VERTICAL STRABISMUS

BY

[Link]
[Link]
ASSISTANT PROFESSOR
CONTENT
 INTRODUCTION
 CLASSIFICATION
 ETIOLOGY
 CLINICAL FEATURES
 INVESTIGATION
 TREATMENT
 INTRODUCTION

 Misalignment of visual axis of the two eyes

in the vertical direction in any of the nine
cardinal positions of gaze, latent or manifest,
constant or intermittent is called vertical
strabismus.

[Link] strabismus
[Link]
 Vertical strabismus is more symptomatic
than horizontal strabismus.
 Usually the vertical recti or the oblique
muscles are involved.
 Diagnosis, analysis and treatment is often
more complex than horizontal strabismus.

[Link] strabismus
CLASSIFICATION
A. Depending upon constancy of deviation
 Hyperphoria
 Intermittent Hypertropia
 Hypertropia

B. Depending upon the direction of deviation in the non-

fixing eye
 Hypertropia
 Hypotropia
C. Depending upon comitance of deviation

I. Comitant vertical deviation

 Induced(Refractive).
 End result of long –standing paralytic deviation
[Link] vertical deviation
 Apparent oblique muscle dysfunction
 Paretic vertical deviation
 Restrictive vertical deviation
[Link] vertical deviation
 Monocular DVD
squintBinocular or alternating DVD
and orthoptics, A.k. khurana, 3rd edition
COMITANT VERTICAL DEVIATION

Comitant strabismus is a common condition affecting infants,

children, and adults.

 Its impact on the affected patient may be severe

resulting in visual loss, lack of binocularity, diplopia , social
stigma and multiple corrective surgeries within the affected
individual’s lifespan.

[Link]
ture
The prevalence of comitant vertical in general is not low. Vertical deviation
may occur as isolated anomalies or in association with horizontal deviation

PREVALANCE

 Approximately, half of the patients with motility disorders have isolated vertical anomalies.

 Approximately, one-third of all patients with motility disorders have isolated vertical
anomalies.

 An associated vertical deviation has

squint andbeen reported
orthoptics, in 43%
A.K. khurana, of all exotropia.
3rd edition
 TYPES OF COMITANT VERTICAL
DEVIATIONS
 Hypertropia
- In this condition, non-fixating eye is higher than the fixating eye

 Hypotropia
- In this condition , non-fixating eye is lower than the fixating eye

squint and orthoptics, A.K. khurana, 3rd edition

[Link]
 ETIOLOGY
• 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

squint and orthoptics, A.K. khurana, 3rd edition

CLINICAL FEATURES
• Symptoms can be marked in hyperdeviation,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 anomalies retinal correspondence
may occur
• In deviation of lesser magnitude, the patient may obtain bifoveal
fusion by tilting the head.
squint and orthoptics, A.K. khurana, 3rd edition
• Typically,patients with small comitant vertical deviation have a
moderate to large horizontal strabismus (exotropia or esotropia)as
well.
• Repeated mesurement in the diagnostic positions of gaze in
majority of patients may reveals a paretic component or a primary
overaction of one or several cyclovertical muscles.

squint and orthoptics, A.K khurana,3 rd edition

 TREATMENT
1. ORTHOPTICS: Amblyopic ,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
suppresion may be indicated prior to surgery. It is almost impossible
to improve vertical fusional vergence through orthoptic training

[Link] program-minnesota/curriculum/
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 infront of hypotropic eye. The
minimal prismatic power that provides comfortable single
binocular vision should be prescribed

[Link]
[Link]: 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 deviation (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.
squint and orthoptics, A.K. khurana, 3rd edition
INCOMITANT VERTICAL DEVIATION

 The angle of deviation varies as the patients move the eye to

look in different parts of the field. Such deviation are incomitant.
 For the most causes of incomitancy, there is a consistency in the
way of angle changes; it increase in one particular direction of
gaze each time the eye are turned in that direction .
 Also, the angle will differ according to which eye is fixating.
 Usually caused by abnormalities in the anatomy of the
oculomotor apparatus are by one are more muscle being unable
to function normally.

