2. Vertical Deviation
Vertical Strabismus refers to a vertical misalignment of the visual axis
Less Common than horizontal
Most commonly associated with horizontal deviations
Also said to have associations with motility disorders
43% of exotropia’ s are resulting in vertical strabismus
It can be hyper or hypotropia (Non fixating eye upper/lower than the fixating
eye)
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vertical deviation
2
4. Restrictive
Misdirected muscle Mechanical restriction
Structural adhesions
Tight EOM Lesions
CCDD EOM
placements
• Duane
• C. Fibrosis
• Mobius
• Browns
• TED
• Blow out fracture
• MED
• Strabismic fixus
Tumors • Post Op
• Scarring
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vertical deviation
4
5. Concomitant – vertical strabismus
Concomitant vertical misalignment of a few diopters is not a rare occurrence
Good fusional Vergence overcome the deviation, resulting in fusion
Also associated with horizontal deviations
Can be hyper or hypo
Idiopathic in many cases
Orbital asymmetry associated with facial and cranial bone disorders can cause a
vertical strabismus
Eg : Plagiocephaly caused by the cranial dysostosis.
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vertical deviation
5
6. Also surgical complication can be one of the cause
Refractive associations are seen
It is intermittent
Suppression, amblyopia, ARC can occur
Treatment
Orthoptics at primary level
Prisms up to 10D
Surgery
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vertical deviation
6
7. Incomitant – vertical strabismus
Oblique muscle dysfunction
IO overactions
SO overactions
IO overactions
Up shoot of eye
Cause : idiopathic mostly
Primary cause : mechanical/ innervational/ or both
Secondary cause : paralysis
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vertical deviation
7
8. Clinical Features
Onset : primary : 2 – 3 yrs
(bilateral)
secondary : any age
(unilateral or bilateral)
Associations
Horizontal D : primary : associated
secondary : isolated
Vertical D : primary : yes with
<5PD
secondary : yes with
10 – 22PD or more
Head tilt : primary : -
secondary : +
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vertical deviation
8
9. Also both primary and secondary deviations are associated with excyclodeviation
Up shoot on adduction (adducted eye over shoots / abducted eye fixates)
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vertical deviation
9
10. Forced duction test : +
DD : DVD
Treatment : surgery – weakening procedure
Recurrence is common complication
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vertical deviation
10
11. Incomitant – vertical strabismus
SO overactions
Down shoot of eye
Cause : idiopathic mostly
Primary cause : mechanical/ innervational/ or both
Secondary cause : paralysis or in association with Browns, Duanes
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vertical deviation
11
12. Clinical Features
Onset : primary : 2 – 3 yrs
(bilateral)
secondary : any age
(unilateral or bilateral)
Associations
Horizontal D : primary : associated
secondary : isolated
Vertical D : primary : +
secondary : -
Head tilt : primary : -
secondary : + towards
affected side
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vertical deviation
12
13. Here incyclodeviation is seen
FDT : +
Treatment : surgery – weakening procedure
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vertical deviation
13
14. Third nerve palsy – paralysis
Oculomotor nerve
Entirely motor in function
Third nerve supplies
EOM - medial rectus, superior rectus, inferior rectus, inferior oblique
IOM - sphincter pupillae and ciliary muscle
Levator palpebrae superioris
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vertical deviation
14
16. Nucleus located in midbrain at the level of superior colliculus, ventral to the
sylvian aqueduct.
Composed of
Unparied levator subnucleus
Paired superior rectus subnuclei
Paired medial rectus ,inferior rectus and inferior oblique subnuclei
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vertical deviation
16
20. Pupillary associations
Parasympathetic fibers
Located superficially between
the brainstem and the
cavernous sinus
Main trunk of 3rd nerve
supplied by the vasa nervorum
Pupillary part by post.
Communicating artery
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vertical deviation
20
22. Third nerve palsy
Eye is down and out
With hypo and large exo
No movement medially and superiorly
No accommodation
Triad
Ptosis
Pupillary dilatation
No accommodation 6/26/2023
vertical deviation
22
29. Treatment
Non surgical
Treat the underlying cause
Diplopia - occlusion patch
Prism in involved eye
Monitor children for development
of amblyopia
Botulinum toxin
Surgical
If it is Complete 3rd nerve palsy
LR recession and MR resection
Anchoring of the globe on medial
wall periosteum
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vertical deviation
29
32. Trochlear nerve palsy
Thinnest and long one - 75mm.
