This document provides information about paralytic strabismus caused by a third cranial nerve palsy. It discusses the anatomy and supply of the oculomotor nerve. Signs of a third nerve palsy include ptosis, divergent squint with intorsion, restricted eye movements, and diplopia. Causes can include lesions of the nerve nuclei, nerve trunk, or intraorbital muscles. Investigation involves assessing eye alignment and movements to localize the site of lesion, with diplopia charting helping to differentiate nerve or muscle involvement.

1. PARALYTIC
STRABISMUS(3rd CN )
DR.PRAKRITI YAGNAM.K

3. Oculomotor N.:
 Third cranial nerve
 Entirely motor
 Supplies all extraocular muscles except
lateral rectus and superior oblique
 Also supplies intraocular muscles like
sphincter pupillae and ciliary muscle

4. - Nucleus is at the midbrain at the level of superior colliculus
- There are main and accessory nucleus which is the Edinger
Westphal nucleus
- Course is broadly divided as :
Fasicular part
Basilar part
Intracavernous part
Intraorbital part

5.  There are mainly two divisions – superior
and inferior
 Superior supplies SR and LPS
 Inferior division supplies the remaining
EOM
 The intraocular muscles are supplied by
the parasympathetic root of nerve from
Edinger Westphal nucleus through ciliary
ganglion

7. Paralytic
squint :
Lesion is situated at the level of
lower neurons affecting the nuclei
, the nerve or the muscles
There will be disturbance in relative
coordination of eyes
The paralysis of the muscles is
called ophthalmoplegia
If EOM affected it is external
ophthalmoplegia

8. If intraocular muscles are affected it is
internal ophthalmoplegia
If all are affected it is total ophthalmoplegia
In paralytic squint afferent pathways and
centers are usually intact but efferent
pathways breakdown

9. Etiology :
 Different mechanisms come into play at
different sites of lesion
 Features help to differentiate the location
of the lesion also
Supranuclear :
Lesions of cerebral cortex and supranuclear
pathway
 Conjugate paresis affects both eyes
equally

10.  Position and movements of eyes are
abnormal but maintain relative
coordination and there will be no
diplopia
Nuclear lesions :
Common causes – Vascular diseases
 Demylienation
 Primary tumors
 Metastasis

11.  Lesions involving entire nucleus –
Ipsilateral third N. palsy with adjacent
fourth N. palsy
 Ipsilateral sparing and contralateral
weakness of elevator is seen
 Involving paired MR subnuclei – wall eyed
bilateral internuclear ophthalmoplegia (
WEBINO )
 There will be defective convergence and
adduction

12. Fasicular lesions :
Causes are similar to nuclear
Syndromic associations seen :
1. Benedikts syndrome
2. Weber syndrome
3. Nothnagels syndrome
4. Claudes syndrome

13. Syndrome Location of pathology Features
Benedikts At intermediate level of midbrain at the
level of red nucleus
I/L 3rd CN.palsy with tremors
and jerky movements on C/L
side
Webers Fasicular part while passing through
cerebral peduncle
I/L 3rd CN.palsy , C/L
hemiplegia and facial palsy of
UMN type
Nothnagel
s
Involving midbrain tectum U/L or B/L 3rd CN.palsy and I/L
cerebellar ataxia
Claudes Brainstem stroke syndrome
Affects oculomotor N.,red nucleus and
brachium conjunctivum
Nothnagels + Benedikts syndromes
I/L 3rd CN.palsy,C/L
hemiparesis,C/L ataxia,C/L
hemiplegia of lower face ,
tongue and shoulder

14. Lesions involving basilar part :
 Isolated 3 rd N. palsies are common
Causes : - Diabetes with pupillary sparing
- Aneurysm at PCA with pupil
involvement
- EDH – fixed dilated pupil with total 3
rd N.palsy

15. Intracavernous part :
•Associated with 4 ,6 and ophthalmic
division of trigeminal nerve
•Pupil is spared
Causes - Diabetes
Pituitary apoplexy
Aneurysms
Meningioma
CCF
Tolosa hunt syndrome

