PARALYTIC STRABISMUS

Oculomotor nerve

Oculomotor nuclear complex:

Site:
- In the midbrain
- At the level of superior colliculus
- Below the aqueduct of Sylvius
- Above: reaches the floor of 3rd ventricle
- Below: reaches the level of the lower border of superior colliculus, it
continues with trochlear nucleus
- Dorsomedial: central gray matter around aqueduct
- Ventrolateral: medial longitudinal bundle

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Parts:

1- Lateral somatic cell columns: (paired)

o Consists of large motor neurons
o Supply EOM:
 Dorsal cell column: supply IR
 Intermediate cell column: supply IO
 Ventral cell column: supply MR
The fibers from these columns are uncrossed
 Medial cell column: supply SR
The fibers from the medial column are crossed

2- Caudal cell nucleus:

o Midline (unpaired group) in lower 1/3 of complex
o Give rise to crossed and uncrossed fibers that supply both levator
palpebrae superioris muscle.

3- Visceral nuclei:
o 2 groups which are in continuity rostrally
a- Edinger-Westphal nucleus:
Consist of 2 slender columns of small cells
b- Cells of anterior median nucleus:
Present in the raphe between rostral parts of lateral
somatic cell columns
o Give rise to uncrossed preganglionic parasympathetic fibers that
run with somatic fibers to ciliary ganglion

2
4- Central nucleus of Perlia:
o Midline (unpaired) group
o Concerned with convergence

Connections:
1- Receive connections from:
i- Superior colliculus through tectobulbar tract
ii- Frontal and occipital cortex through pyramidal tract
iii- Cerebellum through superior cerebellar peduncle
2- Send connections to:
4th, 6th, 7th and 8th cranial nerves of same and opposite side through MLB

Course of fibers:
Fibers pass with lateral convexity through:
i- MLB
ii- Tegmentum to emerge from
iii- Red nucleus sulcus oculomoterius
iv- Medial margin of substantia nigra

Superficial origin:
- By 10-15 rootlets
- From:
a- Sulcus oculomoterius on medial side of cerebral peduncle
b- Adjacent ventral surface of peduncle: small lateral component
- Close to:
a- Upper border of pons
b- Termination of basilar artery
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- Between:
a- PCA: medial and then above nerve
b- SCA: below nerve
- With posterior perforating substance between 2 oculomotor nerves

Course and relations:

A- In posterior cranial fossa

- Passes downwards and forwards between PCA and SCA

- Passes:
a- Above and medial to free margin of tentorium cerebelli and 4th nerve
b- Below and lateral to posterior communicating artery
- Crosses below optic tract from medial to lateral
- Passes below and medial to uncus
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 - Passes in cisterna interpeduncularis where it is in contact with arachnoid
from a point just behind posterior clinoid process to point where the nerve
pierces dura (1 cm).

- Cisterna interpeduncularis is subarachnoid space formed

by bridging across of temporal lobes with arachnoid.
- It contains:
a- Cerebral peduncles
b- Circle of Willis
c- Interpeduncular space
- It is filled with CSF
-
B- In middle cranial fossa

- Passes:
 Lateral to posterior clinoid process and pituitary fossa
 Above attached margin of tentorium cerebelli and cavernous sinus
- At a point midway between anterior and posterior clinoid process, it pierces
dura to run in the lateral wall of cavernous sinus related to:
 Below and lateral:
1- Trochlear nerve
2- Ophthalmic division
3- Maxillary division in the lateral wall of the sinus
 Below and medial:
1- Abducent nerve
2- Internal carotid artery in the sinus
 Receives communication from 1st division of V nerve and
sympathetic fibers around ICA

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- Before it enters SOF:
 It divides into small superior and large inferior divisions
 Trochlear nerve crosses to lie above then medial to it
 Ophthalmic division of V crosses to lie above then divide into 3
branches

C- In superior orbital fissure

The 2 divisions pass through medial part of SOF

within annulus of Zinn between 2 heads of IR

D- Inside the orbit

1- Superior division:
- Passes medially to lie above optic nerve
- Supplies:
i- SR: enters deep surface of muscle at the junction of proximal and
middle 1/3
ii- LPS: passes around or pierce medial border of SR to reach LPS

2- Inferior division:
- Divides immediately into 3 branches:
a- Branch to MR: passes below optic nerve
Enters deep surface of muscle at the junction of proximal and
middle 1/3
b- Branch to IR:
Enters deep surface of muscle at the junction of proximal and
middle 1/3

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 c- Branch to IO:
Run on the lateral border of IR to enter muscle from above
It gives a short branch which relays in ciliary ganglion and
supplies sphincter pupillae and ciliary muscle

Therefore,
It supplies:
a- All EOM except SO and LR
b- LPS
c- Smooth muscles concerned with accommodation (sphincter pupillae and
ciliary muscle)

Structure:
- Number of fibers: 24000
- Types of fibers:
i- Efferent:
 Large motor fibers
 Small fibers  ciliary ganglion
ii- Afferent:
 Small, sensory from V nerve
 Proprioceptives (non-medullated)
- Cross-section:
Nerve is surrounded by a thin perineurium and well-marked pial sheath
It contains:
i- Numerous thick irregular septa from pia
ii- Numerous small vessels
- Pupillomotor fibers:

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 In the precavernous course of 3rd nerve, parasympathetic fibers are
more superficial within the nerve in the superior median part
They are supplied by pial blood vessels, whereas the main trunk of
3rd nerve is supplied by vasa nervosa
i- Surgical lesions e.g. aneurysms
 compression of 3rd nerve
 damage of pupillomotor fibers
 3rd nerve palsy without sparing of pupil
ii- Neuropathy e.g. diabetic microangiopathy
 damage of vasa nervosa
 3rd nerve palsy with sparing of pupil

