN for smooth pursuit (& NOT for OKN)
– Also likely magnocellular input directly from the LGN • Target recognition and selection probably receive
• Output additional input through the reciprocal connections to the
– Area MST posterior parietal cortex (PPC)
– FEF

• Information from the MT and MST : • Dorsolateral pontine nucleus (DLPN)

– Projects via the posterior portion of the internal – Play a large role in maintaining steady-state smooth
capsule pursuit eye velocity
– To dorsolateral pontine nuclei (DLPN) – Serves as a precerebellar relay for both pursuit and
– And lateral pontine nuclei saccade-related information
• From these pontine nuclei, projections are sent to the
cerebellum (paraflocculus and dorsal vermis), with • Nucleus reticularis tegmenti pontis (NRTP)
outflow signals to the vestibular nuclei
– Contributes to both initiation and maintenance of
• The smooth-pursuit system is a double decussating smooth pursuit
pathway (the decussation occurs in both the pons and
– Lies just anterior to rostral portion of the PPRF
cerebellum); therefore, it can be simplistically considered
an ipsilateral system – Also participates in fusional and accommodative
vergence
• MST and FEF also project to NOT to elicit OKN

Pursuit system
• Flocculus • A moving object creates signals in the striate
cortex (V1), and from there to the
– Maintain pursuit eye movements during steady constant extrastriate cortex (V2, V3)
tracking • These signals are subsequently relayed to
the middle temporal (MT) area and medial
• Vermis superior temporal (MST) areas, the posterior
parietal cortex, and the frontal eye field
– Important when the target velocity changes (FEF)
• The descending cortical pathways of the
– Or when initiating pursuit temporal, parietal, and frontal lobes
innervate the ipsilateral dorsal lateral
• The role of the cerebellum is to sort out eye and head pontine nucleus (DLPN)
• The neurons in the DLPN decussate and
rotations in the tracking process and to sort out the ocular project to the vermis and flocculus in the
contralateral cerebellar lobe, which
pursuit signal from visual and eye–head motor inputs innervates the medial vestibular nucleus
(VN)
• From here, activity passes via vestibular nuclei • VN neurons then decussate and project to
the contralateral CN VI nucleus
– Perform necessary neural integration of velocity signal • The nucleus of CN VI initiates conjugate
to a position signal that is sent to the eye muscle motor horizontal eye movements by innervating
the ipsilateral lateral rectus muscle and, via
neurons internuclear neurons that travel in the
medial longitudinal fasciculus, the
contralateral medial rectus muscle

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Accessory optic system for smooth pursuit (Wolff) Cerebellum in Smooth Pursuit (Wolff)
• Comprises regions outside the primary visual cortex • The cerebellar flocculus receives visual input via mossy
which receive retinal projections via the optic tract and possibly climbing fibres and vestibular input via
• Include: mossy fibres
1. The pretectal nuclei of the mid brain which project to • ‘Gaze velocity' Purkinje cells of the flocculus discharge at
the nucleus of the transpeduncular tract a rate which relates to eye velocity during tracking - are
– Lies ventromedial to red nucleus and medial to the thought to sum the vestibular and eye velocity signals to
substantia nigra generate a pursuit gaze velocity in space
– Show increased activity during tracking • The dentate nucleus and vestibular nuclei have been
2. The medial pontine and vestibular nuclei implicated in
3. The nucleus reticularis tegmenti pontis (NRTP) – The control of vertical smooth pursuit
• This system may relay information to the vestibular – Cancellation of the vestibuloocular reflex in
nuclei, a final common pathway for the optokinetic combined head and eye tracing
response

• Accommodative vergence – linked synkinetically to

Vergence Movements accommodation and miosis
– Stimulated by retinal blur
• Binocular retinal disparity of images stimulates fusional
vergence movements – According to AC/A ratio
– Absence of fusional vergence leads to images falling on – Deficiency of accommodative convergence to a near
non-corresponding points on the retina target is taken up by the fusional vergence
mechanism to achieve mutual alignment of the visual
– Lead to object being perceived simultaneously in
axes
separate visual directions
• Vergence results from the combined activity of intrinsic
– Lead to diplopia if outside Panum’s area
tonic activity, accommodative vergence, and fusional
• Tonic vergence vergence
– Due to some inherent innervation tone to EOM when
patient is awake

