REVISION
1. Remember all the laws e.g sherrington and hering
2. Differential diagnosis between mechanical and neurogenic palsies
3. 3rd nerve palsy
4. 4th nerve palsy
5. 6th nerve palsy
6. Myogenic palsy
7. Infantile esotropia and DVD
8. Alphabet pattern
9. Some diseases in aetiology of cranial nerves
10. GO, MG
11. Browns syndrome
12. Duanes
13. CCDD
14. Marcus Gunn, double elevator
15. Aetiology of concomitant strabismus
16. Ptosis
17. Convergence
18. Accommodation
19. Amblyopia
20. Craniostysyonosis
21. Myokimia
22.Functional vision assessment
,LAWS
Differential diagnosis
Congential Acquired
Presentation Symptoms of decompensation Diplopia and occasionally pain
Unaware of abnormal head posture Aware of uncomfortable abnormal head
posture
Unacceptable cosmetic appearance
Ocular motility Binocular function Often full muscle sequelae Muscle sequelae not fully developed.
Presentation Extended vertical fusion range Normal fusion range
Differences between neurogenic and mechanical defects.
Neurogenic Mechanical
Cover test Deviation in primary position reflects the Often only small deviation in primary position
extent of palsy.
Ocular motility Movement is greater on ductions compared Movement is the same on ductions and
to versions versions
No retraction of the globe Retraction may be noted
Hess chart Space between inner and outer fields is equal Outer field is displaced close to inner field in
and proportional the position of greatest limited movement
Fields are displaced away from position of Squashed appearance
greatest limitation
Forced duction Full passive movement Limited passive movement
test Intraocular pressure Same in all positions of gaze Increases when looking away from the
position of limitation
, CN III
Origin- midbrain
Has two branches:
Superior division – superior rectus and levator palpebrae superioris.
Inferior division – Medial rectus, inferior rectus, inferior oblique.
Aetiology of CNIII palsy
Localisation of lesion
• Nuclear- bilateral ptosis (the two levator muscles share a nucleus) and ocular motility
defect.
• Internuclear- internuclear opthalmoplegia (explain)
• Infranuclear- lesion along nerve pathway.
§ Central – pupil sparing (vascular such as diabetes and hypertension)
§ Peripheral- pupil involvement (likely cause is aneurysm)
Other causes include
• Trauma (small percentage)
• Space occupying lesion such as Aneurysm of PCA, tumour compressing CN III, carotid
cavernous fistula and tolosa-hunt syndrome (inflammation in cavernous sinus).
Investigation
Visual acuity - It is necessary to lift the ptotic lid to evaluate visual acuity. This may be reduced
due to mydriasis, particularly for near visual acuity.
Cover test - An exo- and hypo-deviation is present.
Ocular motility - There will be limited elevation, depression and adduction, which may be complete
or partial limitations, depending on the extent of paresis/palsy.
• Always check for the presence of IV nerve function by asking the patient to attempt to
look down and outwards and observe for the presence of incyclo-torsion during this
movement.
• If there’s ptosis, examiner will have to lift it to see eye movements.
• Pupil may be dilated depending on aetiology.
• Check for unilateral and bilateral.
• Extent of limitations, duction versus version.
Convergence - This will be absent if the medial rectus muscle is paralysed.
Binocular function - This is usually absent unless the III nerve paresis is mild and partial.
, Accommodation – Defective accommodation if pupil is involved as the fibres to the ciliary body are
likely to be affected.
Hess chart – Constricted field in affected eye, overaction of muscles in contralateral eye.
Diplopia – Constant diplopia, unless complete ptosis blocks out the diplopic image.
Aberrant regeneration
• Change in the actions of muscles supplied by the third nerve due to regrowth of damaged
nerve fibres following complete or severe third nerve palsy.
• Likely to occur when aetiology is trauma or aneurysm.
• May occur from weeks to months after onset.
• Aberrant regeneration may occur between CN III and CN V.
Generally unexpected things happen such as ptosis (lid) retraction/pupil constriction on attempted
adduction or depression.
Management of CN III palsy
• In children, any associated amblyopia should be treated. Any underlying cause for the lesion
should be investigated and treated.
• As with most conditions affecting the extraocular muscles, it is important to allow a
period for recovery of any muscle function and then wait until stability of this has been
demonstrated.
• Recovery is more common in vascular aetiologies.
• Prisms may be helpful with partial III nerve palsy where there is a small deviation in primary
position that can be joined with prisms. Long-term prisms may be incorporated into a
spectacle correction.
• Occlusion is indicated for diplopia, which cannot be joined by prisms because of a complete
palsy and incomitant ocular motility and where surgery is not (yet) an option. E.g Blanderm,
Bangerter foils, occlusive contact lenses, patch.
• Surgery is indicated to correct the strabismus and any associated ptosis. Squints are
treated initially as the ptosis acts as a mechanical barrier to diplopia and true size of ptosis
is also revealed.
• Adequate bell’s phenomenon is required before ptosis can be repaired.
