In brief the applied anatomy of abducent nerve

1. ABDUCENT NERVE
DR. Nirmal Jayadev
Final year PG student (MS Ophthalmology)
MKCG Medical College
Berhampur
Odisha

2. INTRODUCTION

4. NUCLEUS
• Situated near the midline
in the tegmentum of the
pons ventral to the
colliculus facialis
• colliculus facialis is an
elevation in the floor of
the 4th ventricle ,
produced by the genu of
facial . N

6. The medial longitudinal bundle is
ventromedial
• Partly intermingled with these larger neurons
are more numerous small multipolar cells
which form the so-called nucleus para
abducens

7. CONNECTIONS
ABDUCENT
NERVE NUCLEUS
MEDIAL
LONGITUDINAL
BUNDLE
OCULOMOTOR
NUCLEUS
TROCHLEAR
NUCLEUS
VESTIBULAR
NUCLEUS

8. PARA PONTINE RETICULAR
FORMATION (PPRF)
• The gaze motor command involves specialized
areas of the reticular formation of the brain
stem which receive a variety of supra nuclear
inputs.
The main region for horizontal gaze is the
paramedian pontine reticular formation
(PPRF)

10. PPRF
IPSILATERAL
ABDUCENT
NUCLEUS
MLF
CONTRALATERAL
OCULOMOTOR
NERVE

11. ANATOMICAL LANDMARKS

12. SUPERFICIAL EMERGENCE
• Emerges between lower
border of the pons &
lateral part of the
pyramid
• Emerge as seven or
eight rootlets

13. COURSE
• Passes upwards & anterolaterally in
subarachnoid space of posterior cranial fossa
• Pierces the arachnoid & dura lateral to the
dorsum sellae

14. • Ascends between the layers of dura on the
posterior surface of the petrous bone near its
apex
• Turns anteriorly to traverse the cavernous
sinus

15. • Enters the orbit through the superior orbital
fissure within the annular tendon to supply
the lateral rectus muscle

16. COURSE OF ABDUCENT. N

17. RELATIONS OF ABDUCENT .N

18. 1.AT EMERGENCE
• Abducent nerves are
about 1 cm apart
Between them is the
Basilary . A at its
formation from the 2
vertebral . A
• Lateral to each abducent
is the emergence of the
facial. N at the lateral
side of the olive

19. 2.POSTERIOR CRANIAL FOSSA
Just after its emergence , the nerve is crossed
by the ANTERIOR INFERIOR CEREBELLAR. A
• Usually the artery is ventral , but it may be
dorsal or pass between the abducent rootlets.

20. • Sleeved by the piamater
, it ascends
anterolaterally in the
cisterna pontis of the
subarachnoid space
between pons &
occipital bone

23. • At the upper border of the bone, it turns forward
at a right – angle under the Petro sphenoidal
ligament ( Gruber’s ligament )
• Thus passing through a canal called the Dorello’s
canal – to enter the cavernous sinus with the
inferior petrosal sinus
• Often the nerve pierces the inferior sinus,
entering the cavernous sinus within the inferior
petrosal sinus

26. 3.CAVERNOUS SINUS
• Here the nerve
lies within the
cavernous sinus

27. Nerve is inferolateral to the horizontal portion
of the internal carotid artery with its
sympathetic plexus , which may communicate
with the nerve

28. • In the lateral wall of the
sinus , in descending
order are
• Oculomotor .N
• Trochlear . N
• Ophthalmic. N
• Maxillary. N
 Abducent .N is usually in
the sinus, with a separate
sheath

29. 4.SUPERIOR ORBITAL FISSURE
 Traverses the fissure
within the annulus of
Zinn
• At 1st below the division
of oculomotor.N
• Then between them &
lateral to nasociliary
nerve

30. 5.IN THE ORBIT
• Nerve divides into 3 or
4 filaments which enter
the ocular surface of
lateral rectus muscle
behind its midpoint

31. CLINICAL ASPECTS
LESIONSAT NUCLEUS
AT FASCICULUS
PONTOMEDULLARY
JUNCTION
BASILAR
COURSE
IN
CAVERNOUS
SINUS

32. 1. At the level of nucleus
• ipsilateral weakness of
abduction
• failure of horizontal
gaze towards the side of
lesion
• ipsilateral LMN palsy of
facial nerve

33. AN ISOLATED 6TH NERVE PALSY IS THEREFORE
NEVER NUCLEAR IN ORIGIN

34. 2.PONTINE SYNDROMES – AT THE
LEVEL OF FASCICULUS
M
•MILLARD GUBLER SYNDROME
R
•RAYMOND CESTON SYNDROME
F
•FOVILLE SYNDROME