Arterial supply:
- Supplied by branches of neighboring arteries which
divide into ascending and descending branches which
anastomose with other branches in epineurium
- From epineural vessels, vessels penetrate into perineurium where further
anastomosis occur
- From perineural vessels, vessels pass to fascicules and form an
intrafasicular longitudinal displaced plexus which run all through the
nerve and supply individual fibers

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 Third cranial nerve palsy

Causes of third cranial nerve palsy:

A- Nuclear lesions:
- Congenital: aplasia
- Traumatic
- Inflammatory
- Neoplastic: primary and metastases
- Vascular diseases e.g. aneurysms
- Demyelinating diseases
- Diabetes mellitus
Effect:
1- Entire nucleus:
Ipsilateral 3rd nerve palsy with ipsilateral sparing and contralateral
paralysis of SR
2- Caudal nucleus:
Bilateral ptosis
3- Ventral cell column:
Wall-eyed bilateral internuclear ophthalmoplegia (WEBINO):
defective convergence and adduction

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B- Fasicular lesions:
Causes: as nuclear lesions (usually vascular – occlusion of branches of
PCA to midbrain)
Effect:
1- Benedikt syndrome:
Injury of nerve at the red nucleus
Effect:
i- Ipsilateral 3rd nerve palsy
ii- Contralateral UMNL facial paralysis
iii- Contralateral hemiplegia
iv- Contralateral ataxia + flappy tremors
v- Contralateral hemianesthesia due to involvement of medial lemniscus
2- Weber syndrome:
Injury of nerve at the cerebral peduncle
Effect:
i- Ipsilateral 3rd nerve palsy
ii- Contralateral UMNL facial paralysis
iii- Contralateral hemiplegia
3- Nothnagel’s syndrome:
Ipsilateral 3rd nerve palsy +cerebellar ataxia

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C- Basilar lesions:
Causes:
1- Aneurysms of junction of PCA and ICA: usually presents with
acute painful 3rd nerve palsy with damage of pupillomotor fibers
2- Trauma  extradural and subdural haematoma  tentorial
pressure cone with downward herniation of temporal lobe 
compression of 3rd cranial nerve  dilated fixed pupil followed
by 3rd nerve palsy
3- Chronic meningitis e.g. TB, syphilis and Zoster
4- Tumours of base of brain
Effect:
Isolated 3rd cranial nerve palsy

D- Intracavernous lesions:
Causes:
1- Diabetes mellitus
2- Pituitary apoplexy  haemorrhagic infarction of pituitary gland with
lateral extension to cavernous sinus
3- Intracavernous lesions e.g.
i- Aneurysms (affect abducent nerve first)
ii- Meningioma
iii- Carotid-cavernous fistula
iv- Tolosa-Hunt syndrome
Effect:
Usually associated with paralysis of 4th, 6th and first division of 5th
nerve

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E- Orbital part
Causes:
i- Traumatic
ii- Retrobulbar tumours e.g. optic nerve glioma and Meningioma
iii- Vascular
Effect:
1- Proptosis
2- Alteration in vision
3- Paralysis of abducent and nasociliary nerve

Causes of isolated third nerve palsy:

1- Idiopathic (25%): most common
2- Vascular e.g. diabetes and hypertension
Usually presents with acute painful 3rd nerve palsy with sparing of
pupillomotor fibers
3- Trauma: If trivial and not associated with loss of consciousness, basal
cell tumour should be excluded
4- Aneurysms of junction of PCA and ICA: usually presents with acute
painful 3rd nerve palsy with damage of pupillomotor fibers
5- Others e.g. tumours, vasculitis associated with collagen vascular
disease, syphilis

Clinical picture:

1-Complete division of oculomotor nerve:

a- Ptosis due to paralysis of levator
b- Limitation of elevation, depression and adduction due to paralysis
of SR, IR and MR
c- Eye look laterally due to:
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 1- Unopposed action of LR
2- Depressant action of SO is nil in abduction
There is inability to look upwards, downwards or medially beyond
midline
d- Intorsion when the eye looks down and out due to overaction of
SO
e- Fixed dilated irreactive pupil due to paralysis of sphincter pupillae
and unopposed action of dilator pupillae
f- Paralysis of accommodation
g- No diplopia due to ptosis

2- Incomplete lesion of oculomotor nerve:

i- Internal ophthalmoplegia:
Paralysis of sphincter pupillae and ciliary muscle sparing EOM
ii- External ophthalmoplegia:
Paralysis of EOM sparing sphincter pupillae and ciliary muscle

3- Congenital third nerve palsy:

a- Clinical picture of third nerve palsy
b- Pupil abnormalities:
1- Fixed dilated irreactive pupil due to paralysis of sphincter pupillae
and unopposed action of dilator pupillae
2- Pupillary constriction on attempted adduction, depression or
elevation (aberrant regeneration)
c- Compensatory head posture (torticollis)
1- Chin elevation
2- Head turn to opposite direction
d- Amblyopia and severe loss of BSV
e- Associated neurological problems
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4- Aberrant regeneration
- After traumatic and aneuysmal not vascular lesions
- Clinical picture: abnormal ocular motility e.g.
a- Elevation of upper eye lid (pseudo-Graefe)
b- Pupillary constriction
on attempted adduction, depression or elevation

Right third nerve paresis with ptosis and exotropia. On adduction and
depression, there is elevation of right upper eyelid

Investigations:
1- Blood pressure
2- Blood and urine glucose
3- MRA or angiography mandatory whenever a surgical cause of third
nerve palsy is suspected
a- Pupil dilatation
b- Aberrant innervation

