Facial nerve injuries: Bell's palsy and other causes of paralysis

By Cristiano Antonino On Jul 15, 2022

Bell’s palsy, an overview: the facial (or ‘facial’) nerve is the seventh cranial nerve and comprises two distinct nerves: the facial nerve proper, which contains somatic motor fibres for the innervation of the mimic muscles and other muscles derived from the second branchial arch; the intermediate nerve (Wrisberg’s), which includes somatic and visceral sensory fibres that have a common origin in the geniculate ganglion and lead to the anterior 2/3 of the tongue and to a small area of the auricle, and parasympathetic preganglionic fibres for the lacrimal glands, the submandibular and sublingual salivary glands and the glands of the mucosa of the nose and palate

Facial nerve injuries may manifest as facial paralysis, a situation 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 frequent affliction of the facial nerve (seventh cranial nerve), with an annual incidence of 23 cases per 100,000 individuals.

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

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

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

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

Symptoms and signs

Symptoms and signs are typical: all the mimic muscles on one side of the face are hyposthenic or paralysed: it is impossible to close the eyelid, the corner of the mouth tends to droop and the patient is unable to wrinkle the forehead.

Objective disturbances of sensations are not present, although the patient may report a feeling of ‘weight’ in the face or other abnormal sensations, which may be referred to as ‘numbness’.

In cases of facial nerve involvement proximal to the point of origin of the tympanic cord, there is a loss of gustatory sensitivity of the anterior two-thirds of the tongue.

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

Course and prognosis of facial and Bell’s nerve palsies

Approximately 80% of patients recover within a few weeks or 1-2 months; in about 15%, recovery occurs 3-6 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 5-7 days is a favourable prognostic sign.

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

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

The diagnosis obviously makes use of the anamnesis and, above all, the objective examination.

Differential diagnosis makes use of imaging (CT and MRI).

The anatomo-pathological changes have not been adequately investigated, but the nerve appears swollen and on magnetic resonance imaging (MRI) of the petrous bone a contrast intensification is detected after gadolinium infusion.

Treatment

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From the point of view of therapy, the administration of corticosteroids during the first week is believed to accelerate healing time.

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

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

So-called ‘smile surgery’ is useful in some cases.

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

Permanent facial palsy leads to an abrupt decline in the patient’s quality of life, both socially and professionally, especially in the case of individuals who use the appearance of their face as a work tool (e.g. models, TV presenters…).

The patient with facial palsy tends to isolate himself and has an increased risk of suffering from depression and suicidal ideation: antidepressant medication and psychotherapy are useful here.

Other causes of facial nerve palsy

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

Lyme disease: this is a cause of facial palsy in endemic areas, after tick bites or after a chronic migratory eri theme.
HIV infection: this virus, even in the absence of the manifestations of AIDS, has been identified as a cause of mono- or bilateral facial paralysis in individuals 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 palsies. A rare but typical mode of presentation of sarcoidosis is the association of an acute febrile syndrome with increased volume of the parotid gland and uveitis (Heerfordt syndrome).
Iatrogenic causes: the facial nerve may be accidentally injured during surgery, e.g. to remove a brain tumour.
Compression of the facial nerve by a tumour mass: these masses are usually represented by schwannomas, meningiomas, cholesteatomas, dermoids, carotid glomus tumours or mixed parotid neoplasms.
Herpes zoster: is characterised by inflammation of the facial nerve, geniculate ganglion and contiguous ganglia, manifested by vesicles at the concha of the acoustic meatus and external auditory canal (Ramsay-Hunt syndrome).
Facial dysplegia: most often due to Guillain-Barré polyneuropathy and less often secondary to sarcoidosis (uveoparotid fever or Heerfordt syndrome) or Lyme disease.
Melkersson-Rosenthal syndrome: this is a rare condition whose cause is unknown and is characterised by recurrent facial paralysis, labial oedema and formation of folds on the tongue.
Facial palsy associated with bridge lesions: this condition must be distinguished from supranuclear facial hyposthenia: it may be secondary to infarcts, neoplasms and demyelinating lesions. Association with gaze paralysis or ocular abduction is common.
Facial haemispasm: 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, surgical decompression of the facial root (which is compressed by a small adjacent vessel).
Congenital facial palsy: this is secondary to birth trauma or Mobius syndrome (congenital facial palsy associated with abducens palsy or horizontal gaze palsy); the latter form can be bilateral.
Romberg’s hemiatrophy (facial pseudoparalysis): this is a rare unilateral facial lipodystrophy of unknown aetiology, not associated with hyposthenia.