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266 Theory and Practice of Squint and Orthoptics
Fig. 10.13 A patient with esotropia (A), who developed
consecutive exotropia after surgery (B), which was surgically
corrected to orthotropia (C).
2. Assess state of binocular sensory cooperation:
i. If normal retinal correspondence and bifoveal
fusion can be demonstrated (especially in
patients with overcorrected esotropia):
• Overcome suppression
• Improve fusional convergence
• Perform surgery
ii. If bifoveal fusion cannot be demonstrated, assess
cosmetic appearance:
• If good, leave alone.
• If poor, perform cosmetic surgery.
BIBLIOGRAPHY
1. Burian HM: Pathophysiology of exodeviations.
In Manlev DR (ed): Symposium on Horizontal
Ocular Deviations. St. Louis. Mosby, 1971. p 119
2. Burian HM, Noorden GK von: Binocular Vision
and Ocular Motility. St. Louis, Mosby, 1974.
3. Burian HM: Exodeviations : Their classification,
diagnosis and treatment. Am J Ophthalmol
62:1161, 1966.
4. Cooper El: Purposeful overcorrection in
exotropia. In Arruga A(ed): International
Strabismus Symposium (University of Geissen,
1966). Basel/New York, S Karger, 1968, p 311.
5. Costenbader FD: Roundtable discussion. In
Allen JH (ed): Strabismic Ophthalmic
Symposium II. St. Louis, Mosby, 1958, p 484.
6. Costenbader FD: Infantile esotropia. Trans Am
Ophthalmol Soc. 59:397, 1961
7. Calhou JC, Nelson LB, Harley RD Atlas of Ped.
Ophthal Surgery Philadelphia Saunders. 1987
pp 8-10.
8. Crone RA. Everhard-Halm Y: Cyclofusion. In
Moore 5, Mein J (eds): Orthoptics: Past, Present,
and Future. New York, Stratton Intercontinental,
1976, p 409.
9. Dell' Osso LF, Ellenberger CJr, Abel LA et al:
The nystagmus blockage syndrome: Congenital
nystagmus, manifest latent nystagmus or both?
Invest Ophthalmol Vis Sci. 24: 1580-87, 1983.
10. Duane A: A new classification of the motor
anomalies of the eye based upon physiological
principles, together with their symptoms,
diagnosis and treatment. Ann Ophthalmol
Otolaryngol 5:969, 1896; 6:84, 247, 1897.
11. Helveston EM: Cyclic strabismus. Am Orthopt
J 23: 48-51, 1973.
12. Havener WH: Ocular Pharmacology, St. Louis,
Mosby, 1978.
13. Henson DB, Williams DE: Depth perception in
strabismus. Br J Ophthalmol 64:349, 1980.
14. Hiles DA: Surgery for congenital esotropia. Int
Ophthalmol Clin 16 (3) : 75, 1976.
15. Hoyt WF, Daroff RB: Supranuclear disorders of
ocular control systems in man: Clinical,
anatomical and physiological correlations. In
Bach-y-rita P, Collins CC, Hyde JE(eds): The
Control of Eye Movements New York. Academic
Press, 1971, p 175.
16. Ing MR: Early surgical alignment for congenital
esotropia. J Pediatr Ophthalmol Strabismus
20:11-18, 1983.
17. Jotterand VH, Isenberg SJ: Enhancing surgery
for accommodative esotropia, Ophthalmic Surg
19:263-266, 1988.
18. Krzystkowa, K and Paja Kowa J, The sensorial
state in divergent strabismus. In orthoptics,
Proceeding of the second international
orthoptics congress, Amsterdam, 1972, Excerpta
media foundation, p 72.
19. Kushner BJ: Exotropic deviations: A functional
classification and approach to treatment. Am
Orthoptic J 38:81-93, 1988.
20. Manle DR: Classification of the exodeviations, in
Manley DR (ed): Symposium on Horizontal
Ocular Deviations. St. Louis. Mosby, 1971.p 128.
Concomitant Esotropias and Exotropias
267
21. Nelson LB Bacal Da Burke MJ An alternative
approach to the surgical management of
exotropia : the unilateral lateral rectus recession.
J.Ped. Ophthalmol strabismus 1992. 29 (6) 357–
60.
22. Noorden GK von: Divergence excess and
simulated divergence excess, diagnosis and
surgical management, Ophthalmologica 26: 719,
1969.
