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98 Theory and Practice of Squint and Orthoptics
5
Strabismus: Definition,
Classification and Etiology
DEFINITION AND CLASSIFICATION
Definition
• Orthoposition
• Orthophoria
• Strabismus
Classification
• Apparent squint
• Latent squint
• Manifest squint
Clinical types of ocular
deviations
• Esodeviations
• Exodeviations
DEFINITION AND CLASSIFICATION
DEFINITION
Normally visual axes of the two eyes are parallel
to each other in the primary positions of gaze
and this alignment is maintained in all positions
of gaze, except in convergence and divergence.
Perfect alignment of the two eyes is denoted by
the terms orthoposition and orthophoria.
Orthoposition may be defined as the position
of fusional demand in which both primary lines
of sight intersect at the fixation point (Fig. 5.1).
When fusion is interrupted by means such as
covering one eye, the eyes in a small number of
persons will remain in the orthoposition. Such
binocular co-operation in the absence of fusion
is called orthophoria.
Orthophoria, thus, may be defined as a position
of the eyes in which the primary lines of sight
intersect at the fixation point, without any fusion
adjustment being necessary to attain or maintain
this position. A person may be orthophoric only
for one particular fixation distance, whereas at
• Vertical deviations
• Cyclodeviations
Symbols used for phorias and tropias
ETIOLOGY OF STRABISMUS
• Obstacles in the development of normal
binocular vision and coordination
– Sensory
– Motor
– Central
• Role of heredity
• Influence of age on the
development of strabismus
• Development of strabismus in a blind eye
Fig. 5.1 Diagram illustrating orthoposition—the position of
fusional demand in which both primary lines of sight intersect
at the fixation point.
other distances, an adjustment of the relative
position of the eyes by the fusion reflex is
necessary to obtain bifoveal fixation.
Strabismus or squint or simply deviation of the
eye refers to a misalignment of the visual axes
of the two eyes. The term strabismus is derived
99Strabismus: Definition, Classification and Etiology
from the Greek word strabismos (to look
obliquely or askance). The term squint comes
from the fact that strabismic patients often close
one eye or squint to block out one image.
Practically, the term eye deviation describes a
deviation from the orthoposition. Thus strabismus
refers to misalignment of eyes in which the fovea
of one eye is aligned with the fixation target and
the fovea of the fellow eye is off the target and the
image of fixation target is formed at a point nasal
to fovea in esotropia (Fig. 5.2A) and temporal to
fovea in exotropia (Fig. 5.2B).
CLASSIFICATION
Strabismus has been variously classified.
However, no classification is perfect or all
inclusive. Broadly, strabismus can be classified
into latent and manifest strabismus.
Apparent squint or pseudostrabismus
It refers to certain conditions in which visual
axes of the two eyes are in fact parallel in all
positions of gaze and actually there exists a
normal bifoveal vision; but the eyes apparently
seem to have a squint.
1. Pseudoesotropia or apparent convergent
squint may be associated with:
• A prominent epicanthal fold, which covers the
normally visible nasal aspect of the globe and
gives a false impression of esotropia (Fig. 5.3).
• A negative angle kappa
• A too small interpupillary distance.
• An excessively broad nasal bridge
2. Pseudoexotropia or an apparent divergent
squint may be associated with:
• Hypertelorism, a condition of wide separation
of two eyes.
• A positive angle kappa.
• An excessively narrow nasal bridge.
• A too large interpupillary distance.
• Narrowing of lateral canthi (Fig. 5.4)
3. Pseudohypertropia. Pseudohypertropia or
apparent hypertropia may be associated with:
Fig. 5.2 Diagram illustrating formation of image in tropia:
(A) nasal to fovea in esotropia and; (B) temporal to fovea in
exotropia.
Fig. 5.3 Pseudoesotropia in a child with prominent epican-
thal fold (A), Corrected by pinching the skin fold (B)
(Courtesy: Dr Kalpna and Dr. Sandra).
Fig. 5.4 Pseudoexotropia in a child with marked narrowing
of lateral canthus.
100 Theory and Practice of Squint and Orthoptics
• Orbital dystopia
• Anterior segment anomalies
• Vertical angle kappa (e.g. due to a displaced
fovea secondary to retinopathy of prematurity
or other causes of retinal dragging).