• Vergence movements are slow – 200/sec and disjugate Cortical centers for Vergence
• Result from a sudden step change in tonic innervation of • The sensory afferent signals for binocular disparity and
the horizontal eye muscles acting against the viscous retinal blur are coded in
drag of the orbital contents
1. Primary visual cortex (area V1)
• May take up to a second to complete
• Some cells in V1 incorporate vergence to code
• Reaction time for fusional vergence is under 20 ms egocentric (head-referenced) distance
• For accommodative vergence is about 200 ms 2. Area MT and MST (included in area 19)
• During convergence
• Respond to retinal disparity and changing size
– Medial rectus receives a step increase in innervation 3. Parietal cortex
– Lateral rectus has a step decrease in innervation
• Respond to motion in depth
• The neural substrate for vergence is not fully known – Accommodation due to stimulation of area 18
• The premotor command passes directly to the medial • Efferent commands for vergence
rectus portion of the oculomotor nucleus
1. Frontal eye fields

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Subcortical centers for vergence Cerebellum in vergence:

– NRTP projects to the cerebellum
• Nucleus reticularis tegmenti pontis - NRTP – Dorsal vermis is involved in the conversion of 3D
– Premotor pursuit signals to control signals for vergence eye
– In the midbrain movements
– Located just ventral to the rostral portion of the – The interpositus nucleus of the cerebellum projects to
PPRF supraoculomotor regions that contain near response
– Receives projections from the frontal eye fields and cells in the mesencephalic reticular formation (MRF)
the superior colliculus
– Lesions in this region result in deficits of slow-
continuous and fast-step vergence control

• Supraoculomotor nucleus of MRF Vergence in accommodation - Adler

• Relays control of both accommodative and disparity
vergence • Controlled by supraoculomotor nucleus in the
– Has burst and tonic neurons mesencephalic reticular formation (MRF)
– Burst neurons code velocity signals for smooth • Has near response cells
vergence • Is a heterogeneous group of cells that respond to
– Tonic neurons code position signals to maintain accommodative stimuli, or vergence stimuli or a
static vergence angle combination of accommodation and vergence stimuli
• Excitatory connections of the supraoculomotor nucleus • This nucleus contains burst, tonic, and burst-tonic cells
project to the oculomotor nucleus similar as for saccades
– Drives medial recti • Velocity signals related to disparity stimuli activate burst
cells
• Inhibitory connections project to the abducens nucleus
to inhibit the lateral rectus • A position signal from tonic innervation is derived by
integration of the burst cell activity

• These cells provide velocity and position signals to • Omnipause cells in midbrain inhibit both saccades and
– Medial rectus motor neurons in the control of vergence burst cells
vergence • Accelerated vergence caused by saccadic facilitation is
– Edinger–Westphal nucleus to stimulate due to a release from inhibition of vergence bursters
accommodation which share their inhibition with saccadic and near
• The Edinger–Westphal nucleus, located at the rostral response bursters.
portion of the midbrain at the oculomotor nucleus, • This also causes saccadic facilitation of accommodation
contains parasympathetic motor neurons that project to • Because near response cells provide innervation for both
the ciliary muscle and drive accommodation.9 accommodation and vergence, release of inhibition
• EW-nucleus projects to its ipsilateral eye from OPNs augments activity of both accommodation
• Also results in miosis and vergence when associated with saccades
• Inhibition of the EWN causes pupil dilation.
• Saccades enhance the velocity of both vergence and
accommodation

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• The term square waves derives from the appearance of

Ocular Fixation System eye movement tracings, in which eye movements of
equal amplitude and speed to the left and right have a
• The ocular fixation system holds the image of a stationary brief intersaccadic interval that produces tracings in the
object on the fovea when the head is immobile shape of square waves
• Eye movement recordings show that the eye is not • The to-and-fro movements are small enough that the
completely still during ocular fixation; subclinical eye image is maintained within the field of the fovea but
movements prevent attenuation of neuronal responses in large enough to provide a constantly changing image to
the retina photoreceptors, thereby enhancing perceptual quality.
• The degradation of image quality that would result if the
eye were completely still is countered by microsaccadic
refixation movements
• These eye movements are continuous, very small
amplitude (0.1°–0.2° of visual angle) square waves

