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Causes of facial nerve paresis. Peripheral and central paresis of the facial nerve

The facial nerve runs in a narrow canal, which causes its possible damage due to infections, injuries, and hormonal imbalances. When this happens, facial nerve paresis (paralysis) occurs, with possible pain. This disease usually involves weakening of the facial muscles; its symptoms are noticeable: one half of the face “sags”, the folds on it are smoothed out, and the mouth warps to one side. When it is severe, it becomes difficult to cover the eye with the eyelid.

The disease has acute course, develops in a few hours and lasts two weeks (as can be judged from the patient’s medical histories), after which the symptoms, under therapeutic influence or on their own, weaken and go away. Treatment should be prescribed from the first days of the onset of paresis to avoid the development of complications.

When doctors talk about paresis, they mean weakened function. Paralysis means its complete loss and absence of voluntary movements.

When does paresis develop?

The main possible reasons for the development of the disease:

  • traumatic brain injury;
  • infectious diseases (borreliosis, herpes, chicken pox, flu, measles, etc.);
  • hypothermia (mainly, infection develops against its background);
  • circulatory disorders, stroke;
  • otitis;
  • neuro surgical treatment;
  • inflammation of the brain and its membranes;
  • tumors and cysts that can compress the nerve;
  • hormonal imbalance;
  • autoimmune diseases.

If facial nerve paresis is diagnosed in a newborn child, the main cause is birth trauma. Much less often, nerve damage occurs in utero as a result of infection or developmental abnormalities. In an older child, the disease may develop against the background of otitis (since the facial nerve canal originates in the internal auditory canal) or during chickenpox (the facial nerve is exposed to the varicella-zoster virus).

If symptoms of paresis (paralysis) of the facial nerve are recorded, the doctor is faced with the task of finding the causes of this pathology, since it may be concomitant with a serious illness ( tick-borne borreliosis, stroke, tumor). But in most cases, the exact reasons remain unknown.

Types of disease

Facial nerve palsy is divided into two types:

  • peripheral;
  • central.

The first is the most common; it is its symptoms that were described at the beginning of the article. Other signs that accompany the disease:

  • swelling of the cheeks when pronouncing vowels (sail syndrome);
  • rolling the eye upward when trying to close it (lagophthalmos);
  • pain symptoms in some areas of the face, behind the ear and in the ear, back of the head, eyeball;
  • impaired diction;
  • saliva leaking from the corner of the lips;
  • drying of the oral mucosa;
  • increased sensitivity to sounds, ringing in the ears;
  • hearing loss;
  • decreased taste sensitivity;
  • symptoms of eye damage on the affected side: lacrimation or, conversely, drying out of the mucous membrane.

IN mild stage Peripheral facial paresis is sometimes difficult to establish. To do this, they perform a series of tests: they close their eyes and evaluate how difficult it was to do it (one eye can be closed with effort), they stretch out their lips with a tube, frown their forehead, and puff out their cheeks.

Central paresis affects the lower part of the face - one (it is opposite to the lesion) or both.

Its main symptoms:

  • weakening of the muscles of the lower facial part;
  • hemiparesis (partial paralysis of half the body);
  • preservation of the eye and muscles of the upper facial part;
  • unchanged taste sensitivity.

Central paresis is mainly due to or secondary to stroke.

Diagnostic procedures

Treatment of the disease should begin as soon as it is detected. Sometimes paresis of the facial nerve can go away on its own, but in which cases this will happen is difficult to predict.

The symptoms of the disease are quite clear, but before treatment, you must try to determine the reasons that caused the paresis (paralysis). In some cases, elimination of the underlying disease leads to restoration of the function of the facial nerve (this can happen, for example, with a brain tumor). For this purpose, tomography (computer or magnetic resonance imaging) is performed.

In addition, an examination of reflexes on an electroneuromyograph should be prescribed. The procedure allows you to evaluate the speed of impulses passing through the fibers, their number, as well as the location of the lesion. One way to determine the degree of paresis (paralysis) is to conduct electrogustometry.

This procedure is performed using an electroodontometer. An anode is applied to the front of the tongue, the electrodes are located 1.5 cm from the midline. The current strength is gradually increased until the patient registers a sensation of sour or metallic taste.

Paresis therapy

Treatment in the acute period is aimed at relieving swelling and inflammation and improving microcirculation. For these purposes the following is used:

  • corticosteroids;
  • diuretics;
  • antiviral drugs (if the disease occurs due to herpes or chickenpox);
  • antibiotics (with the development of paresis during infection, otitis media).

Gymnastics and massage can be prescribed no earlier than the third day from the onset of the disease and only under the supervision of a doctor, since self-treatment And misuse techniques threatens the appearance of contractures and synkinesis.

  1. The phenomenon of contracture consists of increased muscle tone with pain on the affected side and twitching of the facial muscles. There is a feeling of tightening of the face.
  2. Synkinesis - movements that appear simultaneously with the main ones. This may include wrinkling the forehead or raising the corner of the mouth when closing the eyes. Either raising the ears or flaring the wings of the nose when closing the eyes with effort, etc.

These complications appear, as can be learned from medical histories, in 30% of all cases of facial nerve paresis. If this happens, massage and physiotherapy are temporarily canceled and the muscles are given rest.

Principles of gymnastics and massage

Therapeutic gymnastics consists of certain techniques. It could be:

  • puffing out the cheeks (alternating, simultaneous);
  • snorting, pronunciation of the letter “p” with a delay at the initial stage of movement;
  • manual assistance when performing movements (closing eyes, wrinkling the forehead, etc.), which is performed by a specialist.

One of the recovery methods is post-isometric muscle relaxation, which is alternate short-term isometric work of the muscles and their passive stretching afterwards. This type of gymnastics is performed only under the supervision of a doctor, since it has many nuances in its implementation, failure to do which can lead to complications.

The main massage is carried out from the inside of the mouth, which allows you to define the muscles and increase blood circulation in them. In addition, there is acupressure, since the classic one can lead to muscle strain.