Other conditions in which an eye may look to
have an apparent strabismus are:
• Marked facial asymmetry
• Enophthalmos
• Exophthalmos
Latent squint (heterophoria)
Heterophoria, the term introduced by Stevens,
refers to a condition in which the tendency of
the eyes to deviate is overcome (kept latent) by
the fusion reflex during binocular vision.
Therefore, when the influence of fusion is
interrupted, the visual axis of the non-fixing eye
deviates from the orthoposition.
Depending upon the direction of deviation,
heterophoria may be classified into:
• Esophoria
• Exophoria
• Right hyperphoria
• Left hyperphoria
• Incyclophoria
• Excyclophoria
Manifest squint (heterotropia)
Heterotropia is a manifest deviation of the eyes
from the orthoposition that cannot be overcome
by the fusion reflex.
Heterotropia can be variously classified as
follows.
(A) Depending upon concomitance of deviation
1. Comitant strabismus. It is a type of manifest
squint in which the angle of squint remains
constant (unaltered) in all directions of gaze with
either eye fixating.
The term concomitant is considered synonymous with the term comitant. However, the
recent literature prefers the term comitant over
concomitant.
2. Incomitant strabismus. It is a type of
heterotropia in which the angle of deviation
varies with the direction of gaze and/or with the
eye used to fixate. Incomitance may be caused
by innervational, mechanical or restrictive factors.
It includes the following conditions:
• 'A' and 'V' pattern heterotropias
• Special ocular motility defects such as Duane's
retraction syndrome.
• Paralytic squint
(B) Depending upon the direction of deviation
(Fig. 5.5)
1. Esotropia or convergent squint. It denotes
inward deviation of the globe (Fig. 5.5A).
2. Exotropia or divergent squint. It implies
outward deviation of the eyeball (Fig. 5.5B).
3. Right hypertropia. The right eye is elevated
relative to the left (any of the eye may be fixing
eye) (Fig. 5.5C).
4. Left hypertropia. The left eye is elevated
relative to right (any of the eye may be fixing)
(Fig. 5.5D).
5. Incyclotropia. The deviated eye is intorted,
i.e. 12 O'clock meridian of the cornea is rotated
inward (Fig. 5.5E).
6. Excyclotropia. The deviated eye is extorted,
i.e. 12 O'clock meridian of the cornea is rotated
outward (Fig. 5.5F).
(C) Depending upon the constancy of deviation
1. Constant squint. When the deviation remains
constant in all directions of gaze, at all times and
at all distances of fixation.
2. Intermittent squint. When the deviation may
be present sometimes and absent at other times,
under similar conditions of vision and fixation
distances. It may develop in conditions of stress
and strain and also in patients with decompensated heterophoria.
3. Periodic squint. It appears repeatedly under
the same set of conditions, e.g. a squint may
always be present for a particular distance of
fixation and absent for others. This term is not
commonly used and such patients are also
labelled as having intermittent squint.
(D) Depending upon fixation behaviour
1. Unilateral squint. The same eye always
deviates and the second normal eye fixates
(Fig. 5.6A).
Fig. 5.5 Diagrammatic depiction of types of strabismus
depending upon the direction of deviation. (A) left exotropia
(LXT); (B) left esotropia (LET); (C) left hypertropia (LHT);
(D) left hypotropia or right hypertropia (RHT); (E) left
incyclotropia and; (F) left excyclotropia.
2. Alternating squint. Either of the two eyes can
deviate and the other eye fixates (Fig. 5.6B).
3. Bilateral squint. In it, both eyes are squinting
simultaneously. It is seen very rarely.
(E) Depending upon the time of onset
1. Congenital strabismus. A deviation that is
present at birth or appears in first a few months
of life. In the recent literature, the term congenital
strabismus has been almost replaced or is used
synonymously with the infantile strabismus, which
includes all forms of deviations with an onset
during first 6 months of life.
2. Acquired strabismus. A deviation that
develops after 6 months of life.
101Strabismus: Definition, Classification and Etiology
Fig. 5.6 A patient with primary alternate divergent squint
(ADS): (A) Right exotropia while fixing with left eye; and (B)
left exotropia while fixing with right eye.
(F) Depending upon the etiology
Depending upon the etiology/causative
mechanism, following terms are in vogue:
A. Paralytic strabismus, in which one or more
of the extraocular muscles are paralysed.
B. Non-paralytic strabismus. Depending upon
the etiology, non-paralytic strabismus may be
of following types.
1. Accommodative heterotropia. In it, act of
accommodation has a major influence on the
deviation.
