6th cranial nerve

where is the 6th nerve nucleus located?

Nucleus: pons – beneath floor of 4^th ventricle

-          Cavernous sinus + subarachnoid space

describe the course of the 6th nerve

• under 4th ventricle in caudal pons.

→ Fibers pass thru pons.
→ Pass thru corticospinal tract.
→ Exit midbrain & enter brainstem at pontomedullary junction.

→ Subarachnoid Space:

• Runs upward between pons & clivus.

→ Pierces dura mater:

• Runs between dura & skull in Dorello’s canal.

→ Enters cavernous sinus:

• Adjacent to internal carotid artery.

→ Enters orbit via Superior Orbital Fissure:

• Supplies (LR).

nucleus in the pons, traverses brainstem and leaves to enter the subarachnoid space, makes a vertical ascent over the petrous apex bone over the clivus, enters cavernous sinus

why is cavernous sinus an important anatomic feature for the 6th nerve?

it is adjacent to and wraps around the internal carotid artery - any issues affecting the ICA affect the 6th

briefly joined by oculosympathetic fibres responsible for pupil dilation, issues in this area can cause pupil abnormalities where pupil cant dilate

medial to 5th nerve (trigeminal) V1

possible aetiologies that can affect the 6th nerve?

-          Aneurysm

-          Trauma

-          Tumour

-          Arnold Chiari malformation – herniated cerebellum

o    Brainstem displacement = 6^th n impact

-          ↑ ICP= 6^th N stretch – FLC – tether at Dorello’s canal = tumour, hydrocephalus, pseudo tumour

-          False localising sign – press ↓on sharp petrous apex = flc presents as 6^th – but aetiology elsewhere

-          Gradenigos S: post middle ear infection – inflammation of petrous apex = pressure in 6^th

o    Symptoms: hearing loss, facial palsy

-          Petrous bone F

-          Closed head injury- damages 6^th

what is an arnold-chiari malformation?

herniated cerebellum pushes down and pulls tissue along the spinal cord
causes displacement of structures in the brainstem
causing direct effect onto 6th nerve

how does increased intracranial pressure cause a 6th?

6th is stretched and tethered
could be due to mass
can cause a non-localising sign/false localising sign

what is a false localising sign

↑ICP - chiari malformation

• 6th presses down on sharp petrous apex- due to long course form brainstem & passage thru CS, affecting its function

• = false localizing sign - presents as 6th but aetiology elsewhere in brain not along the course of 6th

• ↑ ICP stretch 6th nerve - tethered at Dorello’s canal = 6th NP horizontal diplopia &esotropia

• The lesion causing raised ICP may be remote, such as:

  • Tumors in the posterior fossa.

  • Hydrocephalus.

  • Pseudotumor cerebri.

what is pseudo Gradenigo's

presents in a similr way to Gradenigos
nasopharyngeal carcinoma

how can a petrous bone fracture cause a 6th?

closed head injury damages the 6th

list aetiologies within the CAVENOUS SINUS causing a 6th

vascular lesion e.g. ICA aneurysm

• thrombosis, tumour e.g. pituitary, meningioma, infection

• Inflammation, ischaemia, trauma - skull fracture

• Carotid-cavernous fistula (CCF)

  
  

would diplopia be worse at N or D

worse at D, may be phoric at near

Dip - Horiztonal

lateral gaze e.g. left LR 6th CNP, looks worse looking right

what is the general health like in someone with a 6th CNP?

vascular problems tend to occur in those 50+

what would the CHP be like in a 6th nerve palsy

face turn to the affected side e.g. right 6th CNP, turn to the right, eyes move to the left

6th

• SOL

• trauma

• vascular

• inflammation

• secondary to raised IOP = false localising sign

• MS

• viral infection

congenital

• birth trauma

• hereditary

• infection - maternal

• failure of LR development

acuired

• children

  • SOL

  • infections -

    • bacterial - gradinegos syndrome - infection of middle ear - spread to 6th nerve at petrous temporal bone

    • or viral - benign 6th np - follows infection, viral illness, immunization

INV

CH

• vascular issues < 50yrs

• H dip - worse in D

• eso - AHP

• CHP: worse in lat gaze - toward affected side e.g. R6th - turn right

VA

• reduced if marked dev

• ambylopia develop in unilateral strab

CT

• eso D>N

• c & s AHP

• N - phoric/ sm ET

OM

• primary u/a LR = limited abduction

• o/a of contralteral & ipsilateral MR

• secondary u/a - LR

BV

• c AHP - bsv

• head trauma - fusion may be lost

Hess

field of BSV

• BSV displaced from affected side

Diplopia

• uncrossed - worse in D

mx - congenital/ ac

Management

-          Consider false localizing sign

Congenital

-          Tx amblyopia

-          Occlusion therapy

-          Sx – cosmetic

-          Teach use AHP

Acquired

-          Treat underlying cause

-          Wait for spontaneous rec

Botulinum Toxin A:

• Inject into MR in recent onset cases.

• Prevents contracture, helps restore binocular single vision.

• May be combined with surgical transposition.

mx - sugery

Timing:

• Performed after ≥6 months of stable deviation.

Non-surgical:

-          Prism when dev static

-          Occlusion for dip

-          BT- to MR prevent contracture

-          Bupivacaine

Surgical >6m

-          Sm/mod: MR recession only

-          LR resection

-          Complete palsy

-          MR recession + V recuts transposition to LR = Jensen

-          ALX – transposition full tendon MR recession

-          Residual income – recession of Faden of contralateral MR

Notes:

• 3 muscle sx = higher ischemia risk.

• Botulinum toxin A showed subjective improvement, but no difference in ultimate outcomes in trials.

DD

• trauma

• raised IOP

• decom eso

• infntile eso w cross fixaton

• mobius syndrome

-          Nystagmus block

-          Medial wall F