23. Noorden GK von: Some aspects of exotropia,
presented before meeting of the Wilmer
Resident Association, John Hopkins Hospital,
April 26, 1966.
24. Noorden GK von: The nystagmus compensation
(blockage) syndrome. Am J Ophthalmol 82:283,
1976.
25. Noorden GK von: Indications of the posterior
fixation operation in strabismus. Ophthalmology
(Rochester) 85:512, 1979.
26. Parks MM: The monofixation syndrome. Trans
Am Ophthalmol Soc 67:609. 1969.
27. Prism Adaptation Study Group: Efficacy of
prism adaptation in the surgica management of
acquired esotropia. Arch Ophthalmol 108:12281256, 1993.
28. Reinecke RD: Accommodative esotropia. J
Continuing Educ Ophthalmol 40:11,1978.
29. Rogers GL, Chazen S, Fellows R, et al:
Strabismus surgery and its effect upon infant
development in congenital esotropia.
Ophthalmology 89:479-483, 1982.
30. Sanfilippo S. clahane AC The effectiveness of
orthoptics alone in selected cases of
exodeviations the immediate result and several
years later Am Orthopt J. 1970: 20: 104-17.
31. Tychsen L, Lisberger SG: Maldevelopment of
visual motion processing in humans who had
strabismus with onset in infancy. J Neurosci
6:2495-2508, 1986.
32. Wright KW, Bruce-Lyle L: Augmented surgery
for esotropia associated with high hypermetropia.
J Pediatr Ophthalmol Strabismus 30:167-170, 1993.
268 Theory and Practice of Squint and Orthoptics
11
Vertical Strabismus and
Cyclodeviations
VERTICAL STRABISMUS
Classification
•
Comitant vertical deviations
•
Incomitant vertical deviations
•
– Classification
– Apparent oblique muscle dysfunction
Dissociated vertical deviations
•
Dissociated horizontal deviation
•
CYCLODEVIATIONS
Classification
•
VERTICAL STRABISMUS
CLASSIFICATION
A. Depending upon constancy of deviation
1. Hyperphoria (H)
2. Intermittent hypertropia (H [T])
3. Hypertropia (HT)
B. Depending upon the direction of deviation in
the non-fixing eye
1. Hypertropia
2. Hypotropia
C. Depending upon comitance of deviation
I. Comitant vertical deviation
1. Induced (refractive)
2. End result of long-standing paralytic
deviation
II. Incomitant vertical deviations
Depending upon the innervational etiology,
the incomitant vertical deviations can be
further subdivided into following types:
1. Apparent oblique muscle dysfunction
2. Paretic vertical deviations
3. Restrictive vertical deviations
Etiology
•
Clinical characteristics
•
Diagnostic tests
•
– Subjective tests
– Objective tests
Treatment
•
– Cyclovertical deviation
– Cyclodeviation without vertical deviation
III. Dissociated vertical deviation (DVD)
• Monocular DVD
• Bionocular or alternating DVD
COMITANT VERTICAL DEVIATIONS
The prevalence of comitant vertical deviations
in general is not low. Vertical deviations may
occur as isolated anomalies or in association
with horizontal deviations.
Prevalence. Following observations have been
made regarding prevalence of vertical deviations:
• Approximately, half of the patients with
motility disorders have isolated vertical
anomalies.
• Approximately, one-third of all patients with
motility disorders have a combined horizontal
and vertical deviation.
• An associated vertical deviation has been
reported in 43% of all exotropias.
Types. Comitant vertical deviations include:
1. Hypertropia. In this condition, non-fixating
eye is higher than the fixating eye.
2. Hypotropia. In this condition, non-fixating eye
is lower than the fixing eye.
269Vertical Strabismus and Cyclodeviations
Etiology
Exact etiology is not known. Following factors
have been blamed:
• Correction of unequal refractive error may induce
comitant hyperdeviations.
• Anomalous position of rest caused by orbital or
other anatomical anomalies or mechanical
factors or abnormal innervation may be
causative mechanism.
• Convertion of incomitant paralytic hyperdeviation
to comitant with the passage of time (as
secondary changes occur) is also common to
find.
Clinical features
• Symptoms can be marked in hyperdeviations,
even when the magnitude is low. Patients
often present with frontal headache, diplopia,
ocular discomfort or pain, due to overuse of
fusional vergence.