During the recovery period, drugs of group B and alpha lipoic acid, UHF, phonophoresis.

If the lesion is severe, treatment should be aimed at preserving the eye on the affected side of the face. Drops are used to eliminate and prevent dry mucous membranes, but if the eyelid does not droop at all, this threatens the development of keratopathy and blindness. Doctors can stitch the eyelids together, insert upper eyelid implants for its forced lowering. Currently, the injection of botulinum toxin is popular, which lasts 2-3 weeks. Injections are also effective in combating contractures and can be used for aesthetic facial correction in the future.

During the acute period of the disease, it is not recommended to treat the affected side of the face mechanically, using treatment methods such as massage and gymnastics. At home, you need to use a patch that will fix the weakened muscles on the sore side of the face. Your doctor will show you how best to do this.

Features of the course of the disease and treatment in childhood

A disease in children that is secondary in nature (that is, another disease is the cause of its occurrence) is usually accompanied by pain in the parotid region. In some cases, pain and discomfort may be experienced in various parts of the face and back of the head, depending on the location of the nerve damage.

In a child, paresis of the facial nerve usually goes away faster than in an adult.. In this case, complications may be completely absent or their degree may be minimal. Symptoms of the disease in childhood more often than in adults they can regress on their own. However, it is necessary to treat paresis, since there is no guarantee that it will go away without therapy.

In a newborn who has suffered nerve damage during childbirth, in addition to visual signs, damage to some reflexes is noted: palatine, search, sucking, proboscis. A complication that occurs with this pathology in an infant is difficulty or complete inability to suck on the mother’s breast. In this case, feeding is carried out from a bottle with a lightweight nipple.

Therapy

Treatment for paresis begins in the maternity hospital. standard scheme. In some cases, doctors do not use corticosteroids because their use infancy may result in complications.

A child with damage to the facial nerve often suffers from hyperacusis - it is necessary to protect him from loud sounds and not use rattles.

After the maternity hospital, treatment for paresis continues on an outpatient basis: during the recovery period, massage and physiotherapy can be prescribed. Available to parents at home therapeutic exercises, with the help of which reflexes are evoked in a child.

  1. The palmo-oral reflex is caused by pressing the parent's fingers on the middle of the child's palm: the baby's mouth opens slightly.
  2. To trigger the proboscis reflex, you need to lightly touch the baby’s lips with your finger: his lips should stretch into a tube.
  3. The search reflex is caused by stroking the baby's cheek near the corner of the lips, after which the baby moves his mouth towards.
  4. The sucking reflex is formed thanks to the pacifier.

Also, at home, parents continue treatment with medications prescribed by the doctor. Massage, heating and any other influences should not be carried out independently - only in a clinic with a specialist. This will avoid the appearance of contractures and synkinesis.

If the pathology at birth is diagnosed as congenital, surgical treatment is indicated.

So, facial nerve paresis - pathological condition, which occurs acutely and is characterized by weakening of the muscles of one side of the face (peripheral paresis) or the lower facial part (with the central type). The causes of this phenomenon often remain unclear, but they may include tumors, infections, neurosurgical interventions, and in newborns, birth trauma. Treatment of the disease begins with medication from the first day to avoid complications. During the recovery period, massage and therapeutic exercises can be added.

Treatment of facial paralysis represents a difficult problem for both the doctor and the patient. This potentially disabling disease can have many causes, so a detailed understanding of the differential diagnosis and available treatments is necessary to select the correct management.

For optimal cosmetic and functional results all patients with facial paralysis treatment should be provided taking into account individual characteristics course of the disease with the participation of a team of various specialists.

Frequency of occurrence facial paralysis depends on its etiology. More detailed information is provided to the following articles on the site - we recommend using the search form on home page site.

A) Classification of facial paralysis. A reliable method for assessing facial nerve function is the House-Brackmann scale. It is not applicable to patients with facial synkinesis. Other scales have also been proposed that assess the degree to which paralysis affects the physical and mental state of the patient.

b) Anatomy of the facial nerve. The facial nerve enters the temporal bone through the internal auditory canal and then follows the bony fallopian canal. Most often, compression and paralysis of the nerve due to various inflammatory processes occur precisely in this segment of the nerve. After emerging from the stylomastoid foramen, the facial nerve passes through the parenchyma of the parotid salivary gland, therefore, in the preauricular region, the nerve is protected by glandular tissue.

Then, within its thickness, the facial nerve divides into five main branches, which leave the gland deeper from the superficial muscular aponeurotic system (SMAS). Anterior to the parotid salivary gland, the distal branches of the nerve communicate with each other, so here the fibers of the facial muscles can be innervated by several nerves at once.


Educational video of the anatomy of the facial nerve and the projection of its branches

If you have problems watching, download the video from the page

V) Congenital causes of facial paralysis:

1. Birth trauma. During childbirth, several factors can contribute to injury to the facial nerve with subsequent paralysis. These include the use obstetric forceps, birth weight more than 3.5 kg, first pregnancy. The provoking factor is compression of the fetus as it passes through the birth canal. Under these conditions, the facial nerve is extremely susceptible to injury from stretching, and it takes time to restore normal function.

In general, the prognosis is extremely favorable; 90% of children experience full recovery functions of the facial nerve without any surgical or pharmacological interventions. In rare cases when there is high risk Nerve rupture may require surgical exploration.

2. Mobius syndrome. Mobius syndrome, first described in the 19th century, is characterized by combined paralysis of the facial and abducens nerves, which may be caused by underdevelopment of the peripheral part of the nerves or insufficient functioning of the nuclei of the brain stem. Sometimes there is damage to other cranial nerves. Clinically, there is a violation of the mobility of facial muscles; it is difficult for patients to display any emotions on their faces.

Other symptoms and signs include incomplete lip closure, drooling, decreased self-esteem, and social isolation. All these factors aggravate the general condition. In patients with this syndrome, free muscle tissue transplantation is successfully used to restore the function of facial muscles. It is highly advisable to carry out surgical treatment before starting school in order to prevent psychological trauma that a child may receive due to insults from peers in reality. early stage your life path.

