anatomy Abducens nerve palsy is the most common ocular motor paralysis. The abducens (sixth) cranial nerve controls the lateral rectus muscle, which abducts the eye. Abducens nerve palsy causes an esotropia due to the unopposed action of the antagonistic medial rectus muscle. The affected eye turns in toward the nose and is unable to abduct properly. The deviation is constant and is usually greater at distance fixation than at near. The esotropia is also worse when the patient is looking toward the affected side.

1. VI th Cranial Nerve Palsy
Dr. Vinit Kumar

3. Abducens ( VI th CN ) nerve palsy
• Abducens nerve palsy is the m/c ocular motor paralysis.
• The abducens (sixth) cranial nerve controls the lateral rectus muscle, which
abducts the eye.
• Abducens nerve palsy causes an esotropia due to the unopposed action of the
antagonistic medial rectus muscle. The affected eye turns in toward the nose
& is unable to abduct properly. The deviation is constant & is usually greater at
distance fixation than at near. The esotropia is also worse when the patient is
looking toward the affected side.

4. Etiology ( Pediatrics )
• Congenital.
• Palsies can occur rare. They can sometimes be associated with birth trauma & with
neurological conditions such as hydrocephalus & cerebral palsy.
• Acquired.
• Acquired VI th CN palsies in childhood can be due to neoplasm, trauma,
inflammation & idiopathic etiologies. Nontraumatic acquired sixth nerve palsies may
be due to benign recurrent sixth nerve palsy, elevated or low intracranial pressure,
or pontine gliomas. Benign isolated abducens nerve palsy can occur in childhood
following ear or throat infections or viral illness.

5. • Trauma, secondary to open or closed head injuries . Trauma causes indirect
pressure on the nerve, to which it is very susceptible to trauma as it passes over
the apex of the petrous temporal bone to the cavernous sinus . In addition,
traumatic abducens nerve palsy can occur secondary to bruising and/or
hemorrhage causing pressure on the nerve.
• Closed head trauma may cause elevated intracranial pressure and secondarily
produce a non-localizing sixth nerve palsy.

6. • Pontine glioma.
• Brainstem gliomas are one of the common tumors seen in the pediatric
population & more than 80% arise from the pons with the peak age of onset
between 5-8 years of age.
• Presenting symptoms include ataxia, disturbance of gait & unilateral or bilateral
abducens nerve palsy.

7. • Elevated or low intracranial pressure = Elevated ICP can cause stretching of the
sixth cranial nerves which are tethered in Dorello’s canal. Their steep course over
the petrous apex & the tethering make the sixth nerve susceptible to injury. The
same mechanism can explain the reason for the non-localizing sixth nerve palsy that
can be seen with either elevated or reduced ICP .
• Elevated ICP can occur secondary to a variety of different causes, including shunt
failure, pseudotumor cerebri, posterior fossa tumors, neurosurgical trauma, venous
sinus thrombosis, meningitis, or Lyme disease

9. • Intracranial tumor , Posterior fossa tumors, such as pontine glioma,
medulloblastoma, ependymoma, or cystic cerebellar astrocytoma can produce
unilateral or bilateral abducens nerve palsies in children.
• Skull base tumors (meningioma, chordoma, nasopharyngeal carcinoma,
metastasis) predominate in the adult population. Abducens nerve palsy can also
present as a postoperative complication after resection of posterior fossa
tumors in the pediatric population .
• Meningitis ( least common cause )

10. In Adults ( etiology )
• Microvascular ischemia.
• Trauma.
• Idiopathic.
• Less likely: Multiple sclerosis.
• Neoplasm.
• Stroke.
• Sarcoidosis/vasculitis.
• Increased intracranial pressure.(ICT)
• Giant cell arteritis.(GCA / Temporal arteritis )

11. Lesions causing abducens nerve palsy are usually classified by
the location of the lesion.
• Fascicular. Demyelination, vascular disease & metastatic tumors are likely causes of
fascicular damage. Lesions in this area can cause Foville’s syndrome (damage to the
pontine tegmentum) which is classified by partial sixth nerve palsy, ipsilateral facial
weakness, loss of taste in the anterior portion of the tongue, ipsilateral Horner’s
syndrome, ipsilateral facial sensory loss & ipsilateral peripheral deafness.

