1) LR palsy is caused by infections, trauma, neoplasms, systemic disorders or neurological disorders and affects the 6th cranial nerve that controls lateral eye movement. 2) Clinical features include esotropia that is worse for distance vision, limited abduction of the affected eye, and compensatory head turning. 3) Evaluation includes assessing eye alignment, diplopia, and ruling out underlying causes by reviewing medical history and performing examinations of other cranial nerves and neurological function.

1. LR PALSY
DR.ANISHA RATHOD
MS,FPOS
(PEDIATRIC OPHTHALMOLOGY AND

2. FINANCIAL DISCLOSURE
• THE AUTHOR HAS NO FINANCIAL INTEREST IN THE SUBJECT
MATTER BEING PRESENTED

3. ETIOLOGY
• Infections
• Trauma
• Neoplasm
• Systemic disorders
• Neurologic disorders
Route of the sixth nerve from the pons to the lateral rectus
Anatomy of nerve VI
Nucleus + caudal portion of pontine tegmentum beneath floor 4th ventricle
VII fibers loop around VI MLF passes medial of VI , Medial longitudinal fasciculus (
conjugate horizontal gaze)

4. CONGENITAL 6 TH NERVE PALSY
• Esotropia at 6-8 weeks of life
• Sequelae of perinatal cranial trauma
• Two types-
• Neonatal esotropia with unilateral abduction deficit-Resolves in 1st month of life
• Second is without obvious abduction deficit

5. FUNCTIONAL COMPONENT
• Somatic efferent-Lateral movement
• General somatic afferent-proprioreceptive impulses from LR muscle-reach
mesencephalic nucleus of trigeminal nerve

6. NUCLEUS
• Mid level of pons-ventral to floor of 4 th ventricle-horizontal gaze centre.
• Fasciculus of 7th nerve lies around abducent nerve +produces elevation of floor of 4th
ventricle. Hence isolated 6 th nerve palsy never nuclear in origin

7. THE FORAMINA ROTUNDUM AND OVALE- LOCATED THE FLOOR OF THE MIDDLE CRANIAL
FOSSA.
THE PETROCLINOID LIGAMENT EXTENDS, AT AN ANGLE OF APPROXIMATELY 30
DEGREES, FROM THE MEDIAL THIRD OF THE PETROUS RIDGE TO THE POSTERIOR
CLINOID.
IT THEREBY CREATES THE COMPARTMENT (DORELLO’S CANAL) THROUGH WHICH THE
ABDUCENS NERVE TRAVELS

8. NUCLEUS
• Two types of cells-large and small
• Large-Fibres give rise to abducent nerve
• Small-Fibres relay in oculomotor nucleus via medial longitudinal
fasciculus

9. CONNECTIONS OF NUCLEUS
1.Cerebral cortex
• Motor gyrus-(Precentral gyrus)-Afferent corticonuclear fibres from both cerebral
hemispheres
• Visual cortex-Superior colliculus and tactobulbar tract
• Frontal cortex(Frontal eye fields)
2.Nuclei of 3,4,8th nerve via medial longitudinal bundle
3.Pretectal nucleus
4.Horizontal gaze centra(paramedian pontine reticular formation) through medial
longitudinal bundle
5.Cerebellum through vestibular tract

10. CLINICAL FEATURES
• Ipsilateral weakness of abduction
• Failure of horizontal gaze towards side of lesion
• Ipsilateral lower motor neuron facial nerve palsy caused by comittant involvement of
facial nucleus

11. FASCICULUS
• Passes ventrally upto ponto medullary junction
• Efferent fibres start via medial lemiscus and pyramidal tract
• 7-8 rootlets arise from pons and medulla lateral to pyramidal prominenece of medulla
• Rootlets join to form one nerve

12. FOVILLE SYNDROME
• Involves fasciculus
• Caused by vascular disease/tumours involving dorsal pons
• Ipsilateral involvement of 5-8th cranial nerves and central sympathetic fibres
• 5 nerve-facial anaesthesia
• 6 nerve palsy with gaze palsy
• 7 th nerve(nuclear/fascicular damage)-facial weakness
• 8 nerve-deafness
• Central Horner syndrome