• Hypertropias are more frequently intermittent
than constant deviations.
• Suppression, amblyopia, or vertical anomalous
retinal correspondence may occur.
• In deviation of lesser magnitude, the patient
may obtain bifoveal fusion by tilting the head.
• Typically, patients with small comitant
vertical deviations have a moderate to large
horizontal strabismus (exotropia or esotropia)
as well.
• Repeated measurements in the diagnostic
positions of gaze in majority of patients may
reveal a paretic component or a primary
overaction of one or several cyclovertical
muscles.
Note. Large primary comitant vertical deviations
are rare. The primary vertical deviation must
be differentiated from skew deviation, which is
rather abrupt in onset, variable, and associated
with symptoms caused by intracranial or
labyrinthine disease.
Treatment
1. Orthoptics. Amblyopia, when present,
should be treated. If a bifoveal fusion potential
and normal correspondence can be demonstrated in patients in whom the deviation was
acquired after a period of normal binocular
vision, orthoptic treatment to eliminate
suppression may be indicated prior to surgery.
It is almost impossible to improve vertical
fusional vergence through orthoptic training.
2. Prismotherapy. Comitant vertical deviations
smaller than 10D can be corrected with prism.
The prism power should be distributed equally
before the two eyes with a base-down prism in
front of the hypertropic eye and a base-up prism
infront of hypotropic eye. The minimal
prismatic power that provides comfortable
single binocular vision should be prescribed.
3. Surgery. Following procedures are indicated:
• A comitant vertical deviation up to 11D to 14D
associated with horizontal deviation can be
eliminated by simply lowering the horizontal
muscle insertion (by 5 to 8 mm) of the
hypertropic eye or by raising the insertions of
hypotropic eye; while performing the
horizontal squint surgery.
• For large vertical deviations (between 15D and
25D), a 3 to 4 mm recession of the appropriate
vertical rectus muscle is recommended. For
example, in a patient with right hypertropia
of 25D, the right superior rectus and left
inferior rectus should each be recessed by
4–5 mm.
INCOMITANT VERTICAL DEVIATIONS
CLASSIFICATION
Incomitant vertical deviations can be classified
as below:
1. Apparent oblique muscle dysfunction
i. Inferior oblique overaction (strabismus surso-
adductorious) is now termed as over-elevation
in adduction (OEA). It can be:
• Primary OEA, or
• Secondary OEA.
ii. Inferior oblique underaction, is now termed as
under-elevation in adduction (UEA). It can be:
• Primary UEA, or
• Secondary UEA
iii. Superior oblique overaction (strabismus
deorsadductorious) is now termed as overdepression in adduction (ODA). It can be:
• Primary ODA, or
• Secondary ODA.
270 Theory and Practice of Squint and Orthoptics
iv. Superior oblique underaction is now termed as
under-depression in adduction (UDA). It can be:
• 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.
• Inferior oblique paresis
3. Restrictive vertical deviations
A. Restrictive vertical deviations due to misdirected
muscle force, as seen in:
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 deviation due to mechanical
restrictions as seen in:
i. Tight extraocular muscles, e.g.
• Congenital Brown’s syndrome (new name
restrictive hypotropia in adduction, i.e.
RHA).
• Hypotropia due to incarceration of
inferior rectus in blow-out fracture of
orbital floor.
• Hypotropia due to inferior rectus
thickening in thyroid ophthalmopathy.
• Hypotropia in monocular elevation
deficiency (MED) caused by fibrotic
inferior rectus muscle.
ii. Restrictive vertical deviation due to structural
adhesions (induced adhesive syndromes), e.g.:
• Acquired Brown’s syndrome due to
scarring around the trochlea.
• Due to fat adherence as seen after retinal
detachment surgery.
• Post-radiation orbital scarring.
• Due to conjunctival and Tenon’s capsule
scarring:
– Postoperative
– Post-traumatic
– Post-chemical burns
iii. Restrictive vertical deviation due to orbital mass
lesions, e.g. as in:
• Orbital tumours
• Glaucoma explant with large bleb causing
mass effect.
Note. Incomitant vertical deviations caused by
overaction of superior and inferior oblique
muscles are discussed here.
Incomitant vertical deviations caused by
weakness, paralysis or restriction of the
cyclovertical muscles are discussed in Chapter
12.
