This document discusses the anatomy, etiology, signs, symptoms, diagnosis and management of fourth cranial nerve (trochlear nerve) palsy, also known as paralytic strabismus. It begins with the anatomy of the fourth cranial nerve and then discusses the various causes of fourth nerve palsy including congenital, traumatic, idiopathic, vascular and neurological etiologies. The document outlines the clinical features, diagnostic workup including tests like Hess chart and double Maddox rod test, as well as treatment options based on the Knapp classification system for superior oblique palsies. Surgical management aims to correct vertical and torsional diplopia through techniques like superior oblique t

1. PARALYTIC
STRABISMUS
DR.PRAKRITI YAGNAM.K

2. Of Fourth cranial nerve :
Anatomy :
- Also called trochlear nerve
- Arises from the nucleus present at the dorsal part of
midbrain at the level of inferior colliculus
- The nerve crosses completely onto the other
side…Nerve arises from contralateral nucleus
- Longest and thinnest of all
- Entirely motor and supplies superior oblique muscle

3. COURSE : NUCLEUS
FASICULUS WITH EFFERENT
FIBRES
DECUSSATE IN ANTERIOR
MEDULLARY VELUM
TROCHLEAR NERVE TRUNK PRECAVERNOUS PART
EMERGES FROM SUPERIOR
MEDULLARY VELUM AND
WINDS AROUND SUPERIOR
CEREBELLAR AND
CEREBRAL PEDUNCLES

4. passes between
posterior cerebral
and superior
cerebellar A.
Pierces dura at roof
of posterior corner
of cavernous sinus
Cavernous part
In cavernous sinus
lies between Third
and fifth cranial
nerves
Intraorbital part
Passes through
lateral part of
superior orbital
fissure
Supplies superior
oblique muscle

5. Etiology :
- Superior oblique paralysis is the most common form of
paralytic squint
- Congenital – 40 %
- Trauma – 34 % - frequently due to impact in the area
of anterior medullary velum
- Idiopathic – 20 %
- Vascular and neurologic – 3 to 5 %

6. - Supranuclear lesions – loss of conjugate movements of eyeball
- Nuclear and fasicular – Haemorrhage
Infarction Paralysis of C/L SO
Demylienation.
Trauma
- Precavernous – Trauma
Basal meningitis
- Cavernous – Cavernous sinus syndromes along with 3 , 5 , 6 CN. and
ocular sympathetic paralysis
- Intraorbital – Trauma , inflammation and tumors – along with 3,5,6 CN.

7. Causes of isolated
fourth cranial nerve
palsy :
Congenital
Acquired – DM , HTN ,
Atherosclerosis , HZV
infection
Tumors , aneurysm, MS
and iatrogenic injury
are initially isolated but
later combined with
other nerve palsies

8. - Trauma is one of the most common causes – sometimes
trivial also
- Due to its unusual fasicular decussation from dorsal side of
brain stem – making it more vulnerable to compression
against bony skull in countercoup head injuries
- Its long intracranial course may also be another reason

9. Pathophysiology :
- Congenital – Dysgenesis of fourth nucleus
Abnormality of peripheral nerve
Abnormal Superior oblique muscle or tendon
Tendon abnormalities – Lax or abnormal insertion or
absence
- Acquired – Depends on the etiology

10. Symptoms :
- Vertical diplopia with tilting of objects – more on downgaze
- Abnormal head posture
- Vertigo
- Near work is affected as superior oblique integrity is more trivial for
near work – depression and intorsion – reading position
- Adults with congenital palsy – asthenopia and neck pains

11. Signs :
- Hyper deviation – Involved eye is higher due to weakness of SO muscle
Deviation increases when head is tilted towards
ipsilateral shoulder
- Movements – Depression is limited in adduction
Extorsion is also limited
- Diplopia – Homonymous vertical diplopia on looking downwards
Vision is single as long as eyes look above horizontal
plane

12. - Abnormal head posture – Face slightly turned towards opposite side
Chin is depressed
Head tilted towards ipsilateral shoulder
- In congenital palsies – facial asymmetry is also seen
Shallowing of mid facial region between
lateral canthus and edge of mouth
Due to long standing tilt