Fixation Movements Physiological Nystagmus

• Even within the 15-degree range, the fixating eye is not
• Foveal gaze lock for stationary objects completely stationary
– Gaze is mainly controlled by eye position for targets • Exhibits physiological nystagmus that is composed of :
lying in eccentricities of less than 150 from primary – Slow horizontal, vertical, and torsional drifts (0.1
position deg/sec)
– For steady fixation for larger gaze eccentricities – – Micro-saccades (<0.25 deg)
need both head and eye position – Small amplitude (<0.01 deg) high frequency tremor
– >30 degree fixation without head movements is (40–80 Hz)
difficult – eyes drift intermittently towards primary
position
– Ie; gaze evoked nyastagmus
– This drift exacerbated by alcohol

• Mechanisms Pathway for fixation

– Rapid : • Stimulus : Visual interest
• Microsaccades (less than 0.25 degrees) • Cortical centers
• Microtremors (less than 0.01 degrees at 40-80Hz) – Dorsolateral prefrontal cortex
– Slow – Supplementary eye field
• Microdrifts – avoid fading of retinal image : Troxler – Parietal eye field
effect – Regions V5 and V5a
• Occur 2-3 per second, Velocity 1 min of arc/sec – Basal ganglia
• Less than 0.5 degrees – Superior colliculi
• Clinical evaluation of ocular stability involves observing
the patient’s ability to fixate on a target when the head
and body are held stationary.

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• Venous return
Blood Supply of Midbrain Centers
– Partly by cortical veins
• Tectum of midbrain – Partly by basal vein which runs close to posterior
– Supplied by pial plexus from posterior cerebral and cerebral artery
superior cerebellar arteries
• Superior colliculi – main supply by posterior cerebral
artery
• Oculomotor and trochlear nuclei
– Supplied by specific end arteries from posterior
cerebral artery
– Enter midbrain through posterior perforated
substance
• Abducent nuclei – from perforating branches from
basilar artery

EOM physiology
• Pull of EOM depends on
1. Size (cross-sectional area) and length of muscle
2. Direction of pull
3. Innervation
Physiology of EOM movements 4. Mechanical characteristics of muscles
• MR is thickest. Next is LR
• Horizontal muscles work alone
• SR and IR come next
• SO and IO are thinnest
• 1 mm change in length produces 4.5-5 degree of
rotation

• Functional origin of EOM :

– From fibrous slings attached anteriorly and posteriorly
Actions of EOM
– Anterior slings act as suspension fibers attaching • Center of rotation
pulleys to intermuscular membrane
– Globe can be considered to rotate around a fixed point
– Posterior fibrous slings attach pulleys to bony orbital
that lies 13.5mm behind corneal apex
walls – check ligaments
• Functional insertion of EOM – It lies 1.6mm nasal to geometric center
– Point of tangency : point at which EOM first touch
sclera – In big myopic eyes, center of rotation is a bit farther
– Arc of contact : length from point of first contact posterior
(tangency) to anatomical insertion of musce – In small hyperopic eyes, center of rotation is a bit
• Changes according to direction of gaze anterior
– Functional insertion is point of tangency
– At extreme rotation, arc of contact is zero – functional
and anatomical insertions coincide

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• Fick’s axes • Listing’s plane

– Movements of globe are described around 3 axes – A frontal plane fixed in the skull and roughly
meeting at the center of rotation corresponds to the equatorial plane of the globe in
– Vertical movements occur around horizontal X axis the primary position
– Horizontal movements occur around vertical Z axis
– Torsional movements occur around AP Y axis
– X and Z axes lie in Listings plane, Y axis is
perpendicular
• Primary position of gaze – position of eyes with head
erect, object lying at infinity
• Secondary positions : direct up/down, left/right
• Tertiary positions : all other positions of gaze. They are
always associated with some degree of cyclotorsion

• Donder’s law • Listing’s law

– For any tertiary position of gaze, there is a predictable – Elaborates Donder’s law
amount of torsion, irrespective of how the eyes reach – States : Eyes rotate to a tertiary position around a
this position single axis perpendicular to the primary position of
gaze and lying in Listing’s plane
– Eg: 100 vertical + 100 horizontal = 10 torsion – This axis is perpendicular to the anteroposterior Y axis
– 200 vertical + 200 horizontal = 30 torsion
– 300 vertical + 300 horizontal = 80 torsion
– 400 vertical + 400 horizontal = 150 torsion