13. MILLARD GUBLER SYNDROME
• Involves fasciculus via pyramidal
tract
• Vascular
disease/tumours/demyelination
• Ipsilateral 6 th nerve palsy
• Contralateral hemiplegia

14. BASILAR
• Prepontine basilar cistern
• Passes upwards close to base of the
skull
• Crossed by anterior inferior cerebral
artery
• Pierces of dura 1 cm below posterior
clinoids(the crest of petrous bone) ,
• Angles forward on tip of petrous bone
• Around inferior petrosal sinus via Dorello

15. ACOUSTIC NEUROMA
• Damage at pontomedulaary junction
• First symptom-hearing loss,
• Sign-Diminished corneal sensitivity

16. RAISED ICT
• Downward displacement of
brainstem
• Stretch 6 th nerve over petrous
tip from brainstem to point of
entry at cavernous sinus
• In this case 6 th nerve-false
localising sign

17. BASAL SKULL FRACTURE
May damage petrous segment of abducent segment-penetration of dura and
passed beneath the petroclinoid ligament

18. GRADENIGO SYNDROME
• Mastoiditis/acute petrositis at petrous tip
• Acute petrositis associated with facial weakness ,pain and hearing difficulties.
• In 1904 the syndrome was introduced by Giuseppe Gradenigo described as a
constellation of sixth nerve palsy,
• ipsilateral decreased hearing (VIII nerve involvement),
• ipsilateral facial pain in distribution of cranial nerve V
• ipsilateral facial paralysis (VII nerve involvement).

19. PSEUDO-GRADENIGO’S SYNDROME
• Hearing deficits +sixth nerve palsy+trigeminal symptoms may be due to brianstem
lesions, such as cerebello-pontine angle tumor.
• Nasopharyngeal carcinoma may also mimic Gradenigo’s syndrome, since it can
obstruct the Eustachian tube, resulting in serous otitis media.
• The carcinoma may subsequently invade the cavernous sinus, causing sixth nerve
paresis.

20. INTRACAVERNOUS AND INTRAORBITAL
• Intracavernous
• Runs below 3,4th nerve+1 st division of 5th.
• 6th nerve located most medially and through middle of sinus in close relation to
ICA(hence more prone to damage)
• 6 th nerve palsy+ postganglionic Horner syndrome(Parkinson sign) as
intracavernous course of 6th nerve by sympathetic branches from paracarotid plexus
• Intraorbital-enters through superior orbital fissure with Annulus of Zinn

21. THE COMPOSITE DIAGRAM CAN BE DIVIDED
INTO THE FIVE SECTIONS THAT MAY AID IN
DETERMINING THE DIAGNOSIS OF SIXTH
NERVE PALSY:12
VI1: THE BRAINSTEM SYNDROME
VI2: THE ELEVATED INTRACRANIAL
PRESSURE SYNDROME
VI3: THE PETROUS APEX SYNDROME
VI4: THE CAVERNOUS SINUS SYNDROME
VI5: THE ORBITAL SYNDROME

22. BRAINSTEM SYNDROME
• Lesion in the posterior
fossa(compressive, ischemic,
inflammatory)
• Most commonly multiple sclerosis in
young adults) or degenerative
• May involve the fifth, seventh and
eighth cranial nerves+pyramidal
tract(anterior aspect of the pons and
the cerebellum )behind .
• Cross-sectional diagram of the lower pons the
central neuron of oculosympathetic pathway, the
spinal tract of five cranial nerves, the medial

23. INFLAMMATORY
• Viral infections-bilateral sixth nerve palsy, impaired adduction and vertical movements-
diffuse ophthalmoplegia
• Areflexia, distal parathesias, CSF albuminocytologic dissociation(Mild form of Millard
Fischer)
• Abducent nerve more susceptible to ANTI GQ1IgG antibody than other cranial nerves
and bilateral abducent nerve palsy is characteristic.
• Anti GQ1b detected in Miller Fischer, Bickerstaff’s brainstem encephalitis , Guillian
Barre syndrome with Ophthalmoparesis .
• Bilateral 6 th nerve palsy+ Mild neurologic symptoms=Atypical Miller Fischer syndrome
• Above syndrome can cause ataxia in absence of ophthalmoplegia

24. ELEVATED INTRACRANIAL PRESSURE
SYNDROME
• Subarachnoid space syndrome
• The second syndrome of the sixth nerve corresponds to the vertical course of the nerve as it
ascends the clivus and turns 90 degrees anteriorly to enter Dorello’s canal
• Lesions located elsewhere intracranially can secondarily affect the sixth nerve; (poor localizing
value of a sixth nerve palsy.)
• Changes in intracranial pressure (ICP) increased or decreased - result in downward
displacement of the brainstem causing stretching of the sixth nerve as its exits the pons and
inside Dorello’s canal.

