NON-CONCOMITANT STRABISMUS

INTRODUCTION
• Strabismus is the Misalignment of one or both
eyes so as the eye (eyes) is not looking straight at
the object of regard.
• It is also known as SQUINT
Significance In Children

• Children need normally aligned eyes to develop

vision.
• Strabismus in childhood is the second most
common presentation of retinoblastoma.
• Strabismus is a common presentation for
refractive errors.
Significance in Adults
• Frequent sign of neurological disease
• Frequent presentation of systemic disease
• ( Thyroid disease & Myasthenia)
• Cosmetology
Strabismus secondary to loss of vision
from Cataract in Lt. eye
Types of Eye Movements
• Horizontal direction
• Vertical direction
• Torsional direction
All superior muscles are intortors.
All inferior muscles are extortors
 Anatomy & Physiology
Muscle Nerve Function Testing

MR 3rd Nasal Look to

nose
LR 6th Temporal Look away

SR 3rd Elevates, Up and out

intorts
ADDucts
IR 3rd Depress, Down and out
extorts,
ADDucts
 Anatomy and Physiology
Muscle Nerve Functio Testing
n
Superior 4th Intorts, Look Down
Oblique depress, & In
abducts

Inferior 3rd Extrorts, Look Up &

Oblique elevates, In
abducts
CLASSIFICATION
• Apparent strabismus or pseudo strabismus
• Latent squint or Heterophoria
• Manifest squint or Heterotropia
• 1. Concomitant squint
• 2. Non concomitant squint
Types of Strabismus
• Esodeviation  eye turned in

• Exodeviation  eye turned out

• Hyperdeviation  eye turned up

• Hypodeviation  eye turned down

Classification of Strabismus
• Constant or intermittent
• Latent or manifest (phoria or tropia)
• Unilateral or alternating
• Comitant or incomitant (restrictive or paralytic)
• Paralytic or non-paralytic
• Nuclear or supranuclear
Esotropia
Esotropia
Alternating Esotropia
Exotropia
Causes of Strabismus
• Congenital: Imbalance between innervations
and contraction