Supplies only the SO in eye
Only CN that comes out from the dorsal aspect
of the brainstem.
Only CN that crosses completely to the opposite
side.
Thus originates from the contralateral nucleus.
Nucleus lies at the level of the inferior colliculus
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vertical deviation
32
33. Course and Distribution
1. Nucleus
2. Fasciculus
3. Trunk
4. Intracavernous
5. Intraorbital
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vertical deviation
33
34. Intracavernous part of CN IV runs in the lateral wall
of the sinus inferior to CN III and above the 1st
division of CN V
Also meets 4 CN
Then leaves the sinus at the level of superior orbital
fissure lateral to annulus of zinn
Travels temporal and inferior to innervate the
superior oblique muscle – Intraorbital part
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vertical deviation
34
35. Causes of isolated fourth nerve palsy
Idiopathic lesions are common, and many of these are thought to be congenital
although symptoms may not develop until decompensation occurs in adult life
due to reduced fusional ability.
In contrast - acquired lesions patients are not usually aware of the torsional
aspect, but may develop vertical double vision
Examination of old photographs for the presence of a compensatory head posture
may be helpful, as is the presence of an increased vertical prism fusional range.
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vertical deviation
35
36. Trauma frequently causes bilateral fourth nerve palsy.
The long and slender nerves are particularly vulnerable as they decussate in the
anterior medullary velum, through impact with the tentorial edge.
Microvascular lesions are relatively common
Aneurysms and tumours are extremely rare.
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vertical deviation
36
37. Signs and symptoms
The acute onset of vertical diplopia in the absence of ptosis, combined with a
characteristic head posture, strongly suggests fourth nerve disease.
Peripheral lesions cause ipsilateral and nuclear lesions contralateral superior
oblique weakness
Signs
Left hypertropia (‘left over right’) in the primary position and increasing on right
gaze
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vertical deviation
37
38. Limitation of left depression, most marked in adduction
Left extorsion, greatest in abduction.
Normal abduction of the left eye
Normal elevation of the left eye
A compensatory head posture
Always unilateral if bilateral involvement seen should be because of head trauma
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vertical deviation
38
40. Investigation
Vascular investigation is sometimes indicated; neuroimaging is not required
routinely for an isolated non-progressive fourth nerve palsy, but should be
considered if improvement does not occur.
Park three step
Double Maddox – in unilateral cyclodeviation is less than 10 deg where as in
bilateral its > 10 deg
Hess chart
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vertical deviation
40
46. Treatment
Microvascular palsies commonly resolve spontaneously
Up to 10D prisms can be used
Underlying cause to be known and treated
Then surgery is the option – weakening or tucking procedure done
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vertical deviation
46
48. Sixth nerve palsy
6th cranial nerve entirely motor in
function
It supplies the lateral rectus
muscle
Abduction of the eye
The nucleus of the sixth nerve lies
at the mid-level of the pons,
ventral to the floor of the fourth
ventricle
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48
49. Course and Distribution
1. Nucleus
2. Fasciculus
3. sub arachnoid space
4. petrous part
5. Intracavernous
6. Intraorbital
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49
50. The intracavernous section runs below the
third and fourth, and the first division of
the fifth nerves
Then leaves the sinus at the level of
superior orbital fissure superior to annulus
of zinn
Travels to innervate the lateral rectus
muscle – Intraorbital part
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vertical deviation
50
52. It can be congenital (rare) or acquired (common).
Can be unilateral or bilateral 6th nerve palsy.
Occasionally, intracavernous sixth nerve palsy is accompanied by a
postganglionic Horner syndrome due to damage to the paracarotid sympathetic
plexus.
The causes of intracavernous sixth nerve and third nerve lesions are similar.
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vertical deviation
52
54. Signs and symptoms
Double vision is characteristically worse for a distant target and less or absent for
near fixation
Should look for about other neurological symptoms, giant cell arteritis, trauma
and symptoms of ear disease
Esotropia in the primary position
Limitation of abduction on the side of the lesion
Normal adduction of the affected eye
A compensatory face turn
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vertical deviation
54
56. Investigation
Routines
FDT
Vascular data
Diplopia charting
Hess chart
Neuro imaging is must done here
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vertical deviation
56
L R
58. Treatment
Observation with monocular occlusion or prismatic correction of diplopia is
appropriate or even head tilt is allowed
In idiopathic and presumed microvascular lesions; up to 90% will recover
spontaneously, usually over weeks to several months.