15. Long standing paralysis :
Initially incomitant hypertropia is greater in adducted and depressed field.
Contracture of ipsilateral inferior oblique occurs
Hypertropia maximum Overelevation of eye in
In field of action of IO adducted position

16. Features Unilateral Bilateral
Etiology Congenital or acuired Mostly acquired – trauma
Esotropia in downgaze A little V pattern due to unopposed action of IR
Subjective torsion Absent Present
Objective torsion - Double Maddox
rod
Excyclodeviation < 10 degree > 10 degree
Ductions of SO Normal or diminished Diminished
Head tilt test Deviation increase on tilting head towards I/L
shoulder
Increases on tilting towards either shoulder
Chin down position Absent Usually present

17. Features Congenital Acquired
Diplopia Not common unless
decompensated SO
paralysis
Marked
AHP From childhood Recent onset
Vertical vergence Increased range Normal range
Floppy SO -
Intraoperative
Present Absent
Facial asymmetry Present Absent

18. Work up and Diagnosis :
- Visual acuity
- Head position and facial asymmetry
- Ocular movements and assessment of
deviation in all fields of gaze
- Head tilt test
- Maddox rod and double Maddox rod tests
- Diplopia charting
- Hess chart

19. Park three step test
Step 1 :
■ Identify hypertropia in primary gaze
■ Weak muscle may be
Elevators of Depressors of
Hypotropic eye Hypertropic eye
SR / IO IR / SO
■ If Right eye hypertropia
■ Either RE SO/IR or LE SR/IO can be
affected

20. Step 2 :
■ Move eyes in either right or left gaze
■ Deviation increases in which gaze
noted
■ Deviation increases In the action of
paralyzed muscle
■ In Right hypertropia
■ If deviation increases
Right gaze Left gaze
RE IR or RE SO or
LE IO LE SR

21. Step 3 :
■ Tilt the head towards each shoulder
■ And notice the deviation
■ Eye on the same side intorts and
opposite side extorts
■ It is called Beilschowsky sign and is
also the basis of Beilschowsky head
tilt test
■ If Right hypertropia increases on left
gaze
RE SO or LE SR
■ Head tilt done and deviation
increases
Right Left
RE SO LE SR

22. In SO palsy :
- Deviation increases in opposite horizontal gaze
- And increases with same side head tilt
In right SO palsy :
- Deviation increases in left gaze
- And with right side head tilt
- Even after spread of comitance head tilt test will be positive

25. Diplopia charting :
- False image is lower and upper end tilted towards
true image
- Image is intorted because eye is extorted
- Distance between the images increases on looking
down and towards sound side
- Inclination of false image increases on looking down
to paralyzed side

27. Hess chart :
Congenital palsy :
•No difference in chart size
•Primary and secondary
deviations are almost same
•Hypertropia increases with
gaze towards sound side and
dcreases towards paralyzed
side
•In involved eye under action of
SO and overaction of IO seen
•In non paralyzed eye
Overaction of IR and SR is seen

29. Acquired palsy :
•Paralyzed eye chart smaller than the other
•Under action of SO and overaction of IO seen
•In non paralyzed eye over action of IR and under action of SR is seen

31. For late presentations to note down long standing changes
- In older children and adults – double Maddox rod test done to note torsion
- In younger children – IO and fundus photography done for cyclo deviation
- In normal fundus – fovea is 1/3rd DD below center of ONH
- If lower than that – ex cyclotorsion is suspected
- In Indirect Ophthalmoscopy it is above ( as image is inverted )

33. Systemic workup :
- Blood sugars
- Blood pressure
- Lipid profile
- Hemogram
- ESR
- CRP
- Thyroid profile
- VDRL and FTA-ABS

34. DD :
•Skew
deviation :
Vertical
alignment of
visual axes
Transient ,
constant /
alternating ,
comitant or
incomitant
Due to
imbalance of
supranuclear
inputs
Associated
with brain
stem or
cerebellar
signs and
symptoms
Not
associated
with torsional
or
cyclodeviation