35. A. Foville syndrome
 Involves fasciculus as it
passes through PPRF
 5th nerve – facial
anaesthesia
 6th nerve + gaze palsy
 7th nerve – facial
weakness
 8th nerve - deafness

36. B. Millard – Gubler syndrome
 Involves fasciculus as it
passes through the
pyramidal tract
 Ipsilateral 6th nerve
palsy
 Contralateral
hemiplegia

37. C. Raymond – Ceston syndrome
Due to tumor of cerebral peduncles
Red nucleus – speech & gait disorder
Paralysis of lateral conjugate gaze
Ipsilateral 6th N palsy
5th nerve – facial anaesthesia
Contralateral hemiparesis

38. 3. At the pontomedullary junction:
 ACOUSTIC NEUROMA:
• 1ST symptom – hearing
loss
• 1st sign - ↓ corneal
sensitivity

39. It is very important to test hearing &
corneal sensation in all patients with
6th nerve palsy

40. 4. In the basilar course
 A. ↑ intracranial
tension:
• - downward
displacement of
brainstem
• - stretching of 6th nerve
over petrous tip
• b/l 6th nerve palsy –
false localizing sign

41.  B. nasopharyngeal
tumors
 C. base of skull fractures

42.  D. Gradenigo’s
syndrome:
• Mastoiditis/Petrositis
• - damage to 6th nerve at
the Dorello’s canal
• Facial weakness
• Pain
• Hearing difficulties

43. 5. INTRACAVERNOUS PART
• Situated close to the
internal carotid A
• More prone to damage
than other cranial
nerves
 Intra cavernous 6th
nerve palsy is
accompanied by a
postganglionic Horner’s
syndrome

44. CLINICAL PRESENTATION
• HISTORY:
– Esotropia
– Head-turn
– Binocular diplopia (worse at distance)
– Vision loss
– Pain
– Hearing loss
– Symptoms of vasculitis, particularly giant cell arteritis
– Trauma

45. PHYSICAL FINDINGS
• An eso deviation that ↑
on ipsilateral gaze
• An isolated abduction
deficit
• Slowed ipsilateral
saccades
• Papilloedema
• Nystagmus
• Otitis media
• Orbital wall fracture
• Tender , non pulsatile
temporal arteries

46. CAUSES OF 6TH NERVE PALSY
ELEVATED INTRACRANIAL
TENSION
NEOPLASM
SUBARACHNOID SPACE
LESIONS
CONGENITAL ABSENCE
VASCULAR TRAUMATIC
METABOLIC POST LUMBAR TAP
DEMYELINATING DISEASE INFECTIONS

47. Classic teaching in pediatric ophthalmology
held that isolated sixth nerve palsies in
childhood should be considered the result of a
PONTINE GLIOMA until proven otherwise

48. DIFFERENTIAL DIAGNOSIS
1. myasthenia gravis
2. restrictive thyroid myopathy
3. medial orbital wall blow out fracture
4. orbital myositis
5. duane syndrome
6. convergence spasm
7. divergence paralysis
8. early onset esotropia

49. WORK UP
• LAB TESTS:
• CBC
• Glucose levels
• HbA1C
• ESR/C – reactive protein
• Rapid plasma reagin tests
• Fluorescent treponemal antibody – absorption test
• Lyme titre
• Anti nuclear antibody test
• IMAGING STUDIES

50. IMAGING STUDIES
• CT
• MRI
• CEREBRAL ANGIOGRAPHY

51. Indications of MRI
• Age < 45 years
• Associated pain or neurologic abnormality
• History of cancer
• Bilateral 6th nerve palsy
• Papilloedema
• In the event no marked improvement is seen
or other nerves become involved

52. OTHER TESTS
• Lumbar puncture
• Thyroid function tests
• Otoscopic examination
• Temporal artery biopsy

53. MANAGEMENT
• Medical Care
• Truly isolated cases often are benign.
• They can be followed with a serial
examination, at least every 6 weeks, over a 6-
month period to note decreasing symptoms
(diplopia) and resolution of the paretic lateral
rectus (increasing motility)

54. • Children : Amblyopia treatment
• Older patients in whom giant cell arteritis is a
consideration should start the standard
treatment with prednisone or intravenous
methylprednisolone as soon as possible.

55. SURGICAL CARE
• INDICATION:
• If after 6 months of follow up care the
remaining deviation is still unacceptable & is
too large to be corrected with prisms

56. residual function exists
graded recession/resection

57. little or no residual function
transposition procedure
( weakening of antagonist
ipsilateral medial rectus
in appropiate patients )

58. THANK YOU