25. ELEVATED INTRACRANIAL PRESSURE
SYNDROME
• Approximately 30% of patients with pseudotumor cerebri have sixth nerve paresis as
the only neurologic deficit, (papilledema,concomitant visual field changes that result in
blind spot enlargement).
• Normal or small-sized ventricles are often present on magnetic resonance imaging.
• Other pathologies in the subarachnoid space - hemorrhage, meningeal or
parameningeal infections (viral, bacterial, fungal), inflammation (sarcoidosis) or
infiltrations (lymphoma, leukemia, carcinoma

26. PETROUS APEX SYNDROME
• Contact with the tip of the petrous pyramid makes the portion of the sixth nerve within Dorello’s canal
susceptible to pathologic processes.
• Important in cases secondary to localized inflammations or extra-dural abscesses due to complicated
otitis media.
• Cerebellopontine angle (especially acoustic neuroma or meningioma) may involve the sixth and other
contiguous cranial nerves, cause decreased hearing with vestibular symptoms, and decrease corneal
sensitivity that can imitate the petrous apex syndrome.

27. • Chiari 1 malformation causes bilateral palsy
• Chiari malformation is associated with pseudotumour cerebri
• Hence in cases of non resolving papilloedema after successful treatment, this
malformation to be ruled out.

28. NASOPHARYNGEAL TUMOURS
• Invade foramen and damage basilar course

29. CAVERNOUS SINUS SYNDROME (CSS)
• The course of the sixth nerve through the cavernous sinus associates it with third,
fourth and fifth (ophthalmic and maxillary divisions) cranial nerves as well as the
internal carotid artery and the carotid sympathetic plexus.
• The cavernous sinus syndrome may consist of deficits of two or more of these
structures.
• The pituitary gland, optic nerve, and chiasm may also become affected.

30. INTRA CAVERNOUS INTERNAL CAROTID ARTERY
ANEURYSM
• The prominent, tortuous course of the internal carotid artery in the cavernous
sinus The sixth and third cranial nerves are most vulnerable
• Schrader1 found no case of aneurysm in 104 patients with isolated sixth nerve
palsy.
• Locksley28, reported that out of 2,695 cases of single aneurysms (ruptured and
unruptured) only 50 (1.9%) were located in the intracavernous portion of the

31. CAROTID-CAVERNOUS FISTULA (CCF)
• A defect of the internal carotid artery within the cavernous
sinus will result in arterialization of the sinus, and of the
orbital and ocular veins-result in the following signs and
symptoms:
• pain,
• proptosis,
• bruit,
• ocular pulsation, red eye,
• chemosis and tearing,
• double vision and decreased vision.

32. TOLOSA -HUNT SYNDROME
• Tolosa-Hunt syndrome is an idiopathic, sterile inflammation that primarily affects the
anterior portion of the cavernous sinus.
• “Painful ophthalmoplegia”.
• Trauma, syphilitic periostitis,neoplasms in the superior orbital fissure.
• Orbital pain, ipsilateral involvement of 2nd through 6th cranial nerves, oculosympathetic
palsy (Horner syndrome).
• Spontaneous remission occurs after some days or weeks
• Response to corticosteroid therapy is good.

33. MENINGIOMA
• Located along the medial aspect of the sphenoid ridge, the anterior clinoid process/
tuberculum sellae.
• Exophthalmos and visual loss
• Visual field defects such as bitemporal hemianopia,
• Monocular blindness
• Upper-temporal field defects in the other eye (junctional scotoma).