[Link]
INCOMITANT VERTICAL DEVIATION

 The angle of deviation varies as the patients move the eye to

look in different parts of the field. Such deviation are incomitant.
 For the most causes of incomitancy, there is a consistency in the
way of angle changes; it increase in one particular direction of
gaze each time the eye are turned in that direction .
 Also, the angle will differ according to which eye is fixating.
 Usually caused by abnormalities in the anatomy of the
oculomotor apparatus are by one are more muscle being unable
to function normally.

[Link]
CLASSIFICATION

 Apparent oblique muscle dysfunction

I. Inferior oblique overaction is now termed as over-elevation in

adduction(OEA).
II . Inferior
oblique underaction is now termed as under-elevation in
adduction(UEA).
III. Superior oblique overaction is now termed as over-depression in
adduction(ODA).
IV. Superior oblique underaction is now termed as under-depression
in adduction(UDA).
 Paretic vertical deviation
 Restrictive vertical deviation
squint and orthoptics, A.K. khurana, 3rd edition
 APPARENT OBLIQUE MUSCLE
DYSFUNCTION
 Inferior oblique overaction ,also referred to as strabismus
sursoadductorious,is now termed as over-elevation in
adduction(OEA).

 It is characterized by an upshoot of the in adduction

squint and orthoptics, A.K. khurana, 3rd edition

[Link]
 ETIOLOGY
• Primary overaction of the inferior oblique muscle is etiologically not well
[Link] it may be due to mechanical or innervational causes or a combination
of the two.
• Its may occur as an isolated phenomenon or in association with esotropia or exotropia often
of v-pattern

• 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 overactionof the inferior oblique ,unrelated to
paralysis is non-parallelism of the plane of superior and inferior oblique muscles.

squint and orthoptics, A.K. khurana, 3rd edition

 CLINICAL FEATURES
 Age of onset.
 Bilaterality
 Upshoot or over-elevation of the eye in adduction
 Associated horizontal deviation in primary position
 Associated vertical deviation in primary position
 Head tilt
 Associated excylodeviation
 Forced duction test

squint and orthoptics, A.K. khurana, 3rd edition

 DIFFERENTIAL DIAGNOSIS
 Dissociated vertical deviation: Inferior oblique overaction should
be differentiated from dissociated vertical deviation
 SIOOA: Primary inferior oblique overaction can be differentiated
from the secondary inferior oblique overaction as described in
clinical features.
 Pseudo v pattern due to DVD ,Duanes syndrome and large
intermittent exotropia also needs to be differentiated from PIOO

squint and orthoptics, A.K. khurana, 3rd edition

 TREATMENT
 When hyperdeviation of the adducted eye become clinically significant,a
weakening procedure on the inferior oblique muscle is indicated.

 Mostly, surgery 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.

squint and orthoptics, A.K. khurana, 3rd edition

 INFERIOR OBLIQUE WEAKENING
PROCEDURES
 Disinsertion
 Myectomy
 Denervation and extirpation
 Reccession
 Reccession with anterior transposition
 Bilateral asymmetry
 Graded response
 Effect on associated horizontal deviation
 Effect on associated vertical deviation
 Associated dissociated vertical deviation
 Effect on head tilt test and excyclodeviation
 Recurrent of overaction
squint and orthoptics, A.K. khurana, 3rd edition
Schematic diagram demonstrating the key differences
among the various inferior oblique weakening
techniques. Each panel depicts the patient's right eye
viewed from below; (a) natural position of the inferior
oblique muscle indicating the fields of action and the
axes of Fick (x, y, and z); (b) recession; (c) anterior
transposition; (d) anterior nasal transposition; (e and f)
nasal myectomy. See text for details. IO: Inferior oblique
muscle; IR: Inferior rectus muscle; LR: Lateral rectus
muscle; NFVB: Neurofibrovascular bundle
https;//[Link]/paper/The-inferior-oblique-muscle-adherence-syndrome.-kushner/d4fd
37105fc54ab90c34cd17afeb849b421cf995
a) Minimal upshoot (+1) of adducting eye when taken straight across. Upshoot is
better seen when the abducting eye is moved up and out.
(b) Upshoot (+2) of adducting eye is obvious when the abducting eye looks
straight across at the lateral canthus.
(c) Severe upshoot (+3) of the adducting eye is seen even with the abducting eye
in straight abduction.
(d) Very severe upshoot (+4) of the adducting eye is seen as the fixing eye moves
straight across into abduction
MYECTOMY. A)Cross-hatching represents the portion of the temporal
inferior oblique (IO) muscle removed in the myectomy procedure.

