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 a decrease (paresis) or complete absence (paralysis) of facial movements and the appearance of facial asymmetry. The symptoms depend on which part of the nerve was involved in the pathological process. In this regard, there is a distinction between central and peripheral neuritis of the facial nerve. A typical clinic of facial neuritis does not raise doubts about the diagnosis. However, to exclude the secondary nature of the disease, an instrumental examination is necessary.
ICD 10
G51.0 Bell’s Palsy
General information
The facial nerve passes through a narrow bone canal, where it may be pinched (tunnel syndrome) in inflammatory processes or blood supply disorders. People with an anatomically narrow canal or with facial nerve structure features are more predisposed to the occurrence of facial nerve neuritis. The cause of the development of facial neuritis may be hypothermia of the neck and ear, especially under the influence of a draft or air conditioning.
Classification
There are primary Bell’s palsy, which develops in healthy people after hypothermia (catarrhal facial neuritis), and secondary — as a result of other diseases. Diseases in which facial nerve neuritis can develop include: herpes infection, mumps, otitis media (inflammation of the middle ear), Melkerson-Rosenthal syndrome. Possible traumatic damage to the facial nerve, its defeat in violation of cerebral circulation (ischemic or hemorrhagic stroke), tumors or neuroinfections.
Symptoms
Usually Bell’s palsy develops gradually. At the beginning there is pain behind the ear, after 1-2 days the asymmetry of the face becomes noticeable. On the side of the affected nerve, the nasolabial fold is smoothed, the corner of the mouth is lowered and the face is distorted to the healthy side. The patient cannot close his eyelids. When he tries to do this, his eye turns up (Bell’s symptom). The weakness of the facial muscles is manifested by the inability to make movements with them: smile, grin, frown or raise an eyebrow, pull out the lips with a tube. In a patient with facial neuritis, the eyelids are wide open on the diseased side and lagophthalmos (“hare’s eye”) is observed – a white strip of sclera between the iris and the lower eyelid.
There is a decrease or complete absence of taste sensations on the front of the tongue, also innervated by the facial nerve. Dryness of the eye or lacrimation may occur. In some cases, the symptom of “crocodile tears” develops – against the background of constant dryness of the patient’s eye, lacrimation occurs during meals. Salivation is observed. On the side of Bell’s palsy, auditory sensitivity (hyperacusis) may increase and ordinary sounds seem louder to the patient.
The clinical picture of neuritis may be different depending on the location of the lesion of the facial nerve. Thus, with pathology of the nucleus of the facial nerve (for example, with the stem form of polio), only weakness of the facial muscles is observed in patients. When the process is localized in the bridge of the brain (for example, a stem stroke), not only the root of the facial nerve is involved in it, but also the nucleus of the abductor nerve innervating the external muscle of the eye, which is manifested by a combination of facial muscle paresis with converging strabismus. Hearing disorders in combination with symptoms of facial neuritis are observed when the facial nerve is affected at the exit from the brainstem, since concomitant damage to the auditory nerve occurs. This pattern is often observed with neurinoma in the area of the internal auditory input.
If the pathological process is located in the bone channel of the pyramid of the temporal bone to the exit point of the superficial stony nerve, then mimic paralysis is combined with dryness of the eye, impaired taste and salivation, hyperacusis. When neuritis occurs in the area from the point of departure of the stony nerve to the departure of the strep nerve, instead of dryness of the eye, lacrimation is observed. Bell’s palsy at the level of its exit from the shilosocular opening of the skull to the face is manifested only by motor disorders in the facial muscles.
Hunt syndrome is distinguished — a herpetic lesion of the cranial ganglion, through which the innervation of the external auditory canal, tympanic cavity, auricle, palate and tonsils passes. The motor fibers of the facial nerve located nearby are also involved in the process. The disease begins with severe pain in the ear, giving in the face, neck and back of the head. Herpes rashes are observed on the auricle, in the external auditory canal, on the mucous membrane of the pharynx and in the front of the tongue. Paresis of facial muscles on the affected side and impaired taste perception on the anterior third of the tongue are characteristic. There may be ringing in the ears, hearing loss, dizziness and horizontal nystagmus.