• Position of rest • Pure version and vergence movements are described

– Is the position that eyes adopt in orbit under deep respectively by the isovergence and isoversion contours
GA and complete muscle relaxation • The isovergence circle
– Dictated by anatomical factors – Describes the locus of points that stimulate the same
• Direction of orbital axis vergence angle in all directions of gaze
• Elastic pull of muscles and their fibrous – A different isovergence circle exists at each viewing
attachments distance
• Normal orthophoric individuals show 2.250 of • The isoversion lines
exotropia in each eye – Describe the locus of points that stimulate the same
• Is 350 in newborn version angle over a range of viewing distances in a
common direction of gaze relative to the head
• Pure vergence movements occur along any of the
isoversion lines and not just along the central or
midsagittal plan

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Functional classification of ocular

movements (1)
• Conjugate
1. Saccades
2. Smooth pursuit
3. VOR
4. OKN
5. Fixation
• Disjugate
6. Vergence

Functional classification of ocular movements (2) Summary of Saccades

• Saccades are very fast, yoked eye movements that have
1. Stabilization of gaze relative to the external world
a variety of functions
– Extraretinal – VOR
• Produce the quick phase of VOR and OKN to avoid
– Retinal – OKR
turning the eyes to their mechanical limits
2. Foveal gaze lock on stationary and slow moving targets
• Reflexively shift gaze in response to novel stimuli that
– Fixation for stationary targets
appear unexpectedly away from point of fixation
– Conjugate smooth pursuit for slow moving targets at
constant distance • Saccades shift gaze during reading from one group of
words to another
– Smooth vergence tracking targets with changing depth (at
changing distances) • Saccades search novel scenes to assist us in acquiring
3. Foveal gaze shifts information
– Saccades • Return gaze to remembered spatial locations
– Near response • Velocities can approach 10000/sec

• As saccade amplitude increases from 0.1 to 10 degrees, • Normally the perceived head-centric direction of a target
duration increases from 20 to 40 msec and peak velocity does not change when the eye changes position
increases from 10 to 400 deg/ sec • However, spectacle refractive corrections that magnify or
• Peak velocity saturates for saccades larger than 20 minify the retinal image produce changes in perceived
degrees direction with eye position
• Therefore amplitude of larger saccades increases mainly • Due to prismatic effect of corrective lenses
with duration • The prismatic power of the lens increases with increased
• The normal latency of a saccade to an unpredictable distance from the center of the lens such that the
stimulus is 180–200 msec saccade amplitude needed to fixate an eccentric target is
• Corrective saccades occur with shorter latencies (100– larger (magnifier)/smaller than the gaze eccentricity
150 msec) sensed prior to the saccade
• Saccade latency can be reduced by a blank or gap interval
before the saccade – results express saccades with
latency less than 100 ms

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• In natural viewing conditions it is rare for the eyes to Summary of Smooth Pursuit
converge symmetrically from one distance to another
• Usually, gaze is shifted between targets located at • Pursuit eye movements are able to track a moving target
both when the head is immobile and when it is in motion
different directions and distances from the head
• In order to track when head is in motion, the pursuit
• Rapid gaze shifts to these targets require a combination system must override the VOR
of conjugate saccades and disjunctive vergence. • For example, rightward head rotation stimulates the VOR
• In asymmetric convergence, the velocity of disparity to move the eyes in the opposite direction, toward the left.
vergence, accommodative vergence and accommodation Therefore, in order to track a rightward-moving object with
are enhanced when accompanied by gaze shifting simultaneous rightward head rotation, the pursuit system
(which tracks the object by moving the eyes toward the
saccades
right) must cancel the VOR (which drives the eyes in the
opposite direction, toward the left).
• Pursuit movements cannot be generated without a
moving target; attempts to pursue an imaginary target will
result in a series of saccades.

