3rd NP Flashcards

1
Q

pathway of 3rd - LEARN

A

The oculomotor nerve originates from the oculomotor nucleus – located within the midbrain of the brainstem, ventral to the cerebral aqueduct.

It emerges from the anterior aspect of the midbrain- passing inferiorly to the posterior cerebral artery and superiorly to the superior cerebellar artery.

The nerve then pierces the dura mater and enters the lateral aspect of the cavernous sinus.

Within the cavernous sinus, it receives sympathetic branches from the internal carotid plexus. These fibres do not combine with the oculomotor nerve – they merely travel within its sheath.

The nerve leaves the cranial cavity via the superior orbital fissure.
At this point, it divides into superior and inferior branches:

.

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2
Q

what do the superior and inferior branches provide in 3rd nerve

A

Superior branch – provides motor innervation to the superior rectus and levator palpabrae superioris.
- Sympathetic fibres run with the superior branch to innervate the superior tarsal muscle.

Inferior branch – provides motor innervation to the inferior rectus, medial rectus and inferior oblique.

  • Also supplies pre-ganglionic parasympathetic fibres to the ciliary ganglion, which ultimately innervates the sphincter pupillae and ciliary muscles
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3
Q

Types of 3rd nerve palsy

A

Congenital or acquired
* Unilateral or bilateral
Complete or incomplete

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4
Q

Aetiology of congenital 3rd nerve palsy

A

Congenital 3rd occurs far less commonly than acquired palsy. Most cases are bilateral and involve some degree of ptosis and paresis of the muscles.

Abnormalities may be caused by absent or incomplete development of the nerve nucleus or nerve itself.

Most cases will have involvement of the pupils but in some case the pupil may be miosed rather than dilated due to aberrant regeneration.

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5
Q

Aetiology of acquired 3rd nerve palsy

A

Trauma (SEVERE)

Aneurysm PCA (posterior cerebral artery)

Space occupying lesion

Microvascular

Inflammatory - MS

Viral or Bacterial infections

Vasculitis

Demyelination

Ophthalmoplegic Migraine - transient 3rd - vascular (not enough blood supply to certain parts of brain)

Miller Fisher Syndrome

Guillain Barre Syndrome

Acquired Immunodeficiency Syndrome

Tolosa Hunt Syndrome

Most important to know are trauma, aneurysm, microvascular

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6
Q

7 syndromes OF 3RD

A

Nuclear Palsy

Fascicular Lesions - on the nerve pathway

Uncal Herniation Syndrome
Very serious, px is bedbound

Posterior Communicating Artery Aneurysm - most common and serious case of 3NP as px can die

Pupil Sparing 3rd N Palsy - pupil reacting to light - 3NP that doesn’t affect pupil is usually vascular

Cavernous Sinus Syndrome

Orbital Syndromes

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7
Q

Summary of Acquired Causes of 3rd nerve

A

Ischaemic causes such as hypertension, aneurysm , haemorrhaging in the brain or orbit may cause IIIrd nerve palsy. MOST IMPORTANT AETIOLOGY

Space Occupying lesions along the path of the IIIrd nerve may result in paresis.

Inflammatory conditions such as granulomas, orbital cellulitis, meningitis, encephalitis and herpes zoster may result in IIIrd nerve. MS may cause IIIrd nerve but is usually partial. CS thrombosis

Metabolic disorders such as diabetes and systemic lupus erythmatosous can give rise to IIIrd nerve.

Ophthalmoplegic migraine may also cause IIIrd.

Trauma.

Rare cases have been reported after dental anaesthesia.

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8
Q

Diabetic 3rd N Palsy

A

Diabetes

Usually pupil sparing (central)

Blood vessels Vasa vasorum supply the inner aspect of the nerve, sparing the outer pupillary fibres

Painful headache often reported

Myasthenia Gravis can mimic a pupil sparing 3rd nerve palsy.

