Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5507_Библиотеки_им_академика_М_И_Перельмана.pdf
316 Theory and Practice of Squint and Orthoptics
if the eyeball jumps across the tendon, tightness
of the superior oblique is indicated.
Tightness of the inferior oblique is also tested
in the similar manner, except that instead of
elevating and adducting, the eyeball is pushed
down and nasally.
3. Spring-back balance test
It is a continuation of the FDT, when performed
under general anaesthesia. It is of specific use
in patients who are suspected (after FDT) of
having mechanical restriction and not a weak
muscle. In this test, after holding near the
limbus, eyeball is rotated back and forth
vigorously for 2–3 times and then released
suddenly. After settling, normally, the globe
comes to rest in straight ahead position.
However, in the presence of a significant
mechanical restriction, the eyeball will be drawn
towards the direction of the mechanical pull, e.g.
the eyeball will be adducted, if the cause of
mechanical restriction is located medially.
Fig. 12.18 Technique of judging active force generated
during ocular movement (muscle contraction). (For
explanation, see text).
• Lid fissure widening and a relative proptosis
is noted in paralytic squint as the patient
looks into the field of action of paretic rectus
muscle.
4. Active force generation test
In this test, eyeball is stabilized with the forceps
applied at the limbus under topical anaesthesia
and patient is asked to move his/her both eyes
in the direction of the muscle to be tested. For
example, if right lateral rectus muscle is to be
tested, patient is asked to move his/her eyes in
dextroversion. During this movement, the force
generated by the contracting muscle of the eye
being tested (e.g. Rt LR) is transmitted through
the forceps to the examiner's fingers. From the
feel of the transmitted force, examiner can judge
subjectively whether the contracting muscle is
weak or normal (Fig. 12.18). For objectively
quantifying this test, calibrated forceps are
available which indicate the amount of force
generated in grams. A normally acting muscle
generates a force of 60–80 g in extreme gaze. This
test is quite useful in diagnosing the weak
muscle. However, it can only be performed in
alert and co-operative patients.
5. Lid fissure changes on eye movements
• Narrowing of lid fissure along with globe
retraction is seen in restrictive squints, as in
Duane’s retraction syndrome.
6. Electro-oculographic measurement
of saccadic velocity
Saccades are sudden, jerky conjugate eye
movements, that occur as the gaze shifts from
one object to another. These movements bring
the object of regard quickly on the fovea with
an average velocity of 250°/second in the field
of action of the muscle concerned. Measurement of saccadic velocity with the help of
specially designed electro-oculographic (EOG)
recorder can help in differentiating muscle
restrictions from the muscle weakness. The
saccadic velocity is decreased in paretic muscle,
while it is near normal in mechanical muscle
restrictions.
7. Positional tonometry
It has been reported that intraocular pressure
rises from the compression of a non-relaxing stiff
muscle, when attempts are made to move the
eye into the field of its antagonist. Perkin's handheld applanation tonometer or Digilab Pneumotonometer can be used to measure the IOP in
different gaze positions. A pressure increase of
over 5 mm Hg in a particular field of gaze is
indicative of a restriction.
Incomitant Strabismus
317
CLINICAL VARIETIES OF OCULAR PALSIES
1. Isolated ocular muscle palsies.
2. Palsy of 3rd cranial nerve
3. External ophthalmoplegia
4. Total ophthalmoplegia
5. Internuclear ophthalmoplegia
ISOLATED OCULAR MUSCLE PALSIES
Superior oblique (4th nerve palsy) and lateral
rectus (6th nerve palsy) are the most common
muscles to be paralysed singly, as they have
separate nerve supply. Isolated paralysis of the
remaining four extraocular muscles is less known.
FOURTH CRANIAL NERVE PALSY
(SUPERIOR OBLIQUE MUSCLE PARESIS)
The fourth cranial nerve (trochlear) is entirely
motor in function and supplies only the superior
oblique muscle of the eyeball. It differs from
other cranial nerves in being:
• The only cranial nerve to arise from the dorsal
aspect of the brain (midbrain);
• The only cranial nerve to cross completely on
the other side (i.e. the trochlear nerve arises
from the contralateral nucleus; and
• The longest and thinnest of all cranial nerves.
