Facial Nerve Palsy

How may a facial nerve palsy present?

A facial nerve palsy may be partial or complete. It may be upper or lower motor neurone. Reviewing the diagram of the pathway of the facial nerve, there are several levels where the nerve may be affected by pathology. The cerebello-pontine angle, temporal bone and parotid gland are common sites to be affected.

Clinical symptoms and signs reflect the level of the lesion.

The commonest cause of a facial nerve palsy is a cerebrovascular accident (ie a supranuclear lesion), whcih is an upper motor neurone lesion. This results in a hemiparesis and weakness of the lower part of the face on the side opposite to the lesion. Frontalis muscle is spared as this has bilateral cortical innervation, so eye closure, wrinkling of the forehead and blinking are not affected. Other causes of an upper motor neurone facial nerve palsy include intracranial tumours and multiple sclerosis.

Lesions in the pons or below will cause a lower motor neurone lesion. Here, there is weakness of all the muscles of facial expression on the same side of the lesion. Other symptoms include loss of taste, hyperacusis (sensitivity to loud noises) and dry eye due to reduced lacrimation, if the lesion is within or above the level of the temporal bone.

Cranial nerve VI (abducens) nucleus is encircled by the VIIth (facial) nerve, and is sometimes affected in pontine lesions, leading to a lateral rectus palsy.

Cranial nerves V (trigeminal), VI, VIII, (acoustic and vestibular) lie in the cerebello-pontine angle, and these may also be affected by lesions at this site (e.g. acoustic neuroma, meningioma).

Consider causes of facial nerve palsy at the various stages along the facial nerve pathway:-

  • INTRACRANIAL – Neoplastic (acoustic neuroma, meningioma, metatases, Traumatic (neurosurgery), Neurological (MS, Gullain-Barre, CVA).
  • INTRATEMPORAL – Infective (acute and chronic otitis media, malignant otitis externa), Neoplastic (cholesteatoma, glomus jugulare), Traumatic (middle ear surgery, temporal bone fracture)
  • EXTRATEMPORAL – Neoplastic (malignant parotid tumours), Traumatic (parotid surgery, facial trauma, mandibular fracture, birth trauma).
  • Other more general causes include:

    Infections such as herpes simplex, herpes zoster, viral neuronitis, Lyme disease, syphilis. Ramsey Hunt syndrome typically presents with pain and vesicles in the ear on the affected side. Vesicles sometimes appear on the hard palate and anterior two thirds of the tongue. Hearing loss and vertigo may also occur. Other cranial nerves can be involved too.

    Neoplasia such as leukaemia and lymphoma

    Sarcoidosis

    Idiopathic, more commonly known as “Bells palsy.”

    How should I assess someone who presents with a facial nerve palsy?

    A good history will help you to identify the aetiology and level of the facial nerve palsy. Ask about:

  • Onset (in children, facial nerve palsy may follow acute otitis media)
  • Progression (progressive palsies may indicate neoplasia)
  • Pain (e.g. seen in herpes zoster oticus – Ramsey-Hunt syndrome)
  • Malaise (suspect infective cause)
  • Altered taste or lacrimation?
  • Previous trauma to head or neck?
  • Associated otological symptoms?
  • A full ENT and cranial nerve examination is essential.

  • Is there forehead sparing (ie an upper motor neurone lesion)?
  • Is there a blink reflex? If not, the eye is vulnerable and the cornea may ulcerate.
  • Don’t forget to feel for any parotid swellings. Look in the mouth to assess the deep lobe of the parotid gland that may push the tonsil medially.
  • Is the facial paralysis partial or complete?
  • Where an upper motor neurone lesion is suspected, a detailed cardiovascular examination is required, as well as a full neurological assessment.

    Are any further investigations helpful?

    Consider:

  • Blood Tests – FBC/ESR/HSV titres
  • Audiometry to exclude asymmetrical sensory hearing loss, indicating VIII nerve involvement
  • Stapedial reflex may be absent in a LMN VII palsy affecting the intratemporal portion of the nerve
  • Assess lacrimation (Schrimers test)
  • CT (e.g. in head trauma, suspected CVA)
  • MRI scan if a space occupying lesion or MS is suspected
  • Electrophysiological testing is helpful in assessing nerve recovery
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