16. Herpes zoster inflammation
SLE
MS
Sarcoidosis
Wegeners granulomatosis
Intraorbital lesions :
- Isolated or combined
- Orbital tumors , psueudo tumors , trauma or
vascular diseases

17. Lesions of
pupillomotor fibres :
Pupillomotor fibres are located
superficial B/W brainstem and
cavernous sinus
- Blood supply is from pial blood
vessels
- affected by surgical lesions like
aneurysm , trauma and uncal
herniation
Main trunk is deeper and supplied
by vasa nervosum
- affected by microangiopathy in
conditions like diabetes ,
hypertension
- due to infarction of nerve fibres
Therefore diabetes spares the pupil

18. Isolated third nerve palsy :
- Idiopathic – 25 %
- Vascular – DM , HTN
- Trauma
- Aneurysm at junction of PCA and ICA – painful
condition
- Other painful miscellaneous conditions are migraine ,
tolosa hunt syndrome , DM , tumors , vasculitis
associated with collagen disordes , syphilis and TB
- Infections of CNS ( encephalitis , polio )

19.  Toxins – endogenous – diptheria
 - exogenous – lead , botulinum
 Thiamine Deficiency
Symptoms :
 Blurred vision with pain sometimes
 Deviation of eye with limitation of movements with
drooping of eyelids
 Diplopia
 Reduced contrast sensitivity
 Abnormal position of head
 Vertigo

20. General
signs of
paralytic
squint :
Magnitude of squint – varies with
eye position ( Incomitant )
Diplopia – usually present
Ocular movements – restricted
False projection – present
Abnormal head posture – Usually
present
Secondary deviation greater than
primary

21. Signs
:
Ptosis – due to paralysis of LPS
Squint with deviation of eye – downwards
, outwards and slightly intorted due to
unopposed action of LR and SO muscles
Movements restricted are – adduction ,
elevation , depression and extorsion
Head posture – turns on the opposite side
, tilted towards the same side and chin is
slightly raised

24. Squint :
- Magnitude of squint or abnormal alignment of eyes is of
variable degree – depends on degree of paralysis and in
which direction patient is looking
- Amount of squint determined by angle of deviation is
more if paralysis is severe
- More if patient is looking in the direction in which
paralysed muscle comes into play

25. For
oculomotor
N. palsy :
Divergent squint or exotropia with
intorsion seen
Pupil is semidilated and immobile
if involved
Accomodation is paralysed
Slight degree of proptosis – owing
to the tone of paralysed muscles

27. Diplopia
:
If both eyes are functioning and one
deviates – binocular diplopia
Diplopia occurs only over that part of field
of fixation towards which affected muscles
move the eye
Image seen by the squinting eye – false or
apparent image
Image seen by fixing eye is true image
False image is less distinct than true image
because the latter falls on fovea centralis

28.  Angular displacement of false image =
angle of deviation of eye
In 3rd CN.palsy –
 Crossed or heteronymous diplopia
 Tested by Diplopia charting

29. Crossed
diplopia :

30. False
orientation
:
Necessary accompianment of
binocular diplopia
Same principle as the increase of
secondary deviation for the object
is projected according to the
amount of nervous energy exerted
As this is greater than that exerted
in normal circumstances , object is
projected too far in the direction
of action of paralyzed muscle

31. Test :
patient fixes with paretic eye to an object
quickly points with index finger
finger moves past the object
- In long standing paralysis may compensate the error

32. Position of head :
•To eliminate diplopia
•Patient holds his head , so that his face is
turned in the direction of action of
paralyzed muscle so that eyes are
rotated away from field of action
•In defective vertical movements – tilting
of head present
DD : ocular torticollis