The fourth cranial nerve palsy (superior
oblique muscle paralysis) is the most common
isolated cyclovertical muscle palsy encountered
by the ophthalmologists. Fourth cranial nerve
palsy may be unilateral or bilateral. Bilateral
palsies are almost always acquired. Unilateral
palsy (more common than bilateral) may be
congenital or acquired.
Note. The applied anatomy of fourth cranial
nerve (see page 12 and Fig. 1.12) should be
reviewed before proceeding further.
Etiology
In order of frequency, following are the causes
of fourth cranial nerve paralysis:
1. Congenital paralysis is quite frequent (about
40% cases). Congenital paralysis may result from
a defect in the nucleus or the motor portion of
the nerve (hypoplasia or even oplasia rarely).
High definition magnetic resonance imaging
(MRI) studies have identified two groups of
congenital SOP:
• The most frequent type, present in 73% of
cases, is a congenital cranial dysinnervation
syndrome where the trochlear nerve is absent
and results in secondary atrophy of the
superior oblique muscle.
• The second type has a normal trochlear nerve
and size of the superior oblique muscle, but
has an abnormal laxity of superior oblique
tendon.
Note. It has been reported that sometimes a
spontaneous manifestation of fourth cranial
nerve palsy in adult age might be due to
decompensation of fusion mechanism in a
patient with congenital palsy.
2. Trauma is another frequent cause of fourth
nerve paralysis (about 34% cases). Because of
the position of the trochlear nerves with respect
to the tentorial edge, closed head injury (even
minor) can result in fourth nerve palsy. Due to
an impact in the area of anterior medullary
velum, where the two nerves decussate, bilateral
trochlear nerve palsies are quite common in
head injury. Iatrogenic trauma, occurring after
SO tenectomy and ethmoid sinus surgery, now
has become rare due to refinement in the
surgical techniques.
3. Idiopathic. In about 20% cases of 4th nerve
palsy, cause could not be ascertained.
4. Vascular and neurogenic causes account for
about 3 to 5% cases, seen in elderly age group,
having acute onset and small angle hypertropia
(<6 prism diopters).
• Aneurysms and tumours (trochlear Schwannoma
and brain tumours) are rare causes.
• Ocular myasthenia gravis may present as an
isolated unilateral superior oblique paralysis
with an insidious course. Therefore, as a
general rule, a patient who presents with an
unexplained diplopia of any type should
undergo a tensilon test.
• Diabetic neuropathy may occasionally involve
the trochlear nerve. Therefore, in an undiagnosed case of 4th nerve paralysis, a glucose
tolerance test should also be done to rule out
diabetic cranial mononeuropathy.
• Herpes zoster can also be considered a
potential etiologic agent.
• Hydrocephalus may be a cause of acquired
unilateral or bilateral fourth nerve palsies.
• Idiopathic intracranial hypertension can also lead
to fourth nerve palsies.
318 Theory and Practice of Squint and Orthoptics
5. Cavernous sinus and superior orbital fissure
syndrome may be considered a cause of 4th
nerve paralysis in association with 3rd and 6th
cranial nerves (see pages 325 and 341).
Clinical features
Clinical features in a patient with 4th nerve
paralysis (Fig.12.19) are as follows:
1. Cyclovertical deviation.
When the patient fixates with normal eye,
usually the involved eye is elevated, slightly
adducted and extorted following weakness of
the superior oblique muscle (Fig. 12.19K).
The hyperdeviation becomes more obvious,
when the head is tilted towards ipsilateral
shoulder (Bielschowsky head tilt test) (Fig.
12.19M). Depending upon severity, deviation
seen is as below:
• Mild cases show hypertropia in down and
adducted position.
• Modirate cases hypertropia in adduction only
(without depression).
• Severe cases show hypertropia in primary
position.
When the patient fixes with the paretic eye, the
normal eye is hypotropic (depressed), adducted
and extorted more than the primary deviation.
