Facial nerve damage can manifest as facial paralysis, a condition in which a person is unable to move the muscles on one or both sides of their face.

Bell’s palsy

Bell’s palsy is the most common condition of the facial nerve (seventh cranial nerve), with an annual incidence of 23 cases per 100,000 individuals.

It affects men and women of all ages equally and at any time of the year. Pregnant women are particularly affected.

Causes and risk factors of facial nerve palsy and Bell’s nerve palsy in particular

From an etiological point of view, whereas it was previously thought to be an idiopathic form, it is now clear that the most common cause of Bell’s palsy is an infection with the virus of the herpes simplex type 1 and it is likely that other viruses and inflammatory processes may be responsible in other cases.

The onset is acute and the disorder reaches its maximum intensity after a few hours or a few days: it is frequently preceded by one or two days of retro-auricular pain.

Symptoms and signs

Symptoms and signs are typical: all mimic muscles on one side of the face are hyposthenic or paralyzed: the eyelid cannot be closed, the corner of the mouth tends to droop, and the patient is unable to wrinkle the forehead.

Objective disturbances of sensation are not present, although the patient may report a feeling of “heaviness” in the face or other abnormal sensations, which may be called “numbness”.

In case of damage to the facial nerve upstream of the point of origin of the tympanic cord, there is a loss of taste sensitivity of the anterior two-thirds of the tongue.

If, on the contrary, the nerve leading to the stapedium muscle is involved, hyperacusis is detected and the patient experiences a distortion of sounds.

Evolution and prognosis of facial and Bell’s nerve palsies

About 80% of patients recover within a few weeks or 1-2 months; in about 15%, recovery occurs 3 to 6 months later; in about 5% of cases recovery is very poor or does not occur at all.

The presence of incomplete paralysis in the first 5 to 7 days is a favorable prognostic sign.

A complete and persistent paralysis, indicating the total interruption of nerve fibers, suggests that recovery will begin late (after about 3 months): in these cases, recovery is by nerve regeneration, which can take up to 2 years and be incomplete, leaving as sequelae spasms and contractures of the facial musculature and signs of aberrant regeneration of nerve fibers (“crocodile tears”, mandibular dysfunction, dyskinesias).

Bell’s palsy is usually a diagnosis of exclusion: the diagnosis is therefore made after excluding other pathologies that cause similar symptoms

The diagnosis obviously relies on the anamnesis and especially on the objective examination.

The differential diagnosis uses imaging (scanner and MRI).

The pathological changes have not been sufficiently studied, but the nerve appears swollen and on magnetic resonance imaging (MRI) of petrous bone, an intensification of contrast is detected after gadolinium infusion.


From a therapeutic point of view, the administration of corticosteroids during the first week is supposed to accelerate the healing time.

Many, but not all, studies have shown that the same goal can be achieved by administering antiviral drugs.

The cornea should also be protected by goggles, the instillation of artificial tears and gauze until healing allows the eyelids to close.

The so-called “smile surgery” is useful in some cases.

Physiotherapy and speech therapy are indicated for patients with facial paralysis.

Permanent facial paralysis leads to a sharp drop in the patient’s quality of life, both socially and professionally, especially in people who use the appearance of their face as a work tool (eg models, TV presenters, etc.).

The patient with facial paralysis tends to isolate themselves and has an increased risk of suffering from depression and suicidal thoughts: antidepressants and psychotherapy are useful here.

Other Causes of Facial Nerve Paralysis

Other causes of facial palsy are considerably less common than Bell’s palsy and are briefly listed here:

  • Lyme disease: this is a cause of facial paralysis in endemic areas, after tick bites or after a chronic eri-migratory theme.
  • HIV infection: this virus, even in the absence of the manifestations of AIDS, has been identified as the cause of mono- or bilateral facial paralysis in people with the disease.
  • Sarcoidosis: Sarcoid granulomas tend to infiltrate the 7th nerve more than any other cranial nerve. Sarcoidosis is a common cause of alternating or sequential facial paralysis. A rare but typical presentation of sarcoidosis is the association of an acute febrile syndrome with enlargement of the parotid gland and uveitis (Heerfordt syndrome).
  • Iatrogenic causes: the facial nerve can be accidentally injured during surgery, for example to remove a brain tumour.
  • Compression of the facial nerve by a tumor mass: these masses are usually represented by schwannomas, meningiomas, cholesteatomas, dermoids, carotid glomus tumors or mixed parotid neoplasms.
  • Herpes zoster: is characterized by inflammation of the facial nerve, the geniculate ganglion and the contiguous ganglia, manifesting as vesicles at the level of the concha of the acoustic meatus and the external auditory canal (Ramsay-Hunt syndrome).
  • Facial dysplegia: most often due to Guillain-Barré polyneuropathy and less often secondary to sarcoidosis (uveo-parotid fever or Heerfordt syndrome) or Lyme disease.
  • Melkersson-Rosenthal Syndrome: This is a rare condition with an unknown cause and characterized by recurrent facial paralysis, lip edema, and the formation of folds on the tongue.
  • Facial paralysis associated with bridge lesions: this condition must be distinguished from supranuclear facial hyposthenia: it can be secondary to infarctions, neoplasms and demyelinating lesions. The association with gaze paralysis or ocular abduction is frequent.
  • Facial hemispasm: is often idiopathic in nature, but may follow Bell’s palsy; it responds to periodic injection of botulinum toxin into the muscles and, in many cases, to surgical decompression of the facial root (which is compressed by a small adjacent vessel).
  • Congenital facial palsy: it is secondary to birth trauma or Mobius syndrome (congenital facial palsy associated with abducens palsy or horizontal gaze palsy); this last form can be bilateral.
  • Romberg’s hemiatrophy (facial pseudoparalysis): this is a rare unilateral facial lipodystrophy of unknown etiology, not associated with hyposthenia.

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