33. Vertigo :
- Leading to nausea and vomiting due to diplopia or false
projection
- When gaze is turned from region of correct to that of
false localization , objects appear to move with
increasing velocity in the direction in which eye is moving
- Occurs chiefly when paralysed muscle is called upon to
exert itself
- Counteracted partially by altering position of head or
completely by shutting or covering the affected eye

34. In paralyses of long standing , relief is
gradually obtained – learns to ignore
Changes in long standing paralysis :
•Secondary contractures in antagonist
muscles and soft tissues such as
conjunctiva , tenon capsule and muscle
sheaths
•Extent of incomitance decreases
•Gradually resembles comitant squint

35. Paresis of one muscle
Overaction of I/L antagonist
Overaction of C/L yoke muscle
Secondary inhibitional paresis of C/L antagonist
Phenomenon of comitization :

36. Workup and
Investigation :
Evaluation of squint
and determination of
involved N. or muscle
2. Investigation to find
out underlying causes
based on history and
examination

37. History taking :
Ophthalmoplegia – Onset , duration and
progression
 Associated ocular symptoms – loss of
vision diplopia , pain
 eyelid signs like retraction , ptosis ,
edema , fatiguability , proptosis
 Associated systemic symptoms –
headache , generalized asthenia etc…
 Associated systemic comorbities ( DM ,
HTN )

38. Examination :
 Visual acuity
 Pupillary examination
 Ocular alignment –
 Angle of deviation by Hirschberg test
or synaptophore
 Movements in all directions noted for
overaction and under action

40. Cover , cover and uncover test and
Alternate cover test done
 To determine relative movements of two
eyes when each eye is used for fixation
 The position of eyes with normal eye
fixing – primary deviation
 Deviation of sound eye when paralyzed
eye fixates the target – secondary
deviation
 In paralytic squint
 secondary deviation > primary
deviation
- Due to overaction of C/L synergist of
palsied muscle

43. Diplopia charting :
 Dark room – Red googles in front of right
eye
 Green in front of left eye
 Bar of light through stenopaeic slit with a
hand torch moved about in the field of
binocular fixation
 Distance – 120cm. From the patient

44. Data
derived
:
Area of single vision and diplopia
Distance between two images in
areas of diplopia
Whether images are at same level
or not
One image in inclined or both are
erect
Diplopia is homonymous or
crossed

45. False image – Frequently tilted and
fainter of the two
• Determined by direction in which images are
most separated from each other
• Displaced farthest in the direction of normal
action of paralysed muscle
• By covering one eye we can show which eye
the image belongs to
• Deviation of false image is most easily
determined when eye is turned in cardinal
positions

46.  Should be plotted with either eye fixing if
possible
 In paralytic squint greater separation of
images when the affected eye is fixing
on target ( secondary deviation )

47. Diplopia charting for different muscle palsies

49. Limitations
:
Subjective test
Contracture of antagonist muscle
may develop
Paresis may unmask latent squint
Patient may fix with paralyzed
muscle if that eye has greater
visual acuity

50. To measure degree of deviation especially if
torsional and to have a record to assess
recovery – HESS charting or LESS screen is
used
Inner and outer charts are parallel to each
other

51. HESS charting
for 3rd
CN.palsy

52. Ocular positioning – Exophthalmos or
enophthalmos is noted
Anterior segment evaluation
Posterior segment evaluation
Ocular and orbital U/S – for combined
nerves involvement

53. Forced Duction Test :
•To assess passive function of the muscle
•Positive – resistance to full passive
movement
•Seen in restrictive squint
•Negative – passively can rotate eye fully
with forceps
•Seen in paralytic squint

54. Forced Generation Test :
•Patient made to look in direction of
deviation and restriction is noted
•If Tug is present – Mechanical restriction
present
•No tug – Only paralytic squint

55. Pharmacological tests :
- To rule out myasthenia
- Tensilon test

56. Systemic
workup :
Blood sugars
Blood pressure
Lipid profile
ESR ( to rule out GCA )
Hemogram
Thyroid profile
CRP
VDRL,FTA-ABS for syphilis