Young children should be treated with alternate patching to prevent amblyopia
Botulinum toxin injection
Surgery should be considered only when adequate time has been allowed for
maximal spontaneous recovery say 6 – 12 months
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58
61. IO palsy
Isolated inferior oblique palsy (IOP) is a rare clinical entity and the least frequent
palsy among all those involving the 6 extraocular muscles.
The main clinical features of isolated IOP consist of hypotropia and under
elevation in adduction of the affected eye, along with absence of restriction on
forced duction testing
The inferior oblique muscle is innervated by the inferior branch of oculomotor
nerve
Unlike superior oblique palsy, isolated IOP palsy is inherently troubling
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61
62. Clinically, a patient exhibits limitations of elevation in adduction
Brown syndrome is strongly suggested, but here a positive forced duction test
which differentiates it from IOP
The possible etiology for this condition may be congenital or acquired.
The acquired basis for this condition can result from damage of the inferior
oblique nucleus or terminal branches of the oculomotor nerve serving only the
inferior oblique, or direct inferior oblique muscle injury, such as orbital trauma,
vascular lesion or myasthenia gravis
But mostly remains to still understand over it
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vertical deviation
62
63. Investigation
Only MRI could help
The diagnostic criteria for isolated IOP:
1. Presence of hypotropia and under
elevation in adduction of the
affected eye
2. FDT : -
3. Vertical deviations increased on
gaze to the unaffected side
4. Incyclotorsion in one or both eyes
5. Increased hypotropia in
contralateral head tilt
6. A head tilt toward the paralytic
side, face rotation to the unaffected
side and an elevated chin.
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63
64. Treatment
Observation 6 – 12 months
Patching if sensory adaptations
Prisms
Weakening of the ipsilateral superior oblique muscle and/or contralateral superior
rectus recession often resulted in favorable surgical outcomes with a surgical
success rate of 61.5%.
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vertical deviation
64
66. DEP/DDP
Monocular elevation deficiency (MED) is defined as the inability to elevate one
eye equally in abduction, adduction, and primary gaze.
MED was originally termed double elevator palsy (DEP) when the disorder was
thought to be caused by paresis of the two eye elevators, the superior rectus (SR)
and inferior oblique (IO)
When the sound eye is fixed, the paralyzed eye appears to be hypotropic and
pseudoptotic.
When the paralyzed eye is fixed, the ptosis disappears, and the sound eye appears
to be hypertropic.
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66
67. Pseudoptosis may cover the true vertical deviation, leading clinicians to
misdiagnose it as congenital ptosis and then to perform a ptosis correction
surgery
This entity is not known to be hereditary (inherited).
It is a rare condition, and can be congenital (present at birth) or acquired after
birth.
Treatment : only surgery
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vertical deviation
67
68. DDP
Similar to that this is monocular depressor deficiency
Either be palsy or even by restriction
Etiology is still not clear
Simultaneous paralysis of IR & SO in same eye
Hypertropia is seen in primary gaze
It shows reduced depression in field of gazes
Treatment : again surgical process
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68
69. Ophthalmoplegia
Ophthalmoplegia : paralysis of the muscles within or surrounding the eye
Chronic progressive external ophthalmoplegia (CPEO) usually begins in
childhood with:
Ptosis
Slowly progresses to total paralysis of the eyelids and extraocular muscles
CPEO may be sporadic
Although a true Pigmentary retinal dystrophy usually is absent, constricted fields
and electro diagnostic abnormalities can occur.
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69
70. Affected individuals have to turn their head to see in different directions,
especially as the ophthalmoplegia worsens.
People with progressive external ophthalmoplegia may also have general
weakness of the muscles used for movement (myopathy), particularly those in the
neck, arms, or legs.
The weakness may be especially noticeable during exercise
Muscle weakness may also cause difficulty swallowing (dysphagia).
Absence of bells phenomenon
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70
71. Etiology is unclear but still defects in mitochondrial DNA have been found in
some patients. (oxidative phosphorylation)
The triad of :
Retinal pigmentary changes
CPEO
Cardiomyopathy (especially heart block) is called Kearns-Sayre syndrome
Treatment options are limited.
