#7531 - Optic Nerve Palsies - Medical Finals & OSCEs Notes

Optic Nerve Palsies

Cranial Nerve III: Oculomotor nerve

Functions of oculomotor:

• The efferent for the pupillary reflex (i.e. constricts) since it carries parasympathetic fibres

• Innervates all extraocular muscles except lateral rectus and superior oblique:

  • Medial rectus adduction (move medially)

  • Superior rectus up

  • Inferior rectus down

  • Inferior obliqueup and out

  • Levator palpebraelift eyelid

A lesion therefore produces:

• Levator palpebrae damageptosis

• Parasympathetic efferent damagefixed dilated pupil

• Unopposed lateral rectusabducted eye

• Unopposed superior obliquedown

• Muscle damageeye fixed down and out

Pathway:

• Originates in midbrain

• Travels near the posterior communicating artery near the Circle of Willis

• Travels through the cavernous sinus (below the pituitary gland)

• Travels through the superior orbital fissure

Anatomy:

• Parasympathetic fibres carried on the outside

• The muscle nerves are in the middle

• There are small arteries that supply the middle nerve

Mechanisms of damage:

• Iatrogenic CNIII palsycomplete palsy d/t severing during an operation (e.g. to fix a posterior communicating artery aneurysm)

• Surgical CNIII palsy:

  • Aneurysm of posterior communicating artery or internal carotid artery in the cavernous sinuscompress CNIIIouter parasympathetic fibres firstpupil dilated first

  • Increased ICP compressing CNIIIouter parasympathetic fibres firstpupil dilated first

  • Uncal herniation down into the midbrain compresses CNIII nucleus almost before anything elseevolving CNIII palsy

    • Uncal herniation may be unilateral but give bilateral CNIII palsies as it pushes across

    • Unilateral pressure (e.g. haematoma)unilateral uncal herniation

    • Bilateral pressure (e.g. hydrocephalus)bilateral uncal herniation

• Medical CNIII palsy:

  • Oculomotor middle nerve blood supply damaged d/t:

    • Small ischaemic episodes

    • Vasculitides

  • Oculomotor nerve damaged d/t:

    • Mononeuritis multiplex

    • MS

    • Diabetic polyneuropathy

• Cavernous Sinus Syndrome

Patterns of damage:

• A surgical CNIII palsy will theoretically compress the outer parasympathetic fibres first and cause a dilated pupil without motor involvement.

• A medical CNIII palsy will theoretically damage the inner motor fibres first and cause a ptosis and ophthalmoplegia without a dilated pupil.

• Practically, all features (lid ptosis, pupil dilation, eye down-and-out) occur simultaneously.

Cranial Nerve IV: Trochlear nerve

Functions of trochlear:

• Innervation of superior oblique muscle

  • pulls the eye nasally

  • pulls the eye down when it is facing inwards

  • makes the eye look at the nose

  • the gaze for going downstairs or reading the newspaper

  • cannot turn nasally when the oculomotor muscles are paralysed

  • when the oculomotor muscles are paralysed it can only turn downwards

  • when the oculomotor muscles are paralysed it cannot counteract the lateral rectuseye moves down and out

A lesion therefore produces:

• An inability to turn the eye nasally when it is turned downwards

• Difficulties with going downstairs or reading the newspaper

• Double vision on looking down, especially on looking down and nasally

• Impaired ability to turn the eye downwards

• The resting position of the affected eye is slightly higher than the unaffected eye

• Affected eye ‘stuck’ higher up than the unaffected eye, especially on downgazevertical diplopia

• A compensatory position of tilting the chin down and turning the head towards the affected eye so that the unaffected eye is now at the same level as the affected eyepatient appears to have torticollis

Pathway:

• Originates in the dorsal midbrain

• Travels up the dorsum of the midbrain

• Decussates! under the inferior colliculi

• Travels through cavernous sinus

• Travels through the superior orbital fissure

Mechanisms of damage:

• Isolated lesions are rare

• Neuropathies: MS, diabetic neuropathy, etc.