(b) Recession. The muscle is dissected, disinserted, and then reattached

along the path of the inferior oblique muscle, but closer to its origin
a) The least amount of anteriorization, for minimal inferior oblique (IO)
overaction.
(b) For moderate overaction, the muscle is placed 4 mm posterior to the
inferior rectus (IR) insertion.
(c) The anteriorization procedure for severe overaction.
(d) Anteriorization of the entire inferior oblique insertion, including the
posterior fibers
 SUPERIOR OBLIQUE OVERACTION
 Superior oblique overaction, also referred to as strabismus
deosoadductorius, is now termed as over-depression in adduction (ODA).

 It is characterized by a downshoot of the eye in adduction

Etiology:
• 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
squint and orthoptics, A.K. khurana, 3rd edition
https;//[Link]/en/a-chilads-eye/special-forms-of-stabismus/hyperfunction of /the-sup
[Link]
 • Secondary overaction of the superior oblique muscle is caused by a
paralysis or paresis of either its antagonists muscle (ipsilateral inferior
oblique muscle) or its yoke muscle (contralateral inferior rectus muscle).
• Other causes of causes of secondary overaction of the superior oblique,
unrelated to paralysis are, brown’s syndrome and duane’s syndrome with
contraction of the horizontal rectus muscles.

squint and orthoptics, A.K. khurana, 3rd edition

CLINICAL FEATURES

 Age of onset.
 Bilaterality
 Downshoot or over-depression of the eye in adduction
 Associated horizontal deviation in primary position
 Associated vertical deviation in primary position
 Head tilt
 Associated incylodeviation
 Forced duction test
 Differential diagnosis
Brown syndrome can be differentiated from primary SOOA, on clinical
basis:
• An ability to elevate the paretic eye in adduction effectively rules out
brown syndrome.
• In contrast to SOOA where hypotropia is maximum in downgaze , Brown
syndrome is associated with a restriction of elevation thus causing a
hypotropia that is greatest in upgaze.
• “A” pattern in SOOA, while there is ‘v’ pattern in brown syndrome .
• FDT positive in brown syndrome.(unable to move the eye)
Inferior oblique paresis, there is positive head tilt , hypotropia is
greatest when patients looks up and in.
In IO palsy , the deviation worses with tilt.
 TREATMENT

1. SUPERIOR OBLIQUE TENOTOMY AND

TENECTOMY:
It is indicated for treating ‘A’ pattern strabismus and can correct 20 PD or more of A-
pattern in the primary position and up to 45 PD in downgaze. The amount of correction
achieved depends mostly on the size of preoperative pattern and the amount of SOOA .
. This usually causes postoperative SO palsy and torsional diplopia in patient with fusion .

squint and orthoptics, A.K. khurana, 3rd edition

Tenotomy involves cutting the tendon at
its insertion point, while tenectomy
involves removing a portion of the
tendon. Tenotomy is generally considered
to be a more predictable procedure for
correcting A-pattern strabismus,
 [Link] TENECTOMY OF SUPERIOR OBLIQUE
(PTSO)

 The anterior fibres of so tendon responsible for torsion, where as

the posterior fiber are implicated in downward rotation and
abduction.
 This procedures prefered over tenotomy in patient with bifoveal
fusion because negligible extorsion is induced.
 This surgery can correct moderate A-pattern upto 20PD with
SOOA.