Cautious surgical elevation (suspension) of the upper eyelids indicated to lessen a
severe chin-up head position.
72. Total Ophthalmoplegia
Total ophthalmoplegia thus refers to the paralysis of all the muscles in the eye,
which in turn results in ptosis, immobility of the eye, dilated non reacting pupil
and loss of accommodation.
The condition may be myopathic, that means the muscles controlling eye
movement are directly involved or neurogenic, that means the nerve pathways
controlling eye muscles are affected
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72
74. Investigation
The patient's medical history, family history and detailed examination.
In addition Computed tomography scan (CT scan) or magnetic resonance
imaging (MRI) scan of the brain, orbit and sinuses are needed to rule out
underlying sinus pathology, brain tumour, stroke, aneurysm, or multiple sclerosis.
Other tests like hearing test (audiogram) and the Tensilon (edrophonium) test
should be done in suspected cases.
Thyroid disease and diabetes mellitus should be excluded by appropriate blood
test.
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vertical deviation
74
75. Treatment
Underlying cause
Relieving diplopia
Monitoring exposure keratitis
Surgery for cause
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vertical deviation
75
77. CCDDs - Congenital Cranial dysinnervation
disorders
A number of well-defined syndromes characterized by congenital limitation of eye
movements from abnormal innervation or miswiring of EOM have recently been
grouped as the congenital Cranial dysinnervation disorders
Congenital disorders resulting from aberrant innervation of the ocular and facial
musculature
They are
• Duane – HD of ocular motility
• C. Fibrosis - HD of ocular motility
• Mobius - facial motility and ocular abduction deficit
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77
78. Duanes
Which occur due to result of developmental errors in the innervation of ocular and
facial muscles
Congenital non progressive ocular motility defect.
It was first described by Stilling and Turk.
The syndrome is characterized by limitation or absence of abduction and/or adduction
of the eyes.
There is also retraction of the globe and narrowing of the palpebral fissure on
adduction, which is often associated with elevation or depression of the globes.
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vertical deviation
78
79. Etiology
Pathological studies of DRS have
provided clear evidence that
innervational deficiencies can cause
fibrotic muscle changes.
Most cases are due to innervational
defects, which correlate with aplasia of
the sixth nerve nucleus and the VI cranial
nerve itself
Autosomal dominant DRS- CHN1 gene
mutation
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vertical deviation
79
80. Hubers classification
Type I : due to agenisis of 6th nerve
Esotropia on primary gaze
Limitation / absence of abduction
Normal / slightly defective adduction
Narrowing of palpebral fissure & retraction of globe on adduction
Widening of fissure on abduction.
Head tilt in direction of duanes eye
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80
82. Type II : both 3rd and 6th nerve supplies LR – strong innervation
Exotropia seen
Limitation / absence of adduction
Normal / slightly defective abduction
Narrowing of PF & retraction of globe on attempted adduction
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82
83. Type III
Limitation /absence of both abduction & adduction of affected eye
Retraction of globe & narrowing of PF on attempted adduction.
No eso or exo
Equal innervation to MR/LR
No AHP
Upsoots and downshoots are associated with duanes irrespective of its type
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vertical deviation
83
85. Treatment
The value of botulinum injection into the medial rectus muscle to improve
abduction is controversial
Surgical treatment
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vertical deviation
85
86. Congenital fibrosis of EOM
Congenital fibrosis of the extraocular muscles (CFEOM) describes a group of
rare congenital eye movement disorders that result from the dysfunction of all or
part of the oculomotor (CN 3) and the trochlear (CN 4) nerves, and/or the
muscles these nerves innervate.
Etiology : Recently, CFEOM has been accepted to be of neurogenic origin rather
than primary muscle pathology.
α motor neurons of sup. division of III are present very early in development, but
disappear later (apoptosis, necrosis)
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vertical deviation
86
87. Causes
These disorders have been classified as CFEOM1, CFEOM2, and CFEOM3
based on ophthalmologic findings and molecular genetic testing.
CFEOM 1 and CFEOM 3 are inherited as autosomal dominant genetic
conditions. (abnormal gene)
CFEOM 2 and Tukel syndrome are inherited as autosomal recessive genetic
conditions
CFEOM3 can be characterized by additional involvement of the peripheral and
central nervous system in addition to the eye findings.