APPARENT OBLIQUE MUSCLE DYSFUNCTION
INFERIOR OBLIQUE OVERACTION
Inferior oblique muscle overaction, also referred
to as strabismus sursoadductorious, is now termed
as over-elevation in adduction (OEA). It is
characterized by an upshoot of the eye in
adduction.
Etiology
1. Primary overaction of the inferior oblique
muscle is etiologically not well understood.
Perhaps it may be due to mechanical or
innervational causes or a combination of the
two. It may occur as an isolated phenomenon
or in association with esotropia or exotropiaoften of V-pattern.
2. Secondary overaction of the inferior oblique
muscle is caused by paralysis or paresis of either
its antagonist muscle (ipsilateral superior
oblique muscle) or its yoke muscle (contralateral
superior rectus muscle). Another cause of
secondary overaction of the inferior oblique,
unrelated to paralysis is non-parallelism of the
plane of superior and inferior oblique muscles.
(The term desagittalization has been suggested
to describe this dysfunction.)
271Vertical Strabismus and Cyclodeviations
Clinical features
Clinical features of primary inferior oblique
overaction (PIOO) versus secondary inferior
oblique overaction (SIOO) are as follows:
1. Age of onset. PIOO usually occurs after one
year of age, while SIOO can occur at any age.
SIOO occurs either spontaneously or few weeks
to months following paresis of the ipsilateral
superior oblique muscle or contralateral
superior rectus muscle.
2. Bilaterality. PIOO is frequently bilateral
(72%) and often asymmetric while SIOO is
occasionally bilateral.
3. Upshoot or over-elevation of the eye in
adduction is the clinical characteristic of primary
as well as secondary inferior oblique overaction.
That is, with the eyes in lateral gaze and the
abducting eye fixing, the adducted eye is over
elevated. When the eyes are in lateral gaze and
the adducting eye is made to fix, the abducted
eye will be depressed and manifest a hypotropia
on alternate cover testing. (c.f. DVD see page
281). Clinically, the upshoot of the eye can be
graded on a scale of +1 to +4 (see page 122). In a
+4 overaction, the cornea nearly disappears
(Fig. 11.1).
4. Associated horizontal deviation in primary
position. PIOO is commonly (but not universally)
associated with some horizontal deviation such
as infantile esotropia (72%), accommodative
esotropia (34%) and intermittent exotropia
(32%). The associated horizontal deviation is
usually of V-pattern. It may be a part of infantile
esotropia syndrome (see page 231). In contradiction to it, SIOO is usually not associated with
any form of concomitant deviation.
5. Associated vertical deviation in primary
position is either absent or less than 5PD in
PIOO. While a vertical deviation of 10–22PD is
characteristic of SIOO, a vertical deviation of
more than 22PD usually suggests a coexisting
vertical rectus muscle weakness. Bilateral
inferior oblique overaction produces a left
hypertropia in right gaze, a right hypertropia
in left gaze and little or no vertical deviation in
primary position. Further, primary IOOA is
commonly associated with DVD also.
6. Head tilt is typically present in patients with
SIOO, when the onset is after 6 years of age,
while it is usually absent in patients with PIOO.
Distinguishing PIOOA from SIOOA is largely
dependent on the head tilt test. If the head tilt
test is negative this indicates a PIOOA, whereas
a positive head tilt test (increasing hypertropia
with tilt to the side of IOOA ) indicates a superior
oblique paresis or secondary inferior oblique
overaction.
7. Associated excyclodeviation. Objective
excyclodeviation, as evidenced by a disturbed
relationship of the optic disc with foveola
(normally the foveola is aligned approximately
with the junction of the middle and lower third
of disc), can be demonstrated both in patients
Fig. 11.1 A patient with bilateral primary inferior oblique overaction. (A) no vertical deviation in primary position; (B) +4
inferior oblique overaction in left eye on dextroversion; and (C) +4 inferior oblique overaction in right eye on levoversion.
272 Theory and Practice of Squint and Orthoptics
Fig. 11.2 Fundus photograph showing relation of optic disc with foveola in a normal subject (A) and in a patient with inferior
oblique overaction (B) direct view; (C) indirect ophthalmoscopic view.
with primary as well as secondary inferior
oblique muscle overaction (Fig. 11.2). However,
subjective excyclodeviation (as demonstrated by
double Maddox rod test, Hess screen test, the
major amblyoscope or the Lancaster red-green
test) is typically present in patients with SIOO
(and extorsion is maximum in downgaze),
when the onset is after 6 years of age, but is
absent in patients with PIOO. Absence of
subjective excyclodeviation in PIOO might be
due to the development of some sensory
adaptation in such patients owing to early onset
of the condition.