12. • Lesions in the fascicular area can also cause Millard-Gubler syndrome, which is a
result of damage to the ventral pons, is characterized by sixth nerve palsy and
contralateral hemiplegia & may or may not also have ipsilateral facial paralysis .

13. • Peripheral.
• Causes of peripheral nerve damage include closed head injury, compression &
bacterial infection of the inner ear.
• Localized compression can be caused by a primary pituitary tumor,
craniopharyngioma or meningioma. Metastatic tumors & aneurysms involving
the basilar artery can also cause an abducens nerve palsy.

14. Risk Factors
• Inflammatory & microvascular conditions are risk factors for abducens nerve
palsy.
• Other risk factors include multiple sclerosis, encephalitis, meningitis, cavernous
sinus thrombosis, hypertension, hypercholesterolemia, aneurysm, diabetes,
arteriosclerosis & birth trauma.

15. 6th CN anatomy
•

17. 6th CN anatomy ( Brainstem )
• The nucleus of the sixth (abducens or abducent) nerve lies at the mid-level of the
pons, ventral to the floor of the fourth ventricle . The fibres (fasciculus) leave the
brainstem ventrally at the pontomedullary junction. • Nuclear lesion. A nuclear
sixth nerve lesion also causes a failure of horizontal gaze towards the side of the
damage due to involvement of the adjacent horizontal gaze centre (paramedian
pontine reticular formation). Facial (seventh) nerve fibres wrap around the sixth
nerve nucleus, so ipsilateral lower motor neurone (LMN) facial nerve palsy is also
common. Isolated sixth nerve palsy is never nuclear in origin.

18. DIAGNOSIS & HISTORY
• The pattern of onset & associated symptoms can be very important in
determining the etiology of an abducens nerve palsy.
• Sudden onset suggests a vascular etiology…………
• while slowly progressive onset suggests a compressive etiology.
• Subacute onset suggests a demyelinating process.

19. PHYSICAL EXAMINATION
• All patients with 6th CN palsy need a complete ophthalmologic examination, including
visual acuity, binocular function & stereopsis, motility evaluation, strabismus
measurements at near, distance & in the cardinal positions of gaze, measurement of
fusional amplitudes, cycloplegic refraction, & evaluation of ocular structures in the
anterior &posterior segments.
• Precise assessment of ductions & versions, as well as precise orthoptic measurements
in lateral gazes are helpful in determining incomitance associated with abducens nerve
palsy.

20. SIGNS
• Because the greatest motility deficit occurs on attempt to abduct the palsied eye,
palpebral fissure widening upon abduction may be seen with maximal abduction
effort.
• The patient may also present with a head turn toward the affected eye, to keep their
eye opposite the field of gaze of the affected lateral rectus muscle & there by avoid
or minimize diplopia. It is important to differentiate isolated 6th nerve associated
abduction deficit from a gaze palsy or INO as this would localize the lesion to the
nucleus/internuclei of the 6th and 3rd nerve .

21. Symptoms
• Diplopia is the most common symptom.
• Patients will have horizontal uncrossed diplopia which is greater at distance than
at near.
• The diplopia is also worse in the direction of the palsied muscle & gets better in
the contralateral gaze (incomitant). In recent onset palsies, the deviation
measures greater when the paretic eye is fixating and smaller when the
nonparetic eye is fixing (primary and secondary deviations).

22. • In cases of abducens nerve palsy due to raised intracranial pressure, patients may
experience associated symptoms of headache, pain around the eyes, nausea,
vomiting, or tinnitus.
• Low ICP from a CSF leak can also cause abducens palsy & can present with
symptoms of headache & can hence present clinically very similarly to raised ICP.
• MRI brain & orbits can sometimes help distinguish between high or low ICP.

23. • If a patient has a lesion causing the abducens nerve palsy which affects other
structures in the brain, other neurologic signs may be observed.
• If the etiology of the abducens nerve palsy is a brainstem lesion affecting the sixth
cranial nerve fasciculus, there may be associated ipsilateral facial weakness,
contralateral hemiparesis, or sensory abnormalities.
• If the abducens nerve palsy presents together with other ipsilateral cranial nerve
palsies, etiology could be a lesion involving the meninges, superior orbital fissure,
orbital apex, or cavernous sinus.
• Presence of orbital signs or pulse synchronous tinnitus can suggest an
arteriovenous fistula .