Tukel syndrome is characterized by missing and webbed fingers and toes in
addition to the eye findings. These disorders do not worsen over time.
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vertical deviation
87
88. C/F
Affected individuals have limited ability to move their eyes vertically (upward and
downward) and can have variable limitations in moving their eyes horizontally.
CFEOM is also frequently associated with droopy eyelids (ptosis) and eyes that
are fixed in an abnormal position.
Eyes fixed in a downward position, and elevation of the chin is seen.
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vertical deviation
88
90. Management
Molecular test is required here
Routines
The standard management of CFEOM may involve surgery
Non surgical management
Correction of refractive error
Treatment of amblyopia,
Surgical management-
Correction of hypotropia, exotropia followed by ptosis correction
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vertical deviation
90
91. Mobius syndrome
Mobius syndrome is an extremely rare congenital neurological disorder which is
characterized by facial paralysis and the inability to move the eyes from side to
side.
Moebius syndrome is caused by the absence or underdevelopment of the 6th and
7th cranial nerves, which control eye movement and facial expression
It is thought to result from a vascular disruption (temporary loss of blood flow) in
the brain during prenatal development.
The use of drugs and a traumatic pregnancy may also be linked to the
development
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vertical deviation
91
92. C/F
Most likely, Moebius syndrome is multifactorial,
which means that both genetic and
environmental factors play some causative role
Dental issues
Weak muscle tone (hypotonia)
Abnormal curvature of the spine (scoliosis)
Respiratory disorders
Sleep problems
Upper body weakness which can lead to delays
in motor function
Ear abnormalities - Hearing loss (if certain
cranial nerves are affected) 6/26/2023
92
95. Diagnosis
A diagnosis of Moebius syndrome is based upon the characteristic
signs/symptoms, a detailed patient history, and a thorough clinical evaluation.
There are no diagnostic tests that confirm a diagnosis of Moebius syndrome.
Some specialized tests may be performed to rule out other causes of facial palsy.
GTR done, CT Scanning, MRI, and Ultrasonography
Diagnostic Criteria
Paralysis or weakness of at least one side of the face (usually both)
Sideways movement of the eyes is paralyzed
Vertical movement of the eyes is intact
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vertical deviation
95
96. Management
Each person with Moebius syndrome will have different needs.
While there's no definitive treatment or cure for the condition, a multi model
approach is needed
Since the diagnosis can usually be made at birth or soon after, early interventions,
such as physical, occupational, and speech therapy can be made early.
A thorough eye exam to address vision problems.
Squint surgery
If hearing is impaired, an audiologist may be consulted.
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vertical deviation
96
100. Tight EOM – Brown’s
Brown syndrome was described by Harold W. Brown in 1950 as the superior
oblique tendon sheath syndrome.
Brown syndrome is a condition involving mechanical restriction, typically of the
superior oblique tendon.
It is usually congenital but occasionally acquired
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vertical deviation
100
101. Causes
Congenital
Idiopathic.
‘Congenital click syndrome’ where
there is impaired movement of the
superior oblique tendon through the
trochlea.
Acquired
Trauma to the trochlea or superior
oblique tendon.
Inflammation of the tendon, which
may be caused by rheumatoid
arthritis, pan sinusitis or scleritis.
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vertical deviation
101
103. Signs
Usually straight with BSV in the
primary position
Limited elevation in adduction
Limited elevation on up gaze is
common
Normal elevation in abduction
Absence of superior oblique
overaction
Rarely - Down-shoot in adduction.
Hypotropia in primary position.
CHP with chin elevation and
ipsilateral head tilt
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vertical deviation
103
106. Brown syndrome OS
Divergence in up gaze
Down shoot in attempted elevation in adduction?
Down shoot in attempted elev. in adduct. (different than IO palsy)
107. Treatment
Congenital cases do not usually require treatment as long as binocular function
is maintained with an acceptable head posture
Spontaneous improvement can be seen at the end of 1st decade of life
Indications for treatment include significant primary position hypotropia,
deteriorating control and/or an unacceptable head posture.
The recommended procedure for congenital cases is lengthening of the superior
oblique tendon.