• Acute head trauma

• Compression pathologies (e.g. haematoma, haemorrhage, oedema, hydrocephalus, space-occupying lesion) usually affect CNVI abducens first, thus producing a horizontal diplopia not a vertical diplopia!

• Infection: meningitis, herpes zoster virus

• Cavernous Sinus Syndrome

Patterns of damage:

• The lesion is ipsilateral if after the decussation i.e. after passing above the midbrain

• The lesion is contralateral if before the decussation i.e. in the nucleus

• Lesions will almost always be in association with other neurological pathology

Cranial Nerve VI: Abducens nerve

Functions of abducens:

• Innervation of lateral rectus muscleeye abduction i.e. looking outwards away from the nose

• Turns to see the surrounding environment

A lesion therefore produces:

• An inability to abduct the affected eye

• An eye that ‘sticks’ when it tries to look outwards past the midpoint

• A diplopia on turning the eye towards the affected eye

• A compensatory mechanism of moving the head to look towards the environment on the affected eye’s side, to avoid diplopia and gain visual field

Pathway:

• It has a very long coursefalse localising sign!

• It emerges at the pontine-medullary junction

• Travels upwards past midbrain

• Travels along the petrous temporal bone

• Travels through the cavernous sinus

• Passes very close to the internal carotid artery

• Emerges through the superior orbital fissure

Mechanisms of damage:

• Pontine-medullary junctionpontine stroke

• Petrous temporal bonebasal skull fractures

• Cavernous Sinus Syndrome

• Internal carotid aneurysm

• Any compression pathology or raise in intracranial pressure (e.g. space-occupying lesion, hydrocephalus, haemorrhage, haematoma, oedema) will often affect the abducens nerve

• It is sensitive to changes in intracranial pressure and thus can be the first sign, as a false localising sign

Cavernous Sinus Syndrome

The cavernous sinus contains:

• CNIII Oculomotor nerve

• CNIV Trochlear nerve

• CNV V₁ Ophthalmic branch of the Trigeminal nerve

• CNV V₂ Maxillary branch of the Trigeminal nerve

• CNVI Abducens nerve

• Internal carotid artery

• Sympathetic chain around the internal carotid artery

It connects through the midline so is continuous bilaterally. In the middle it is the space under the pituitary fossa. It is the space above and behind the backmost nasal sinuses. It is an area where congenital AV fistulae arise due to the passage of an artery through a venous sinus.

Causes of cavernous sinus syndrome:

• Thrombosis of the cavernous sinus, commonly d/t trauma to the ‘danger zone’ of triangle around the nose, rarely d/t thrombophilia syndromes

• Mass effect from a tumour, commonly a pituitary adenoma

• Severe sinusitis erosion backwards into the skull, commonly Staph aureus

• Aneurysmal haemorrhage of the internal carotid artery

Symptoms of cavernous sinus syndrome:

• Bilateral acute complete palsies of oculomotor, trochlear, abducens, ophthalmic and maxillary nerves

  • Complete ophthalmoplegia!

  • Bilateral ptosis d/t levator palpebrae muscle inactivation

  • Bilateral chemosis (eyelid swelling) and proptosis (eyes pushed forwards)

  • Bilateral fixed dilated pupils

  • Bilateral loss of face sensation in V₁ and V₂ distributions

• Bilateral Horner’s Syndrome d/t sympathetic chain damage

  • Bilateral ptosis d/t superior tarsal muscle inactivation

  • Bilateral anhidrosis

  • The parasympathetic nerves are damaged, so the pupil physically cannot constrict; even though the sympathetic nerves are damaged, there are bilateral fixed dilated pupils, hence miosis is missing from this particular Horner’s Syndrome

Management of cavernous sinus syndrome:

• A medical emergency!

• Treat the cause

• In dire straits, can...