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9
Q

Hypertensive 3rd N Palsy

A

Similar to the Diabetic Occlusive Nerve Palsies

Not usually associated with pain

Patient may have severe atheromatous blood vessel disease without hypertension or diabetes

Extensive palsies may be the result of brainstem stroke

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10
Q

orthoptic investigations of 3rd

A

CT - exotropia with hypotropia

OM - underacting MR, IR, SR, IO

Pupils - dilation, no pupillary reaction, iin pupil sparing/ diabetic 3rd will react normally

Ptosis - normal palpebral apperture = 10mm - less = ptosis, no diplopia due to ptosis

PCT - vertical and horizontal, bigger at near
Hess/Lees

Convergence - MR palsy convergence may be affected , does pupil constrict on conv and accom

Accommodation

Muscle sequelae

Torsion

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11
Q

non orthoptic investiagtion of 3rd

A

Blood Pressure

Blood count

Erythrocyte sedimentation rate

Blood glucose

Acetylcholine receptor antibodies - checking for MG

Lumbar puncture - cerebral spinal puncture and infection - to check pressure in cerebral cortex
CT scans and MRI - checking for aneurysm

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12
Q

Complete 3rd N Palsy

A

Superior, inferior, and medial rectus muscles, the inferior oblique muscle, the levator palpebrae, the sphincter pupillae and the ciliary muscle all involved

Eye exotropic, intorted and slightly hypotropic

Pupil dilated and ptosis, no AHP or face turn as everything is double

Accommodative palsy

AHP absent since ptosis prevents diplopia

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13
Q

Incomplete 3rdN Palsy

A

Paresis of all the EOM’s

Palsy of the superior division

Palsy of the inferior division

Double elevator palsy

Single muscle palsies

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14
Q

Superior Division 3rd N Palsy

A

Superior rectus and levator palpebrae

Eye hypotropic giving rise to pseudo ptosis in addition to true ptosis which must be assessed with the affected eye fixing

AHP chin elevation with both head tilt and face turn to affected side

More likely to be congenital than acquired

Hold fretalis - measure px looking straight, depression, elevation to see if levator muscle is working

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15
Q

Inferior Division 3rd N Palsy

A

Inferior and medial rectus, inferior oblique, sphincter pupillae and ciliary muscle

Eye exotropic, intorted and hypertropic - depressor is problem rather than elevator

Pupil dilated

Accommodative palsy - check accom in younger px

AHP both head tilt and face turn to unaffected side

Rare as congenital or acquired

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16
Q

Double Elevator Palsy

A

Superior rectus and inferior oblique

Eye hypotropic and some pseudo ptosis. True ptosis unlikely

AHP chin elevation

Restriction of elevation in both adduction and abduction

Likely to be congenital

17
Q

Differential diagnosis for 3rd

A

Trauma (blowout fracture) - eye unable to elevate

  • Mechanical limitation (TED)
  • Brown’s syndrome
  • Congenital fibrosis of the inferior rectus muscle
18
Q

Aberrant Regeneration
LEARN

A

Aberrant regeneration most commonly results from trauma, aneurysms and tumours. It does not occur following microvascular causes, (Ansons & Davis, 2014)

Only from traumatic , compressive or congenital 3rd NP
Not from microvascular

The most common presentations include:
* Eyelid retraction with adduction, elevation or depression
* Abnormal EOM firing i.e. adduction with elevation
* Pupillary miosis with adduction, elevation or depression

→ Pseudo Von-Graefe Sign:” elevation of upper eyelid on downward gaze or adduction
→ Adduction of the eye on attempted upward or downward gaze
→ Limitation of elevation and depression of the eye with retraction of the globe on attempted vertical movement
→ “Pseudo-Argyll Robertson pupil”: greater constriction of pupil to convergence than to light and gaze-evoked pupillary constriction - changes to the pupil happens in the edinger westphal nucleus

19
Q

Prognosis in Congenital 3RD cases

A

Congenital Palsy / Palsy acquired in childhood

  • The main concern is the prevention of stimulus deprivation amblyopia by the ptosis.
  • This may require lid surgery if the ptosis is significant. If the child can see below ptosis by using an AHP then prescribing occlusion treatment may reduce the impact of the amblyopia
  • If the ptosis is not likely to give amblyopia the child is still at risk of developing strabismic amblyopia so occlusion will still be required.
  • Squint surgery may be undertaken to improve cosmesis.
  • Prognosis is usually very poor for these cases
20
Q

Prognosis in acquired 3RD cases

A

Diplopia may not be a problem initially if ptosis covers the pupil however the lid is usually the first muscle to recover and the patient will then experience diplopia.

  • Investigations should be carried out to try and determine the cause of the palsy
  • Many cases will have complete recovery and the Orthoptist should see the patient regularly ( every 3-4 weeks ) to monitor the improvement
  • Recovery is more common in vascular aetiologies