Facial palsy refers to the neurological syndrome of facial paralysis. It can result from a broad range of physiological insults to the facial nerve or its central nervous system origins. The most common causes of this is Bell palsy.
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Terminology
While facial palsy refers to the clinical presentation of facial paralysis and associated symptoms of facial nerve compromise it can sometimes be used interchangeably with facial nerve palsy which refers specifically to paralysis caused by a lesion in the facial nerve.
The distinction is important as facial nerve palsy implies almost an exclusively lower motor neurone cause of facial paralysis while the term facial palsy can include upper motor neurone lesions as well.
Clinical presentation
The facial nerve provides innervation to the facial muscles, middle ear, tongue, salivary and lacrimal glands. Accordingly signs and symptoms of facial nerve palsy include:
dropping mouth
loss of ipsilateral eye closure (lagophthalmos)
altered or reduced sense of taste
hyperacusis
dry mouth and/or eyes
mild dysarthria
synkinesis (late sign in lower motor neurone causes)
An important clinical discriminator between upper and lower motor neurone presentations of facial nerve palsy is that in the former there is sparing of the ipsilateral forehead muscles which allow patients to ipsilaterally wrinkle the forehead, raise the eyebrow, and completely close the eye. This finding is important in trying to localise the lesion and evaluating possible underlying causes, however, can be misleading if the facial palsy is bilateral.
The palsy can be complete or partial with the later carrying a better chance of full recovery. In partial paralysis the lower facial muscles are more prominently affected while loss of taste and sensation to the anterior two-thirds of the tongue occurs more frequently in complete lesions. The House-Brackmann grading system is used to score the severity of presenting facial nerve palsy to help guide treatment and follow up.
Pathology
As above, the pathophysiology of facial nerve palsy depends on the underlying disease and can include all variety of causes summarised in the surgical sieve. Traditionally the preservation of forehead muscles in upper motor neurone lesions has been thought to be due the bilateral innervation of upper facial muscles by the cerebral cortices. However, this may not be supported by the literature 4.
Aetiology
Upper motor neurone facial palsy
Causes of upper motor neurone facial palsy include 5,7:
It should be noted that bilateral pathology (e.g. bilateral stroke) can result in a pseudo-lower motor neurone pattern of facial palsy (e.g. Foix-Chavany-Marie syndrome).
Lower motor neurone facial palsy
Causes of lower motor neurone facial palsy, including neuromuscular junction and myopathic causes, include 6,7:
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idiopathic
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iatrogenic
local anaesthetic from dental surgery
post-parotidectomy
botulinum toxin A administration (e.g. for cosmesis)
post-acupuncture haematoma
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infective
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vascular
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mononeuropathy
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neoplastic
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trauma
skull base fracture (e.g. temporal bone)
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autoimmune
Guillain-Barré syndrome (and variants)
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myopathies
mitochondrial myopathies
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other
Practical points
if bilateral consider Guillain-Barré syndrome or Lyme disease
if recurrent consider lymphoma, sarcoidosis or Lyme disease
in children particularly consider Lyme disease and otitis media
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