Such a condition has been labelled as fallen eye
syndrome.
In congenital cases, typically, parents may
notice that one eye of this infant is higher than
the other and that there is abnormal head posture.
2. Abnormal head posture occurs towards the
action of paralysed superior oblique, i.e. chin is
depressed, face is slightly turned towards the
opposite side and the head is tilted towards the
opposite shoulder (Fig. 12.19A). The degree of
abnormal head posture is not always
proportional to the size of the hypertropia.
Compensatory head posture is the most
common presenting sign of SO palsy.
• In congenital SO palsy, there is a large head tilt
which is confirmed on the family album
photography or FAT scan.
• In bilateral acquired palsies, there is a chin down
posture to compensate for V esotropia.
Note. Rarely there may be head tilt towards
affected side to increase separation of images
and hence to ignore the second image.
3. Facial asymmetry. Another important clinical
sign is facial asymmetry, which is a
characteristic finding of congenital palsy. There
occurs typical shallowing of mid-facial region
between lateral canthus and the angle of the
mouth on the side of head tilt. This is indication
of long-standing SO palsy.
4. Diplopia is seldom noticed, if onset is during
visual immaturity. However, when onset is after
visual maturity, i.e. adult patients will
experience homonymous vertical, diagonal or
torsional diplopia. Image seen by the involved
eye is lower, uncrossed and intorted. If principal
complaint is of torsional diplopia then bilateral
palsy should be suspected. Vertical separation
increases while looking down, therefore,
diplopia is particularly noticed by the patient
while coming down the stairs. Further, such a
patient may not have much problem as long as
the eyes look above the horizontal plane.
5. Ocular movements. Three abnormalities may
be observed:
• Ipsilateral SO under action is seen in patients
with marked paresis or lax SO tendons.
• Ipsilateral IOOA is present in most of the
cases.
• Contralateral SO overaction or pseudo SO
overaction which are clinically indistinguishable due to decreased infraduction in
abduction of the involved eye, there is
apparent over depression of the fellow eye.
Note. Long-standing hypertropia can cause
contracture of SR muscle which causes
restrictions in depression and can be tested by
forced duction test.
Ocular movements in a patient with superior oblique
paralysis, e.g. of right eye, are affected as below:
• Movements of left eye are limited, when
looking down and to right (Fig. 12.19H) (angle
of deviation is also greatest in this direction).
• Overaction of left eye as looking up and
to right (Fig. 12.19B).
• Overaction of right eye on looking down and
to right (Fig. 12.19H).
• Underaction of right eye on looking up and
to right (Fig. 12.19B).
• In a long-standing palsy with the paretic eye
fixing, the inferior rectus of the hypotropic
non-paretic eye can undergo hypertrophy,
then contracture, resulting in limited elevation
of the non-paretic eye on both ductions and
Incomitant Strabismus
319
Fig. 12.19 Left superior oblique palsy. (A) Abnormal head posture, note head is tilted to the right shoulder, face is slightly
turned to the right and chin is slightly depressed. (B to J) Eyeballs in nine positions of gaze, note left hypertropia (F)
which increases on right gaze (E). Also note left hypertropia (K) which increases on tilting the head to the left shoulder
(M) and no change in hypertropia on tilting the head to the right shoulder (L). (Courtesy: Dr Kanwar Mohan).
320 Theory and Practice of Squint and Orthoptics
versions. The effect can simulate a double
elevator palsy in the non-paretic eye, but this
can be ruled out with the forced duction and
head tilt tests.
Diagnosis
In the diagnosis of superior oblique palsy, one
needs to consider the following:
• Differentiation of superior oblique paresis
from other cyclovertical deviations.
• Unilateral versus bilateral superior oblique
paresis.
• Congenital versus acquired superior oblique
paresis.
Diagnosis of superior oblique paralysis
Differential diagnosis is made by performing
following tests:
1. Park three-step test The key to diagnose SO
palsy is Park 3-step test which requires motility
measurement in primary gaze, right and left
lateral gaze and right and left head tilts (for
details see page 307).