24. Clinical Diagnosis
• There is a limitation to abduction in the affected eye.
• Abducens nerve palsy causes an esotropia due to the unopposed action of the
antagonistic medial rectus muscle. The affected eye turns in toward the nose & is
unable to abduct properly.
• The deviation is constant and is usually greater at distance fixation than at near,
& also greater when the patient is looking toward the affected side.

25. Diagnostic Procedures
• There is no universal consensus about diagnostic relevance of MRI in abducens
nerve palsy.
• In general, if unilateral abducens nerve palsy presents acutely, MRI could be
performed, especially if there is no evidence of vasculopathic risk factors.
• Some clinicians may prefer to routinely perform MRI in all patients with abducens
nerve palsy, even with evidence of vasculopathy .

26. • However, according to a 2017 review by Elder et al, the most recent input to the MRI
debate was a 2013 prospective study of 109 patients > 50 years old with isolated
ocular motor neuropathies who received MRI. An etiology other than ischemia was
found in 16.5% of patients, including brainstem infarction, petroclival meningioma, &
cavernous sinus B cell lymphoma .

27. • Due to the possiblility of dangerous diseases presenting with an isolated cranial
motor neuropathy, the authors recommended MR imaging even if a microvascular
cause is suspected.
• The authors stress that high-resolution brain & orbital MRI with gadolinium, fat
suppression,& thin coronal & axial cuts through the orbits are necessary, as sixth
nerve palsy mimics (e.g. thyroid eye disease) may be missed by a standard MRI brain

28. Lab investigations
• Complete blood cell (CBC) count
• Glucose levels
• Glycosylated hemoglobin (HbA1C)
• Erythrocyte sedimentation rate and/or C-reactive protein
• Fluorescent treponemal antibody-absorption test, VDRL or RPR
• Lyme titer
• Glucose tolerance test
• Antinuclear antibody test
• Rheumatoid Factor test

29. • MRI could be performed for the following:
• Patients younger than 45 years
• Associated pain or other neurologic abnormality
• History of cancer
• Bilateral sixth nerve palsy
• Papilledema
• If no marked improvement is seen or other nerves become involved
• An LP can be considered if MRI results are negative.

30. D/D of 6th CN palsy
• Duane’s retraction syndrome (Types 1 and 3), congenital esotropia, thyroid eye
disease (TED) spasm of the near reflex, longstanding esotropia with medial rectus
contracture, ocular neuromyotonia, & lateral rectus myositis.
• An abduction deficit can be produced by orbital disease, such as a blowout fracture
with entrapment of the medial rectus muscle, or by neuromuscular disease such as
ocular myasthenia gravis or Miller-Fisher syndrome..

31. • Clinical assessment for orbital, neuromuscular, & brainstem disease is the first
step in evaluation for this condition, and after this, an abducens nerve palsy can
be diagnosed by exclusion .

32. Diagnostic syndrome associated with 6th CN palsy
• Millard Gubler ( ventral pontine ) syndrome
• Raymond syndrome
• Foville (inferior medial pontine) syndrome
• Acoustic neuroma (C-P angle tumor )
• Nasopharyngeal tumours
• Raised ICT
• Basal skull fracture
• Gradenigo syndrome / mastoiditis / petrositis .
• Superior orbital fissure synd., orbital apex syndrome , tolasa hunt
Fascicular Nucleus
Basilar lesion
Intercavernous &
intraorbital

33. • Millard–Gubler (ventral pontine) syndrome involves the fasciculus as it passes
through the pyramidal tract & is most frequently caused by vascular disease,
tumours or demyelination.
• As well as ipsilateral sixth nerve palsy, there is contralateral hemiplegia & often
an ipsilateral LMN facial nerve palsy.

34. • Foville (inferior medial pontine) syndrome is most frequently caused by vascular
disease or tumours involving the dorsal pons. It is characterized by ipsilateral
involvement of the fifth to eighth cranial nerves, central sympathetic fibres
(Horner syndrome) & horizontal gaze palsy.