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vertical deviation
107
108. Acquired: treatable aetiology should be addressed specifically. Depending on the
cause, acquired cases may benefit from steroids, either orally or by injection near
the trochlea.
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vertical deviation
108
109. TED – thyroid eye diseases
Thyroid eye disease (TED), also known as thyroid-associated orbitopathy and
Graves ophthalmopathy, is a very common orbital disorder, and is the most
common cause of both bilateral and unilateral proptosis in an adult
Graves disease, the most common form of hyperthyroidism, is an autoimmune
disorder in which IgG antibodies bind to thyroid stimulating hormone (TSH)
receptors in the thyroid gland and stimulate secretion of thyroid hormones.
It is more common in females
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vertical deviation
109
110. Presentation is often in the fourth or fifth decades with symptoms including
o Weight loss despite good appetite,
o Increased bowel frequency,
o Sweating,
o Heat intolerance,
o Nervousness,
o Irritability,
o Palpitations,
o Weakness and fatigue
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vertical deviation
110
112. May be associated with other autoimmune disorders
R/F
Smoking
Women are five times more likely to be affected by TED than men
Radioactive iodine used to treat hyperthyroidism can worsen TED.
Hyperthyroidism 94%
Euthyroid 4%
Hypothyroid 2%
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vertical deviation
112
113. Pathogenesis
Circulating T cells in patients with Graves’ disease directed against an
antigen on thyroid follicular cells
But these lymphocytes came to be directed against a self -antigen,
escaping deletion by the immune system, is unknown
An interaction between the activated CD4 T cells and local fibroblasts
results in release of cytokines into the surrounding tissue
They then develop the autoimmune response in the orbital connective
tissue.
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vertical deviation
113
114. 6/26/2023
vertical deviation
114
Stimulate glycosaminoglycan production in fibroblasts, proliferation of
fibroblasts, or both
leading to the accumulation of glycosaminoglycan's and oedema in
the orbital connective tissue.
The increase in connective-tissue volume and the fibrotic restriction
of extraocular-muscle movement resulting from fibroblast stimulation
lead to the clinical manifestations of ophthalmopathy
115. Clinical features
Lid signs: Retraction of the upper lids producing the characteristic staring and
frightened appearance (Dalrymple’s sign)
Lid lag (von Graefe’s sign)
Fullness of eyelids due to puffy oedematous swelling (Enroth’s sign);
Difficulty in eversion of upper lid (Gifford’s sign);
Infrequent blinking (Stellwag’s sign).
Conjunctival signs. These include ‘deep injection’ and ‘chemosis’.
Pupillary signs. These are of less importance and may be evident as inequality
of dilatation of pupils.
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vertical deviation
115
116. Convergence weakness (Mobius’s sign)
Exophthalmos
Exposure keratitis and symptoms of ocular surface discomfort
Optic neuropathy. It occurs due to direct compression of the nerve or its blood
supply by the enlarged rectus muscles at the orbital apex.
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vertical deviation
116
120. Investigations
Thyroid function tests. These should include: serum T3, T4, TSH and estimation
of radioactive iodine uptake.
Positional tonometry.
Ultrasonography.
Computerised tomographic scanning
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vertical deviation
120
121. Treatment
When
Optic nerve compression
Corneal exposure
Diplopia
Proptosis
AHP
Artificial tears
Steroids
Orbital decompression
Eye muscle surgery
Eyelid surgery
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vertical deviation
121
122. MED restrictive
It is thought to manifest primarily with a tight or contracted inferior rectus
muscle or a hypo plastic or ineffective superior rectus muscle.
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vertical deviation
122
124. Blow out fracture
These are isolated comminuted fractures which occur when the orbital walls are
pressed indirectly, ‘Blowout fractures’ mainly involve orbital floor and medial
wall.
A blow-out fracture of the orbital floor is typically caused by a sudden increase in
the orbital pressure from an impacting object that is greater in diameter than the
orbital aperture (about 5 cm), such as a fist or tennis ball, so that the eyeball itself
is displaced and transmits rather than absorbs the impact
Roof and lateral wall can withstand
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vertical deviation
124
126. C/F
Visual function, especially acuity, should be recorded and monitored as
necessary, particularly in the acute situation.