2. Non-accommodative heterotropia. In it,
accommodation has not much role to play.
3. Primary heterotropia. Wherein no obvious
cause is found. Duane suggested following
terms:
• Convergence excess type of esodeviation
which is more for near than distance fixation.
• Divergence insufficiency type of
esodeviation which is more for distance
fixation than the near.
• Convergence insufficient type of
esodeviation which is more for near fixation
than the distance.
• Divergence excess type of exodeviation
which is more for distance fixation than near.
4. Secondary/sensory heterotropia is the term
used to describe a deviation which results
from some known cause of visual deprivation/
102 Theory and Practice of Squint and Orthoptics
sight impairing disease of one eye, e.g.
anisometropia, central chorioretinitis, etc.
5. Consecutive heterotropia is the term used to
describe the deviation resulting from surgical
overcorrection or spontaneous conversion of
an esotropic eye into an exodeviation.
CLINICAL TYPES OF OCULAR DEVIATIONS
In day-to-day clinical practice, the ocular
deviations are classified as below.
ESODEVIATIONS
A. Esophoria (E)
B. Intermittent esotropia (E [T])
C. Esotropia (ET)
I. Concomitant esotropia
1. Infantile (congenital) esotropia
2. Accommodative esotropia
i. Refractive (normal AC/A ratio)
ii. Non-refractive accommodative
– Hyperaccommodative (high AC/A ratio)
– Hypoaccommodative
(weak accommodation)
iii. Mixed or partially accommodative
3. Non-accommodative esotropia
i. Acquired or late onset non-accommo-
dative esotropia
– Basic esotropia
– Convergence excess type
– Divergence insufficiency type
ii. Acute concomitant esotropia
iii. Microtropia
iv. Nystagmus blockage syndrome
v. Cyclic esotropia
vi. Stress-induced esotropia
vii. Esotropia in myopia
viii. Esotropia due to spasm of near reflex
4. Sensory esotropias
5. Consecutive esotropia
II. Incomitant esotropia
1. Paralytic esotropia
i. Lateral rectus paralysis
ii. Divergence paralysis
iii. Mobius syndrome
2. A- and V-pattern esotropias
3. Special types of restrictive esotropia
i. Duane's retraction syndrome (with
esotropia)
ii. Thyroid myopathy
iii. Medial orbital wall fracture
iv. Strabismus fixus
v. Excessively resected medial rectus muscle
EXODEVIATIONS
A. Exophoria (X)
B. Intermittent exotropia (X [T])
C. Exotropia (XT)
I. Concomitant exotropias
1. Primary exotropias
i. Divergence excess type
ii. Convergence insufficiency type
iii. Basic exotropia
iv. Pseudodivergence excess type
2. Sensory exotropia
3. Consecutive exotropia
II. Incomitant exotropias
1. Paralytic exotropias
i. Isolated medial rectus paresis
ii. Complete third nerve paralysis
iii. Paralysis of convergence
2. A-, V- and X-pattern exotropias
3. Special types of restrictive exotropias
i. Duane's retraction syndrome (with exotropia)
ii. Craniofacial anomalies with divergent orbit
iii. Thyroid myopathy
iv. Restriction due to trauma or excessive surgery
VERTICAL DEVIATIONS
A. Hyperphoria (H)
B. Intermittent hypertropia [H (T)]
C. Hypertropia (HT)
I. Comitant hypertropia
1. Induced (refractive)
2. End result of long-standing paralytic
deviation.
II. Incomitant vertical deviations
1. Apparent oblique muscle dysfunction
i. Inferior oblique overaction (strabismus
surso-adductorious) now termed as over
elevation in adduction (OEA).
103Strabismus: Definition, Classification and Etiology
• Primary OEA, or
• Secondary OEA.
ii. Inferior oblique underaction, now termed
as under-elevation in adduction (UEA).
• Primary UEA, or
• Seconday UEA
iii. Superior oblique overaction (strabismus
deorsodductorious), now termed as over
depression in adduction (ODA).
• Primary ODA, or
• Secondary ODA.
iv. Superior oblique underaction is now
termed as under-depression in adduction
(UDA).
• Primary UDA, or
• Secondary UDA.
2. Paretic vertical deviations
• Congenital unilateral superior oblique
paresis.
• Non-congenital superior oblique paresis.
• Bilateral superior oblique paresis.
• Monocular elevation deficiency (MED),
(old name: Double elevator palsy).