Treatment:
Aim:
Removal of diplopia and achievement of BSV in many gazes
Restoration of ocular motility is not possible

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A- Conservative: for 6 months – 3 years
1- Occlusion to prevent diplopia
2- Prisms
3- Botulinum toxin to lateral rectus to prevent permanent contracture
4- Prevention of amblyopia in children

B- Surgery when no further recovery is expected

1- Treatment of strabismus first
a- Supermaximum resection-recession of MR and LR. May be
combined with traction suture to keep the globe adducted
b- Lateral rectus orbital wall fixation
c- Transposition of SO near MR insertion with or without removal
from the trochlea
d- Transposition of LR near MR insertion. LR is split into upper and
lower halves and passed under SR and IR to reach MR
e- Fixation of sclera to a medial periosteal flap
2- Treatment of ptosis after:
a. Correction of diplopia
b. Good Bell’s phenomenon
However it should be done earlier in children to prevent amblyopia

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 Trochlear nerve

Nucleus:

Site:
- In tegmentum of midbrain
- At the level of upper part of inferior colliculus
- Dorsomedial: central gray matter around aqueduct
- Ventrolateral: medial longitudinal bundle
- Above it continues with oculomotor nucleus

Connections:
1- Cortico-bulbar tract
2- Tecto-bulbar tract
3- MLB to 3rd, 5th, 6th cranial nerves of same and opposite side
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Course of fibers:
- Fibers pass laterally to medial surface of 5th nucleus
- Passes down parallel to aqueduct of Sylvius to lower border of
inferior colliculus
- Passes medially to decussated completely in superior medullary
velum to emerge at the medial border of superior cerebellar peduncle

Special characters:
1- Longest intracranial course 75 mm
2- Only cranial nerve to emerge from the dorsal aspect of the brain
3- Crossed cranial nerve: fourth nerve nucleus supplies contralateral
SO muscle

Superficial origin:
- By 2-3 rootlets
At the medial border of superior cerebellar peduncle
Just below inferior colliculus
At the level of superior medullary velum
i.e. it arises from dorsal aspect of brain

Course and relations:

A- In posterior cranial fossa

 Passes laterally behind superior cerebellar peduncle

where it is crossed from below upwards
by a branch of superior cerebellar artery to inferior colliculus
 Passes forwards on upper border of pons between

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 posterior cerebral artery and superior cerebellar artery
 Appears on ventral aspect of brain between temporal lobe and pons
 Passes:
a- Below and medial to the free margin of tentorium cerebelli
and 3rd nerve
 Above and medial to trigeminal nerve

B- In middle cranial fossa

Passes:
i- Lateral to posterior clinoid process and pituitary fossa
ii- Above and medial to trigeminal ganglion
It pierces dura to lie in the lateral wall of cavernous sinus related to:
i- Above and medial: oculomotor nerve
ii- Below and lateral: ophthalmic and maxillary division
iii- Below and medial: abducent nerve and ICA
Receives communication from 1st division of V (containing
proprioceptive fibers) and sympathetic plexus around ICA
Before it enters SOF, trochlear nerve crosses to lie above then
medial to it before it enters SOF

C- In superior orbital fissure

It passes through wide part of SOF above annulus of Zinn related to:
- Laterally: frontal and lacrimal nerve
- Below: ophthalmic vein

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 D- In the orbit

It passes forwards and medially below periorbital and SR and levator

Divides into 3-4 branches which enters muscle from above near its lateral
border
Most anterior: at the junction of posterior and middle 1/3
Most posterior: 8 mm from the origin

Communications and varieties:

1- Branches to:
i- Orbicularis oculi
ii- Supratrochlear, infratrochlear and nasociliary nerves
2- Rarely it pierces levator to reach SO

Structure: 3400 large-sized fibers

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 Fourth nerve palsy
Superior oblique palsy

Causes:
A- Nuclear lesions:
- Congenital: aplasia
- Traumatic
- Inflammatory
- Neoplastic: primary and metastases
- Vascular diseases e.g. aneurysms
- Demyelinating diseases
- Diabetes mellitus
Effect: paralysis of contralateral SO muscle

B- Fasicular lesions:
Causes: as nuclear lesions (usually vascular – occlusion of
branches of PCA to midbrain)
Effect: paralysis of contralateral SO muscle

C- Basilar lesions:
Causes:
1- Trauma may cause bilateral fourth nerve palsy as
they decussate in the anterior medullary velum due
to injury by edge of tentorium cerebelli
2- Aneurysms of junction of PCA and ICA
3- Chronic meningitis e.g. TB, syphilis and Zoster
4- Tumours of base of brain

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Effect:
Paralysis of ipsilateral SO muscle – may be bilateral

D- Intracavernous lesions:
Causes:
1- Diabetes mellitus
2- Pituitary apoplexy  haemorrhagic infarction of
pituitary gland with lateral extension to cavernous sinus
3- Intracavernous lesions e.g.
i- Aneurysms (affect abducent nerve first)
ii- Meningioma
iii- Carotid-cavernous fistula
iv- Tolosa-Hunt syndrome
Effect:
Usually associated with paralysis of 3rd, 6th and first
division of 5th nerve

E- Orbital part
Causes:
1- Traumatic
2- Retrobulbar tumours e.g. optic nerve glioma and Meningioma
3- Vascular
Effect:
i- Proptosis
ii- Alteration in vision
iii- Paralysis of abducent and nasociliary nerve

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 Causes of isolated fourth nerve palsy:
1- Congenital (MOST COMMON): symptoms may not develop until
adult life. Examination of old unposed photographs are helpful
2- Trauma: may cause bilateral fourth nerve palsy as they decussate in
the anterior medullary velum due to injury by edge of tentorium
cerebelli
3- Vascular lesions
4- Aneurysms and tumours: less common
5- Absent SO muscle or tendon in craniofacial anomalies