• Moving target generates signals from M ganglion cells in • The descending cortical pathways of the temporal,
the retina that are relayed through the magnocellular parietal, and frontal lobes converge and pass through the
layers of the LGN to the striate cortex V1 posterior limb of the internal capsule to innervate the
• From there relay to extrastriate cortex (V2, V3) ipsilateral dorsal lateral pontine nucleus (DLPN)
• Subsequently relayed to the • The pathway that follows the DLPN comprises 2
– Middle temporal (MT) area- where neurons decussations
preferentially respond to the speed and direction of • First, the neurons in the DLPN decussate and project to
moving stimuli the contralateral cerebellar lobe (the first decussation),
– Medial superior temporal (MST) area which in turn innervates the medial vestibular nucleus
– Posterior parietal cortex • Thereafter, neurons in the medial vestibular nucleus
decussate and project to the contralateral CN VI nucleus
– FEF (the second decussation)
• The MT and MST areas are part of the dorsal visual
processing stream, which plays an important role in
detecting moving visual stimuli

• The CN VI nucleus initiates conjugate horizontal eye

movements by innervating the ipsilateral lateral rectus
muscle and, via internuclear neurons that travel in the
MLF, the contralateral medial rectus muscle
• Thus, the cortical regions control ipsilateral pursuit
movements as a result of the double decussation
pathway
• Vertical pursuit movements are generated by similar
pathways that ultimately stimulate CN III and CN IV

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2. Stare mode
Optokinetic Reflex – This is a true reflex
– Subject is inattentively staring towards the object
• Occurs when subject view a series of moving objects
– Amplitude is small and frequency is higher (200 at
• Eg: When looking at a house from a train window 2Hz)
• Eyes tend to lock on the object, follow it for some time, – Continues for about 1 minute after cessation of
then saccade in the opposite direction object movement – after nystagmus (OKAN)
• Modes of OKN – Some subjects show and after-after nystagmus in the
1. Look mode opposite direction (OKAAN)
• Subject is attentive to the moving object
• Look mode starts with a quick anticipatory saccade to
• Movements are of large amplitude and low the direction where the stripes come from
frequency (400 at 1Hz)
• Stare mode starts with slow pursuit with the stripe
• Nystagmus stops abruptly with cessation of the movement
motion of the object

• Velocity of OKN • Clinical uses of OKN

– Below 300/sec – good correpondence 1. Localize cerebral lesions – frontal and parietal
– From 300-1000/sec – there is a lag phase
2. Measure vision in prevertebral infants
– Above 1000/sec – OKN cannot be evoked
– Here suppression of OKN by interposing an object
• Components of OKN
that has a certain size is more accurate
1. Slow phase
3. Reversal of OKN in congenital nystagmus
– In the direction of movement of object
4. Elicit convergence retraction nystagmus on attempting
– A slow pursuit movement
to elicit vertical OKN
– Lesions deep in parietal lobe abolish ipsilateral slow
phase and produce contralateral homonymous 5. Used to diagnose myasthaenia – and improves with
hemianopia edrophonium
– Positive OKN sign : slow phase cannot be elicited
when object moves away from hemianopia
2. Fast phase : corrective saccade mediated by FEF

• Can compensate upto rotations of 3000/sec

Vestibulo-ocular Reflex
• Most body rotations do not exceed this
• Is a statokinetic reflex • However, when body rotates at great speed around a
• Are innate and unconditioned vertical axis (eg; skater performing a spin), eye
movements show oculovestibular nystagmus
• Occur even in blindness
– Slow motion of eyes in opposite direction of rotation –
• Causes conjugate deviation of the eyes to the opposite
initiated by vestibular mechanism
direction
– Followed by quick jerky binocular return movement in
• Can be tested by inducing vestibular nystagmus
direction of rotation
1. Caloric test (caloric vestibular nystagmus ) – COWS
– This sequence repeated as long as angular
2. Rotating subject in revolving chair – rotatory acceleration lasts
vestibular nystagmus
• VOR gets fatigued after about 30 sec – OKN takes over

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Neurological disorders - Strabismus Neurological disorders – Gaze Restrictions