35. 2.
Myasthenia
gravis :
Ocular MG can
presented as isolated
U/L SO palsy
- Involves SO
muscle and mimic
palsy
Shows diurnal
variation
Can involve other
extraocular muscles
also
Tensilon test is
positive
EMG and ACh
antibodies are
positive and
diagnostic

36. 3. Thyroid Ophthalmopathy :
• Hypertropia worse in upgaze
• Other signs of hyperthyroidism will be present
• T3 , T4 and TSH levels are suggestive
4. Orbital diseases – tumors , inflammation , blow out fractures
5. Partial third nerve paresis
6. Brown syndrome

37. Management :
- Patching – for symptomatic diplopia
- Prisms – for small deviations and diplopia without torsional component
- Based on clinical evaluation of spread of hypertropia Knapp classified superior
oblique palsy into seven classes
- These aid both in diagnosis and subsequent management

38. Class 1 :
Greater hypertropia
is in the field of
ipsilateral IO
After partial or
complete recovery
of SO palsy IO still
remains spastic
Simulates
contralateral SR
palsy
Head tilt test is
positive
Management : IO
weakening

39. Class 2 :
• Greater deviation in the field of action of paretic SO muscle
Management : Strengthening of SO muscle – tucking
If no significant head tilt and difficulty in isolating
Contralateral yoke muscle Inferior rectus can be recessed
To decrease incomitance and enlarge filed of BV in downgaze

40. Class 3 :
•Hypertropia significant and similar in both fields
Management :
•< 25 PD – IO recession before proceeding to surgery on
superior oblique
•> 30 PD – IO weakening + SO strengthening + C/L IR
recession

41. Class 4 :
- Class three with hypertropia towards ipsilateral inferior rectus
Management :
IO weakening + SO strengthening + C/L IR recession
Observe effect on horizontal hypertropia
observe and if does not resolve
Resection of I/L IR or weakening of C/L SO

42. Class 5 :
Hypertropia greatest in
lower gaze with greatest
incomitance in field of
action of ipsilateral
inferior rectus
Called double depressor
palsy
Management :
- Strengthening Of
ipsilateral SO and IR and
weakening of
contralateral yoke
muscles

43. Class 6 :
•Bilateral SO palsy sequale to
closed head trauma
•Diplopia on downgaze present
•Hallmark – Alternating
hypertropia , torsional diplopia
and V pattern esotropia
Management :
•B/L SO strengthening +
B/L IO weakening
•Downward transposition
of MR + recession – for
esotropia

44. Class 7 :
- Trauma to upper eyelid area near trochlea
- Paresis of ipsilateral SO muscle with reverse hypertropia in the field of I/L IO
due to mechanical inability of affected SO to alter contraction or relaxation
- Subsequent to dog bites
- Also called canine tooth syndrome
- Treatment is customized

46. Indications for surgery :
• Diplopia
• AHP
• Hypertropia
Factors that influence surgical decision are
- Angle of deviation in primary gaze
- Presence or absence of IO overaction
- Measurements in down gaze
- Force duction test
- Presence and absence of torsion

47. Requisitions :
- Assessment of deviation in all fields of gaze and stability is noted
- Ocular movements evaluated for overaction of IO and underaction of SO
- Patch test to differentiate between ocular and non ocular torticollis
Monocular patching for 20 minutes
Improvement in AHP No
Ocular Non ocular

48. - Superior oblique tendon laxity assessed intraoperatively with FDT
Tucking useful

49. Individual
surgeries :
Bilateral SO palsies –
SO strengthening
procedures
Overaction of IO –
myectomy / recession
Ipsilateral SR tight – SR
recession
No IO overaction / SO
laxity – Contralateral IR
recession
If > 25 PD – Ipsilateral
IO weakening +
Contralateral IR
recession

50. If torsional diplopia is
the primary problem
– Harada – Ito
procedure with Feels
modification done
Here anterior half of
SO tendon is
displaced to anterior
and temporal location
above LR
- If marked
incomitance is
present – Bilateral IO
weakening is done