57. - X ray skull lateral view – to rule out sellar lesions involving
cavernous sinus
- MRI/MRA for aneurysms
- In isolated 3rd CN.palsies with no pupillary involvement ischemic
vascular evaluation and daily pupil evaluation is indicated
- Pupillary involvement may sometimes be delayed by five to
seven days after onset of motor ophthalmoplegia

58. Cerebral angiography – for any berry
aneurysm usually in patients less than 50
years age if no pupillary involvement also
because ischemic cause is unlikely
Any age with complete or partial 3rd
CN.palsy with pupillary involvement –
medical emergency – aneurysm
In children less than 14 years most common
cause is congenital or traumatic

59. - Lumbar puncture – For any blood
in CSF or inflammatory reaction or
infiltration or infection
- Cytogenic examination to
diagnose meningeal
carcinomatosis or lymphomatoses
or leukemic infiltration

60. Evaluation of other cranial
nerves including 4 ,5,6,7
and 8
Other focal neurological
deficits ( DTR,sensory and
motor evaluation and
cerebellar signs )
Clinical photography in
every visit is necessary for
objective followup

61. DD :
- Ophthalmoplegic migraine
- Internuclear ophthalmoplegia
- Acquired ptosis
- Anisocoria
- Congenital ptosis
- Myasthenia gravis
- Thyroid ophthalmopathy

62. Management :
•Principles include symptomatic and etiologic
management
•Symptomatic mainly for diplopia
•Patching of one eye if patient has severe diplopia

63. Etiologic
:
Pupil sparing secondary to
ischemic causes – spontaneous
resolution in 6 to 8 weeks
Physician referral required for
evaluation of atherosclerotic risk
factors and control of blood
sugars
Recurrences may occur
affecting the same N. or any
other

64. Aneurysms or other intracranial lesions –
Immediate referral to a NeuroSurgeon
Other etiologies are treated accordingly
Palsies in children younger than 8 years are
associated with poor outcomes if there is a
traumatic or neoplastic cause – improved
alignment occurs but poor stereopsis

65. Surgical management :
- For significant and stable deviation for a
period greater than 6 months
Complete palsy :
- Goal is primary position alignment
compromising the ocular motility of
involved eye

66. Options
include
Supramaximal recessions of LR (14-16 ) and
large resection of MR ( 8 – 14mm. )
Here eye may become exotropic again with
time as LR undergoes chronic contracture
and resected muscle elongates
Primary position alignment may be
achieved by surgery on horizontal muscles
and IR muscles
Ocular fixation to nasal periosteum with SO
tendon
Fixing the eye with a Callahan suture after
recessing all of the temporal tissue to lateral
rim of orbital bone

67. Partial
palsy
:
Goals include good primary position
alignment, enlarge field of binocular vision ,
improving motility,alleviation of abnormal
head posture and elimination of diplopia
Isolated MR involvement – MR resection with
LR recession
Paresis of superior division – Transposition of
MR and LR ( Knapp’s procedure ) near
insertion of SR
Transposition of LR to IR, SR to MR with
tenotomy of SO muscle – for inferior division
palsy

68. Selective IR palsy – Horizontal recti transposed
inferiorly in relation to IR
If MR lacks any function due to complete palsy
other surgical options are required to improve
adduction – Transposition of SO tendon
Overacting SO muscle with A pattern – SO
tenotomy
Eyelid surgeries may be required for long
standing ptosis

69. Abberrant regenerations :
• May follow acute traumatic and
compressive but not vacular lesions
• Because of breach of endoneural
nerve sheaths in the former
Clinical presentations :
• Lid gaze dyskinesis :
Pseudo vongraffe sign – IR to LPS
– lid retracts when patient looks
down

70. Inverse duane syndrome – MR to LPS – lid
retracts when patient adducts his eye
2. Pupil gaze dyskinesis :
Pseudo Argyl Robertson pupil – MR to
sphincter pupillae
More pupil constriction to convergence than
to light response

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