Effect of fourth nerve palsy

Unilateral fourth nerve palsy Bilateral fourth nerve palsy
Limited 1- Depression on adduction on one 1- Depression on adduction on both
side  ipsilateral hypertropia in sides  no hypertropia in
primary position primary position (bilateral)
Limited 2- Abduction in downgaze 2- Abduction in downgaze (bilateral)
(unilateral)  insignificant V ET  V-pattern esotropia
Limited 3- Intorsion  objective (indirect 3- Intorsion  objective (indirect
ophthalmoscope) and subjective ophthalmoscope) and subjective
(Maddox rod) extorsion on one (Maddox rod) extorsion (marked >
side 10°)

Diplopia Vertical and cyclic Cyclic (additive)

Head tilt Hypertropia increases on head tilt to Right hypertropia on head tilt to right
test same side (hypertropic eye) side and left hypertropia on head tilt to
left side
CHP Chin depression Chin depression only
Head turn to opposite direction
Head tilt to opposite direction

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Unilateral (Right) Superior Oblique Palsy

Bilateral Superior Oblique Palsy

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Three-step test showing LSO palsy with LHT that increase on right gaze
and head tilt to left side
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 Facial asymmetry:
Causes:
1- Congenital fourth nerve palsy
2- Long-standing fourth nerve palsy
Diagnosis:
Hypoplasia and shortening of ipsilateral side of face
A line drawn through both pupils and a line drawn through corners of
mouth intersect near the face on the side of the tilt (Normally should
be parallel)
Mechanism:
1- Ipsilateral carotid compression
2- Deformational molding from monotonous
positioning during sleep
Reversible by early surgery

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Management:
Aim:
1- Binocular vision
2- Esthetic
3- Avoid changes in head posture

A- Conservative: for 6 months – 3 years

1- Occlusion to prevent diplopia
2- Prisms
i- If there is spread of comitance
ii- Without spread of comitance by correcting deviation in
primary position only
3- Prevention of amblyopia in children (rare)

B- Surgery when no further recovery is expected (usually needed)

One or combination of the following:

1- Weaken the direct antagonist (ipsilateral inferior oblique) 
ipsilateral inferior oblique weakening
- Most common muscle to be done as inferior oblique overaction is
usually present
- Either
- Inferior oblique myectomy (self adjusting), or
- Graded recession depending on degree of inferior oblique
overaction
2- Strengthen the weak muscle (ipsilateral superior oblique) 
ipsilateral superior oblique tucking
- Done only if superior oblique is very lax (not common)
- May cause iatrogenic Brown syndrome
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 3- Weaken the yoke muscle (Contralateral inferior rectus) 
contralateral inferior rectus recession
- Usually done in combination with another muscle if the angle is
large, or there is residual deviation after prior surgery
- 1 mm recession corrects about 3 Δ hypertropia

Decision of surgery depends on:

1- Presence of inferior oblique overaction (usually present)
2- Deviation in primary position
3- Superior oblique laxity

In the presence of IO overaction (more common)

a. Deviation in primary position <15 Δ: ipsilateral IO weakening
(IO is the cause of deviation in primary position)
b. Deviation in primary position > 15 Δ: ipsilateral IO weakening
and another muscle (ipsilateral SO tucking if superior oblique
is lax or contralateral IR recession if SO is not lax)
c. Deviation in primary position >35 Δ: usually needs three
muscle surgery

In the absence of IO overaction (less common)

a- Ipsilateral SO tuck
b- Contralateral IR recession

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In bilateral SO palsy:
a- Harada-Ito procedure: advancement of the anterior fibers of superior
oblique towards the lateral recti to improve the abduction and
intorsion in downgaze and leaving the posterior fibers in place (no
vertical deviation in primary position)
b- Bilateral IO weakening
c- Bilateral SO tucking
d- Bilateral IR recession

Knapp classification

Knapp classified superior oblique palsy according to where the greatest

deviation is (up and in, down and in,, etc…). Surgery is performed on the
muscle that works in that field. For example, if the greatest deviation is up
and in (in the IO field)  inferior oblique weakening is done

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 Greatest LIO weakening
deviation in
I
field of
ipsilateral IO

Greatest LSO strengthening

deviation in
II
field of
ipsilateral SO

Greatest 1- LSO strengthening if <25

deviation in Δ

III
field of 2- LSO strengthening and
ipsilateral IO LIO weakening if > 25 Δ
and SO

Greatest First surgery:

deviation in As III
IV
field of Second surgery
ipsilateral IO LIR strengthening
and SO and IR

Greatest 1- LSO strengthening

V deviation in all 2- RIR weakening

downgazes RSO weakening may
convert it to bilateral SO
palsy

Bilateral SO Bilateral SO strengthening

VI Bilateral Superior Oblique
Palsy palsy (Tucking or Harado-Ito
procedure)
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VII: acquired Brown
 Abducent nerve

Nucleus:

Site:
- Mid portion of pons
- Below the floor of 4th ventricle
- Close to the fasiculus of 7th nerve which causes a small elevation in the
floor of 4th ventricle (facial colliculus)
- Consists of large motor neurons which supply ipsilateral LR muscle

Superficial origin:
Fibers (fasiculus) pass ventrally to emerge:
o at pontomedullary junction
o lateral to pyramidal prominence
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 Course and relations:

I- Basilar part:

1- Passes upwards, forwards and slightly laterally in cisterna pontis covered

by pia
2- Pierces dura matter below and lateral to posterior clinoid process and
medial to inferior petrosal sinus
3- Crosses inferior petrosal sinus from medial to lateral
4- Passes up in a groove on the back of petrous part of temporal bone near its
apex
5- At the sharp upper border of petrous part of temporal bone, it bends
forwards at right angle under petro-sphenoidal ligament and superior
petrosal sinus to enter cavernous sinus