3. Melkersson-Rosenthal syndrome. Melkersson-Rosenthal syndrome is characterized by a triad of recurrent facial nerve paresis, facial swelling, and folded tongue. In the treatment of exacerbations, glucocorticosteroids and anti-inflammatory drugs are used. There is no consensus on how to treat and prevent facial paresis. Some descriptions of individual cases provide information about decompression of the facial nerve (opening the bony walls of its canal to prevent compression of the nerve as swelling increases), according to which the long-term prognosis for restoration of nerve function turns out to be more favorable when using such a fairly aggressive treatment tactic.

4. Hemifacial microsomia. The group of hemifacial microsomia includes a whole series congenital developmental anomalies, which are based on underdevelopment of one half of the face. The syndrome is characterized by a deficiency of soft tissues on one side of the face, underdevelopment of the lower and upper jaw, external ear. In the presence of combined facial nerve paresis, surgery for it can be performed simultaneously with craniofacial reconstruction of the jaws and ear. Particularly useful in restoring facial symmetry and the patient's ability to smile is the use of free muscle grafts, one of the additional effects of which is to add volume to the facial area.


Course of the prepared facial nerve.
Temporal part: 1 - meatal segment; 2 - labyrinth segment; 3 - drum segment; 4 - mastoid segment.
Extratemporal part: 5 - temporal branches; 6 - zygomatic branches; 7 - temporofacial portion;
8 - buccal branches; 9 - cervical branches; 10 - marginal mandibular branch; 11 - neck part; 14 - extratemporal part.
Other structures: 12 - duct of the parotid gland; 13 - parotid gland.

G) Infectious causes of facial paralysis:

1. Bell's palsy. Bell's palsy is also known as idiopathic facial palsy. However, the data recent years indicate that most cases of Bell's palsy are caused by a virus herpes simplex. The incidence is about 30 cases per 100,000 people. Paralysis usually develops within 24-72 hours. It may be accompanied by pain around the ear, decreased taste, and decreased hearing on the affected side. And although in the vast majority of patients, nerve function gradually returns to normal, some of them continue to have limited mobility of the facial muscles, which is often combined with periodic aberrant twitching (syncinesia).

IN acute phase diseases, glucocorticosteroids and antiviral drugs can be successfully used to improve the recovery of nerve function. In some cases where the electrical activity of the nerve is significantly reduced during the first two weeks (see examination section below), surgical decompression of the facial nerve canal should be considered. If restoration of nerve function has not occurred and synkinesis persists, a rehabilitation option that has a chance of success is chemical denervation of the nerve (paralysis) using botulinum toxin A followed by an intensive course of physical therapy.

2. Hunt syndrome. Hunt's syndrome (herpes zoster oticum) occurs when the virus is reactivated Varicella zoster(human herpes virus 3) in the area of ​​the facial nerve. Other symptoms include ear pain and the formation of vesicles (zoster oticus). Other symptoms may also occur: hearing loss, tinnitus, dizziness, nausea and vomiting, which are believed to occur due to irritation of the vestibulocochlear nerve, located near the facial nerve in the thickness temporal bone. Although there are no randomized controlled trials evaluating the effectiveness various methods treatment for this rare pathology, a combination of corticosteroids, antivirals, and analgesics can be used successfully to suppress facial nerve inflammation.

This treatment regimen is based on experience with the treatment of facial paralysis (corticosteroids), as well as Herpes zoster lesions in other parts of the body (which are treated with antiviral drugs). In Hunt syndrome, the prognosis for restoration of facial nerve function is poor. After resolution of the infectious process, patients often continue to be bothered by chronic neuralgia(pain).

3. Otitis media and mastoiditis. Otitis media and mastoiditis are acute inflammation of the mastoid process, which in rare cases (less than 1%) can lead to facial paralysis. It is believed that nerve damage is caused by swelling of the surrounding tissue and exposure to bacterial toxins. Successful treatment consists of timely recognition and eradication of infection, which includes the use of broad-spectrum antibiotics and myringotomy with the installation of a ventilation tube to obtain material for culture. In some cases of mastoiditis, mastoidectomy (removal of the affected mastoid tissue) is indicated. If all of the above measures are performed, the prognosis for restoration of nerve function is favorable.

4. Cholesteatoma. Cholesteatoma is a slowly growing cystic formation epithelial origin, which over time causes destruction of surrounding tissues with their compression and the appearance of lesions chronic inflammation. The incidence of facial paralysis with cholesteatoma reaches 3%. Timely diagnosis And surgical removal cholesteatomas are necessary for the successful elimination of compression of the facial nerve that develops against the background of chronic inflammation and infection. Unfavorable prognostic signs include the spread of cholesteatoma to the apex of the pyramid (deep part of the temporal bone) and untimely surgical treatment. In patients who surgical care was provided in the early stages, the likelihood of restoring the function of the facial nerve is highest.

5. Lyme disease. Lyme disease is caused by the pathogen Borrelia burgdorferi, which enters the human body through the bite of a tick infected with the microorganism. TO typical symptoms and signs acute stage diseases include headache, weakness, fever and chronic migratory erythema (characteristic skin rash, which occurs at the site of a tick bite). And although concomitant damage to the facial nerve can occur in 11% of cases, its function is completely restored in 99.2% of patients. Lyme disease should always be kept in mind when treating patients living in endemic areas who develop symptoms after tick bites in the summer. On the website of the US Centers for Disease Control and Prevention you can find a map that shows the frequency of occurrence of the disease in different US states. To confirm the diagnosis and start antibacterial therapy antibody level determination is required. Treatment is carried out in accordance with the recommendations of the Infectious Diseases Society of the United States.