8. Forced duction test is usually positive in
primary as well as secondary inferior oblique
overaction, indicating there by that both
mechanical and innervational factors contribute
to most inferior oblique overaction, including
primary form.
Differential diagnosis
1. Dissociated vertical deviation. Inferior
oblique overaction should be differentiated from
dissociated vertical deviation (see pages 282 and
283).
2. SIOOA. Primary inferior oblique overaction
can be differentiated from the secondary inferior
oblique overaction as described in clinical
features.
3. Pseudo ‘V’ pattern due to DVD, Duanes
syndrome and large intermittent exotropia also
needs to be differentiated from PIOOA.
Treatment
Treatment for inferior oblique muscle overaction
depends on the severity of the condition and its
impact on the individual's vision and eye
alignment. Here are some common treatment
options:
i. Observation and monitoring: In mild cases
of inferior oblique muscle overaction,
especially in children, your eye care
professional may choose to monitor the
condition and see if it improves on its own
over time. This is often the case when the
overaction is intermittent and not causing
significant symptoms or eye misalignment.
ii. Prism lenses: Prism lenses can be prescribed
to help correct any resulting double vision
(diplopia) caused by the overaction. Prism
lenses shift the image seen by one eye to align
it with the other, reducing the perception of
double vision.
iii. Vision therapy: Vision therapy, also known
as orthoptics or eye muscle exercises, may
be recommended to help improve eye
coordination and control. Vision therapy
exercises are performed under the guidance
of a trained eye care professional and are
designed to strengthen the eye muscles and
improve their coordination.
iv. BOTOX® injections: In some cases, BOTOX
injections can be used to temporarily weaken
the inferior oblique muscle. This can provide
relief from symptoms and help manage the
overaction. BOTOX® injections are typically
administered by an ophthalmologist or
strabismus specialist and may need to be
repeated periodically.
v. Surgery: Surgical intervention may be
considered if the overaction is severe,
persistent, and causing significant eye
misalignment or discomfort.
®
273Vertical Strabismus and Cyclodeviations
When hyperdeviation of the adducted eye
becomes clinically significant, a weakening
procedure on the inferior oblique muscle is
indicated. Mostly, surgery is done for the
functional reasons, that is, when the hypertropia
produced by the overacting inferior oblique
muscle presents an obstacle to fusion in
lateral gaze or a V-pattern exists that prevents
fusion in upward (V-exotropia) or downward
(V-esotropia) gaze.
Inferior oblique weakening procedures that have
been employed are as follows:
1. Disinsertion, i.e. cutting of the muscle from
the globe near its insertion is an effective and
easy technique. However, because of the
unpredictable results and high rate of
recurrences (>50%), this procedure is not much
popular.
2. Myectomy involves excision of approximately
8 mm of inferior oblique muscle. This procedure
is generally performed between the temporal
border of inferior rectus muscle and insertion
of the inferior oblique. It can also be performed
nasally between the origin of inferior oblique
and the nasal border of inferior rectus muscle.
This procedure is also becoming unpopular
because of unpredictable results, a high rate of
recurrences (especially nasally performed
myectomy) and occurrence of postoperative
adhesive syndrome in some cases. However,
temporally performed myectomy is still
preferred by many surgeons especially for
treating recurrent inferior oblique overaction. A
unilateral myectomy will correct 5 to 20 PD of
hypertropia.
3. Denervation and extirpation, i.e. excision of
whole of the muscle with its Tenon's capsule
covering after cauterisation of the neurovascular
bundle has been reported to be effective with
least incidence of recurrence. The procedure is
reported to be effective in severe overaction (+4)
or in residual overaction when recession or
anteriorization has already been performed.
However, it is not being considered necessary
to sacrifice the muscle.