Pneumonic SOS, to remember summary of 3
step test for superior oblique palsy, is very useful
as below:
• S: Hypertropia in primary position occurs in
Same, i.e. involved eye
• O: Hyperdeviation increases in gaze towards
the Opposite side
• S: Hyperdeviation increases on head tilt to the
Same side
2. Torsion is usually measured objectively by
indirect ophthalmoscope and subjectively by
double Maddox rod test.
The following features are observed:
• Congenital SO palsy usually has no torsion.
• Acquired SO palsy is usually associated with
complaints of subjective torsion.
• Cyclotorsion of <10° is seen in unilateral
palsy and >10° in bilateral palsy.
3. Hess screen (Fig. 12.20) or Lancaster red/
green test is useful for a meticulous follow-up
of the patients.
4. Diplopia charting (Fig. 12.21) is also
important as in all cases of acquired strabismus
and should be done in all cases of SO palsy
presenting with complain of vertical and
diagonal diplopia.
5. Measurement of ocular deviation in all 9 diag-
nostic gaze positions, as well as in right and left
head tilt is important in diagnosing and planning
treatment for superior oblique palsy.
6. Force duction test should be done to look for
SR contracture.
Fig. 12.20 Hess chart of a patient with right superior oblique palsy.
Fig. 12.21 Diplopia chart of a patient with right superior
oblique palsy.
7. Oblique traction test. Intraoperative testing
of SO is essential for evaluating patients with
SO palsy, especially in young children where
precise orthoptic measurement cannot be taken.
This not only helps to identify the lax tendon
that should be tucked but also importantly
identifies tendon of normal length which should
not undergo this procedure for the fear of brown
syndrome.
Assessing SO tendon laxity with traction test
known as Guyton's Exaggerated Forced
Duction Test for Superior Oblique
Retro pulse globe and do dynamic traction
testing and Grade (1 to 4)
• Grade 1: Minimal laxity
• Grade 2: Definite laxity
• Grade 3: Marked laxity
• Grade 4: ? Tendon absent
8. Neuroimaging. Most patients with isolated SO
palsy do not need neurological workup.
Indications of neuroimaging are:
• Fresh trauma
• Non-isolated, multiple palsies
• Acquired palsy in absence of trauma
• Presence of associated neurological sign
• Younger patients presenting with acute
symptoms
Modified Knapp and Moore's classification of
superior oblique palsy. Depending upon the
Incomitant Strabismus
321
amount of hypertropia in different diagnostic
positions of gaze, Knapp and Moore have
classified common manifestations of superior
oblique paralysis into 7 classes which has been
modified by other workers by adding class VIII
(Table 12.6).
Table 12.6 Modified Knapp and Moore's classification
of superior oblique palsy into eight classes
Class Pattern of deviation (e.g. in paralysis of LSO)
Description Diagrammatic
depiction
I HT is greatest when eye
is elevated and adducted
II HT greatest when eye is
depressed and adducted
III HT of equal magnitude in
the entire paralysed field
IV HT of equal magnitude in
the entire paralysed field
and the entire inferior field
(L-shaped or reverse Lpattern)
V HT is greatest in the entire
inferior field
VI Underaction of both SO,
overaction of both IO,
V-pattern esotropia,
bilateral positive
Bielschowsky head tilt test
VII Canine tooth syndrome
characterized by underaction of inferior oblique
(acquired Brown's) and
under-action of superior
oblique. It usually occurs
due to trauma in the area
of the trochlea
VIII Comitant hypertropia but with positive head
tilt test
Unilateral versus bilateral superior oblique palsy
1. Esotropia in downgaze is usually little in
unilateral cases while in bilateral cases usually
there is a V-pattern esotropia with chin down
head posture.
322 Theory and Practice of Squint and Orthoptics
2. Torsion, when measured by the double
Maddox rod test, usually shows an excyclodeviation of less than 10° in unilateral cases and
more than 10° in bilateral cases.
3. Ductions of the superior oblique muscles are
usually diminished in bilateral cases while in
unilateral cases, actions may be normal or
diminished.