Surgical options
1. Remember all the laws e.g sherrington and hering
2. Differential diagnosis between mechanical and neurogenic palsies
3. 3rd nerve palsy
4. 4th nerve palsy
5. 6th nerve palsy
6. Myogenic palsy
7. Infantile esotropia and DVD
8. Alphabet pattern
9. Some diseases in aetiology of cranial nerves
10. GO, MG
11. Browns syndrome
12. Duanes
13. CCDD
14. Marcus Gunn, double elevator
15. Aetiology of concomitant strabismus
16. Ptosis
17. Convergence
18. Accommodation
19. Amblyopia
20. Craniostysyonosis
21. Myokimia
22.Functional vision assessment
,LAWS
Differential diagnosis
Congential Acquired
Presentation Symptoms of decompensation Diplopia and occasionally pain
Unaware of abnormal head posture Aware of uncomfortable abnormal head
posture
Unacceptable cosmetic appearance
Ocular motility Binocular function Often full muscle sequelae Muscle sequelae not fully developed.
Presentation Extended vertical fusion range Normal fusion range
Differences between neurogenic and mechanical defects.
Neurogenic Mechanical
Cover test Deviation in primary position reflects the Often only small deviation in primary position
extent of palsy.
Ocular motility Movement is greater on ductions compared Movement is the same on ductions and
to versions versions
No retraction of the globe Retraction may be noted
Hess chart Space between inner and outer fields is equal Outer field is displaced close to inner field in
and proportional the position of greatest limited movement
Fields are displaced away from position of Squashed appearance
greatest limitation
Forced duction Full passive movement Limited passive movement
test Intraocular pressure Same in all positions of gaze Increases when looking away from the
position of limitation
, CN III
Origin- midbrain
Has two branches:
Superior division – superior rectus and levator palpebrae superioris.
Inferior division – Medial rectus, inferior rectus, inferior oblique.
Aetiology of CNIII palsy
Localisation of lesion
• Nuclear- bilateral ptosis (the two levator muscles share a nucleus) and ocular motility
defect.
• Internuclear- internuclear opthalmoplegia (explain)
• Infranuclear- lesion along nerve pathway.
§ Central – pupil sparing (vascular such as diabetes and hypertension)
§ Peripheral- pupil involvement (likely cause is aneurysm)
Other causes include
• Trauma (small percentage)
• Space occupying lesion such as Aneurysm of PCA, tumour compressing CN III, carotid
cavernous fistula and tolosa-hunt syndrome (inflammation in cavernous sinus).
Investigation
Visual acuity - It is necessary to lift the ptotic lid to evaluate visual acuity. This may be reduced
due to mydriasis, particularly for near visual acuity.
Cover test - An exo- and hypo-deviation is present.
Ocular motility - There will be limited elevation, depression and adduction, which may be complete
or partial limitations, depending on the extent of paresis/palsy.
• Always check for the presence of IV nerve function by asking the patient to attempt to
look down and outwards and observe for the presence of incyclo-torsion during this
movement.
• If there’s ptosis, examiner will have to lift it to see eye movements.
• Pupil may be dilated depending on aetiology.
• Check for unilateral and bilateral.
• Extent of limitations, duction versus version.
Convergence - This will be absent if the medial rectus muscle is paralysed.
Binocular function - This is usually absent unless the III nerve paresis is mild and partial.
, Accommodation – Defective accommodation if pupil is involved as the fibres to the ciliary body are
likely to be affected.
Hess chart – Constricted field in affected eye, overaction of muscles in contralateral eye.
Diplopia – Constant diplopia, unless complete ptosis blocks out the diplopic image.
Aberrant regeneration
• Change in the actions of muscles supplied by the third nerve due to regrowth of damaged
nerve fibres following complete or severe third nerve palsy.
• Likely to occur when aetiology is trauma or aneurysm.
• May occur from weeks to months after onset.
• Aberrant regeneration may occur between CN III and CN V.
Generally unexpected things happen such as ptosis (lid) retraction/pupil constriction on attempted
adduction or depression.
Management of CN III palsy
• In children, any associated amblyopia should be treated. Any underlying cause for the lesion
should be investigated and treated.
• As with most conditions affecting the extraocular muscles, it is important to allow a
period for recovery of any muscle function and then wait until stability of this has been
demonstrated.
• Recovery is more common in vascular aetiologies.
• Prisms may be helpful with partial III nerve palsy where there is a small deviation in primary
position that can be joined with prisms. Long-term prisms may be incorporated into a
spectacle correction.
• Occlusion is indicated for diplopia, which cannot be joined by prisms because of a complete
palsy and incomitant ocular motility and where surgery is not (yet) an option. E.g Blanderm,
Bangerter foils, occlusive contact lenses, patch.
• Surgery is indicated to correct the strabismus and any associated ptosis. Squints are
treated initially as the ptosis acts as a mechanical barrier to diplopia and true size of ptosis
is also revealed.
• Adequate bell’s phenomenon is required before ptosis can be repaired.
Surgical options