Bell’s palsy in mumps is accompanied by symptoms of general intoxication (weakness, headache, aching limbs), fever and an increase in salivary glands (the appearance of swelling behind the ear). Bell’s palsy in chronic otitis occurs as a result of the spread of the infectious process from the middle ear. In such cases, paresis of facial muscles develops against the background of shooting pains in the ear. Melkerson-Rosenthal syndrome is a hereditary disease with a paroxysmal course. His clinic combines Bell’s palsy, a characteristic folded tongue and dense swelling of the face. Bilateral Bell’s palsy occurs only in 2% of cases. Recurrent course of neuritis is possible.
Complications
In some cases, especially in the absence of adequate treatment, Bell’s palsy can lead to the development of contractures of facial muscles. This can happen after 4-6 weeks from the moment of the disease, if the motor functions of the facial muscles have not fully recovered. Contractures tighten the affected side of the face, causing discomfort and involuntary muscle contractions. At the same time, the patient’s face looks as if the muscles on the healthy side are paralyzed.
Diagnostics
The clinical picture of facial nerve neuritis is so vivid that the diagnosis does not cause difficulties for a neurologist. Additional examinations (MRI or CT of the brain) are prescribed to exclude the secondary nature of neuritis, for example, tumor or inflammatory processes (abscess, encephalitis).
Electroneurography, electromyography and evoked facial nerve potentials are used to determine the location of the pathological process, the degree of nerve damage and the dynamics of its recovery during treatment.
Treatment
Conservative treatment
In the initial period of Bell’s palsy, glucocorticoids (prednisolone), decongestants (furosemide, triamterene), vasodilators (nicotinic acid, scopolamine, xanthinol nicotinate), group B vitamins are prescribed. Blockades are shown to relieve pain. With secondary Bell’s palsy, the treatment of the underlying disease is carried out. During the first week of the disease, the affected muscles should be at rest. Physiotherapy in the form of non-contact heat (solux) can be used from the first days of the disease. From day 5-6 — UHF (a course of 8-10 procedures) and contact heat in the form of paraffin therapy or ozokerite applications.
Massage and physical therapy for the affected muscles begin from the second week of the disease. The load is gradually increased. To improve conductivity, anticholinesterase drugs (neostigmine, galantamine) and bendazole are prescribed from the end of the second week. Ultrasound or hydrocortisone phonophoresis is used. With slow nerve recovery, drugs that improve metabolic processes in the nervous tissue (methandienone) are prescribed. In some cases, it is possible to conduct electroneurostimulation.
If the complete recovery of the facial nerve did not occur during the first 2-3 months, hyaluronidase and biostimulants are prescribed. When contractures appear, anticholinesterase drugs are canceled, tolperizone is prescribed.
Surgical treatment
Surgical treatment is indicated in the case of congenital Bell’s palsy or complete rupture of the facial nerve as a result of injury. It consists in stitching a nerve or conducting neurolysis. In the absence of the effect of conservative therapy after 8-10 months and the identification of electrophysiological data on nerve degeneration, it is also necessary to decide on the operation. Surgical treatment of Bell’s palsy makes sense only during the first year, since in the future there will be irreversible atrophy of the facial muscles left without innervation, and they will no longer be possible to restore.
Facial nerve plasty is performed by autotransplantation. As a rule, the graft is taken from the patient’s leg. Through it, 2 branches of the facial nerve are sewn to the muscles on the affected half of the face from the healthy side. Thus, a nerve impulse from a healthy facial nerve is transmitted immediately to both sides of the face and causes natural and symmetrical movements. After the operation, a small scar remains near the ear.
Prognosis and prevention
The prognosis of facial nerve neuritis depends on its localization and the presence of concomitant pathology (otitis media, mumps, herpes). In 75% of cases, complete recovery occurs, but with a disease duration of more than 3 months, complete nerve recovery is much less common. The most optimistic prognosis is if the lesion of the facial nerve occurred at its exit from the skull. Recurrent neuritis has a favorable prognosis, but each subsequent relapse is more severe and prolonged.
Prevention of injuries and hypothermia, adequate treatment of inflammatory and infectious diseases of the ear and nasopharynx allow to avoid the development of facial nerve neuritis.