34. ORBITAL SYNDROME OF THE SIXTH NERVE
• Proptosis is an early sign of the orbital syndrome and is frequently accompanied by
congestion of conjunctival vessels and conjunctival chemosis.
• Optic atrophy or papilledema.
• Difficult to distinguish cranial nerve (III, IV and VI) + mechanical displacement of the
globe.
• Horner syndrome may be present, but the ptosis may not be recognized because of
proptosis.

35. BENIGN RECURRENT SIXTH NERVE PALSY
• Viral illness/immunisation
• Acute onset
• Complete absence of abduction
• Antecedant febrile viral illness
• Absence of cranial nerve dysfunction
• Absence of signs of raised ICT
• Repeat Neuroimaging if negative in incomplete resolution to rule out pontine
gliomas s/o symmetrical expansion of pons

36. PONTINE GLIOMA
5-8 years of age
• 80% from pons
• Gait disturbance,6,7th nerve palsy, headaches,nausea,vomiting
• Large tumours elevate floor of 4 th ventricle-Obstructive hydrocephalus
• Intact sensory and motor fusion
• Facial palsy, trigeminal deficits, palsies of cranial nerves 9 and 10
• Differential diagnosis of bilateral 6 th nerve palsies with thickened pons-
• MS,Brainstem vascular malformation,
• Bickerstaff’s brainstem encephalitis,
• Tuberculoma,
• Cysticercosis,
• AIDS

37. • Mechanism of injury-Direct infiltration of pons and elevation of ICP(with/without
hydrocephalus)
• Posterior fossa tumour resection cause 6 th nerve palsy.
• Associated trigeminal dysfunction dysfunction suggests space occupying lesion.
• Vincristine therapy for leukaemia-Unilateral 6 th nerve palsy

38. RARE CAUSES
• Ophthalmolegic migraine
• Infantile botulism-bilateral 6 th nerve palsy
• Ectasy abuse-Transient bilateral 6 th nerve palsy
• Hydrocephalus-shunting procedures/lumbar puncture(caudal displacement of brain after
loss of CSF support in basal cisterns)
• Abducent more susceptible to traction as it changes direction at petrous ridge to pass
forward under petroclinoid ligament

39. ISOLATED SIXTH NERVE PALSY SYNDROME
• Lateral rectus weakness and no data to implicate a specific etiology, is categorized as
“isolated sixth nerve palsy”.
• Vascular risk factors such as diabetes mellitus, hypertension or history of a recent
viral infection.
• Benign, remitting palsies occur in children however, and may be recurrent .
• The main purpose in a case of isolated six nerve palsy is to ensure that signs and
symptoms of the other five syndromes have been assessed and ruled out.

40. • Eye involved-uniocular/binocular
• Direction of deviation-constant/intermittent
• Mode of onset-sudden/gradual
• Double vision
• Precipitating factors
• Duration
• Type of deviation,photophobia,asthenopia,prior
treatment
• Medical History,
HISTORY

41. EVALUATION

42. CLINICAL FEATURES
• Esodeviation greater for distance than near
• Greater on fixation with paretic eye
• Infants and children may appear to have gaze palsy-as they avoid
looking in diplopic field

43. LONG STANDING LEFT 6 TH NERVE PALSY
• Left esotropia in primary position due to unopposed action of left medial rectus
• Deviation worst for distant target and less for near
• Marked limitation of abduction to left
• Normal left adduction
• Compensatory face turn into field of action of paralysed muscle to left to minimise
diplopia

45. COVER TEST

46. DIPLOPIA PRINCIPLE

47. DIPLOPIA CHARTING

48. RECOVERY
• Spontaneous recovery from acute sixth nerve palsy depends on its cause.
• Infectious,vascular (diabetic, hypertensive, atherosclerotic)/ idiopathic sixth nerve
palsy recover.
• Tumor, anatomic abnormality, trauma, or underlying neurologic disease-remission
less likely.