6. Other. A number of other infectious diseases can manifest as dysfunction of the facial nerve. These include HIV infection, tuberculosis, infectious mononucleosis and others. In most cases, these diseases are accompanied by a number of other symptoms; for a correct diagnosis, the doctor must be extremely alert. When carrying out differential diagnosis, it is necessary to take into account the patient’s medical history and the presence of relevant risk factors. The basis of treatment is correctly selected pharmacotherapy, except in cases where mastoiditis is detected as a result of additional examination. In this case, a mastoidectomy is performed to eradicate the infection and reduce swelling around the nerve.

d) System and neurological causes facial paralysis. These include autoimmune diseases, diabetes, sarcoidosis, Guillain-Barre syndrome, multiple sclerosis and others. In rare cases, these diseases manifest as isolated facial paralysis. In most cases, with timely diagnosis and prompt initiation of adequate treatment, it is possible to restore nerve function.

e) Traumatic causes of facial paralysis. Head and skull injuries are one of the most common causes of acquired facial paralysis. If the injury was blunt and there are no fractures or soft tissue injuries, the integrity of the facial nerve is preserved and its function is likely to be restored. If nerve damage is suspected (penetrating injury to the skin and soft tissues of the face), immediate surgical revision of the wound is required to restore the integrity of the nerve. IN ideal conditions surgery should be performed within three hours of injury while stimulation of the distal fragment remains possible to allow identification of the nerve during surgery.

At combination of facial skeleton trauma With a fracture of the temporal bone, damage to the facial nerve occurs in 10-25% of cases. Depending on the relationship of the fracture line to the longitudinal axis of the temporal bone, the following types of fracture are distinguished: longitudinal (80%), transverse (10%) and mixed (10%). Facial nerve paralysis is more often observed with transverse (50%) fractures rather than longitudinal (20%). Complete restoration of nerve function is most often observed with delayed development. On the contrary, in 50% of cases of acute paralysis, recovery is extremely poor. Often, due to existing extensive injuries to the facial area and other emergency conditions, diagnosis and assessment of facial nerve function is not carried out in a timely manner. However, postponed surgery, which can be carried out even several months after the injury, still has a sufficient chance of restoring or improving the function of the facial muscles.

Iatrogenic facial nerve damage may occur during operations on facial tissues, the skull, or during intracranial interventions. The choice of treatment method depends on the extent of nerve damage. In severe cases, restoring the integrity of the nerve is impossible, which is why it is necessary to resort to other methods.

e) Tumors as a cause of facial paralysis. Removal of tumors that penetrate the facial nerve or are located in close proximity to it often requires significant exposure to the nerve, which may result in its partial or complete transection. The most common tumors affecting the facial nerve include acoustic neuroma (vestibular schwannoma), glomus tumors, facial neuroma, and parotid carcinoma. If during the operation the integrity of the facial nerve was preserved, careful monitoring of its condition is required in the postoperative period. To clarify the prognosis, electrical stimulation of the nerve can be performed at the end of the operation. Corticosteroids are not usually used in this situation because several studies have clearly shown their lack of effectiveness in this setting. After surgery, electromyography (EMG) can be used to assess the process of reinnervation of the facial muscles.

Depending from the recovery stage(as well as individual patient preferences and difficulties), several simple techniques can be used to ensure eyelid closure, facial asymmetry, and complete lip closure.

and) Possible complications. If the integrity of the facial nerve has been successfully restored (or was not damaged initially), resolution of the paralysis depends on the regeneration of axons and their growth into the facial muscles. With pathological regeneration, there may be a change in the direction of the axons, or their branching to many fibers at once. As a result of this process, synkinesis occurs, which are involuntary twitches of facial muscles during their contraction.
To others possible complications Paralysis of the facial nerve includes severe dryness of the eyeball with subsequent keratopathy, incomplete closure of the lips with the flow of saliva, and constant biting of the cheek.

Central paralysis of the facial nerve is caused by damage to the nerve at the level of the nuclei and brain stem, peripheral paralysis occurs when the nerve is damaged in the area from the internal auditory canal to the stylomastoid foramen.

With central paralysis of the facial nerve, a dysfunction of the facial muscles of the lower part of the face is characteristic; with peripheral paralysis, all facial muscles suffer.

Peripheral facial paralysis is accompanied by a number of features. Damage to the facial nerve in the internal auditory canal can cause dizziness and hearing loss. When the nerve is damaged at the level of the geniculate ganglion and the petrosal nerve, dry eye (xerophthalmia) appears in the clinical picture. When affected at the level of the stapedius muscle, hyperacusis (painful perception of loud sounds) is characteristic. When the facial nerve is injured at the level of the chorda tympani, taste sensitivity in the anterior 2/3 of the tongue is lost and salivation decreases. To quickly assess the level of damage to the facial nerve, you can use the scheme of N. Curtin (1986).

A comprehensive diagnosis of the area of ​​damage to the facial nerve can be carried out using electrophysiological ones. acoustic and audiological research methods. The first work on acoustic reflexometry (study of thresholds, latency and amplitude characteristics of the stapedial reflex) was carried out by A. I. Lopotko (1976) at the ENT Department of the First Leningrad Medical Institute.

Damage to the VII nerve causes peripheral paralysis of the facial muscles (prosopoplegia). Even with a simple examination, the sharp asymmetry of the face is striking (Fig. 29). The affected side is mask-like, the folds of the forehead and the nasolabial fold are smoothed out, the main fissure is wider, the corner of the mouth is lowered. When the forehead wrinkles, no folds form on the side of paralysis (the m. frontalis is affected); When you close your eyes, the palpebral fissure does not close (lagophtalmus) due to weakness of m. orbicularis oculi. In this case, the eyeball moves upward (Bell's phenomenon), moreover on the affected side than on the healthy side. With lagophthalmos, increased lacrimation is usually observed (for exceptions, see below). When showing teeth, the corner of the mouth on the affected side is not pulled back (m. risorius), and the m. platysma myoides on the neck. Whistling is impossible, speech is somewhat difficult (m. orbicularis oris). As with any peripheral paralysis, a degeneration reaction is observed, the superciliary reflex (and corneal) is lost or weakened.