35. • Nuclear lesion.
• A nuclear sixth nerve lesion also causes a failure of horizontal gaze towards the
side of the damage due to involvement of the adjacent horizontal gaze centre
(paramedian pontine reticular formation).
• Facial (seventh) nerve fibres wrap around the sixth nerve nucleus, so ipsilateral
lower motor neurone (LMN) facial nerve palsy is also common.
• Isolated sixth nerve palsy is never nuclear in origin.

36. Basilar part of 6th CN
• The basilar part of the nerve enters the prepontine basilar cistern, passes upwards
close to the base of the skull & is crossed by the anterior inferior cerebellar artery .
• It pierces the dura below the posterior clinoids & angles forwards over the tip of the
petrous bone, passing through or around the inferior petrosal sinus, through the
Dorello canal (underneath the petroclinoid ligament), to enter the cavernous sinus.

38. • An acoustic neuroma may damage the sixth nerve at the pontomedullary junction
the first symptom of an acoustic neuroma is hearing loss, and the first sign
diminished corneal sensitivity. Hearing & corneal sensation should be checked in
each patient of 6th CN palsy .

39. • Nasopharyngeal tumours may invade the skull & its foramina & damage the
nerve during its basilar course.
• • Raised intracranial pressure may cause a downward displacement of the
brainstem. This may stretch one or both sixth nerves over the petrous tip
• • Basal skull fracture ( may cause uni or bilateral palsy )

40. • Gradenigo syndrome, most frequently caused by mastoiditis or acute petrositis,
may result in damage of the sixth nerve at the petrous tip. The latter is frequently
accompanied by facial weakness and pain, and hearing difficulties.

41. intercavernous & intraorbital part
• The intracavernous section runs below the third & fourth & the first division of the
fifth nerves.
• The sixth nerve is the most medially situated & runs through the middle of the sinus
in close relation to the internal carotid artery.
• Occasionally, intracavernous sixth nerve palsy is accompanied by a postganglionic
Horner syndrome due to damage to the paracarotid sympathetic plexus .

42. Intraorbital part
• The intraorbital part enters the orbit through the superior orbital fissure within
the annulus of Zinn to innervate the lateral rectus

43. Management ( general t/t)
• Treatment depends on etiology of the abducens nerve palsy.
• In general, underlying or systemic conditions are treated primarily.
• Most patients with a microvascular abducens nerve palsy are simply observed &
usually recover within 3-6 months.
• Treatment for the diplopia associated with abducens nerve palsy can be managed
with prisms, occlusion, botulinum toxin, or surgery .

44. • Occlusion using Bangerter filter or pirate patch can eliminate diplopia and confusion,
prevent amblyopia or suppression in younger patients, and decrease the possibility of
ipsilateral medial rectus contracture. Base-out Fresnel prisms can be used to help the
patient maintain binocular single vision in the primary position, but are not usually
useful due to the incomitance of the deviation.

45. • Botulinum toxin injections to the medial rectus of the affected eye are sometimes
used to prevent secondary contraction of the medial rectus, or during
transposition procedures to weaken the non-operative muscle.
• In general, surgical intervention is reserved for patients who have had stable
orthoptic measurements for at least 3-6 months.

46. Bangerter filter or pirate patch

47. Surgery
• Strabismus surgery can be performed for persistent abducens nerve palsies that
demonstrate stable measurements over a 6 month period.
• Forced duction test is performed in the office or in the operating room in order
to assist with surgical planning.
• Often, a resection of the affected lateral rectus & recession of the ipsilateral
medial rectus (recess/resect or “R and R” procedure) is performed.
• Alternatively, a resection of the affected lateral rectus with a recession of the
contralateral medial rectus may be performed.

48. • Various forms of transposition surgeries can be considered (e.g., Jensen,
Hummelsheim, Augmented Hummelsheim with resections +/- Foster
modifications, Knapp's procedure).
• Botulism toxin can also be used as a temporizing treatment.