• Refractive errors

• Loss of vision
• Paralysis or Neuromuscular
• Restrictive: Thyroid eye disease
• Tumours
Presenting symptoms of Strabismus
• Deviation of the eye (cosmesis)
• Double vision
• Torticollis (abnormal head posture)
• Unexplained visual loss in a normal
looking eye (Microtropia)
Abnormal Head Posture
Non- concomitant Strabismus
• Also known as incomitant strabismus or
manifest squint
• This is a type of heterotropia in which the
amount of deviation varies in different directions
of gaze
Non comitant squint
• This includes the following conditions
• Paralytic squint
• A and V pattern heterotropias
• Special Ocular motility defects
Paralytic strabismus
• This is ocular deviation due to complete or
incomplete paralysis of one or more extra-ocular
muscles.
• ETIOLOGY
• Neurogenic lesions
• Myogenic lesions
• Lesions at the level of the neuro-muscular
junction
NEUROGENIC LESIONS
• Congenital: Hypoplasia or absence of nucleus
causing palsies of the CN III and VI. Birth injuries
also mimic congenital lesions.
• Inflammatory lesions: Due to encephalitis,
meningitis, neurosyphilis or peripheral neuritis
(viral) or infectious lesions of cavernous sinus and
orbit.
• Neoplastic lesions: Brain tumours involving
nuclei, nerve roots or intracranial part of the nerves
and intraorbital tumours involving peripheral parts
of the nerves.
NEUROGENIC LESIONS
• Vascular lesions: seen in hypertension,
diabetes mellitus, atherosclerosis in the form of
haemorrhage, thrombosis, embolism, aneurysms
or vascular occlusions. Cerebro vascular
accidents are common in elderly.
• Traumatic lesions: Head injury and direct or
indirect trauma to the nerve trunks.
• Toxic lesions: carbon monoxide poisoning,
diphtheria toxins effect, alcohol and lead
neuropathy.
NEUROGENIC LESIONS
• Demyelinating lesions: Ocular palsy may
occur in multiple sclerosis and diffuse sclerosis.
MYOGENIC LESIONS
• Congenital lesions: absence, hypoplasia,
malinsertion, weakness and musculofacial
anomalies.
• Traumatic lesions: laceration, disinsertion,
haemorrhage into the muscle substance or
sheath and incarceration of muscles in fractures
of the orbital walls.
• Inflammatory lesions: Myositis is usually
viral in origin and may occur in influenza,
measles and other viral fevers.
MYOGENIC LESIONS
• Myopathies: Thyroid myopathy,
carcinomatous myopathy, those due to drugs,
progressive external ophthalmoplegia which is a
bilateral myopathy of extraocular muscles which
may be sporadic or inherited as an autosomal
dominant disorder.
NEUROMUSCULAR JUNCTION LESION
• Myasthenis gravis: This is due to fatigue of
muscle groups which usually starts with small
extra ocular muscles before involving large
muscles.
CLINICAL FEATURES
• Diplopia: main symptom of paralytic squint. It
is more marked towards the action of the
paralysed muscle. It may be
• Crossed: in divergent squint
• Uncrossed: in convergent squint
• Horizontal
• Vertical or oblique depending on paralysed
muscle
• This is due to formation of image on dissimilar
points of the two retinae.
CLINICAL FEATURES
• Confusion: this is due to formation of image of
two different objects on the corresponding
points of two retinae.
• Nausea and vertigo: These are due to diplopia
and confusion
• Ocular deviation: occurs suddenly
CLINICAL SIGNS
• Primary deviation: deviation of the affected
eye and is away from the action of paralysed
muscle, e.g if the lateral rectus is paralysed the
eye is converged.
• Secondary deviation: this is deviation of the
normal eye seen under the cover when the
patient is made to fix with the squinting eye.
• Restriction of the ocular movement:
direction of the action of paralysed muscles.
CLINICAL SIGNS
• Compensatory head posture: the patient does
this to avoid diplopia and confusion. Head is turned
towards the direction of the action of the paralysed
muscle, e.g if the right lateral rectus is paralysed the
patient’s head will be turned right.
• False projection or orientation: this is due to
increased innervational impulse conveyed to the
paralysed muscle. It can be demonstrated by asking
the patient to close the sound eye and then to fix an
object placed on the side of paralysed muscle.
Patient will locate it further away in the same
direction. E.g. Patient with right LR paralysis will
point towards right more than the object actually is.
A and V pattern Heterotropia
• A and V pattern squint are labelled when the
amount of deviation in the squinting eye varies by
more than 10 and 15 degrees respectively between
upward and downward gaze.
• A and V esotropia: In A- the amount of deviation
increases in upward gaze and decreases in
downward gaze. It is vice versa in V esotropia.
• A and V exotropia: In A the amount of deviation
decreases in upward gaze and increases in
downward gaze and vice versa in V exotropia.
SPECIAL OCULAR MOTILITY DEFECTS
• Duane’s retraction syndrome
• It is a congenital motility defect occurring due to
fibrous tightening of lateral or medial or both
rectus muscles.
• Limitation of abduction(type 1) or
adduction(type 2) or both (type 3)
• Retraction of the globe and narrowing of the
palpebral fissure on attempted adduction.
• Eye in primary position may orthotropic,
esotropic or exotropic.
SPECIAL OCULAR MOTILITY DEFECTS
• Brown’s superior oblique tendon sheath
syndrome
• It is congenital ocular motility defect due to
fibrous tightening of the superior oblique tendon.
It is characterized by limitation of elevation of
the eye in adduction(normal elevation in
abduction), usually straight eyes in primary
position and positive forced duction test on
attempts to elevate eye in adduction.
SPECIAL OCULAR MOTILITY DEFECTS
• Strabismus fixus
• This is a rare condition characterised by bilateral
fixation of eyes in convergent position due to
fibrous tightening of the medial recti.

• Double elevator palsy

• This is a congenital condition caused by third
nerve nuclear lesion. It is characterised by
paresis of the superior rectus and the inferior
oblique muscle of the involved eye.
Management of Strabismus
History:
4 most important questions:
1. Age of onset
2. Constant or intermittent
3. Unilateral or alternating
4. Diplopia or torticollis
Management of Strabismus
Examination:
Three objectives:
1. Confirm the diagnosis