The height of the lesion of the facial nerve should be determined depending on the symptoms accompanying the described picture.

When the nucleus or fibers inside the brain stem are damaged (see Fig. 28), damage to the facial nerve is accompanied by central paralysis or paresis of the limbs of the opposite side (Millard-Gubler alternating syndrome), sometimes with the addition of lesion n. abducentis (Fauville syndrome).


Damage to root n. facialis at the site of its exit from the brain stem is usually combined with lesions of n. acustici (deafness) and other symptoms of the lesion cerebellopontine angle(see Fig. 22). Paralysis of the facial nerve in these cases is not accompanied by lacrimation (dry eye), there is a disturbance of taste in the anterior two-thirds of the tongue, and dry mouth may be felt. Hyperakusis is not observed due to concomitant damage to the VIII nerve.

During processes in the area of ​​the bone canal up to genu n. facialis, i.e. above the origin of n. petrosi superficialis majoris, along with paralysis, dry eyes, taste disturbances and salivation are also noted (see Fig. 28); on the hearing side, hyperakusis is observed here (damage to the fibers of the n. stapedii). With a lesion in the bone canal below the origin of n. petrosi, the same disorders of taste, salivation and hyperakusis are observed along with paralysis, but instead of dry eye, increased lacrimation occurs. In case of damage to the facial nerve in the bone canal below the origin of n. stapedii and above chordae tympani (see Fig. 28) paralysis, lacrimation, taste disorders and salivation are observed. Finally, when the nerve is damaged in the bone below the origin of the chordae tympani or after it exits the skull through the foramen stylomastoideum, only paralysis with lacrimation is observed without those accompanying symptoms discussed with higher lesions.

The most common are recent cases with peripheral localization of the process, and paralysis is usually one-sided. Cases of diplegiae facialis are quite rare. It should be noted that with peripheral paralysis of the facial nerve, especially at the onset of the disease, pain in the face, in the ear and in its circumference (especially often in the mastoid region) is very often observed.

This is explained by the presence on the face of rather intimate connections (anastomoses) with branches of the trigeminal nerve, possible passage sensory fibers of the V nerve in the canalis facialis (chorda tympani - canalis Fallopii - n. petrosis superficialis major), simultaneous involvement in the process of the facial nerve and the root of the trigeminal nerve or its node in processes at the base of the brain (see Fig. 22).

Central paralysis (paresis) of the facial muscles is observed, as a rule, in combination with hemiplegia. Isolated lesions of the facial muscles central type are rare and are sometimes observed with damage to the frontal lobe or only the lower part of the anterior central gyrus. It is clear that central paresis facial muscles is the result of a supranuclear lesion of the tractus cortico-bulbaris in any part of it (cerebral cortex, corona radiata, capsula interna, cerebral peduncles, pons). With central paralysis, the upper facial muscles (m. frontalis, m. orbicularis oculi) are almost not affected, and only the lower (oral) muscles are affected. This is explained by the fact that the upper cell group of the nucleus of the VII nerve has bilateral cortical innervation, in contrast to the lower one, the cells of which are approached by fibers of the central nerves (tractus cortico-bulbaris) mainly only from the opposite hemisphere.

With central paralysis of the facial muscles, unlike peripheral paralysis, a degeneration reaction will not be observed; the brow reflex is preserved and even strengthened.

Phenomena of irritation in the area of ​​the facial muscles include various types of tics (a manifestation of neurosis or organic disease), contractures that may be a consequence of peripheral paralysis of the VII nerve, localized spasm, other clonic and tonic convulsions (cortical or subcortical hyperkinesis).

Facial nerve palsy is neurological disease, characterized by impaired functioning of the motor nature of facial muscles localized on one side of the face. The pathogenesis of the development of the disease is based on a change in the transmission of nerve impulses due to damage to the trigeminal nerve.

The main distinguishing feature of the disease is asymmetry and lack of motor activity of part of the face. Such disorders prevent a person from expressing his emotions through facial expressions and speaking fully.

Reasons for development

Trigeminal nerve paresis can act as an independent nosological entity, as well as as a symptom of concomitant pathology. In most cases, the main one is the inflammatory nature of the disease. The causes are different, so it is customary to classify the disease:

  • primary lesion (idiopathic);
  • secondary, as a consequence of an inflammatory process or injury;

The facial trigeminal nerve may lose its ability to conduct impulses, characterized by inflammation and swelling of the nerve. Its main symptom is trigeminal neuralgia. In addition, neuritis can be a complication of otitis media and have an infectious (types of herpes infection) or non-infectious origin (trauma).

The causes of paresis also include disruption of the local blood supply to the nerve and parts of the central nervous system, for example, due to coronary disease, as well as as a result of the appearance of a tumor-like neoplasm or trauma.

Factors that contribute to facial nerve paresis are strong and prolonged exposure low temperatures on the body, background diseases - diabetes mellitus, complications of an existing pathology - stroke due to hypertension, the effect of certain medications in the treatment of atherosclerotic vascular lesions, as well as surgical intervention.

Despite the nature of the disease, treatment should be aimed at restoring the lost functions of the facial nerve and correcting concomitant pathology.

Clinical manifestations of paralysis

The functions of the trigeminal nerve are considered to provide motor activity and sensitive perception of the face. Based on this, we can assume the consequences of paresis of this nerve. Among all the symptoms, the main ones are:

  • loss of movement on one side of the face due to lack of nerve impulses from the brain’s regulatory center;
  • weakness of the muscles responsible for facial expressions;
  • lack of ability to close an eye, raise or frown eyebrows, puff out cheeks;
  • It becomes difficult to reproduce speech correctly and take liquid food;
  • dry eyes along with involuntary lacrimation;
  • an aversion to loud music develops, a change in taste preferences and increased salivation.

Treatment of paresis

Therapeutic tactics for facial nerve paresis should consist of several points:

  1. Removal of the causative factor of the disease.
  2. Drug therapy.
  3. Physiotherapeutic procedures.
  4. Massage.

Thus, an integrated approach makes it possible to cure facial nerve paresis without residual effects. However, it should be remembered that the restoration of previous functions takes a long time and takes up to six months.