4. Head tilt test is positive for the involved eye
in unilateral cases, i.e. hypertropia increases on
tilting the head towards ipsilateral shoulder.
While, in bilateral palsies, tilting to either side
will increase the hypertropia, i.e. right hypertropia on right tilt and left hypertropia on left
tilt. Even after spread of comitance, the headtilt test should be positive in fourth cranial nerve
palsy.
Congenital versus acquired superior oblique palsy
Most patients are congenital, so facial asymmetry
with old photographs showing head tilt, or
asthenopia symptoms of long duration are
sufficient to rule out acquired palsy. Following
points are useful in differentiating congenital
from acquired SO palsy:
1. Amblyopia is uncommon in acquired paresis
but may be present in congenital ones.
2. Excyclodeviation and complaint of apparent
tilting of objects are common in acquired cases.
3. Abnormal head posture may be traced to
childhood from the old family photographs in
patients with congenital palsy while not in those
with acquired palsy.
4. Presence of increased vertical vergence may be
the only suggestion of a previous palsy in some
adult patients who develop spontaneous
manifestations of 4th nerve palsy due to
decompensation of fusion mechanism in old
case of congenital palsy.
5. Long, redundant or floppy superior oblique tendon
seen during surgery may indicate a congenital
palsy.
Table 12.7 summarizes the differences between
congenital and acquired superior oblique
palsy.
Differential diagnosis
1. Thyroid ophthalmopathy is a chronic
restrictive disease in which:
• IR muscle, which is most commonly involved
(positive on FDT).
• Signs of proptosis, lid lag, lid retraction,
lagophthalmos.
• Signs of active disease, i.e. chemosis, orbital
congestion are seen.
• On imaging, enlargement of muscle belly is
seen.
2. Brown syndrome. In it, there is underaction
of ipsilateral IO whereas in SO palsy, there is
ipsilateral IOOA.
3. Primary IOOA. It is usually seen with
infantile esotropia. There is absence of
hyperdeviation in the primary position, lack of
torsion and negative head tilt test.
4. Skew deviation is an acquired, acute, hyper-
deviation which may or may not be comitant.
Presence of neurologic signs refers to brainstem
or cerebellum involvement.
Table 12.7 Differences between congenital and acquired superior oblique palsy
Features Congenital SO palsy Acquired SO palsy
Diplopia No complain of diplopia, only intermittent Usually complain of vertical,
vertical diplopia in decompensated palsy diagonal or torsional diplopia
with incomitant hypertropia
Torsion There is no measurable subjective torsion Excyclotorsion usually seen
more so in bilateral palsy
Head tilt Present since infancy (old photographs) Anytime later following the onset
Traction test Lax SO tendon confirmed by traction test SO traction test is normal
intraoperatively
Facial asymmetry Facial asymmetry is usually present There is no facial asymmetry
Fusional amplitudes Significantly increased (16–30 prism diopters) Normal (2–3 prism diopters)
Amblyopia in the May be present Usually absent
involved eye
Incomitant Strabismus
323
Treatment
I. General principles of therapy are same as
described in therapy of paralysis of sixth
(see page 328) and third (see page 347) nerves.
II. Non-surgical treatment
1. Amblyopia, when present, should be treated
first; if the patient is a child, surgery is usually
indicated.
2. Segmental membrane prisms or segmental
occlusion of the lower third of the spectacle lens
before the paretic eye with semiopaque Scotch
tape may be tried till surgery is undertaken.
3. Alternate occlusion or occlusion of the sound
eye may be performed to create visual comfort
in patients in which binocular single vision
cannot possibly be restored by any means.
4. Prisms may be used to overcome diplopia in
small, symptomatic, comitant or nearly comitant
deviations that do not have a symptomatic
torsional component. If this alleviates the
symptoms, surgery is not warranted.
III. Surgical treatment. Surgical treatment is
indicated for a:
• Significant abnormal head posture,
• Vertical deviation, or
• Diplopia.
A significant head tilt is the main indication
for surgery in children younger than age 5, as it
is thought that the uncorrected torticollis will
lead to progressive facial asymmetry.