4. Recession of the inferior oblique is being
preferred by many surgeons especially for
secondary inferior oblique overaction and for
cases with mild to moderate primary inferior
oblique overaction. Recession of 6–10 mm can
be performed as indicated. In this procedure,
inferior oblique is detached from its insertion and
is reattached to the sclera (along the lateral
margin of the inferior rectus) at a site selected
depending upon the amount of recession to be
done. For example:
• For a maximum recession of 12–14 mm, anterior
border of inferior oblique muscle is placed
4 mm behind the insertion line of inferior
rectus muscle.
• For 10 mm recession, the anterior suture is
placed 6 mm posterior to the lateral border of
the inferior rectus muscle insertion and 4 mm
temporal to the lateral border of the inferior
rectus (approximately at the vortex vein), in
this there occurs anteriorization of IO by
1–1.5 mm, that is why based on long-term
follow ups it is said to be more powerful than
12–14 mm recession.
A recurrence rate to the tune of 15% is
reported with simple recession. The major
advantage of the recession is that it allows the
weakening procedure to be titrated according
to the severity of inferior oblique overaction as
below:
• For 1+ or 2+ overaction, the inferior oblique
muscle is recessed by 12–14 mm.
• For 3+ overaction, inferior oblique muscle is
recessed by 10 mm.
• For 4+ overaction, 10 mm recession or full
anterior transposition of IO is preferred.
5. Recession with anterior transposition is being
considered more effective than simple recession.
Therefore, it is recommended that this
procedure may be preferable for large overactions, particularly those associated with Vpattern due to primary inferior oblique
overaction. In this procedure, after detaching
from the insertion, the inferior oblique is
reattached to the sclera near the lateral end of
the inferior rectus insertion. This technique is
even easier than the simple recession.
Anteriorizing the inferior oblique muscle
insertion, anterior to eyeball’s equator changes
the IO muscle from an elevator to more of a
depressor. The more IO is anteriorized the more
it becomes a depressor and this enhances its
recession effect. Compared with recession,
274 Theory and Practice of Squint and Orthoptics
anteriorization decreases ocular elevation by
approximately 15 PD more.
Graded IO anteriorization (as described below)
works extremely well for both PIOOA and
SIOOA:
• +4 overaction: Full anteriorization, up to the
insertion line of temporal border of inferior
rectus.
• +3 overaction: 1 mm posterior to IR insertion
line
• +2 overaction: 3 to 4 mm posterior to IR
insertion
• +1 overaction: 4 mm posterior and 1 mm lateral
to IR insertion.
It is important to note that full anteriorization
of the IO can be performed with a ‘J’ deformity
of the new insertion, which can limit ocular
elevation and produce a postoperative
hypotropia worse in upgaze. The ‘J’ deformity
is created when the posterior fibres of IO are
anteriorized parallel or in front of inferior rectus
insertion. This is seen mainly with U/L anterior
transposition, so should be reserved for patients
with appreciable hypertropia in upgaze or
patients with superior oblique paresis with
hypertropia >25 PD.
An anterior and nasal transposition procedure
converts inferior oblique from an extorter to
intorter and from an elevator to depressor,
significantly improving large ‘V’ patterns.
Note. For surgical techniques of IO recession,
see page 431.
Some observations about
inferior oblique weakening
1. Bilateral asymmetry. If there is no superior
oblique muscle paresis but there is a marked
asymmetry of the overactions of the inferior
oblique muscles, unilateral surgery on the
muscle with the most marked overaction will
often be followed by a significant degree of
overaction in the unoperated eye. Therefore,
bilateral inferior oblique weakening procedures
are indicated for bilateral overaction, even if
asymmetrical. However, inferior oblique
muscles that are not overacting should not have
a surgical weakening procedure. Further,
recession of the inferior oblique can be graded
depending upon the asymmetry.
2. Graded response. The response to any surgical
weakening procedure on the inferior oblique is
graded one, i.e. the larger overactions will show
a greater response to the same amount of surgery.
3. Effect on associated horizontal deviation.
When PIOO is associated with the V-pattern
horizontal deviation, weakening of the one or
even both inferior oblique muscles has little to
no effect on the horizontal alignment in the
primary position. Therefore, there is no need to
make any adjustment in the amount of
horizontal rectus surgery. Further, the
weakening of the inferior oblique should be
performed along with the horizontal muscle
surgery and that there is no need to do two
separate procedures. It has been observed that
unilateral weakening of overacting inferior
oblique in V-pattern strabismus can be expected
to cause 5–10 prism dioptres and bilateral
weakening 15–25 prism dioptres of eso shift in
upgaze (decrease of an exodeviation or increase
of an esodeviation) but almost little or no effect
in primary gaze and downgaze.