If nerve paresis has developed as a result of otitis, then it is necessary to include in the treatment anti-inflammatory drugs that reduce swelling of the trigeminal nerve trunk. Also, the main focus is to ensure a constant outflow of purulent contents from tympanic cavity. For this purpose, paracentesis is performed. In heavy and advanced cases opening of the mastoid process is used.

If not produced timely treatment otitis, and the inflammatory process persisted for more than 3 weeks, then there is a high probability of facial paralysis due to mastoiditis or toxic damage trigeminal nerve. If there is a persistent impairment of muscle motor ability, surgical intervention is performed - elimination damaging factor nerve in the bone cavity.

Motor disorders, in particular paresis, respond well to integral therapy. The effectiveness directly depends on the start time and duration of use of the course, as well as on the degree of damage to the trigeminal nerve. If started early, the recovery rate reaches 80%.

The therapeutic course consists of physiotherapy and reflexology methods. In particular, electro- and acupuncture, acupressure, electromassage and the use of laser are widely used. IN in some cases courses of electrophoresis, magnetic therapy and mud procedures are used.

The main effects of these procedures are aimed at:

  • elimination of the inflammatory reaction and swelling of the nerve and surrounding tissues;
  • activation of blood circulation and delivery of nutrients to nerve cells;
  • stimulation of restoration processes in the trigeminal nerve;
  • increasing the level of local immune defense;
  • elimination of concomitant pathology.

Physiotherapy and reflexology used to treat the disease can be used by everyone. Their properties ensure safety combined with high efficiency for the body. In addition, their regular use in parallel with medications has a positive effect not only on the affected area, but also on the body as a whole. Physiotherapy can also reduce adverse reactions after taking medications.

The consequence of the full course of treatment is an improvement in the motor activity of facial muscles, a reduction or absence of facial asymmetry and other manifestations of the disease, restoration of the functions of the trigeminal nerve and the elimination of concomitant pathology, which became the causative factor in the occurrence of paresis.

Facial nerve paresis in children

Paresis of the facial nerve in children can be congenital or acquired. As with adults, main reason The development of paralysis is considered to be trigeminal neuritis. At the same time, it should be noted that restoration of lost nerve functions in childhood occurs much faster and more often than in adults. In newborns, the incidence of the disease is at the level of 0.1-0.2%, almost all of which occur due to birth trauma.

The provoking factor for the occurrence of paresis is considered to be the use of forceps during childbirth and the inappropriate size of the woman’s pelvis to the fetal head. In addition, this group includes excess fetal weight (from 3.5 kg), hemorrhage in brain tissue, intrauterine injuries, a long anhydrous period of labor and the damaging effects of drugs or radiation on the body of a pregnant woman. A pathognomonic sign of the traumatic nature of the development of paresis in newborns is hematotympanum and hemorrhage behind the ear.

The tactics for treating facial nerve paresis in children depend on the cause of the pathology. In the case of a congenital anomaly, the chances of recovery are not high enough and treatment does not imply emergency surgery. Diagnosis of paresis should include certain methods that can confirm or exclude the disease. It is necessary to start with assessing the general condition of the baby, identifying all neurological symptoms, as well as identifying concomitant diseases. Next you should use additional instrumental methods diagnostics, such as electroneurography, EMG and tomographic methods for visualizing lesions.

Electroneurography should be performed in the first two days after birth. If there is a reaction of the distal part of the nerve in response to stimulation, then the cause of the development of paresis was injury. The probability of complete restoration of the lost functions of the trigeminal nerve reaches 100%. If the cause of paralysis is serious congenital anomalies that cannot be corrected, then the facial nerve is unable to perform its functions.

To make a diagnosis, they also use questioning of parents for the presence of craniofacial pathology or anomalies of the development of the nervous system in relatives. In some cases, a muscle biopsy may be used.

What is facial nerve paresis? We will discuss the causes of occurrence, diagnosis and treatment methods in the article by Dr. V. N. Efimenko, a neurologist with 41 years of experience.

Definition of disease. Causes of the disease

Facial nerve paresis- this is a polyetiological pathological condition, which is manifested by weakness of the facial muscles innervated by the facial nerve. Found in at different ages, both in adults and children.

Causes of weakness of the facial muscles:

1. Causes due to damage to the central motor neuron:

  • stroke (ischemic - 85%, hemorrhagic - 15%);
  • brain tumors (metastatic or primary, localized in the hemispheres of the brain or its stem);
  • brain abscess;

2. Causes due to damage to the peripheral motor neuron:

  • Bell's palsy;
  • (may be HIV-associated);
  • infection caused by the herpes simplex virus;
  • vasculitis;
  • sarcoidosis, Behçet's disease, periarteritis nodosa, Sjögren's syndrome, ;
  • : bacterial (pneumococcus, meningococcus, Haemophilus influenza, tuberculosis, borreliosis, syphilis, fungal infections);
  • temporal bone fracture;
  • temporal bone tumors: metastatic, invasive meningioma;
  • middle ear infections and tumors;
  • tumors or infections of the parotid gland;
  • traumatic injuries to the face;
  • internal rupture of the carotid artery;
  • effect of drugs (chemotherapeutic agents);
  • consequences of installing a cochlear implant;

3. Diseases that affect neuromuscular synapses:

  • myasthenia gravis;
  • botulism;

4. Diseases that affect the facial muscles:

  • muscular dystrophy;
  • myopathies.