• Monocular depression deficiency (MDD);
(old name: Double depressor palsy).
• Superior rectus paresis (isolated).
• Inferior rectus paresis (isolated).
• Skew deviation.
3. Restrictive vertical deviations
a. Restrictive vertical deviations due to
misdirected muscle force
i. Congenital cranial dysinnervation
disorders (CCDDs) primarily affecting
vertical ocular motility:
• Congenital fibrosis of extraocular
muscles (CFEOMs)
ii. Iatrogenic displacement of inferior oblique
muscle after its anteriorization.
b. Restrictive vertical deviations due to
mechanical restrictions
i. Tight extraocular muscles
ii. Restrictive vertical deviation due to
structural adhesions (induced adhesive
syndromes)
iii. Restrictive vertical deviation due to orbital
mass lesions.
III. Dissociated vertical deviations (DVD)
1. Monocular DVD
2. Binocular or alternating DVD
CYCLODEVIATIONS
A. Cyclophorias
1. Incyclophoria
2. Excyclophoria
B. Intermittent cyclotropias
1. Intermittent incyclotropia
2. Intermittent excyclotropia
C. Cyclotropias
1. Incyclotropia
i. Inferior oblique paralysis
ii. Inferior rectus paralysis
2. Excyclotropias
i. Superior oblique paralysis
ii. Superior rectus paralysis
SYMBOLS USED FOR PHORIAS AND TROPIAS
In medical charts and orthoptic record, the
deviations are usually indicated by the symbols.
Though, variations may exist between different
squint clinics, the symbols listed in Table 5.1 are
fairly uniformly used as abbreviations for
different types of deviations.
Table 5.1 Symbols used for ocular deviations
Phoria Tropia
Deviation
Eso E E
Exo X X
Right hyper RH RH
Left hyper LH LH
Distance Near Distance Near
Constant Intermittent Constant Intermittent
1
1
1
1
ET E (T) ET
XT X(T) XT
RHT RH(T) RHT
LHT LH(T) LHT
1
1
1
1
E(T)
X(T)
RH(T)
LH(T)
1
1
1
1
104 Theory and Practice of Squint and Orthoptics
ETIOLOGY OF STRABISMUS: AN OVERVIEW
Etiology of strabismus varies in different
clinical varieties and has been described there
and then. Further, etiology of strabismus is still
illusive or only presumptive in many cases. As
a general concept, causes of acquired paralytic
strabismus (which is usually acute in onset) are
comparatively better defined and different
from the causes of non-paralytic types of
strabismus, and are described (see page 298).
In general terms, the development of a nonparalytic strabismus is the result of an abnormality
of one or more of the many factors which are
concerned in the establishment of normal
binocular vision. As we know, the binocular vision
and coordination of ocular movements are not
present since birth but are acquired in the early
childhood. The process starts after birth and is, by
and large, completed by the age of 5–6 years.
Therefore, any obstacle to the development of
these processes may result in concomitant
strabismus. Basically, there is no difference
between the causes leading to a heterophoria and
those resulting in a heterotropia. Rather, it is a
matter of degree to which the interference disrupts
a given function. If the interference is minor, the
resulting defect may be compensated during
binocular vision so that only a latent deviation
(heterophoria) results. If it is more severe, a
manifest strabismus may be the result.
General etiological factors which play role in
the development of strabismus can be discussed
as under:
• Obstacles in the development of normal
binocular vision and co-ordination.
• Role of heredity.
• Influence of age on the development of
strabismus.
• Development of squint in a blind eye.
• Binocular similar images (in size and sharpness)
should be formed so that fusion can occur.
• Normal visual pathway from retinal receptors
to visual centres in the brain is required for a
normal visual perception.
• Brain centres must fuse the input from both eyes
into a unified single perception.
• The neural pathway from the various oculo-
motor centres to the extraocular muscles must
function properly.
• The extraocular muscle function should be
normal and symmetrical in two eyes.
• The binocular co-ordination of eye movement must
be such that the fixation object is imaged in
the centre of each fovea.
• Retinal correspondence must be normal.
Malfunction of any of the above factors can be
an obstacle for the development of normal
binocular vision and binocular co-ordination
resulting in strabismus. These obstacles can be
arranged into three groups namely: Sensory,
motor and central.
