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

Abducent nerve clinical anatomy

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Page 1: Abducent nerve clinical anatomy

ABDUCENT NERVE

DR. Nirmal JayadevFinal year PG student (MS Ophthalmology)

MKCG Medical College Berhampur

Odisha

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INTRODUCTION

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Page 4: Abducent nerve clinical anatomy

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

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Page 6: Abducent nerve clinical anatomy

The medial longitudinal bundle is ventromedial

• Partly intermingled with these larger neurons are more numerous small multipolar cells which form the so-called nucleus paraabducens

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CONNECTIONS

ABDUCENT NERVE NUCLEUS

MEDIAL LONGITUDINAL

BUNDLE

OCULOMOTOR

NUCLEUS

TROCHLEAR NUCLEUS

VESTIBULAR

NUCLEUS

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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)

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Page 10: Abducent nerve clinical anatomy

PPRF

IPSILATERAL

ABDUCENT NUCLEUS

MLF

CONTRALATERAL

OCULOMOTOR

NERVE

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ANATOMICAL LANDMARKS

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SUPERFICIAL EMERGENCE

• Emerges between lower border of the pons & lateral part of the pyramid

• Emerge as seven or eight rootlets

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COURSE

• Passes upwards & anterolaterally in subarachnoid space of posterior cranial fossa

• Pierces the arachnoid & dura lateral to the dorsum sellae

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• Ascends between the layers of dura on the posterior surface of the petrous bone near its apex

• Turns anteriorly to traverse the cavernous sinus

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

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COURSE OF ABDUCENT. N

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RELATIONS OF ABDUCENT .N

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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 abducentis the emergence of the facial. N at the lateral side of the olive

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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.

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

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• At the upper border of the bone, it turns forward at a right – angle under the Petro sphenoidalligament ( Gruber’s ligament )

• Thus passing through a canal called the Dorello’scanal – 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

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3.CAVERNOUS SINUS

• Here the nerve lies within the cavernous sinus

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

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• 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

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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 nasociliarynerve

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5.IN THE ORBIT

• Nerve divides into 3 or 4 filaments which enter the ocular surface of lateral rectus muscle behind its midpoint

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CLINICAL ASPECTS

LESIONSAT NUCLEUS

AT FASCICULUS

PONTOMEDULLARY

JUNCTION

BASILAR COURSE

IN CAVERNOUS

SINUS

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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

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

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2.PONTINE SYNDROMES – AT THE LEVEL OF FASCICULUS

M

• MILLARD GUBLER SYNDROME

R

• RAYMOND CESTON SYNDROME

F

•FOVILLE SYNDROME

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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

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B. Millard – Gubler syndrome

Involves fasciculus as it passes through the pyramidal tract

Ipsilateral 6th nerve palsy

Contralateralhemiplegia

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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

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3. At the pontomedullary junction:

ACOUSTIC NEUROMA:

• 1ST symptom – hearing loss

• 1st sign - ↓ corneal sensitivity

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

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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

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B. nasopharyngeal tumors

C. base of skull fractures

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D. Gradenigo’ssyndrome:

• Mastoiditis/Petrositis

• - damage to 6th nerve at the Dorello’s canal

• Facial weakness

• Pain

• Hearing difficulties

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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

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CLINICAL PRESENTATION

• HISTORY:

– Esotropia

– Head-turn

– Binocular diplopia (worse at distance)

– Vision loss

– Pain

– Hearing loss

– Symptoms of vasculitis, particularly giant cell arteritis

– Trauma

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PHYSICAL FINDINGS

• An eso deviation that ↑ on ipsilateral gaze

• An isolated abduction deficit

• Slowed ipsilateralsaccades

• Papilloedema• Nystagmus• Otitis media• Orbital wall fracture• Tender , non pulsatile

temporal arteries

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CAUSES OF 6TH NERVE PALSY

ELEVATED INTRACRANIAL TENSION

NEOPLASM

SUBARACHNOID SPACE LESIONS

CONGENITAL ABSENCE

VASCULAR TRAUMATIC

METABOLIC POST LUMBAR TAP

DEMYELINATING DISEASE INFECTIONS

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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

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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

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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

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IMAGING STUDIES

• CT

• MRI

• CEREBRAL ANGIOGRAPHY

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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

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OTHER TESTS

• Lumbar puncture

• Thyroid function tests

• Otoscopic examination

• Temporal artery biopsy

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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)

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• 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.

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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

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residual function exists

graded recession/resection

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little or no residual function

transposition procedure

( weakening of antagonist

ipsilateral medial rectus

in appropiate patients )

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THANK YOU