Of the most common reasons in 2/3 of cases of paresis of the facial muscles, idiopathic neuropathy of the facial nerve (Bell's palsy) is detected. Infectious lesions of the nerve by the herpes zoster virus can occur in Ramsay Hunt syndrome. Among other infections, neuropathy of the facial nerve can occur with Lyme borreliosis and mumps. In the pontine form of polio, the motor nucleus of the facial nerve may be affected. In addition, damage to the facial nerve can occur with many systemic infections (syphilis, tuberculosis, HIV infection and others). With Guillain-Barré syndrome, paresis of the facial muscles is included in clinical picture diseases. Many authors consider bilateral neuropathy of the facial nerve as erased form of this syndrome. Involvement of the facial nerve can also occur in systemic diseases connective tissue(nodous periarteritis, systemic lupus erythematosus, Sjogren's syndrome and others), as well as sarcoidosis, amyloidosis, etc.

Inflammatory processes in the middle ear can spread to the facial nerve. Recurrent neuropathy of the facial nerve in young people may be a manifestation of Melkerson-Rossolimo-Rosenthal syndrome, which is hereditary and localized in the 9p14 gene.

Other causes include a tumor process, for example, damage to the facial nerve with acoustic neuroma, carcinomatosis of the meninges, arachnoid epithelioma of the base of the skull and others. Traumatic lesions occur with fractures of the base of the skull. Nerve damage can also occur after operations on the middle ear, pyramid of the temporal bone, and salivary gland.

Metabolic disorders with diabetes mellitus may also manifest as involvement of the facial nerve with complex mechanism, characteristic of diabetic neuropathies. In older patients, damage to the facial nerve can occur with hypertension, cerebral atherosclerosis and other angiopathy, when the process involves small vessels that supply the nerves.

Paresis of the facial muscles can also develop with supranuclear damage to the corticonuclear pathways during focal processes in the hemispheres and brain stem above the nucleus of the facial nerve. The so-called “central paresis of the facial nerve” occurs. In rare cases, other causes of facial muscle paresis are possible (for example, myasthenia gravis, facial forms of myopathies, etc.).

Symptoms of facial paresis

It is very important for a practicing physician not only to identify symptoms of damage to the facial nerve, but also to determine the topical (local) level of its damage, which is important for establishing the causes and mechanism of the disease (etiopathogenesis) and targeted treatment.

There are central and peripheral paresis of the facial nerve. Central paresis is different in that it causes weakness of the muscles of only the lower part of the face (smoothness of the nasolabial fold, drooping corner of the mouth, etc.), while the upper part remains intact (undamaged). This is due to the fact that upper part the nerve nuclei have bilateral cortical representation. In addition, on the side of the paresis there may be symptoms of damage to the pyramidal tract in the arm and leg (central hemiparesis, hyperreflexia, pathological reflexes, and others).

In all cases of peripheral damage, the facial muscles are affected: prosoparesis or prosoplegia occurs (decreased or loss of strength of the facial muscles). The patient on the affected side has a reduced number of folds on the forehead, limited eyebrow mobility, the eye does not close completely, and when closing eyeball moves upward (Bell's sign), the nasolabial fold is smoothed, the cheek "sails" when inflated, it is impossible to whistle, liquid pours out of the mouth, does not participate in movement saphenous muscle neck.

The level of nerve damage helps to determine associated symptoms. Most often the nerve is damaged in the canal of the facial nerve of the pyramid of the temporal bone. In this case, prosoparesis is accompanied by symptoms of damage to the intermediate nerve (n. intermedius).

Diagram of the facial and intermediate nerves (n. Intermedius). 1-5 - levels of nerve damage

Symptoms of nerve damage, depending on the level of damage, are presented as follows:

  • when the nerve in the cerebellopontine angle is damaged, symptoms of prosoparesis (VII pair) and hearing impairment (VIII pair) occur;
  • with high damage to the nerve in the canal before it leaves it n. petrosus major the patient has prosoparesis in combination with dry eyes, hyperacusis (perception of any sounds as too loud) and decreased taste in the anterior 2/3 of the same half of the tongue;
  • when the nerve is damaged below the origin of the greater petrosal nerve, prosoparesis, lacrimation, hyperacusis and decreased taste on half of the tongue are detected;
  • with damage to the nerve below the origin n. stapedius there will be prozoparesis in combination with lacrimation and decreased taste in the anterior 2/3 of the same half of the tongue;
  • when the nerve is damaged at the exit from the canal after its departure chorda thympani There will only be prosoparesis and lacrimation.

Tearing due to damage to the facial nerve can be explained by several reasons. On the one hand, when the eye is not completely closed, the mucous membrane is constantly irritated, which, while maintaining lacrimal innervation, leads to increased tear production. On the other hand, when the orbicularis oculi muscle relaxes, the lower eyelid droops somewhat, and the tear, without getting into tear duct, pours out through the eyelid.

Ramsay Hunt's neuralgia, which occurs as a result of herpetic lesions of the geniculate ganglion, is manifested by a combination of paresis of the facial muscles with herpetic rashes on the eardrum, skin auricle and/or external auditory canal. Sometimes there is tinnitus and hearing loss.

Melkerson-Rossolimo-Rosenthal syndrome is characterized by a triad: recurrent angioedema of the face, folded (“geographic”) tongue and peripheral (sometimes recurrent) paralysis of the facial muscles.

Pathogenesis of facial nerve paresis

Central paresis of the facial nerve occurs due to damage to the fibers of the corticonuclear pathway during processes in the hemisphere or brain stem (stroke, tumor, abscess or injury).

When a nerve is damaged in the canal of the pyramid of the temporal bone, the pathogenetic mechanisms may be ischemia, edema and compression of the area of ​​the facial and structures of the intermediate nerves in the canal. This is one of the models of compression-ischemic neuropathy. With Guillain-Barre syndrome and multiple sclerosis autoimmune mechanisms are included in the pathogenesis. In Hunt syndrome, there may be direct damage to nerve structures by the herpes zoster virus, which may cause poor recovery of nerve function.

In the pathogenesis of facial nerve paresis, a special place is given to traumatic injuries with traumatic brain injuries, which are accompanied by a fracture of the pyramid of the temporal bone, and surgical interventions, for example, neurosurgical removal of an acoustic neuroma or operations on the parotid gland.

