Palsies

Question 1

What are the clinical features of a CN III palsy?

Answer 1

• Paralytic squint - the affected eye looks ‘down and out’ due to unopposed abducens and trochlear nerves.
• Ptosis as the levator palpebrae superioris is innervated by oculomotor nerve.
• Horizontal diplopia that is worse when the head is turned away from the side of the nerve palsy. Patients don’t tend to complain about this because of ptosis.
• Pupillary involvement is due to the parasympathetic fibres that control pupil constriction being located on the periphery of the oculomotor nerve. This means it is the first to go for compressive causes, but for ischaemic causes, may still receive enough blood supply:
  
  • Compressive lesions (‘surgical’): a non-reactive, dilated pupil
  • Ischemic microangiopathy (‘medical’) : typically sparing of the pupil

Question 2

What are the causes of a CN III palsy?

Answer 2

Causes of a third-nerve palsy can be split into medical (pupil-sparing) and surgical (fixed-pupil) causes:

• Medical (ischaemic ) causes are mainly due to diabetes microangiopathy or hypertension.
• Surgical (compressive) causes can be due to lesions at multiple levels:
  
  • Midbrain (oculomotor nucleus) lesions can be due to ischaemic stroke of posterior cerebral artery.
  • Basilar segment compression due to posterior communicating artery aneurysm or tentorial herniation
  • Intracavernous lesions such as a meningioma
  • Intraorbital segment lesions such as trauma or orbital cellulitis.

Question 3

What is the management of a CN III palsy?

Answer 3

• Compressive lesions: surgery
  
  • Posterior communicating artery aneurysm: urgent neurosurgical clipping or endovascular coiling
• Ischemic microangiopathy or demyelinating lesions: medical management with adequate control of the underlying disease

Question 4

What is the definition and epidemiology of Bell’s Palsy?

Answer 4

Bell’s Palsy is an idiopathic lower motor neurone facial (VII) nerve palsy. Annual incidence is around 15-40 per 100 000. Although idiopathic, it is preceded by an upper airway infection in 60%, suggesting a viral or post-viral aetiology.

Question 5

What are the clinical features of Bell’s Palsy?

Answer 5

Patients have a prodrome of pre-auricular pain in some cases, followed by acute onset (hours/days)unilateral facial weakness and droop.

Fifty per cent of patients experience pain or numbness in the face, neck or ear. Patients also experience hypersensitivity to sound (due to stapedius muscle paralysis), and tearing or drying of exposed eye. A loss of taste sense is uncommon.

On Examination

There is lower motor neurone weakness of facial muscles(affects all the ipsilateral muscles of facial expression, and does not spare muscles of the upper part of the face as seen in UMN facial nerve palsy).

May elicit Bell’s phenomenon where the eyeball rolls up but eye remains open when trying to close eyes.

The ear should be examined for other causes (e.g, otitis media, herpes zoster infection).

Question 6

What are the potential complications of Bell’s Palsy?

Answer 6

Corneal ulcers and eye infections are likely complications.

Aberrant reinnervation may also occur, e.g. blinking may cause contraction of the angle of the mouth due to simultaneous innervation of obicularis oculi and ori. Parasympathetic fibres may also aberrantly reinnervate causing ‘crocodile tears’ when salivating.

Question 7

How can Bell’s Palsy be investigated?

Answer 7

Usually unnecessary, except to exclude Lyme serology and herpes zoster serology.

An EMG may show local axonal conduction block in facial canal. However, only useful >1 week after onset.

Question 8

How is Bell’s Palsy managed?

Answer 8

Protection of cornea with protective glasses/patches and artificial tears.

High-dose corticosteroids is beneficial if given within 72h of onset. It helps shorten time of recovery and improve long-term outcomes.

• Antiviral agents such as acyclovir gives no additional benefit than corticosteroids alone.