Periocular signs include variable ecchymosis, oedema and occasionally
subcutaneous emphysema
Severe pain
Diplopia may be caused by one of the following mechanisms: Haemorrhage and
oedema in the orbit may be a cause for restricting movement of the globe.
Ocular motility usually improves as the haemorrhage and oedema resolve.
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126
128. Diplopia typically occurs in both upgaze and downgaze.
Forced duction and the differential intraocular pressure (IOP) test are positive
Direct injury to an extraocular muscle, associated with a negative forced duction
test. The muscle fibres usually regenerate and normal function often returns
within about 2 months
Enophthalmos may be present if the fracture is severe, and in the absence of
surgical intervention, enophthalmos may continue to increase for about 6 months
as post-traumatic orbital tissue degeneration and fibrosis develop
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vertical deviation
128
129. Investigations
CT
MRI
Ocular routines and emergencies seen
Hess chart
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vertical deviation
129
131. 6/26/2023
vertical deviation
131
Hess chart of a left orbital floor blow-out fracture shows restriction of left upgaze (superior rectus and inferior
oblique) and restriction on downgaze (inferior rectus). There is also secondary overaction of the right eye
132. Treatment
Initial treatment generally consists of observation, with the prescription of oral
antibiotics; ice packs and nasal decongestants may be helpful
The patient should be instructed not to blow nose, because of the possibility of
forcing infected sinus contents into the orbit
Steroids – if optic nerve is compressed
Fractures involving up to one-half of the orbital floor, with little or no herniation,
no significant enophthalmos and improving diplopia, also do not require
treatment.
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vertical deviation
132
133. Fractures involving more than one-half of the orbital floor will usually develop
significant enophthalmos if left untreated.
Fractures with entrapment of orbital contents, enophthalmos of greater than 2
mm, and/or persistent and significant diplopia in the primary position should be
repaired within 2 weeks.
If surgery is delayed, the results are less satisfactory due to secondary fibrotic
changes.
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vertical deviation
133
134. Very urgent surgical indicative
Enophthalmos
White eyed fracture
Age <18yrs
Surgical repair is performed via a transconjunctival or subciliary incision or via the
maxillary sinus, with elevation of the periosteum from the orbital floor, freeing of
trapped orbital contents and repair of the bony defect with a synthetic implant.
6/26/2023
vertical deviation
134
135. Strabismic fixus
Strabismus fixus is a rare condition in which both eyes are fixed by fibrous
tightening of the medial recti (convergent strabismus) or the lateral recti
(divergent strabismus)
It can be Congenital and acquired forms
This disease may progress over several years from a small degree of esotropia
with free ocular movement to the end stage of large angle fixed esotropia.
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vertical deviation
135
136. Etiology
The underlying etiology of strabismus fixus still remains unclear .
The most recent explanation is that the enlarged globe in high myopia herniates
superotemporally and retroequatorially through the muscle cone
Congenital : Congenital strabismus fixus is caused by fibrosis which explains
loss of elasticity of medial rectus
Lateral rectus palsy: Lateral rectus palsy causes the secondary contracture and
fibrosis of medial rectus
Amyloidosis: Infiltration of extraocular muscle by amyloid
Others : Unspecific, progressive fibrosis, myopathy and myositis
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vertical deviation
136
138. Signs symptoms
Patients are usually old aged, with high myopia, although few cases of
strabismus fixus even in the absence of high myopia have been described
Patients typically complain of there eyes being fixed and there inability to move
the eyes outward
Patients with bilateral strabismus fixus are severely handicapped, one usually is
preferred for vision and immobility of eye necessitates an extreme degree of head
turn in such patients
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vertical deviation
138
139. Investigations and Management
FDT
CT
MRI
Treatment is mainly surgical – resection with recessions carried out
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vertical deviation
139
140. Tumours
Damage to the muscles that move
the eyes or the nerves that control
eye movement can create a diplopia
Eg : thyroid
Stroke
TIA
Aneurysms
Brain tumors
Multiple sclerosis
Trauma
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vertical deviation
140
141. Structural Adhesions
Post Op complications : is most commonly attributed to extraocular muscle
restriction or paresis from surgical trauma or anesthetic myotoxicity.
Scarring : pulls nearby tissues
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vertical deviation
141
143. ‘V’ or ‘A’ patterns occur when the relative contributions of the superior rectus
and inferior oblique to elevation, or of the inferior rectus and superior oblique to
depression, are abnormal, resulting in derangement of the balance of their
horizontal vectors in up and downgaze.