1. Infantile esotropia is associated with latent nystagmus, • Also known as ophthalmoplegias
asymmetric OKN, DVD and cog-wheel temporal ward • Due to lesions in pre-motor or supranuclear sites
pursuit 1. Internuclear Ophthalmoplegia (anterior)
• In DVD, the covered eye rotates upwards • Produced by lesions to the MLF
• This differs from vertical phorias and tropias where one • Interneuron from abducent to contralateral MR
eye is always higher relative to the other subnucleus is interrupted
2. Accommodative esotropia is due to large AC/A ratio • Cause exotropia and slow/failure of adduction of
beyond the ability of fusional vergence to correct or ipsilateral eye
due to abnormal cross-coupling • With usually abducting nystagmus of fellow (good) eye
3. Acquired middle age squints are usually due to motor • Convergence maybe spared
nerve or nuclear affection • INO is named after abnormal eye – right INO causes
right adduction deficit due to lesion in right MLF

2. One-and-a-half syndrome
• Posterior INO
• Combines a complete horizontal gaze palsy one eye and
– Both neurons to ipsilateral LR and to opposite MR INO in the other eye
are interrupted • Caused by a pontine abnormality that is large enough to
– Produce failure of conjugate deviation of both eyes to involve the MLF and the paramedian pontine reticular
the side of the lesion formation (PPRF) or the CN VI nucleus on the same side of
the brainstem
– Similar to an abducent nuclear lesion
• The only horizontal eye movement remaining is abduction
of the eye contralateral to the lesion (ie, horizontal eye
movements are lost in 1 eye, whereas they are “half” lost in
the fellow eye, hence the name).
• Vertical gaze is preserved.
• A lesion that produces one-and-a-half syndrome but also
involves the intra-axial portion of CN VII is termed eight-
and-a-half syndrome (7 + 1.5 = 8.5)
• Stroke is the most common cause of this disorder

• Lesions in PPRF affect saccades to same side • Lesions in MT or MST cause contralateral hemianopia
• Lesions in DLPN affect smooth pursuit to same side – Pursuit to the same side will be affected
• Parinaud’s Syndrome • FEF lesions cause deficits in contralateral saccades
– Due to a lesion rostral to the oculomotor nucleus or • Posterior parietal lesions produce attention deficits,
posterior commissure which is more obvious to small targets
– There is failure of vertical gaze • Saccadic intrusions such as ocular flutter, opsoclonus,
– Unilateral lesions cause skew deviation inappropriate saccades occur due to supranuclear
– Centers affected are riMLF, SC and pretectal nuclei lesions (PSP)
– Causes : strokes, pinealomas
• Lesions in visual cortex will produce homonymous field
defects
– Targets presented to blind areas do not elicit reflex
gaze

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Neurological Disorders - Nystagmus • Congenital Nystagmus

– Also known as infantile nystagmus syndrome
• Nystagmus refers to one form of excessive eye movements of
rhythmic, to-and-fro (eg, horizontal, vertical, torsional, or – Is almost always horizontal
mixed) eye movements that incorporate a slow phase – Has a null point – gaze direction where nystagmus is
• Jerk nystagmus has 2 phases: minimal
– (1) a slow-phase drift from the visual target, followed by – Speed of slow phase increase until fast phase begins
– (2) a corrective saccade (fast phase) back to the target – In all other types of jerk nystagmus, the speed of slow
• Direction of nystagmus is of its fast phase as it is easy to see phase is constant or decrease
• Pendular nystagmus describes back-and-forth, slow-phase – Patients with CN try to block the nystagmus by a head
movements that has no distinctive fast phase turn to bring the null point to the forward direction or
• Abnormal saccadic movements may also drive the eyes off by convergence (nystagmus block esotropia)
fixation. Collectively, these pathologic eye movements are
termed saccadic intrusions or saccadic oscillations; because – Abolished in sleep
they have no slow phase, they do not conform to the – OKN is to opposite side of movement of visual scene
definition of nystagmus

• Latent Nystagmus Gaze-evoked nystagmus

– Also known as fusional maldevelopment nystagmus • Develops because of an inability to maintain fixation in
– Occurs with any condition that disrupts binocular eccentric gaze
development in the first 6 months of life • The eyes drift back to the midline as a result of the
– Most commonly being infantile esotropia elastic properties of the orbit, and a corrective saccade is
– is an early- onset, conjugate, horizontal, jerk generated to reposition the eyes on the eccentric target
nystagmus that is accentuated by monocular fixation • Therefore, the fast phase is always in the direction of
– Eyes with FMN are stable during fusion gaze
– However, when 1 eye is occluded (thereby eliminating • Amplitude of nystagmus increases as eyes are moved in
fusion), the fixating eye slowly drifts toward the nose, the direction of the fast phase
followed by a corrective abducting saccade • This pattern is in accordance with Alexander’s law,
– The eye under the occluder is moving in the same which states that nystagmus increases in intensity
direction and with the same amplitude as the fixating (amplitude and frequency) as the eyes are moved in the
eye (ie, the nystagmus is conjugate) direction of the fast phase