1. Sensory obstacles
These are the factors which hinder the formation
of a clear image in one eye and include the
following:
• Uncorrected refractive errors
• Prolonged use of incorrect spectacles
• Anisometropia
• Opacities in the media such as corneal
opacities, lenticular opacities and vitreous
opacities
• Prolonged covering of one eye with a bandage
or eye shade
• Severe unilateral congenital ptosis
• Prolonged use of one eye as with watch-
maker's eye-glass
• Diseases of macula, e.g. central chorioretinitis.
• Optic atrophy
OBSTACLES IN THE DEVELOPMENT OF NORMAL
BINOCULAR VISION AND CO-ORDINATION
Prerequisites for development of normal
binocular vision and binocular coordination
include the following:
• Normal optical media to produce an image on
the retina of each eye.
2. Motor obstacles
These factors hinder the maintenance of the two
eyes in the correct positional relationship in
primary gaze and/or during different ocular
movements. A few such factors are:
• Congenital abnormalities of the size and shape
of orbit.
105Strabismus: Definition, Classification and Etiology
• Abnormalities of extraocular muscles such as
faulty insertion, faulty innervation, mild
paresis, underdevelopment, overdevelopment and muscle slips.
• Abnormalities of fascial structures such as check
ligaments, intermuscular membranes,
connections between the fascial muscle
sleeves where two muscles cross, etc. may also
lead to deviation.
• Abnormalities of accommodation, convergence and
AC/A ratio play an important role in ocular
deviations.
3. Central obstacles
These may be in the form of:
• Deficient development of fusion faculty.
• Abnormalities of cortical control of ocular
movements as occur in mental trauma, and
hyperexcitability of the central nervous
system during teething.
• Purposive use of the convergence reflex initiated
in the motor area of frontal cortex may
also play a role in the development of
strabismus. This occurs classically in the
voluntary squint which may be produced as
a temporary phenomenon in most normal
individuals; but in children it may be more
sustained often as a result of some psychological upset.
ROLE OF HEREDITY
It is unequivocal that the incidence of strabismus
is higher in certain families than in general
population and that heredity plays a definite
role in the occurrence of this disorder. However,
this role cannot be defined as a distinct genetic
pattern of strabismus; but certain defects such
as a refractive error, usually a high degree of
hypermetropia, which in turn may cause
strabismus are genetically transmitted.
INFLUENCE OF AGE ON THE
DEVELOPMENT OF STRABISMUS
The age of the patient, at the time, when the
strabismogenic factors become operative, plays
an important role in the determination of the
strabismus. In a younger patient, the immature
binocular reflex may be unable to withstand
even small obstacles which mitigate against the
fulfilment of full binocular function, whereas in
an older patient, the more mature binocular
reflexes may be able to overcome quite
formidable obstacles. Chavasse stated that a
very slight and transient paresis in adult patients
with well-developed binocular vision may cause
only heterophoria but in an infant it may be
sufficient to severe the slighter bonds which
associate the two eyes.
DEVELOPMENT OF STRABISMUS IN A BLIND EYE
It has been reported that if the loss of vision in
one eye occurs in the first a few months of life,
there may occur, sensory esotropia or exotropia.
Occurrence of poor vision in adulthood due to
any reason tends to cause a sensory exotropia.
However, Sidkaro and von Noorden have
reported that:
• Infants or young children usually develop
sensory esotropia.
• After 2–4 years of age, definitely there are more
chances of developing sensory exotropia.
Note. The exact mechanism of development of
sensory heterotropia is not known, however,
some views have been put forward (see pages
251–252).
BIBLIOGRAPHY
1. Bielschowsky A. Lectures on motor anomalies.
Hanover NH, 1943 (reprinted 1956). Dartmouth
College Publications.
2. Bredemeyer, HG, and Bullock K. Orthoptics:
theory and practice, St Louis. 1968. Mosby - Year
Book Inc, p.86.
3. Broendstrup P. The squinting position of weaksighted eyes, Acta Ophthalmol 20:386, 1944.
4. Chavasse FB. Worth's squint or the binocular
reflexes and the treatment of strabismus, ed. 7,
Philadelphia, 1939, P Blakiston's Sons & Co.,
Inc.
5. Duane A. A new classification of the motor
anomalies of the eyes based upon physiological
principles together with their symptoms,
diagnosis and treatment, reprinted from Ann.
Ophthalmol Otolaryngol, October, 1896, and
edited by White, JW, nd.
6. Keiner GBJ. New viewpoints on the origin of
squint. The Hague, 1951, Martinus Nijoff's ND.