• Clinical science

Facial nerve palsy

Abstract

Facial (nerve) palsy is a neurological condition in which function of the facial nerve (cranial nerve VII) is partially or completely lost. It is often idiopathic but in some cases, specific causes such as trauma, infections, or metabolic disorders can be identified. Two major types are distinguished: central facial palsy (lesion occurs between cortex and nuclei in the brainstem) and peripheral facial palsy (lesion occurs between nuclei in the brainstem and peripheral organs). Central facial palsy manifests with impairment of the lower contralateral mimic musculature. In contrast, peripheral facial palsy leads to impairment of the ipsilateral mimic muscles and also affects the eyelids and forehead. Additionally, peripheral facial palsy can cause various sensory and autonomic disorders (depending on the exact location of the lesion). Diagnosis can usually be made clinically while patient history often helps in evaluating the underlying etiology. Idiopathic facial nerve palsy is treated with oral glucocorticoids and, in severe cases, antivirals. Treatment of the other types depends on the underlying cause. Most cases of idiopathic facial palsy heal completely within 3 weeks.

Etiology

References:[1][2][3]

Pathophysiology

  • The muscles responsible for eyelid and forehead movements are innervated by fibers from both sides
    • Central facial palsy: unilateral lesion between cortex and brainstem nucleimuscles of the eyelids and forehead are still supplied by input from the other side → function is preserved
    • Peripheral facial palsy: unilateral lesion between nuclei and muscles → no input to the ipsilateral eyelid and forehead musclesparalysis
  • The lower facial muscles are only innervated by fibers from the contralateral hemisphere (via ipsilateral nuclei and the ipsilateral peripheral nerve) → paralyzed in both central and peripheral facial palsy

Clinical features

Motor signs in central and peripheral facial palsy

Central (signs are contralateral to the lesion) Peripheral (signs are ipsilateral to the lesion)
Inability to frown
  • No
  • Yes
Inability to close the eyelids completely
  • No
  • Yes
Mouth drooping
  • Yes

Additional signs of peripheral facial palsy

  • Sensory disturbances; (painful sensation around or behind the ear or numbness of one side of the face; , taste disorders , hyperacusis )
  • Dry mouth (as a result of decreased saliva production)
  • Ocular features (lagophthalmos , decreased lacrimation , ectropion )
  • Synkinetic involuntary movements of the facial muscles; (e.g., facial spasms while closing the eyes)

In central facial palsy, paralysis is contralateral to the lesion and eyelid and forehead muscles are not affected!

References:[3]

Diagnostics

  • Ask about symptom onset and duration, recent infections, and outdoor trips
  • General examination of head and neck (particularly of sensory organs and glands)
  • Ask patient to perform facial movements (e.g., frown, whistle, inflate cheeks, smile, show teeth/grimace, close eyes tightly , blink) → observe inabilities and asymmetries
  • Additional studies diagnosis is inconclusive or disease course is atypical
    • Laboratory: e.g., inflammatory markers, detection of pathogens, blood glucose
    • CT/MRI: if clinical features are atypical, progress for more than 3 weeks or persist for more than 4 months
    • Electrophysiologic studies: e.g., electromyography

References:[1]

Treatment

References:[4][5]

Prognosis

  • Idiopathic facial palsy: complete recovery in ∼ 85% of cases (within 3 weeks)
  • Misdirected regrowth of nerve fibers can lead to persistent disorders (e.g., synkinesias)

References:[4][6]