Possible defeat small vessels, feeding the nerve ( vasa nerve) for diabetes mellitus, hypertension, vasculitis and vasculopathies. Poliomyelitis causes damage to the motor neurons of the facial nerve nucleus.

Classification and stages of development of facial nerve paresis

There are central and peripheral paresis of the facial nerve.

In addition, the disease is divided into primary neuropathy of the facial nerve (idiopathic neuropathy of the facial nerve, Bell's palsy) and secondary neuropathy (due to herpetic infection, tumors, mesotympanitis, trauma and other processes).

  • acute period - the first month from the onset of the disease;
  • subacute period - recovery is delayed by more than 1-1.5 months;
  • residual effects and complications.

The identified courses of illness are important when choosing a method of treatment and rehabilitation (for example, reflexology, electrical stimulation and others).

Complications of facial nerve paresis

Complications in the acute period include damage to the mucous membrane of the eye, especially with high damage to the nerve in the canal, before the separation of tear fibers and the development of keratoconjunctivitis.

TO late complications include spasmoparesis of facial muscles, the development of pathological synkinesis (involuntary muscle contractions) and “crocodile tears” syndrome (lacrimation while eating).

Diagnosis of facial nerve paresis

Anamnesis is studied and possible risk factors and suspected causes are identified. For example, the incidence of facial neuropathy is higher in people suffering from arterial hypertension, diabetes mellitus (about 4 times) and in pregnant women, especially in the third trimester (about 3.3 times). With idiopathic neuropathy of the facial nerve, there may be indications of hypothermia (riding in vehicles with open window, air conditioning, etc.). In addition, it is important to identify associated symptoms, such as fever and other infectious manifestations, damage to other organs and tissues, as well as changes in laboratory tests.

The onset of the disease is usually acute; slow development of symptoms may indicate a tumor process. With Ramsay Hunt syndrome or mastoiditis, at the onset of the disease there may be complaints of pain in the post-auricular area.

A neurological examination allows you to distinguish central paresis of the facial muscles (mainly the lower part of the face suffers) from peripheral paresis, as well as clarify the level of nerve damage. To do this, it is necessary to identify accompanying symptoms, such as lacrimation or dry eyes, hyperacusis, decreased taste in the anterior 2/3 of the tongue.

Consultation with an otolaryngologist is necessary to exclude inflammatory processes in the ear or pyramid of the temporal bone, as well as herpetic rashes on the eardrum or in the ear canal. If you suspect Lyme borreliosis or other infectious disease A consultation with an infectious disease specialist is indicated; if sarcoidosis or tuberculosis is suspected, a consultation with a phthisiatrician is indicated.

From laboratory methods necessary general analysis blood, as well as a blood sugar test. Testing for Lyme borreliosis in some countries is mandatory for mono- and polyneuropathies. In addition, screening for syphilis and HIV infection is carried out.

MRI of the brain is especially indicated if there is a suspected lesion of the brain stem or base of the brain (for example, neuroma of the cochleo-vestibular nerve). Computed tomography is superior in its diagnostic value to MRI in visualizing basal skull fractures. A study of cerebrospinal fluid is indicated for symptoms indicating the possibility of meningitis, encephalitis, vasculitis and other diseases.

Electroneuromyography (needle and stimulation), in addition to confirming the diagnosis, is necessary to assess the dynamics of the reinnervation process in the facial muscles.

Treatment of facial nerve paresis

Treatment goals are aimed at quickly restoring the function of the nerve and paretic muscles, as well as preventing complications. Treatment should begin as early as possible.

For idiopathic neuropathy, treatment traditionally uses a short course of glucocorticoids in high doses, for example, oral prednisolone 1 mg/kg per day for seven days, followed by rapid withdrawal. Timely treatment with glucocorticoids increases the rate of full functional recovery by 17%.

If you suspect herpes infection, including for Hunt syndrome, antiviral drugs are prescribed: 200 mg of acyclovir 5 times a day, or 500 mg of valacyclovir 3 times a day, or 500 mg of famaciclovir 3 times a day. At purulent otitis and mastoiditis, antibacterial therapy is prescribed.

Treatment of paresis of the facial muscles in Guillain-Barre syndrome or multiple sclerosis is carried out in accordance with the recommendations for the treatment of these diseases. For diabetes important has regulation carbohydrate metabolism and microcirculation.

Non-drug treatment includes facial gymnastics. The effectiveness of physiotherapeutic methods and reflexology has not been proven. But in some cases, with slow recovery, properly performed reflexology speeds up the recovery process.

When the first signs of spasmoparesis or synkinesis appear, it is necessary to discontinue anticholinesterase drugs and stimulating methods of physiotherapy. In this situation use thermal procedures facial and muscle relaxation exercises, including post-isometric muscle relaxation (PIRM) and biofeedback (BFE).

Surgical treatment can be used for congenital narrowness of the fallopian canal and deep paresis of the facial muscles in the acute period. The effectiveness of the operation is higher when performed in the first two weeks of the disease. Such operations are performed extremely rarely in specialized centers. Surgical treatment is also carried out for neuroma of the VIII pair or purulent mastoiditis.

Forecast. Prevention

The prognosis for life is favorable. In approximately 2/3 of cases, especially at a young age, complete restoration of function occurs. In 13% of cases, minimal residual symptoms persist; in 16% of patients, recovery is incomplete with the development of spasmoparesis and synkinesis. The prognosis is worse for herpetic lesions of the geniculate ganglion (Ramsay Hunt syndrome), as well as in elderly people, with diabetes mellitus, arterial hypertension, in people with severe paralysis of the facial muscles in the acute period, in cases of nerve damage due to operations. Also worse prognosis with recurrent neuropathy of the facial nerve (for example, with congenital narrowness of the nerve canal or with Melkerson-Rossolimo-Rosenthal syndrome).

Primary prevention the disease does not exist. In cases where congenital narrowness of the canal is detected, surgical treatment is possible. It is also justified to prescribe adequate anti-edematous therapy at the very beginning of prosoparesis in Melkerson-Rossolimo-Rosenthal syndrome.

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