Neuro-ophthalmology

Third Nerve Palsies

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Diagnosis can be difficult

Anatomy nuggets

  • Nucleus in the midbrain at the level of the superior colliculus
  • Bilateral levator innervation
  • Contralateral superior rectus innervation
  • Ipsilateral innervation to the other EOMs
  • Travels through the MLF and lateral to the posterior communicating artery
  • Travels in the lateral wall of the cavernous sinus
  • Superior and inferior branches enter the orbit within the annulus of Zinn
  • Superior branch innervates the superior rectus and levator. Inferior branch does the rest
  • Parasympathetic fibres from the Edinger-Westphal nucleus travel with the branch to inferior oblique to the ciliary ganglion then in the short ciliary nerves

Aetiology

  • Aneurysms, classically of the PCoA (most commonly at the junction of the PCoA and the ICA)
  • Microvascular ischaemia: typically recover over 4 months
  • Tumours
  • Trauma
  • Demyelination
  • Vasculitis including GCA
  • Congenital

Subtypes

  • Complete vs partial

  • Pupil-sparing or involving

  • Nuclear, fascicular or peripheral

    • Nuclear:

      • Unilateral palsy
      • Contralateral superior rectus paresis
      • Bilateral partial ptosis
    • Fascicular: ie. paramedial midbrain lesion eg. infarction of cerebral peduncle with involvement of third nerve fascicle

      • Ipsilateral palsy
      • Contralateral intention tremor, ataxia, anaesthesia (Benedikt syndrome)
      • Contralateral hemiparesis (Weber syndrome)
  • Isolated vs complex (ie. associated with other deficits)

Clinical features

  • Diplopia with horizontal and/or vertical ophthalmoplegia

Hot Topic

Vertical gaze palsy in third nerve lesions. Doll’s head manoeuvre can distinguish supranuclear from nuclear lesions:

  • Eyes elevate on Doll’s head: supranuclear

  • Eyes do not elevate on Doll’s head: nuclear

  • Ptosis: bilateral in nuclear lesions
  • Mydriasis
  • Pain: may be severe and similar to the headache of a SAH
  • Difficulty focussing due to pupil involvement

Hot Topic

Check superior oblique and lateral rectus in third nerve palsy.

  • The eye cannot adduct in third nerve palsies, so to assess function of SO, observe forintorsion(its primary action) in abduction and downgaze.

  • Lateral rectus function can be assessed via saccadic velocity

Aberrant regeneration

  • Typically in longstandingcompressivelesions or trauma (Note: doesnotoccur in vasculopathic lesions)

  • Lid-gaze dyskinesia:

    • Lid elevation on adduction (‘inverse Duanes’) or depression (pseudo Von Graefe’s sign)
  • Pupil-gaze dyskinesia

    • Pupillary constriction on adduction (pseudo Argyll Robertson) or depression

Tests

  • Urgent neuroimaging with angiography (CTA/MRA)

    • Some would observe a pupil-sparing, non-traumatic palsy especially with vasculopathic risk factors/patient over 40 and undertake imaging if no recovery within 3 months.
  • Lumbar puncture

  • Assess vascular risk factors

  • ESR/CRP if over 50

  • Hess chart

Posterior communicating artery aneurysms

  • Rupture in 2/3rd
  • If ruptures, 50% mortality

Brainstem syndromes

  • Raymond syndrome: 6th nerve palsy with contralateral hemiparesis

    • Lesion in the mid-pons (ventral pons) affecting 6th nerve fasciculus and corticospinal tract
  • Weber syndrome: 3rd nerve equivalent of Raymond syndrome

    • Lesion in the midbrain causing fascicular 3rd nerve palsy and contralateral hemiparesis
    • Weber’s is “weak”
  • Claude syndrome: ipsilateral 3rd nerve palsy with contralateral ataxia

    • Lesion in the dorsal midbrain affecting superior cerebellar peduncle and 3rd nerve fasciculus
    • Claude is “cerebellar”
  • Benedikt syndrome: ipsilateral 3rd nerve palsy with contralateral ‘rubral’ tremor (slow tremor at rest and with movement)

    • Lesion in the midbrain (red nucleus) affecting the 3rd nerve fascicle and red nucleus
  • Nothnagel: ipsilateral 3rd nerve palsy and ipsilateral cerebellar ataxia

    • Localises to midbrain

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