• Gaze-evoked nystagmus is most commonly caused by • When eccentric gaze is initiated, the neural integrator
dysfunction of the neural integrator receives a velocity signal (the pulse) from the appropriate
gaze center
• For horizontal gaze, the neural integrator includes the
nucleus prepositus hypoglossi and the medial vestibular • Through the mathematical process of integration, generates
tonic innervation (a step signal) to maintain the eccentric
nuclei position of the eyes after the ocular movements have been
• For vertical gaze, the interstitial nucleus of Cajal serves completed
as the neural integrator • Thus, the neural integrator ensures a level of neural activity
• The cerebellum also participates in neural integration of adequate to maintain the eyes in an eccentric position of
both horizontal and vertical eye movements gaze against the elastic forces of the orbit
• If the neural integrator fails to function properly (ie, becomes
• A few beats of symmetric, low-frequency, small- “leaky”), then the tonic innervation (step signal) that holds
amplitude jerk nystagmus at the extremes of far the eyes in eccentric gaze is deficient
horizontal gaze without other ocular motility dysfunction • Therefore, after completion of eccentric gaze, the eyes
(eg, rebound nystagmus or saccadic dysmetria) constitute slowly drift off the target back to the central position,
physiologic endpoint nystagmus and are not clinically followed by a corrective saccade toward the target—hence
significant the term gaze- evoked nystagmus.

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• The 2 most common etiologies are • Peripheral Vestibular Nystagmus

– (1) toxic effects from drugs and medications (eg, • Patients with peripheral vestibular nystagmus typically
alcohol, sedatives, anticonvulsants, and present with a sudden, sometimes dramatic, onset of
antidepressants) disequilibrium with vertigo, nausea, and vomiting
– (2) cerebellar disease • Patients often recognize that their symptoms are
– Asymmetric :an ipsilateral lesion of the brainstem or worsened by particular head movements or postures
cerebellum—typically stroke, demyelination, or • Oscillopsia, tinnitus, and hearing loss may also occur.
tumor—is presumably present. • After the acute phase of peripheral vestibular loss, which
– Other causes are extraocular myopathies and typically lasts days, patients experience a slow period
myasthenia gravis (lasting weeks to months) of gradually waning symptoms
• Even patients who become asymptomatic may
experience discomfort months to years later when their
vestibular system is challenged, for example when riding
in a fast-moving car or boat

• Central Forms of Vestibular Nystagmus • See-saw nystagmus

• Because the central vestibular structures of the brainstem
and the cerebellum are extensively interconnected, it can • Is a form of disjunctive nystagmus
be difficult, if not impossible, to determine the precise • One eye elevates and intorts while the other eye
location of lesions that produce central nystagmus by depresses and extorts, a movement reminiscent of
clinical examination alone
that of a see-saw
• It is often more useful to think of the central vestibular
pathways as a single system and to obtain neuroimaging if • The eye movements are typically pendular, slow in
more specific information about localization is desired frequency, and similar in amplitude between eyes
• Downbeat nystagmus is the most common form of • See-saw nystagmus may be congenital or acquired
central vestibular nystagmus and results from lesions that and may be caused by lesions that affect the chiasm,
produce defective vertical gaze holding characterized by midbrain, or both
an upward drift of the eyes, which is then corrected with
a downward saccade – patients have occillopsia • Trauma and parasellar-diencephalic tumors, in
• Lesions that cause downbeat nystagmus compromise the particular craniopharyngioma, are frequent causes
vestibulocerebellum

Methods for recording Eye Movements

• Historical
– Using after images
– Mechanical transducer
• Current
– Contact lens with mirror
– Video photography
– Photoelectric oculography
– Corneal reflection
– Motion picture photography
– Ocular EMG

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