Surgical approach employed should take into
consideration:
• Presence of SR contracture,
• SO laxity, and
• Degree of torsion.
Various surgical schemes have been recommended. Knapp and von Noorden's modified
approach depending upon the class of paresis
is summarized in Table 12.8.
Based on the degree of deviation (hypertropia)
and status of muscle sequelae following
paresis of SO muscle, the line of surgical
management is summarized below:
Hypertropia is <20 PD
One muscle surgery as below:
• IO weakening—if IOOA
• SR recession—if contracture of SR positive
• SO tuck—if SO tendon laxity
• Contralateral IR recession—if no SR
contracture and no SO tendon laxity
Hypertropia >20 PD
Two muscle surgery, i.e. ipsilateral IO weakening
+ any of the following:
• SR ipsilateral recession—if contracture of SR
positive
• SO ipsilateral tuck—if SO tendon laxity
• Contralateral IR recession—if no SR
contracture and no SO tendon laxity.
Other recommendations are:
1. Superior oblique muscle tuck is a hard
procedure to quantitate. It is best employed:
• When the deviation is greatest in opposite
downgaze and so muscle is moderately to
markedly underacting.
• For acquired bilateral SO palsy or weakness.
• To reduce or eliminate the head tilt in
congenital SO palsy that presents in early
childhood.
2. Anterior temporal displacement of the
anterior half of the SO muscle tendon (Harada-
Ito procedure) is indicated as an alternative to
SO tuck, when the deviation is primarily
torsional. This procedure does not correct any
vertical deviation in primary position, but
corrects the excyclo-deviation and the abducting
weakness of the SO muscle in downgaze.
• Intraoperative adjustment of Harada–Ito procedure
is possible by visualizing objective torsion of
the fundus using indirect ophthalmoscope.
• Postoperative adjustment of Harada–Ito procedure
has also been described using adjustable
sutures.
3. Fell’s modification of Harada-Ito procedure
involves disinserting the anterior fibres of the
superior oblique tendon and transposing them
8 mm posterior to the superior insertion of the
lateral rectus muscle.
4. Bilateral Harada-Ito procedures are indicated
in some cases of bilateral fourth nerve palsy.
Warning for superior oblique palsy surgery
• Large fusional amplitudes are one directional
• Reverse diplopia is not tolerated well
324 Theory and Practice of Squint and Orthoptics
Table 12.8 Knapp's and von Noorden's surgical schemes for left superior oblique muscle paresis
Modified Knapp’s Pattern of deviation Muscle sequelae associated with Recommended surgical
class of paresis LSO palsy treatment
Class I Maximum HT in Overaction of ipsilateral Weakening of ipsilateral
dextroelevation IO (LIO) IO (LIO)
Class II Maximum HT in Underaction of paretic
dextrodepression LSO
a. If laxity of SO tendon Tuck of ipsilateral SO (LSO)
(grade III and IV laxity) or recession of contralateral
b. If no laxity of SO tendon inferior rectus (RIR)
and IO overaction present Weakening of ipsilateral
IO (LIO)
Class III HT equal in entire Weakness of paretic SO (LSO)
paralysed field (all with overaction of ipsilateral
dextroversion position) IO (LIO)
a. If HT
b. If HT >20 PD with IO (LIO)
Class IV HT equal in entire Contracture of ipsilateral SR
paralysed field and (LSR)
inferior field (i.e. a. If deviation <20 PD LSR recession + LIO
dextroposition and weakening
downgaze positions b. If deviation >20 PD with LSR recession + LIO
(L-shaped) • SO tendon laxity weakening + LSO tuck
Class V HT maximum in all Long-standing SO palsy with
downgaze positions spread of comitance
a. If SO tendon laxity LSR recession + LSO tuck
b. If with IO overaction LSR recession + LIO
Class VI V-pattern esotropia Bilateral SO palsy (underaction)
with reversing with bilateral IO overaction
Bielschowsky head tilt a. If torsion
test b. If torsion >15° Bilateral IO weakening +
Class VII HT in all downgaze Underaction of inferior
