Bell’s palsy

Definition

Facial nerve neuritis (Bell’s palsy) is an inflammatory lesion of the nerve innervating the facial muscles of one-half of the face. As a result, weakness develops in these muscles, leading to reduced (paresis) or complete absence (paralysis) of facial movements and asymmetry. Symptoms of facial neuritis depend on which part of the nerve was involved in the pathological process. In this regard, a distinction is made between central and peripheral facial neuritis. A typical clinic of facial neuritis does not cause doubts about the diagnosis. However, an instrumental examination must be conducted to exclude the secondary nature of the disease.

General information

The facial nerve runs in a narrow bony canal, where it can be pinched (tunnel syndrome) by inflammatory processes or blood supply disorders. People with an anatomically narrow canal or peculiarities of the facial nerve structure are more prone to facial neuritis. Hypothermia of the neck and ear area, especially under the influence of a draft or air conditioning, may also cause facial neuritis.

Classification

A distinction is made between primary facial neuritis, which develops in healthy people after hypothermia, and secondary neuritis due to other diseases. Diseases that can cause facial neuritis include herpetic infection, epidemic mumps, otitis media (middle ear inflammation), and Melkersson-Rosenthal syndrome. Traumatic damage to the facial nerve is possible, as is damage due to cerebral circulatory disorders (ischemic or hemorrhagic stroke), tumors, or neural infections.

Symptoms of facial neuritis

Usually, facial neuritis develops gradually. In the beginning, there is pain behind the ear; facial asymmetry becomes noticeable after 1-2 days. On the side of the affected nerve, the nasolabial fold is smoothed, the corner of the mouth is lowered, and the face is tilted to the healthy side. The patient cannot close his eyelids. His eye turns upward when he tries to do so (Bell’s symptom). Weakness of the mimic muscles is manifested by the inability to make movements with them: smile, grin, frown or raise the eyebrow, pull the lips into a tube. 

There is a decrease or complete absence of taste sensation on the front part of the tongue, also innervated by the facial nerve. Dry eye or lacrimation may occur. In some cases, the symptom of “crocodile tears syndrome” develops – against the background of constant dryness of the eye, the patient has tear production during meals. On the side of facial neuritis, it may increase auditory sensitivity (hyperacusis), and ordinary sounds seem louder to the patient.

The clinical picture of neuritis may be different depending on the location of the facial nerve lesion. Thus, when the pathology of the nucleus of the facial nerve (e.g., in the stem form of poliomyelitis), patients have only weakness of the facial muscles. When the process is localized in the bridge of the brain (e.g., stem stroke), it involves not only the root of the facial nerve but the nucleus of the diverting nerve innervating the external muscle of the eye, which is manifested by a combination of paresis of facial muscles with convergent strabismus. Hearing disorders, in combination with symptoms of facial neuritis, are observed when the facial nerve is affected at the exit of the brainstem because there is a concomitant lesion of the auditory nerve. It is often seen with neurinoma in the area of the internal auditory entrance.

Hunt’s syndrome is a herpetic lesion of the ganglion, which innervates the external auditory canal, tympanic cavity, auricle, palate, and tonsils. The process involves and located nearby motor fibers of the facial nerve. The disease begins with severe pain in the ear, radiating to the face, neck, and back of the head. There are herpes rashes on the ear drum, the external ear canal, the pharynx’s mucous membrane, and the tongue’s front. Paresis of mimic muscles on the affected side and impaired taste perception in the anterior third of the tongue are characteristic. Tinnitus, hearing loss, dizziness, and horizontal nystagmus may occur.

Facial nerve neuritis in epidemic parotitis is accompanied by symptoms of general intoxication (weakness, headache, limb pain), fever, and enlargement of salivary glands (swelling behind the ear). Facial neuritis in chronic otitis media occurs due to the spread of the infectious process from the middle ear. In such cases, paresis of mimic muscles develops against the background of shooting pain in the ear. Melkersson-Rosenthal syndrome is a hereditary disease with an attack-like course. Its clinic combines facial neuritis, characteristic folded tongue, and dense facial edema. Bilateral facial neuritis occurs in only 2% of cases. A recurrent course of neuritis is possible.

Complications

In some cases, especially in the absence of adequate treatment, facial neuritis can lead to the development of contractures of the facial muscles. It can occur 4-6 weeks after the onset of the disease if the motor functions of the mimic muscles have not fully recovered. Contractures tighten the affected side of the face, causing discomfort and involuntary muscle contractions. The patient’s face looks as if the muscles on the healthy side are paralyzed.

Diagnosis

The clinical picture of facial neuritis is so vivid that the diagnosis is not difficult for a neurologist. Additional examinations (MRI or CT of the brain) are prescribed to exclude the secondary nature of neuritis, such as tumor or inflammatory processes (abscess, encephalitis).

Electroneurography, electromyography, and evoked potentials of the facial nerve are used to determine the location of the pathologic process, the degree of nerve damage, and the dynamics of its recovery during treatment.

Treatment of facial neuritis

Conservative treatment

In the initial period of facial neuritis, glucocorticoids (prednisolone), anti-edema agents (furosemide, triamterene), vasodilators (nicotinic acid, scopolamine, xanthinol nicotinate), and B vitamins are prescribed. Blockades are indicated for the treatment of pain syndrome. In secondary neuritis of the facial nerve, the underlying disease is treated. During the first week of the disease, the affected muscles should be at rest. 

Massage and physiotherapy for the affected muscles are started from the second week of the disease. The load is gradually increased. To improve conduction, anticholinesterase drugs (neostigmine, galantamine) are prescribed from the end of the second week. In some cases, electroneurostimulation is possible.

If the facial nerve has not been completely restored during the first 2-3 months, hyaluronidase and biostimulants are prescribed. If contractures appear, anticholinesterase drugs are discontinued, and tolperisone is prescribed.

Surgical treatment

Surgical treatment is indicated in cases of congenital facial neuritis or complete rupture of the facial nerve as a result of trauma. It consists of suturing the nerve or performing neurolysis. If there is no effect from conservative therapy after 8-10 months and the detection of electrophysiological evidence of nerve degeneration, it is also necessary to address the issue of surgery. Surgical treatment of facial neuritis makes sense only during the first year since later, there is irreversible atrophy of mimic muscles left without innervation, and it will be impossible to restore them.

Facial nerve grafting is performed by autotransplantation. The graft is usually taken from the patient’s leg. Through it, 2 branches of the healthy facial nerve are sewn to the muscles in the affected half of the face. In this way, the nerve impulse from the healthy facial nerve is transmitted to both sides of the face simultaneously and causes natural and symmetrical movements. After the operation, a small scar is left near the ear.

All these treatment options are available in more than 700 hospitals worldwide (https://doctor.global/results/diseases/bells-palsy). For example, Facial nerve repair can be done in 28 clinics across Germany for an approximate price of $5,2 K (https://doctor.global/results/europe/germany/all-cities/all-specializations/procedures/facial-nerve-repair). 

Prognosis and prevention

The prognosis of facial neuritis depends on its localization and the presence of concomitant pathology (otitis media, parotitis, herpes). In 75% of cases, the nerve completely recovers, but with the disease lasting more than three months, complete nerve recovery is much rarer. The most optimistic prognosis is if the facial nerve lesion occurred at its exit from the skull. Recurrent neuritis has a favorable prognosis, but each subsequent relapse is more severe and prolonged.

Prevention of trauma and hypothermia and adequate treatment of inflammatory and infectious diseases of the ear and nasopharynx can avoid the development of facial neuritis.