CN6 Palsy Flashcards

1
Q

ANATOMY

Brainstem

  • CN6 nucleus lies at mid pons (level of facial colliculus), fibres leave brainstem anteriorly at ______________
  • Nuclear lesions 🡪 failure of horizontal gaze towards side of lesion (i.e. limitation in ipsilateral abduction AND contralateral adduction)
  • Isolated CN6 palsy is never nuclear in origin!

Basilar part

  • CN6 enters the prepontine basilar cistern, passing upwards close to base of skull (ascending the clivus)
  • Pierces the dura below the posterior clinoids and angles forwards over the tip of the petrous bone, passing through the Dorello canal (underneath the petroclinoid ligament) to enter the cavernous sinus
  • ____________ can damage CN6 at the pontomedullary junction
  • __________ may invade the skull and its foramina 🡪 damage CN6 during its basilar course
  • Raised intracranial pressure (ICP) 🡪 downward displacement of brainstem 🡪 stretch one/both CN6 over the petrous tip 🡪 isolated CN6 palsy as a false localising sign. CN6 is often the first nerve to be compressed in raised ICP!
  • Base of skull fracture (trauma) 🡪 unilateral or bilateral CN6 palsy

Intracavernous

  • This section runs below _____________. CN6 is most medially situated, and runs through the middle of the sinus, in close relation to the ICA
  • Causes of intracavernous CN6 palsy and CN3 palsy are similar

Intra-orbital: Intra-orbital part enters orbit via ________________ to innervate LR

A

pontomedullary junction;

Acoustic neuroma

Nasopharyngeal carcinoma;

B

superior orbital fissure (SOF);

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2
Q

what are the symptoms of CN 6 palsy?

A

Binocular horizontal diplopia

  • Worse for distant target, and less/absent for near fixation
  • Worse on gaze towards affected side

Esotropia (in primary position) due to relatively unopposed action of the medial rectus (MR)

Limitation of abduction on the side of the lesion. Temporal sclera is not buried in lateral gaze

Normal adduction of affected eye

Compensatory head turn towards side of lesion (if unilateral)

ENT symptoms/signs (blood stained mucus, sputum) (thinking of NPC)

Pseudo-CN6: MG 🡪 ptosis, difficulty swallowing, voice changes, limb weakness

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3
Q

What are the causes of CN 6 palsy?

A
  • Vasculopathy (DM, HLD, HTN) (most common)
  • Trapped unilaterally or bilaterally under the petroclinoid ligament (Dorello’s canal at the petrous apex) with acute increased ICP (a false localising sign), e.g. idiopathic intracranial hypertension/pseudotumour cerebri
  • Cavernous sinus lesions, e.g. cavernous sinus thrombosis, carotid-cavernous fistula, ICA aneurysms
  • Demyelination
  • Trauma, e.g. BOS#
  • Tumour
  • Vasculitis
  • Meningitis
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4
Q

what are the causes of pseudo CN6 palsy?

A
  • Myasthenia gravis (MG) (always a differential)
  • Thyroid eye disease (TED) (always a differential) (MR fibrosis 🡪 adducted posn)
  • Duane syndrome
  • Medial orbital wall fracture (🡪 entrapment of MR 🡪 mechanical inability to abduct)
  • Long-standing/congenital esotropia
  • Convergence spasm
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5
Q

what are the investigations for CN6 palsy?

A

Exclude microvascular cause: check ischaemic risk factors (BP, fasting glucose, lipids)

Exclude raised ICP (false localising sign)

  • Fundoscopy/ophthalmoscopy, checking for papilloedema. If present, do:
  • Lumbar puncture (LP), checking for opening pressure
  • Neuroimaging

**Refer ENT to r/o NPC

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6
Q

How is CN6 palsy managed?

A

Observation, management of CVRF in idiopathic and microvascular/vasculopathy

For diplopia

  • Monitor with Hess chart & binocular single vision (BSV) test
  • Occlusion w/ eye patch
  • Fresnel prism
  • Botox injection to paralyse MR of affected eye (prevent contracture) -> but risk of over/under compensation (cannot do for other CN – CN3 affects too many muscles hard to control outcomes) & effect only lasts 2-3 months
  • Surgical correction if no improvement after 3 months
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