4. Effect on associated vertical deviation. In
cases with overaction of inferior oblique,
secondary to paresis of ipsilateral superior
oblique muscle, a weakening of that inferior
oblique muscle could be expected to correct up
to 15 prism dioptres of vertical deviation in
primary position. The amount of vertical
correction is roughly proportional to the degree
of preoperative overaction. If the deviation is
more than 15 PD, then additionally, the yoke
contralateral inferior rectus should also be
recessed (1 mm for every 3 PD deviation).
However, in cases with primary inferior
oblique overaction neither unilateral nor
bilateral weakening of this muscle has any
significant effect on the vertical deviation in
primary position.
5. Associated dissociated vertical deviation.
When DVD is associated with inferior oblique
overaction, the procedure inferior oblique
recession with anterior transposition should be
done. Since in most cases, this procedure alone
can correct DVD, so any other surgical treatment
for DVD should be deferred until later.
6. Effect on head tilt test and excyclodeviation.
Weakening of inferior oblique in primary
275Vertical Strabismus and Cyclodeviations
overaction does not produce a positive head-tilt
test or any effect on subjective cyclodeviation.
However, the objective excyclodeviation (as
evidenced by indirect ophthalmoscopy) is either
fully corrected or greatly reduced.
7. Recurrence of overaction is a common compli-
cation after weakening procedure. Its likelihood
with a particular procedure in order of
increasing frequency is as follows: Extirpation
(least common), recession with anterior
transposition, simple recession (15%), temporally
performed myectomy, disinsertion, and nasally
performed myectomy (33%).
SUPERIOR OBLIQUE OVERACTION
Superior oblique overaction, also referred to as
strabismus deorsoadductorius, is now termed as overdepression in adduction (ODA). It is characterized
by a downshoot of the eye in adduction.
Etiology
1. Primary overaction of the superior oblique
muscle is of unknown etiology. Perhaps it may
be due to mechanical or innervational causes or
a combination of the two. It may occur as an
isolated phenomenon or in association with
exotropia or esotropia—often of A-pattern.
2. Secondary overaction of the superior oblique
muscle is caused by a paralysis or paresis of
either its antagonist muscle (ipsilateral inferior
oblique muscle) or its yoke muscle (contralateral
inferior rectus muscle). Rarely, it can also occur
in cases with contracture of the contralateral
superior rectus muscle, occasionally seen in
conjunction with long-standing paralysis of the
contralateral superior oblique muscle. Other
causes of secondary overaction of the superior
oblique, unrelated to paralysis are, Brown's
syndrome and Duane's syndrome with cocontraction of the horizontal rectus muscles.
oblique overaction (PSOO) versus secondary
superior oblique overaction (SSOO) are as
follows:
1. Age of onset. PSOO usually occurs by the age
of 2–3 years while SSOO can occur at any age.
SSOO occurs either spontaneously or few weeks
to months following paresis of the ipsilateral
inferior oblique muscle or contralateral inferior
rectus muscle.
2. Bilaterality. PSOO is frequently bilateral
although it can be asymmetric or rarely
unilateral; while SSOO is occasionally bilateral.
3. Downshoot of the eye in adduction is the
clinical characteristic of primary as well as
secondary superior oblique overaction. That is
with the eyes in lateral gaze and the abducting
eye fixing the adducted eye downshoots or an
exaggerated rotation of the eye occurs in the field
of action of the superior oblique, i.e. the eye is
over-depressed in adduction. Where the eyes are
in lateral gaze and the adducting eye is made to
fix, the abducted eye will be elevated and
manifest as hypertropia on alternate cover test.
Clinically, overaction of superior oblique can be
graded on a scale of +1 to +4. In a +4 overaction,
the cornea is directed straight down rather than
down and in (Fig. 11.3).
Clinical features
It is important to note that unlike superior
oblique muscle, isolated palsy of inferior oblique
is not much known and so is the secondary
overaction of the superior oblique muscle. So
much so that all bilateral superior oblique
muscle overaction can be considered 'primary'.
Anyhow, clinical features of primary superior
Fig. 11.3 A patient with +4 overaction of superior oblique
muscles. (A) central downgaze; (B) dextrodepression and;
(C) levodepression.