position, primary oblique and superior oblique
position and in (acquired Brown’s syndrome)
dextroversion Usually occur due to trauma
in trochlear area (canine tooth
syndrome)
• If aligned (no deviation) in No procedure
• If ipsilateral hypertropia Recess contralateral IR (RIR)
• If ipsilateral hypotropia Explore trochlea to release
Class VIII Comitant hypertropia Spread of comitance
but with positive head • If IO overaction LIO weakening
tilt test • If tight SR LSR recession
• If lax SO tendon SO tuck or RIR recession
<20 PD Weakening of ipsilateral
• SO tendon laxity LIO weakening + LSO tuck
• No SO tendon laxity LIO weakening + RIR
recession
• No SO tendon laxity LSR recession + LIO
weakening + RIR recession
or RIR recession
weakening
<15° Bilateral IO weakening
B/L Harada-Ito procedure
or B/L IR recession
primary position
restriction
Incomitant Strabismus
325
• Never tuck a SO tendon that is not lax,
otherwise iatrogenic Brown's is a possibility
• The end point of tucking is the symmetry
between two eyes on repeated traction testing
Bilateral SO palsy with torsional problem with V
pattern
The main difference from unilateral to bilateral
palsies are torsion.
Features
• Patients often complain of tilting torsion-door
frames
• More than 10 deviation on DMR
• Mainly chin down posture rather than head
tilt.
• V-pattern esotropia
• Small primary position deviation
• Alternating hypertropia
• LHT on right gaze of left head tilt
• RHT of left gaze or right head tilt.
Surgeries for bilateral SO palsy
Following options are there:
1.Collapse V pattern
• IO weakening
• IR recession
• MR downward transposition
2.Nullify primary position hypertropia
Asymmetric IR recession
3. Reduce torsion
• Harada-Ito
• IR nasal transposition
• SO tuck
LATERAL RECTUS PARALYSIS
The abducent (sixth cranial) nerve is a small
and pure motor nerve that supplies the lateral
rectus muscle. Isolated lateral rectus muscle
paralysis (sixth cranial nerve paralysis) is next
common to isolated paralysis of superior
oblique muscle.
Note. Applied anatomy of sixth cranial nerve
(see page 17) should be reviewed before
proceeding further.
Etiology
A. Congenital sixth nerve palsy due to hypo-
plasia of its nucleus or developmental anomaly
in the motor nerve fibres is quite rare.
• Congenital absence of the 6th nerve nucleus and
aplasia of the nerve is associated with Duane’s
syndrome (congenital cranial dysinnervation
disorder).
• Congenital horizontal gaze palsy due to
involvement of gaze centre may be confused
with congenital 6th nerve palsy.
• However, sixth cranial nerve paresis
occurring shortly after birth had been reported
and usually resolves spontaneously. It is
thought to be caused by the increased
intracranial pressure associated with labour
and delivery.
• Congenital bilateral abducent paralysis
associated with facial diplegia and microglossia
constitutes the Mobius syndrome.
B. Acquired sixth nerve palsy can occur due to
lesions at various levels as follows:
1. Nuclear lesions. Nuclear lesions never cause
isolated sixth nerve palsy. A lesion in and
around the sixth nerve nucleus causes the
following:
• Ipsilateral sixth nerve palsy.
• Ipsilateral seventh nerve palsy of upper motor
neuron type due to concomitant involvement
of facial fasciculus.
• Loss of conjugate movements to the same side
resulting from involvement of horizontal gaze
centre in the pontine paramedian reticular
formation (PPRF).
2. Fascicular lesions may cause:
i. Foville's syndrome. It results due to lesions of
dorsal pons involving sixth nerve fasciculus as
it passes through PPRF and is characterized by
the following:
• Ipsilateral sixth nerve palsy
• Loss of conjugate movement to the same side
• Ipsilateral facial nerve palsy
• Facial analgesia from involvement of the
sensory portion of the fifth nerve.
• Deafness
ii. Raymond's syndrome. It results due to lesions
of the ventral pons involving fasciculus as it