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 B- Cavernous part

Passes forwards through middle of sinus:

- Below 3rd and 4th nerves
- Lateral to ICA

C- Superior orbital fissure

It passes through the medial part of SOF within annulus of Zinn between
the 2 heads of LR

D- Orbital part

Supplies LR through its deep surface just behind its middle

Communication:
1- Sympathetic plexus around ICA in the cavernous sinus
2- Ophthalmic division of V

Structure:
6000-7000 fibers

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 Sixth nerve palsy

Causes of 6th nerve palsy:

A- Nuclear lesions:
Causes:
- Congenital: aplasia
- Traumatic
- Inflammatory
- Neoplastic: primary and metastases
- Vascular diseases e.g. aneurysms
- Demyelinating diseases
- Diabetes mellitus
Effect:
1- Ipsilateral 6th nerve palsy
2- Ipsilateral gaze palsy due to affection of horizontal gaze centre in PPRF
3- Associated ipsilateral 7th nerve palsy due to concomitant affection of
facial colliculus
Therefore, isolated 6th nerve palsy is never nuclear in origin

B- Fasicular lesions:
Causes: as nuclear lesions (usually vascular – occlusion of branches of
PCA to pons)
Effect:
1- Foville syndrome:
Cause: lesion in dorsal pons  affection of fasiculus as it passes through
PPRF

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 Clinical picture:
1- Ipsilateral 6th nerve palsy
2- Ipsilateral gaze palsy due to affection of horizontal gaze centre in PPRF
3- Associated ipsilateral 7th nerve palsy due to concomitant affection of facial
colliculus
4- Ipsilateral hemihyposthesia of face due to affection of sensory part of 5th
nerve
5- Ipsilateral Horner’s syndrome
6- Ipsilateral deafness

2- Millard-Gubler syndrome:
Cause: lesion in ventral pons  affection of fasiculus as it passes through
pyramidal tract
Clinical picture:
a- Foville syndrome
b- Contralateral hemiplegia

C- Basilar lesions:

Causes:
1-
2- Trauma may cause unilateral or bilateral 6th nerve palsy e.g. fracture base
of skull

3- Tumours:
a- Acoustic neruoma:
 compression of 6th nerve as it leaves pontomedullary
junction

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 First symptom: hearing loss
First sign: Impairment of corneal reflex
All patients with 6th nerve palsy should be tested for:
1- Hearing
2- Corneal reflexes
b- Nasopharyngeal tumours especially chinese
 invasion of skull and its foramina
 damage of 6th nerve
c- Chordoma:
Rare midline tumour which arise from notochordal
remanents of clivus
Usually present with unilateral 6th nerve palsy
d- Increased intracranial tension e.g. BIH and posterior fossa tumours
 downward descent of brain stem
 stretch of 6th nerve over petrous tip between point of
emergence from brain stem and its dural attachment to clivus
 6th nerve palsy which may be bilateral (false localized
sign)

3- Inferior petrosal sinus thrombosis

 spread to cavernous sinus  6th nerve palsy

4- Gradenigo's syndrome:
- Occurs in children due to infection of petrous bone from otitis media
- Characterized by:
a- 6th nerve palsy
b- 7th nerve palsy
c- Deafness
d- Severe pain in the distribution of ophthalmic division of 5th nerve

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- Now rare with the use of antibiotics
Effect:
Paralysis of ipsilateral LR muscle – may be bilateral

D- Intracavernous lesions:
Causes:
1- Diabetes mellitus
2- Pituitary apoplexy  haemorrhagic infarction of pituitary gland
with lateral extension to cavernous sinus
3- Intracavernous lesions e.g.
i- Aneurysms (affect abducent nerve first)
ii- Meningioma
iii- Carotid-cavernous fistula
iv- Tolosa-Hunt syndrome
Effect:
Usually associated with paralysis of 3rd, 4th and first division
of 5th nerve

E- Orbital part

Causes:
1- Traumatic
2- Retrobulbar tumours e.g. optic nerve glioma and meningioma
3- Vascular
Effect:
i- Proptosis
ii- Alteration in vision
iii- Paralysis of abducent and nasociliary nerve

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Common causes of isolated 6th nerve palsy:
1- Idiopathic (most common):
a. In children: presumed to be viral – may be recurrent
b. In adults: presumed be immune-mediated e.g. ocular migraine
c. In elderly: presumed to be vasculopathic, in presence of
diabetes, hypertension, or atherosclerosis
2- Traumatic: may be bilateral
3- Increased intracranial tension: may be bilateral

Clinical picture of 6th nerve palsy:

1- Limitation of abduction
2- Esotropia (decreases in long-standing cases)
3- Diplopia: Horizontal: on looking towards the paralyzed side
4- Compensatory head posture:: Head turn to same side

Management:
Aim:
1- Binocular vision
2- Esthetic
3- Avoid changes in head posture

A- Conservative: for 6 months – 3 years

1- Occlusion to prevent diplopia
2- Prisms
3- Botulinum toxin to prevent contracture of medial rectus
4- Prevention of amblyopia in children (rare)

B- Surgery when no further recovery is expected (usually needed)

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1- Ipsilateral medial rectus recession

- Effective alone in small esotropia with recovered lateral rectus

function
- Can be done in combination with other surgeries
2- Contralateral medial rectus recession with Faden operation to

increase innervational tone to paralyzed muscle

3- Lateral rectus resection: if the lateral rectus function recovered

4- Superior and inferior rectus muscle transposition:

- Usually needed in patients with unrecovered lateral rectus

function
- Types:
- Full muscle transposition: carries the risk of anterior
segment ischaemia especially if combined with medial rectus
recession
- Hummelcheim: transposition of only the temporal halves of
superior and inferior recti to lateral recti
- Jensen procedure: suturing of the temporal halves of the
superior and inferior recti to the upper and lower halves of
the lateral recti
- Foster augmentation sutures: suturing of the transposed
muscle to the sclera 8-10 mm behind the LR insertion to
enhance the effect of transposition

38
39
 RESTRICTIVE STRABISMUS
Duane Syndrome

Pathogenesis:
Co-contraction of both medial and lateral recti  retraction of
globe on adduction
May be due to aplasia of abducent nucleus and innervation of LR
by an aberrant branch of oculomotor nerve

Clinical picture: Bilateral in 20%

Types (Huber):
 Type 1: most common
- Limited or absent abduction
- Normal adduction
- Primary position: ortho or slightly eso
 Type 2: least common
- Limited adduction
- Normal abduction
- Primary position: ortho or slightly exo
 Type 3:
- Limited adduction and abduction
- Primary position: ortho or slightly eso

Other features:
A- On adduction: retraction of globe and narrowing of palpebral
fissure

40
 B- On abduction: opening of palpebral fissure and return of globe
to normal position
C- Upshoot or downshoot on adduction (bridle-leash
phenomenon):
- Due to
A- Mechanical theory: tight LR which slips under or
over the globe  anomalous vertical movement
B- Innervational theory: anomalous contraction of
vertical muscles during adduction

Amblyopia is rare
Stereopsis is usually normal

Top: Type I Duane, Middle Type II Duane, Bottom, Type III Duane

41
Systemic associations (30%):

1- Goldenhar syndrome

2- Perceptual deafness and speech disorders

3- Klippel-Fiel syndrome
Congenital fusion of at least two of the seven vertebrae in the
cervical-spine. May be fusion or anomalies of vertebrae in the
thoracic or lumbar-spine. High scapula. More in females
Clinical picture:
1- May be asymptomatic
2- Shortness of the neck, reduced cervical range-of-motion
(torticollis), and a low posterior hairline
3- Sudden neurologic injury or death after minor trauma.

4- Wildervanck association of Duane’s syndrome:

In females only
 Combination of Klippel-Feil syndrome , Duane syndrome,
and congenital perceptive deafness.
 May be associated defects with cleft palate, dental
anomalies, epibulbar epidermoids, epileptic attacks, facial
hypoplasia, facial and cranial asymmetry, preauricular tags,
subconjunctival lipoma, micrognathia, narrow palate, mental
retardation, nystagmus, and heterochromia iridis.

5- Holt-Oram syndrome

6- Fanconi syndrome:
42
 7- Okihiro Syndrome:
Associated with
a- Radial ray anomalies ranging from thenar eminence
hypoplasia with or without abnormally positioned thumbs, to
absent thumbs and radius
b- Congenital perceptive deafness
c- May be Klippel-Fiel syndrome or renal anomalies

8- 22q partial duplication and 22q11.2 deletion syndrome.

9- Fanconi

10- Uveal coloboma

11- Crocodile tears

Management:
Surgery if:
a- Eyes are not straight in the primary position
b- Abnormal head posture
c- Cosmetically unacceptably upshoots, downshoots or severe
retraction

A- To correct strabismus and abnormal head posture:

MR recession in esotropic Duane and LR recession in exotropic
Duane
LR of affected side should not be resected because it increases
retraction

43
B- To decrease globe retraction:
Both MR recession and LR recession
C- Tether phenomenon:
a- Posterior fixation sutures
b- Horizontal splitting of LR into Y with resuturing of muscle
above and below the axis of LR

44
 Brown syndrome
Causes:
A- Congenital:
1- Idiopathic: short anterior sheath of superior oblique tendon
2- Congenital click syndrome: impaired movement of tendon
through trochlea
B- Acquired:
1- Trauma to trochlea or superior oblique tendon:
a- Trauma to orbit or trochlea
b- Buckling
c- Frontal sinusitis or sinus surgery
d- Molteno valve inplant
e- SO tucking if:
1- Tendon sheath is not stripped adequately
2- Surgery close to the trochlea
2- Tenonitis e.g. RA, pansinusitis and scleritis

Incidence:
- F>M
- Right > Left
- Bilateral in 10%

Clinical picture:
1- Eyes: usually orthophoric
2- Limited elevation in adduction and may be primary position (may
improve with repeated testing)
3- Normal elevation in abduction
4- No or minimal SOO
5- Positive forced duction test on elevating globe on adduction
45
 6- Y-pattern exotropia
7- Variable signs:
a- Downshoot on adduction
b- Hypotropia in primary position
c- Head posture:
- Chin up
- Head turn to opposite side
- Head tilt to same side

Differential Diagnosis:
1- IO palsy:
Brown syndrome IO palsy
1- Orthophoric 1- Hypotropia
2- No SOO 2- SOO
3- Y-pattern 3- A-pattern
4- Positive forced duction test 4- Negative forced duction test
2- Monocular elevation deficit: failure to elevate the eye in any position

46
 Left inferior oblique palsy with A-pattern esotropia

Management:
1- Treatment of the cause
2- Steroids: oral or injection near the trochlea in inflammatory causes
3- Prisms in acquired cases
4- Surgery (SO weakening) in:
a- Hypotropia in primary position
b- Abnormal head posture
c- Visual symptoms

47
 Double levator palsy
Monocular elevation deficit

Causes:
Combined weakness of elevators (SR and IO) and restriction of IR
a- Elevator palsy
b- IR restriction
c- Combination
May be:
a- Congenital
b- Acquired e.g. pretectal lesions