squint and orthoptics, A.K. khurana, 3rd edition

[Link] OBLIQUE LENGTHENING BY INSERTION OF A SILICONE
EXPANDER OR a non-absorbable suture also an effective [Link] fact several
surgeons have proposed more controlled weakening by this procedure (rather than
tenotomy)in patients with bifixation and normal stereopsis to eliminate the complication
like torsional diplopia or symptoms of secondary superior oblique palsy with head tilt
observed with simple tenotomy
This correct `A’ pattern from 20to55PD and also the SOOA associated with skew
deviation
Recommended length of spacer according to the magnitude of SOOA
 +1 overaction: 4mm
 +2 overaction: 5mm
 +3 overaction: 6mm
 +4 overaction :7mm

squint and orthoptics, A.K. khurana, 3rd edition

 SUPERIOR OBLIQUE WEAKENING PROCEDURES

 Graded response The response to superior oblique tenotomy is graded one,i.e the larger
overaction will show a greater response to the same amount of surgery.
 Effect on associated horizontal deviation it has been absorbed by several surgeons that
superior oblique tenotomy decreases exotropia and increases the esotropia.
 Effect on associated vertical deviation. Secondary superior oblique overaction is
almost always associated with vertical deviation in primary gaze and in its field of
action. Superior oblique tenotomy is expected to correct almost full vertical deviation in
the field of action of the muscle and of upto15PD in primary gaze
 Tortional diplopia,a positive head tilt test and abnormal posture have been reported
following bilateral superior oblique tenotomy performed for the secondary superior
overaction in adult with a potential for single binocular vision .
squint and orthoptics, A.K. khurana, 3rd edition
[Link]
 Paretic vertical deviation
 Congenital unilateral superior oblique paresis
 Non- congenital superior oblique paresis
 Bilateral superior oblique paresis
 Monocular elevation deficiency (MED) , the old name : double elevator
palsy.
 Monocular depression deficiency (MDD) , the old name : double
depressor palsy.
 Superior rectus paresis
 Inferior rectus paresis
 Skew deviation
 Inferior oblique paresis
Restrictive vertical deviation

Restrictive vertical deviations due to misdirected muscle force,

 congenital cranial dysinnervation disorders(CCDD) primarily affecting
vertical ocular motility
 congenital fibrosis of extraocular muscles (CFEOMs)
Restrictive vertical deviations due to mechanical restrictions
 Tight extraocular muscle
eg i. congenital brown syndrome (restrictive hypotropia in
adduction RHA)
ii. Hypotropia due to inferior rectus in blow out fracture of
orbital floor
iii. Hypotropia due to inferior rectus thickening in thyroid
ophthalmmopathy
[Link] in monocularelevation deficiency (MED) caused by
fibrotic inferior rectus muscle
Restrictive vertical deviation due to structural adhesions
o Acquired brown’s syndrome due to scarring around the trochlea
o Due to fat adherence as seen after retinal detachment surgery
o Post- radiation orbital scarring
o Due to conjuctival and tenon’s capsule scarring;
- Post operative
- Post traumatic
- Post chemical burns
Restrictive vertical deviation due to orbital mass lesions,
eg..orbital tumours
DISSOCIATED VERTICAL DEVIATIONS
 Dissociated vertical deviation basically characterized by a hyperdeviation in one eye that is present
while the other eye is fixing . The non-fixing eye is also extorted and slightly abducted .

 The dissociated vertical deviation (DVD) can be defined as an intermittent anomaly of the non-fixing
eye consisting of upward excursion , excyclotorsion and lateral deviation .

 The term dissociated vertical deviation is preferred because in it the two eyes are more independent of
each other (dissociated movements ) and do not follow the hering’s law of ocular motility , i.e in
contrast to a true vertical deviation , in DVD , the fellow eye does not exhibit refixation movement in
the opposite direction .

 Since the upward drifting of the non-fixing eye is often associated with the lateral deviation and
excyclotorsion , the term ‘dissociated strabismus complex (DSC)’ has been suggested to denote all the
components , i.e. dissociated vertical deviation (DVD),dissociated horizontal deviation (DHD) and
dissociated torsional deviation (DTD).

squint and orthoptics, A.K. khurana, 3rd edition

ETIOLOGY
 Exact etiology of the DVD is not known. Numerous theories have been forward to
explain the occurrence of DVD. A few theories are

i. Bielschowsky’s theory of positive and negative subcortical vertical divergence centres

 Bielschowsky theorized that DVD occurs due to altenating and intermittent excitation of
both subcortical vertical divergence centers.
 However this theory has not been further substantiated
ii. Theory of imbalance of binocular stimulation
 Spielmann postulated that DVD is caused by an imbalance of binocular stimulation.
 This theory explains the frequent occurrence of DVD in essential infantile esotropia and
occasional occurrence with sensory heterotropia .
 However , This theory does not explain the occurrence of DVD in patient with otherwise
squintnormal binocular
and orthoptics, function.
A.K. khurana, 3rd edition
 CLINICAL FEATURES
 Deviation
 Association of DVD.