49. • Overall,20% to 50% of patients fail to recover from acute sixth nerve palsy.
• Mean recovery times range from 2.4 to 5.4 months.
• A third of patients recover within the first 2months, and 94% recover by 6 months
• Esotropia may persist despite full recovery of abduction –residual imbalance in ratio of
phasic to tonic LR innervation -secondary medial rectus contracture/decompression
preeexisting esophoria.
• Small palsies unleash small hyperphorias-persist with head tilt to either side –
peripheral lesions and switch with head tilt to either side of central lesions

50. RECURRENCE
• Recurrences of sixth nerve palsy may occur more than once and have been reported in both children
and adults.
• They are usually painless and occur on the same side.
• Increased susceptibility of the sixth nerve once it has been exposed to inflammation.
• An aberrant antero inferior cerebellar artery may intermittently constrict the abducens nerve.
• Childhood ophthalmoplegic migraine may also be associated with recurrent palsy.
• Intervals between episodes range -1 week to 12 years.

51. D/D UNILATERAL PALSY
• Congenital absence of lateral rectus
• Congenital fibrosis
• Duane syndrome, types I and III
• Lost lateral rectus
• Scarring and restriction on the medial aspect of globe
• Tight medial rectus
• Graves Ophthalmopathy
• Medial orbital wall fracture
• High myopia with restriction
• Neurologic Disorders
• Myasthenia gravis
• Inflammatory orbital disease

52. D/D BILATERAL PALSY
• Convergence spasm.
• Divergence palsy
• Graves Ophthalmopathy
• Bilateral high myopia with compression or restriction
• Horizontal gaze palsy.
• Infantile esotropia

53. LABORATORY DIAGNOSIS
• Complete blood cell (CBC) count
• Glucose levels
• (HbA1C)
• Erythrocyte sedimentation rate /CRP
• Fluorescent treponemal antibody-
absorption test, VDRL
• Lyme titer
• Glucose tolerance test
• Antinuclear antibody test
• Rheumatoid Factor test
•MRI :
•Associated pain or other
neurologic abnormality
•History of malignancy
•Bilateral sixth nerve palsy
•Papilledema
•Patients younger than 55 years
with no vasculopathic history
•No marked improvement or other
nerves become involved
•An LP considered if MRI results
are negative.

54. NON SURGICAL MANAGEMENT
• Alternate occlusion to prevent secondary contracture of the MR may be tried.
• Patching also relieves diplopia.
• Occlusion of the good eye may lead to disorientation and vertigo.
• For small deviations, Fresnel add-on prisms may be given and reduced as the sixth
nerve palsy
• improves.
• Vision may be blurred by the prisms
• Prisms are rarely useful due to horizontal incomitancy

55. • In adults with acute sixth nerve palsy, intervention- preventing secondary contracture
of the antagonist MR muscle ,creating a area of single binocular vision during the
recovery period.
• If involvement is total, some surgeons may elect to use botulinum toxin as early as 2
weeks.
• If a child loses binocularity and is not recovering sixth nerve function,
chemodenervation of the antagonist MR may help to rapidly restore binocularity.

56. CLINICAL ESTIMATION
• Measurement of saccadic velocity
• Forced duction test
• Forced generation test
• Floating saccade-adduction to primary gaze-Complete sixth nerve palsy
• Absent muscle function-OKN sluggish response-drum rotation temporal to nasal
viewing in adduction

57. SURGICAL MANAGEMENT
• Surgical Strategies for Sixth Nerve Palsy
• Partial Sixth Nerve Palsy
• Medial rectus (MR) recession
• Lateral rectus (LR) resection
• MR recession and LR resection (R & R)
• R & R and contralateral MR recession
• Total Sixth Nerve Palsy
• Partial vertical rectus transposition + MR weakening
• (botulinum toxin or recession)
• Full tendon vertical rectus transposition + MR weakening
• Rectus muscle union + MR weakening

58. COMPLICATIONS
• Induced Vertical Deviation
• Overcorrection
• Undercorrection
• Anterior Segment Ischemia(Microdiisection of anterior ciliary vessels of
vertical recti prior to transposition reduced risk of anterior segment
ischaemia)

59. DIFFERENTIAL DIAGNOSIS
• MYASTHENIA GRAVIS
• RESTRICTED THYROID
MYOPATHY
• MEDIAL ORBITAL BLOW OUT #
• ORBITAL MYOSITIS
• DUANE SYNDROME
• CONVERGENCE SPASM
• DIVERGENCE PARALYSIS
• EARLY ONSET ESOTROPIA

60. THANK YOU