51. Doesnot improve
improves

52. Complications : It is better to undercorrect than to
overcorrect
Adjustable suture surgery
minimizes the risk
Iatrogenic Brown syndrome –
Severe limitation in elevation in
adduction is seen
To minimize it preoperative and
intraoperative assessment of SO
tendon laxity is necessary

53. Of sixth cranial nerve :
- Also called abducent nerve
- Nucleus is beneath the floor of fourth ventricle at lower part of pons in
close relation to horizontal gaze centre and fasiculus of seventh cranial
nerve
- Small nerve
- Supplies lateral rectus muscle ( Ipsilateral )

54. Course :
Nucleus. – Infarction , demyelination,tumors , pontine syndromes
Fasiculus Fasiculus with efferent fibres
Traversing medial lemniscus and pyramidal tract
Basilar part Dorellos canal ( at apex of
petrous bone )

55. INTRACAVERNOUS
CAVERNOUS SINUS
LATERAL AND BELOW
INTERNAL CAROTID ARTERY
INTRAORBITAL
MIDDLE PART OF SUPERIOR
ORBITAL FISSURE
ENTERS OCULAR SURFACE
OF LATERAL RECTUS

56. Etiology :
Nuclear – Isolated sixth cranial nerve palsy
Sometimes ipsilateral PPRF can get involved with
Ipsilateral LMN type facial palsy
Fasicular –
1. Foville syndrome
2. Millard Gubler syndrome
3. Raymond syndrome

57. Fovilles Millar Gubler Raymond
Site Dorsal pons involving fasiculus
as it passes through PPRF
( 5th + 6th +7th CN. )
Ventral pons involving
fasiculus as it passes
through pyramidal tracts
Features I/L 6th N. palsy
Loss of conjugate movements to
same side
I/L facial N.palsy
Facial analgesia
Deafness
I/L 6th N. palsy
C/L Hemiplegia
Other signs of dorsal
pontine lesions
I/L 6th N. palsy
C/L hemiparesis

58. Basilar part – CP angle lesions
•Acoustic neuroma – 5th +6th +7th+8th CN.palsy
•First symptom – hearing loss
•First sign – loss of corneal sensations
•Along with ataxia and papilledema
Middle fossa lesions – Tumors , Inflammation of
medial aspect of petrous bone , fracture of skull
Meningioma
Clivus lesions – Nasopharyngeal Ca. , clivus
chordoma

59. Features – 6th N.palsy associated with facial pain or numbness
and facial palsy
- Gradinego syndrome. - Involvement of petrous bone from otitis
media
Features – I/L 6th N.palsy
Deafness
Neuralgia in the distribution of V1
Facial weakness

60. - Raised ICT – commonest false localizing sign
- Due to long course in cisterna pontis to its sharp bend over superior
border of petrous part of temporal bone
- When high rise in ICT downward shift of brainstem towards foramen
magnum occurs compressing the nerve

61. Intracavernous part –
Aneurysms ( rare ) Meningioma CCF
Tolosa Hunt syndrome
Vascular – DM , HTN
•In intracavernous part as the
nerve is joined by sympathetic
branch from paracarotid plexus
associated with postganglionic
Horners syndrome
Intraorbital part – Orbital
apex syndrome
Superior orbital fissure
syndrome

62. Non localizing causes :
- Raised ICT
- Intracranial hypotension
- Head trauma
- LP / Spinal anaesthesia
- Vascular like HTN , microvascular like DM
- Parainfectious processes – post viral ,middle
ear infections in children
- Basal meningitis

63. Common
causes :
Collier
sphenoidal
palsy
Superior orbital
fissure
syndrome
Arteriosclerosis HTN , DM
Trauma and
raised ICT

64. Causes of isolated sixth nerve palsy :
- Post viral – CMV , HZV , EBV , Influenza ( MCC < 9 yrs. )
- Ischemia – DM , HTN , Atherosclerosis ( MCC > 40 yrs. )
- Neoplasms like astrocytoma , medulloblastoma , neuroblastoma
- Trauma
- Neurological disorders like hydrocephalus , pseudotumor cerebri and other causes
of raised intra cranial tension
- Miscellaneous – post immunization and congenital