Clinical picture:
1- Failure to elevate one eye in any position
2- Hypotropia which increases in upgaze
3- Abnormal head posture: chin up
4- Ptosis or pseudoptosis
5- Positive forced duction test for IR
6- IR restriction: extra or deep lower lid fold
7- Bell’s phenomenon: usually asymmetric: absent or weak in IR
restriction

Differential Diagnosis:
Causes of restricted elevation in primary position:
1- Orbital floor fracture
2- Dysthyroid ophthalmopathy
3- Congenital fibrosis syndrome
4- Brown syndrome

48
 Left monocular elevation deficit with limited elevation of left eye in
abduction, adduction, and straight up

Top: Pseudoptosis, caused by hypotropia, disappears when the hypotropic eye fixes and
moves up. Bottom: True ptosis, remains even when the hypotropic eye fixes
49
Treatment:
Surgery:
a- Large vertical deviation in primary position
b- Abnormal head posture
Surgical approaches:
a- IR restriction: IR recession
b- No IR restriction: Knapp procedure Transposition of MR and LR
towards SR

50
 Congenital fibrosis syndrome
Inheritance: autosomal dominant
Pathology: Replacement of muscular tissue with fibrous tissue
Clinical picture:
A- Congenital IR fibrosis:
1- Hypotropia with limitation of elevation ± other movement
2- Compensatory head posture: chin elevation
3- Blepharoptosis
4- On trial of elevation  convergence may occur
B- Vertical retraction syndrome:
Hypertropia with limitation of depression
C- Strabismus fixus:
Contraction and fibrosis of both MR
Both eyes do not cross the midline even by forced duction test
D- Congenital unilateral fibrosis: with enophthalmos and ptosis:
Fibrosis of all extraocular muscles and levator on one side

Differential diagnosis: see before

Treatment:
 IR recession
 Conservative treatment of ptosis to prevent exposure (no Bell’s
phenomenon)
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 Adherence syndrome
Types:
1- Congenital:
a- Adhesion of SR and SO
b- Adhesion of LR and IO
2- Acquired:
After IO surgery  violation of Tenon’s capsule 
fibrofatty proliferation of orbita fat on the sclera 
hypotropia and restriction of elevation
Treatment:
Removal of adhesions + implantation of Supramid sleeve or cap to
prevent reformation.

52
 Mobius syndrome

Pathogenesis:
- 6th + 7th nerve palsy
- Gaze palsy due to abnormality in PPRF

Clinical picture:
A- Ocular:
A- Bilateral 6th nerve palsy
B- Primary position: eyes may be:
a- Esotropic (50%)
b- Normal
c- Pseudoesotropia due to cross-fixation as convergence is
intact
C- Horizontal gaze palsy in 50%: vertical gaze is usually normal
B- Neurological:
1- Bilateral UMNL 7th nerve palsy (upper face): usually
asymmetrical 
a- Mask face with absent nasolabial fold
b- Lagophthalmos
2- 9th and 12th cranial nerve palsy  atrophy of tongue
C- Systemic:
1- Limb anomalies e.g. absent pectoralis muscle, polydactyly,
syndactyly, brachydactyly and clubbed feet (Poland’s
anomaly)
2- MR
3- Abnormal brainstem auditory evoked response

53
Treatment:
1. Gaze palsy alone: no treatment
2. Esotropia: MR recession (difficult due to tight muscle). Double
overlapping marginal myotomies may be safer. No value in
resection of LR

54
 Dysthyroid ophthalmopathy
(Ballet’s sign)

Incidence: 30-50% of dysthyroid ophthalmopathy

Pathogenesis:
1- Edema: infiltrative phase
2- Fibrosis: fibrotic phase

Ocular motility defects: in order of frequency (I'M SLOW)

1- Elevation defect: due to fibrosis of IR
2- Abduction defect: due to fibrosis of MR
3- Depression defect: due to fibrosis of SR
4- Adduction defect: due to fibrosis of LR
a- Early: Limitation of movement in the opposite direction of action
of restricted muscle
b- Then: deviation in the field of action of restricted muscle
Usually asymmetrical

Investigations:
1- Assessment of thyroid status
2- Investigations for non-comitant squint
3- CT scan, MRI and B-scan ultrasound: enlargement of muscles
sparing tendons
4- Differential IOP test:
Measurement of IOP in primary position, upgaze and downgaze
Elevation of IOP when the eye moves in the opposite direction of
action of restricted muscle (usually upwards)

55
Treatment:
A- Conservative treatment: in active phase
1- Treatment of thyroid status
2- Prisms
3- Botulinum toxin to prevent permanent contracture
B- Surgery:
Indications
Diplopia in primary or reading positions provided:
a- Inactive phase
b- Stable angle of deviation for >6mnths
Aim:
 To achieve BSV in primary and reading positions
 Patients may not have BSV in all positions because
dysthyroid ophthalmopathy causes non-comitant squint
 With time, field of BSV increases due to increased
vergences
Surgical technique:
- According to affected muscle e.g. IR and MR recession
(better than resection of normal muscle)
- Adjustable sutures are preferred and patient is
encouraged to practice achieving BSV on a distant target

56
 Fracture floor of orbit

Mechanism:
Striking eye by object > 5cm e.g. tennis ball or fist
 fracture floor (thin wall)

Types:
Pure: does not involve orbital rim
Impure: involve orbital rim and facial bones