49. post surgery follow up
• Patients may be managed closely postoperatively, and any residual or intractable
diplopia can be managed with prisms.
• Complications
• The most likely complication following surgical correction of abducens nerve
palsy is the risk of over- or under-correction, which can be managed
postoperatively with prisms.
• The prognosis for sixth nerve palsy depends on the underlying etiology

50. in summary (management of 6th CN palsy)
• Clinicoinvestigative work up & T/T of cause
• Careful history : antecedent infection,head trauma
• Child <16 yrs with no neurological sign & symptoms : no work up is required , close
follow up every 2 weeks initially then monthly required
• 16 to 40 yrs : risk factors should be ruled out
• > 40 yrs – look for vascular cause like DM/HTN/Atherosclerosis etc
• > 55 yrs – GCA / temporal arteritis ruled out.
• Haematological : BSL (F/PP),ESR,CBC,ANA,FTA Titre )
• Lumbar puncture for raised ICT
• Orbtal USG : for TAO / thyroid /fibrosis of EOMs
• binocular diplopia charting.

51. • Neuroimaging : indication : in presence of multiple cranial nerve palsy & in
younger pt. without muscular cause with neurophysician consultation .
• CONSERVATIVE MEASURES : wait + watch for 6-8 months for self improvement
• Vitamin B complex – acts as neurotonic
• Systemic steroids – hasten recovery in non specific inflammation
• Prevent diplopia & amblyopia in children & preserve BSV
• Patching /occlusion : in case of mild esodeviation & residual LR function intact, occlusion of
unaffected eye is adviced to stimulate fixation with affected eye in Abduction & relaxation of ipsilateral MR to
prevent contracture of MR

52. • Fresnel press on prism useful to correct diplopia
• BOTOX : in to antagonist MR causes paralysis of MR & eye will be in primary gaze
(effect lst for 2-3 months)
• Spontaneous recovery of 6th CN palsy ocures in idiopathic cases ( so progress is
determined by Hess screen )
• SURGICAL INDICATION :
• When spontaneous recovery not ocure after 6 months /more
• To correct incomitant esotropia
• Improve abduction
• Provide BSV
• Eliminate AHP

53. 1. Recess – resect operation - a supra maximal 12-16 mm recession of the antagonist
MR with about 8-10 mm resection of LR is often successful first operation in most pt.
with incomplete palsy. (eliminate AHP & maintain BSV ) . In case mild paresis still
present , weaking of contralateral MR with or without Faden procedure consider as
second operation. Adjustable suture surg. Help ful for final adjustment .
2. Muscle transposition procedures : for complete LR palsy (FDT to rule out MR contracture )
3. Jensens procedure combined with MR recession : the SR ,IR & paralysed LR muscle
are split for 8-10 mm from their insertion backward with the help of muscle hook.
Then superior half of LR is united with lateral half of SR & inferior half of LR with the lateral half of IR
with non absorbable suture ( 5-0 mersilene ) & knot should be tied near equator .

56. 4. Hummelscheim operation
• After splitting of SR & IR their lateral halves are disinserted & sutured to tendon of LR
muscle ( this operation rarely done now days ) mainly of historical interest .
• 5 . BERENS & GIRARD PROCEDURE : in this operation the full SR & IR tendon are
disinserted & sutured with tendon of LR at its insertion. This procedure combines
with recession of MR is recommended by Von Noorden in children with complete
paralysis of 6th CN palsy .

59. 6. Carlson & Jampolsky transposition procedure
• MR muscle spared . After splitting of verical recti their temporal halves are inserted
under the LR . It is essential to separate the halves of vertical recti to the deepest
point towards the apex of orbit allowing the transposed parts of vertical recti to
slide towards the LR, which also minimizes vertical deviations. This procedure
reduces the angle of deviation below 10PD improve abduction , prevent relapses &
also prevents anterior segment ischemia.

61. 7. Superior rectus transposition with MR recession
• This procedure is successfully tried in LR palsy & also in abduction deficit condition
like Duanes retraction syndrome & Mobius syndrome , especially if hypertropia is
also associated.
• Limitation of this procedure is = it induces vertical deviation .
• 8. contralateral MR recession with or without Faden operation can be considered an
option for residual LR abduction deficit or residual esotropia .