They can also be caused by anomalies in the position of the rectus muscle
pulleys.
Assessment is by measuring horizontal deviations in the primary position, upgaze
and downgaze.
They can occur in both concomitant and Incomitant deviations.
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vertical deviation
143
144. V pattern
A ‘V’ pattern is said to be significant when the difference between upgaze and
downgaze is ≥15 Δ.
It also have subtypes or sub patterns
Y pattern and
Arrow
6/26/2023
vertical deviation
144
145. Causes
Inferior oblique overaction associated with fourth nerve palsy.
Superior oblique underaction with subsequent inferior oblique overaction, seen in
infantile esotropia as well as other childhood esotropias. The eyes are often
straight in upgaze with a marked esodeviation in downgaze.
Superior rectus underaction.
Brown syndrome.
Craniofacial anomalies featuring shallow orbits and down-slanting palpebral
fissures.
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vertical deviation
145
146. V pattern for ESO & EXO
ESO
Increased deviation in downgaze
With decreased deviation in upgaze
Eg 10 PD : UP
20 PD : Primary position
30 PD : Down
EXO
Decreased deviation in downgaze
With Increased deviation in upgaze
Eg 30 PD : UP
20 PD : Primary position
10 PD : Down
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vertical deviation
146
149. V pattern SUBTYPES
Y pattern
Divergence in upgaze with change in
deviation between primary and down
gaze is seen
Eg 30 PD : UP
15 PD : Primary position
10 PD : Down
Arrow
Convergence that largely occurs
between down and primary gaze
Eg 05 PD : UP
15 PD : Primary position
30 PD : Down
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vertical deviation
149
150. Treatment
Treatment is by inferior oblique weakening or superior oblique strengthening
when oblique dysfunction is present.
Without oblique muscle dysfunction treatment is as follows:
‘V’ pattern esotropia can be treated by bilateral medial rectus recessions and
downward transposition of the tendons.
‘V’ pattern exotropia can be treated by bilateral lateral rectus recessions and
upward transposition of the tendons.
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vertical deviation
150
151. A pattern
A ‘a’ pattern is said to be significant when the difference between downgaze and
upgaze is ≥15 Δ.
It also have subtypes or sub patterns
Lamda pattern and
X pattern
6/26/2023
vertical deviation
151
152. Causes
Primary superior oblique overaction is usually associated with exo deviation in
the primary position of gaze.
Inferior oblique underaction/palsy with subsequent superior oblique overaction.
Inferior rectus underaction.
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vertical deviation
152
153. A pattern for ESO & EXO
ESO
Increased deviation in downgaze
With decreased deviation in upgaze
Eg 10 PD : UP
20 PD : Primary position
30 PD : Down
EXO
Decreased deviation in downgaze
With Increased deviation in upgaze
Eg 30 PD : UP
20 PD : Primary position
10 PD : Down
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vertical deviation
153
156. A pattern SUBTYPES
Lamda pattern
Divergence in downgaze with change in
Horizontal deviation between primary
and up gaze is seen
Eg 10 PD : UP
20 PD : Primary position
35 PD : Down
X pattern
Convergence that largely occurs
between down and primary gaze
Eg 40 PD : UP
20 PD : Primary position
40 PD : Down
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vertical deviation
156
157. Treatment
Patients with oblique dysfunction are treated by superior oblique posterior
tenotomy.
Treatment of cases without oblique muscle dysfunction is as follows:
‘A’ pattern esotropia is treated by bilateral medial rectus recessions and upward
transposition of the tendons.
‘A’ pattern exotropia is treated by bilateral lateral rectus recessions and
downward transposition of the tendons.
6/26/2023
vertical deviation
157
158. Surgical and non surgical management of
squint
Non surgical
Optical correction
Prisms
Pharmacological agents
Orthoptics
VT
Surgical
Recession
Resection at primary lane
Or both
And other procedures like (fadens
operation, tucking procedure etc…)
6/26/2023
vertical deviation
158
Left Brown syndrome. (A) Straight in the primary position; (B) limited left elevation in adduction; (C) limited left elevation on upgaze; (D) normal left elevation in abduction; (E) absence of left superior oblique overaction; (F) chin elevation and left head tilt