3rd NP Flashcards
pathway of 3rd - LEARN
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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what do the superior and inferior branches provide in 3rd nerve
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
Types of 3rd nerve palsy
Congenital or acquired
* Unilateral or bilateral
Complete or incomplete
Aetiology of congenital 3rd nerve palsy
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.
Aetiology of acquired 3rd nerve palsy
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
7 syndromes OF 3RD
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
Summary of Acquired Causes of 3rd nerve
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.
Diabetic 3rd N Palsy
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.
Hypertensive 3rd N Palsy
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
orthoptic investigations of 3rd
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
non orthoptic investiagtion of 3rd
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
Complete 3rd N Palsy
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
Incomplete 3rdN Palsy
Paresis of all the EOM’s
Palsy of the superior division
Palsy of the inferior division
Double elevator palsy
Single muscle palsies
Superior Division 3rd N Palsy
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
Inferior Division 3rd N Palsy
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
Double Elevator Palsy
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
Differential diagnosis for 3rd
Trauma (blowout fracture) - eye unable to elevate
- Mechanical limitation (TED)
- Brown’s syndrome
- Congenital fibrosis of the inferior rectus muscle
Aberrant Regeneration
LEARN
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
Prognosis in Congenital 3RD cases
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
Prognosis in acquired 3RD cases
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