2. Diagnose type of strabismus

3. Differentiate paralysis from no paralysis

DIFFERENCE BETWEEN PARALYTIC AND
NON-PARALYTIC STRABISMUS
PARALYTIC SQUINT NON -PARALYTIC SQUINT
• Onset is sudden • Onset is slow
• Diplopia present • Diplopia is absent
• Ocular movt is limited in • Full ocular movt
direction of actin of paralysed
mzl. • False projection is negative
• False projection is positive • Head posture is normal
• Head posture depends on the • Nausea and vertigo are absent
presence of muscle paralysed. • Secondary deviation is equal to
• Nausea and vertigo are primary deviation
present • In old cases pathological
• Secondary deviation is more sequelae in mzls are absent.
than primary deviation
• In old cases pathological
sequelae in mzls are present
Examination of Strab Patient

1. Simple observation for the nasal

white of the eye
2. Corneal light reflex

3. Cover test
METHODS OF EXAMINATION
• Inspection: Large degree squint (convergent or
divergent)
• Ocular movements: Both uniocular as well as
binocular movements should be tested in all
cardinal positions of gaze.
• Pupillary reactions: may be abnormal in patients
with secondary deviations due to diseases of retina
and optic nerve.
• Media and fundus examination: may reveal
associated disease of ocular media, retina or optic
nerve.
METHODS OF EXAMINATION
• Testing and refractive error: this is the most
important because a refractive error may be
responsible for the symptoms of the patient or
for the deviation itself. Preferably, refraction
should be done under full cycloplegia especially
in children.
• Cover test: Direct will confirm the presence of
manifest squint.
• Alternate will reveal whether the squint is
unilateral or bilateral
METHODS OF EXAMINATION
• Estimation of angle of deviation
• 1. Hirschberg corneal reflex test
• 2.Prism and cover test
• 3. krimsky corneal reflex test
• 4.Measurement of deviation with synoptophore
Tests for grade of binocular vision and
sensory functions
1.Worth’s 4-dot test
2.Test for fixation
METHODS OF EXAMINATION
• 4. After image test
• 5. Sensory function test
• 6. Neutral density filter test
ADDITIONAL METHODS OF
INVESTIGATION
• Evaluation for squint
• 1. Diplopia charting
• 2. Hess/Lees screen test
• 3. Field of binocular vision
• 4. Forced duction test
Investigations to find out the cause of
paralysis
• 5. orbital ultrasonography
• 6. orbital and skull CT scan
• 7. Neurological investigation
DIPLOPIA CHARTING
• This is indicated in patients complaining of
confusion or double vision. The patient is asked
to wear red and green diplopia charting glasses.
Red glass-right eye, green-left eye. In a semi-
dark room, he is shown a fine linear light from
about 4 ft and asked about the images in
primary position and in other positions about
gaze. Patients tells about the position and
seperation of the 2 images in different fields.
Hess screen test
• Shows paralysed muscles and the pathological
results of paralysis like overaction, contracture
and secondary inhibitional palsy. When the two
charts are compared, the smaller chart belongs
to the eye with paretic muscle and the larger to
the eye with overacting muscle.
HESS CHART
Field of binocular fixation
• This can be used in patients with paralytic squint
where applicable, so if the patient has some field
of single vision. This test is performed on the
perimeter (with the central chin test)
Forced Duction Test
• This is done to differentiate between the
incomitant squint due to paralysis of extraocular
muscle and that due to mechanical restriction of
the ocular movements.
• FDT is positive(resistance encountered during
passive rotation) in cases of incomitant squint
due to mechanical restriction and negative in
cases of extraocular muscle palsy.
TREATMENT
• Treatment of the cause
• Conservative measures: wait and watch for self
improvement for 6 months, vit.B-complex as
neurotonic and systemic steroids for non-specific
inflammations
• Treatment of annoying diplopia using occluder
on the affected eye with intermittent use of both eyes
with changed head posture to avoid suppression
ambylopia.
• Surgery, in case recovery does not occur in 6
months is done to provide a comfortable field of
binocular fixation i.e. Central fields and lower
quadrants. To strengthen the paralysed muscle by
resection and weakening of the overacting muscle by
recession.
SURGICAL TREATMENT
• Procedures that change the direction of muscle
action
• a) vertical transposition of horizontal recti to
correct A and V patterns
• b) posterior fixation suture (Faden Operation) to
correct dissociated vertical deviation
• c) transplant of muscles in paralytic squints
REFERENCES
• www.wikipedia.com
• www.eyedoctor.com
• www.eyecare.com
• Ophthalmology by A.K.KHURANA 3rd edition
THANKS FOR YOUR ATTENTION