65. Clinical features :
Deviation – Eyeballs
are converged –
Esotropia ( distance
> near )
Ocular movements
– abduction is
limited
Diplopia –
Uncrossed
horizontal diplopia
Head posture –
Towards action of
paralyzed muscle

67. Workup and Diagnosis :
•Visual acuity
•Angle of deviation
•Ocular movements
•Head posture

68. Diplopia charting :
- Images are on the same level and erect , becoming more separated on
looking towards paralyzed side
- False image is slightly tilted on looking up or down towards paralysed
side because of imbalanced effect of oblique muscles in these positions

70. Hess chart :
- Paralysed side is smaller
- Primary deviation < Secondary deviation
- Esotropia with marked underaction of LR and slight over action of MR
seen
- In the non paralyzed side marked overaction of MR is seen

72. DIFFERENTIATION
BETWEEN
PARTIAL AND
TOTAL PALSY IS
IMPORTANT
Paresis Total palsy
Saccadic velocity
of LR
> 175 degree / sec < 100 degree / sec
Abd Limitation Can usually move
beyond midline
No movement
beyond midline
FDT No restriction
unless contracture
of MR is present
Same as paresis
Active FGT Reduced Absent

73. - Neuroimaging – CT /MRI
Indications : Young age
evolving or painful paresis
Systemic workup :
- Blood sugars
- CBC , ESR
- Antinuclear antibodies and FTA – ABS and others

74. DD :
•Myasthenia Gravis
•Restrictive thyroid myopathy
•Medial orbital wall fractures
•Orbital myositis
•Duanes syndrome ( 1 and 3 )
•Convergence spasm and

75. Divergence paralysis
Acute onset esotropia ( infantile )
Mobius syndrome
Inflammatory orbital diseases
Strabismus fixus
Tight MR
Congenital fibrosis of extraocular muscles

76. Management :
Non surgical –
Children
Goal in acute stage – To prevent amblyopia and preserve BSV
- Standard occlusion therapy to prevent suppression
- Patching also relieves diplopia
- Must be permitted to maintain AHP till spontaneous resolution occurs or until surgery
- Disappearance of head turn – alarming sign

77. - Alternating patching is recommended to prevent contracture of MR
- Smaller deviations are treated with prisms
- Botulinum toxin can be injected to MR to preserve binocularity abd to prevent contracture

78. Adults :
Aim – to relieve
diplopia and
enlarge area of BSV
Monocular
occlusion or prisms
are used
Layer deviation –
Fresnel prism
Botulinum (
Chemodenervation
)of MR – 3 – 6
months paralysis

79. Surgery :
- Goal – To correct incomitant squint
To improve abduction
To increase the size and to centre the binocular diplopia free
field
- Requisites
FDT – done prior and during surgery to assess MR contracture
FGT – to assess muscle recovery

80. Partial LR palsy :
- MR recession
- LR resection
- Both combined
- And associated with C/L MR recession or Faden

81. Total palsy :
- Partial vertical rectus transposition with MR weakening either by recession or botulinum toxin
- Full tendon vertical rectus transposition with MR weakening
- Rectus muscle union with MR weakening

82. Good Lateral rectus
function :
80 – 100 % recovery
Esotropia 10 – 20 PD
in primary gaze – U/L
or B/L MR recessions
Good results with C/L
MR recession than
ipsilateral MR
recession
Faden if done
increases the field of
diplopia free Binocular
Single Vision

83. Fair LR :
- Significant FGT
- < 20 PD – Unilateral LR resection ( 5.5 to 7 mm. ) and MR recession if
coexisting contracture is present with adjustable suture on MR
- > 40 PD – U/L LR resection + MR recession + C/L MR recession

84. - In total sixth nerve palsy resection of LR gives poor long term alignment
- So if preoperative FGT is poor – transposition of vertical recti muscles is
done – SR and IR to LR
- And along with it recession of MR and/or posterior fixation suture
- This gives good result if MR contracture is present
- Weakening can also be done by botulinum toxin as recession has a
disadvantage of anterior segment ischemia

86. THANK YOU !!!