i. Infantile esotropia
ii. Infantile exotropia
iii. Excycloduction and latent nystagmus
 Head posture
 Laterality

i. Monocular dissociated hyperdeviation

ii. Bilateral DVD or alternating sursumduction
iii. Symmetric versus asymmetric DVD
Comitance DVD

i. Comitant DVD
ii. Incomitant DVD
 Superior rectus contracture syndrome in DVD.
 Binocular vision and sensory adaptations.
squint and orthoptics, A.K. khurana, 3rd edition
 DIAGNOSIS
 Cover-uncover test.
 Spielmann’s translucent occluder test.
 Head tilt test.
 Red glass (filter) test.
 Demonstration of Bielschowsky phenomenon.
 Measurement of DVD

squint and orthoptics, A.K. khurana, 3rd edition

 Differentiated diagnosis
s/no Feature Dissociated Inferior oblique
vertical deviation overaction
1 Hyperdeviation Present in primary Maximum in
position in adduction adduction, never in
and abduction abduction

2 Incycloduction Present Absent

3 Speed of upward Slow (2-200/sec) Rapid (200-400/sec)

movement in
deviating eye

4 Bielschowsky Present Absent

phenomenon
5 V pattern Absent Present
6 Superior oblique May overact Usually underaction
action
S/No Feature Dissociated Inferior oblique
vertical overaction
deviation

7 Pseudoparesis of Absent Present

contralateral
superior rectus

8 Latent nystagmus Often present Absent

9 External rotation Absent Present

of fundus on
indirect
ophthalmoscopy
 TREATMENT
NON-SURGICAL TREATMENT . IS not so effective in DVD . However measures may
be useful.
I. Conservative therapy to strengthen the fusional mechanisms

 Optimal spectacle correction should be prescribed . As the blurred vision may cause a latent DVD to
become a manifest more frequently providing a clear images to both eyes encourages fusion .
 Correcting an associated horizontal deviation either surgically or with prisms , promotes the possibility of
peripheral fusion.
 Treating amblyopia by occlusion therapy also promotes peripheral fusion.
 Treating heterophorias by orthoptics also promotes peripheral fusion .

squint and orthoptics, A.K. khurana, 3rd edition

 ii. Conservative therapy in the form of changing the fixation
pattern
 BY patching or optical means may be useful , especially in patients with
asymmetric involvement or those accustomed to wearing a glasses.

For example , if a patient is having significant DVD of left eye while fixing
with right eye and an insignificant DVD of right eye while fixing with left
eye ; a slight optical blurr induced in the right eye by addition of +2.0 D
lens will shift the fixation preference to the left and DVD may no longer be
a cosmetic problem.

squint and orthoptics, A.K. khurana, 3rd edition

SURGICAL TREATMENT

Surgical procedures for comitant DVD

 Faden operation with superior rectus recession.

 Large recession of superior rectus muscle.

 Resection of the inferior rectus .

 Recess-resect procedure.

squint and orthoptics, A.K. khurana, 3rd edition

 FADEN OPERATION:
Strabismus surgery technique that
weakens the superior rectus
muscle by combining a Faden
procedure (posterior fixation
suture) with a recession of the
muscle insertion.
 Surgical procedures for incomitant DVD

1. When DVD is larger in the field of inferior oblique of the non-fixing eye,
that is adducted position

 The inferior oblique weakening procedures like IOAT is preferred.

squint and orthoptics, A.K. khurana, 3rd edition

 2. When the DVD is larger in adducted position but significant in abduction (>5PD).
 In these patients, both SR recession and IO weakening procedures are preferred .

3. When DVD is more in abduction due to associated SOOA and ‘A’ pattern.

 Bilateral SR recession should be in patient with small degree of A pattern(upto 12PD)

 Additional SO weakening procedure like posterior SO tenectomy is required with bilateral

SR recession in Patient with large amount of A-pattern (12-25PD).

squint and orthoptics, A.K. khurana, 3rd edition