Onset: variable

Site:
Thin bone over infraorbital canal and extends nasally

Signs:
1- External e.g. edema or echymosis
2- Anesthesia along the course of infraorbital nerve, lower lid, cheeks,
side of nose, upper lip, teeth and gums
3- Limitation of:
a- Elevation
b- Depression
4- Diplopia:
a- Hge and edema of orbital fat  restriction of movement of
muscles. Improve with time
b- Mechanical entrapment of IR, IO and orbital tissue in
fracture  diplopia in upgaze and downgaze (double
diplopia)
Diagnosis:
i. Positive forced duction test
ii. Positive differential IOP test
57
 May:
i. Improve with time: in tissue prolapse only
ii. Persist: in muscle prolapse
c- Direct injury to EOM:
Diagnosis: negative forced duction test
Improve in 2 months due to regeneration
5- Intraocular damage e.g.
6- Enophthalmos which increases in first 6 months due to orbital
degeneration and fibrosis

Investigations:
1- Investigations for non-comitant squint
2- X-ray Waters view: Opacification with fluid level in maxillary sinus
or tear drop sign
3- CT scan, coronal section
a- Extent
b- Damage
c- Herniation
4- Differential IOP test:
Measurement of IOP in primary position, upgaze and downgaze
Elevation of IOP when the eye moves in the opposite direction of
action of restricted muscle (usually upwards)

58
Treatment:
A- Conservative:
1- Systemic antibiotics
2- Systemic steroids 1 mg/Kg
3- Instruct patient not to blow his nose
4- Follow up

B- Surgery:

Indications:
1- Large fracture >1/2 orbital floor especially if associated with
large medial wall fracture to avoid enophthalmos
2- Enophthalmos > 2 mm in first 2 weeks to avoid increasing
enophthalmos
3- Obvious entrapment of IR by:
a- CT-scan
b- Confirmed by forced duction
c- Diplopia: limitation of upgaze and/or downgaze
within 30º of primary position

Time of surgery:
- Best results in first 2 weeks
- Earlier: after 7-10 days in significant entrapment of IR
- Late: poor results due to fibrosis

59
Incision:
A- Transcutaneous
1- Infraciliary blepharoplasty incision:
Infraciliary incision
 dissection under orbicularis to expose inferior
orbital septum and inferior orbital rim
Incision of periosteum  exposure of extraperiosteal
space  repair of fracture
2- LL crease  scar contracture and ectropion
3- Orbital rim  bad scar
B- Transconjunctival
Inferior fornix (conjunctiva and lower lid retractors) 
peripheral surgical space and orbital floor
Advantages:
1- Entry to episcleral and intraconal space if IR is detached
2- Lateral canthotomy and cantholysis  better exposure

Orbital implant:
A- Autogenous: free autogenous bone graft
From outer table cranial bone
Disadvantages:
1- Contour defects of skull
2- Inadvertent dural perforation
3- Prolonged surgical time
B- Alloplastic:
1- Absorbable:
a- Vicryl
b- Gel foam

60
 Disadvantages:
a- Lack rigidity
b- Leave defect
2- Non-porous:
a- Supramide: stiff
b- Silicone
c- Silastic
d- Teflon
e- Titanium
f- Vitalium
3- Porous:
a- High density porous polyethylene
b- Hydroxyapatite

NB: IR may remain paralytic and need a second surgery

Fracture medial wall

Cause:
Usually associated with fracture floor, rarely isolated

Clinical picture:
1- External e.g. edema, echymosis, Subacutaneous emphysema:
increase with blowing of nose
2- Limitation of:
a. Abduction
b. Adduction
3- Diplopia: in abduction and adduction

61
 4- May be Duane I-like picture (retraction of globe and narrowing of
palpebral fissure on adduction)
5- Intraocular damage e.g.

Treatment
A- Conservative:
1- Systemic antibiotics
2- Systemic steroids 1 mg/Kg
3- Instruct patient not to blow his nose
4- Follow up
B- Surgery:

Time of surgery:
- Best results in first 2 weeks
- Earlier: after 7-10 days in significant entrapment of MR
- Late: poor results due to fibrosis

Incision:
A- Transcutaneous
1- Subperiosteal (Lynch)
From brow to lateral side of nose
May cause injury to trochlear or SO
2- Nasal:
10-12 mm from medial canthus
May cause injury to anterior ethmoidal artery
 subperiosteal space
 medial canthal tendon is reflected with periosteum
B- Transconjunctival
Medial bulbar conjunctiva  peripheral surgical space

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 Advantages:
1- Entry to episcleral and intraconal space if MR is
detached
2- Lateral canthotomy and cantholysis  better exposure
C- Transcaruncular:
Caruncle  posterior to lacrimal sac  subperiosteal space
Advantages:
1- More cosmetic
2- Better access

Consecutive non-comitant squint

1- Lost muscle:
Definition: Retraction of muscle within posterior Tenon’s capsule
against medial orbital wall.
Incidence: Most common in medial rectus due to absence of
fascial connection with oblique muscles
Treatment:
a- Discovered intraoperatively:
i. Good illumination
ii. Scleral retraction sutures to maintain globe in abduction
iii. Meticulous examination with preservation of Tenon’s
capsule to prevent adherence syndrome
iv. Pull Tenon’s capsule forward in a “hand over hand”
fashion
b- Discovered postoperatively:
1- Early intervention before contracture

63
 2- Localization of muscle by:
a- MRI
b- Intraoperatively: oculocardiac reflex may
help
3- If muscle is found: reattachment of muscle according
to amount of strabismus and amount of contracture
4- If muscle is not found: translation of an adjacent
muscle and recession of direct antagonist

B- Slipped muscle:
Definition: Retraction of muscle within its muscle sheath leaving
sheath only attached to sclera
Effect: underaction but not paresis
Prevention: full-thickness sutures through the muscle
Treatment: readvancement of muscle within its muscle sheath to
sclera.
C- Excessive recession
D- Excessive resection
E- Faden procedure

64