Neuropathy of the facial nerve in children. Causes, symptoms and treatments for neuritis in children Neuritis in children symptoms and treatment

The causes of mononeuritis of the facial nerve can be very diverse, but most often they are of an infectious nature. Diseases such as influenza, parotitis (mumps), anicteric leptospirosis, tick-borne encephalitis, meningitis of various origins, Infectious mononucleosis, toxoplasmosis and many others, can further lead to the development of complete or partial paralysis of the facial nerve.

The most common factor that can provoke mononeuritis of the facial nerve are banal respiratory diseases, most often of viral origin. Very often, the disease occurs as a complication of the inflammatory process in neighboring organs, especially the ear, since the facial nerve passes in close proximity to it. A special type of lesions of the facial nerve are lesions of a traumatic nature, the causes of which are most often: surgical interventions on the ear, most often due to the inflammatory process, fracture temporal bone, traumatic injuries of bones and soft tissues of the face. Previously, injuries of the facial nerve of newborns associated with the application of obstetric forceps were also separately isolated, but recently such manipulation during childbirth is practically not used.

Often the location of damage to the facial nerve directly depends on its cause. For example, in poliomyelitis and encephalitis, damage occurs most often directly to the nucleus of the facial nerve, which is located in the brain. Other factors most often lead to damage to the underlying parts of the nerve. Especially often mononeuritis of the facial nerve as a complication of inflammation in the ear occurs in children. early age under the age of 1 year.

Clinic, diagnostics

Signs of the disease can be different, which is determined by the level of nerve damage.

Common symptom for all forms of the disease- violation of the functions of the muscles responsible for facial expressions. On the side where the affected nerve is located, facial expressions are almost or completely absent. This is manifested in the smoothness of the frontal folds, the lowering of the eyebrow.

characteristic feature- the so-called "hare's eye", when the eye on the affected side seems to be more widely opened. In addition, due to motor disorders, the patient cannot close it completely, as a result of which constant lacrimation is observed.

When examining a child, it is noticeable that the fold between the nose and upper lip on the side of the damage is smoothed, the cheek is slightly sagging. Some patients bite their lip or cheek slightly on the affected side. One of the corners of the mouth is down. With more significant lesions of the facial nerve, the entire nose and mouth can be completely displaced to the healthy side. As a result of violations of movement and tone in the ear muscles, there is also a displacement of the "sick" ear: it turns slightly forward and to the side. In children infancy violations are even more severe: they cannot even take and suck the breast on their own, as the movements in the muscles of the lips are impaired. In older children, all the above violations are most noticeable when crying, laughing, and various grimaces.

Sometimes it happens that with mononeuritis of the facial nerve, movements are disturbed, while sensitivity does not suffer. Such conditions are observed when the pathological process is localized in the brain, the nucleus of the facial nerve.

When a section of the facial nerve passing inside the facial bone is affected, the signs of the disease are distinctive. There is a combination of movement disorders in the mimic muscles, skin sensitivity disorders, and disorders of lacrimation and blood supply.

A slightly different picture is observed in lower nerve lesions. In this case, a violation of the perception of taste by the tongue within its anterior two-thirds, a violation of the release of tears, an increase in sensitivity to sound stimuli, a violation of skin sensitivity in one or another area of the face, can be detected. Often there are quite strong vascular disorders: redness of the eyes due to the expansion of the vessels of the conjunctiva, uneven coloring of the cheeks. Sometimes lesions of the facial nerve are combined with other neuritis, in these cases other relevant signs are revealed.

In contrast to nerve lesions at other levels, in this case, there is a discharge a large number lacrimal fluid and lacrimation. Also characteristic is the presence of dilations of the vessels of the conjunctiva of the eye on one side and different intensity colors of the right and left cheeks.

In the clinic, there are a number of methods for assessing the severity of certain disorders. For example, to detect violations from the side of the vessels, a test is used, named after the author of the Remka test. For this purpose, solutions are applied to the lower eyelid, leading to vasodilation. Subsequently, the result is evaluated by the degree of expansion of the vessels of the conjunctiva.

In order to determine violations of taste, solutions of common salt and sugar of various concentrations are used. This violation appears at the beginning of the disease and after 1 month is completely restored. At the same time, the rate of recovery of taste sensations in no way depends on the rate of recovery of motor functions of the facial muscles.

In the presence of a lesion from the side of the trunk of the facial nerve itself, it is very hallmark is a violation of sweating, resulting in increased sweating on the affected side.

After 2-3 weeks from the onset of the disease, friendly movements, twitches and muscle tics begin to appear on the affected side of the face, then a violation of their mobility increases. The facial expression of the patient on the side of the lesion becomes poor, the facial expression becomes monotonous (the so-called masked face). Such disorders can be observed only when the nerve trunk is directly affected and never develop during the pathological process in the brain centers. In this case, there may be complaints from the patient about constant causeless pain behind the ear, in the back of the head, in the cheek area, which is most typical for the onset and height of the disease. The pain syndrome develops about a week after the onset of the disease, often it is ahead of movement disorders. In the future, it can last from 1 week to 1 month, its extinction always occurs gradually. Very often, pain does not occur by itself, for no reason, but is associated with hypothermia.

When the brain nuclei of the facial nerve are affected, a very typical symptom is disorders of the balance organs. In the pathological process directly in the nerve trunk, such disorders can also occur, but are extremely rare. They manifest themselves in twitching of the eyeballs, impaired stability in the vertical position of the body, impaired gait, and coordination of movements.

The defeat of the facial nerve in some cases can be combined with herpetic eruptions on the face.

In some cases, during recovery, even after complete restoration of impaired motor functions of the nerve, the patient continues to be disturbed by lacrimation for a long time. Rarely, increased excitability of the facial muscles may persist, which manifests itself in the following: when tapping on the zygomatic arch with a neurological hammer, the facial muscles contract on the side of the same name.

When diagnosing neuritis of the facial nerve, very great importance has an electromyographic study, during which the excitability of the nerve and facial muscles, their contractility and the speed of nerve impulses are determined. Laboratory tests are also used (bacteriological, virological, serological method, etc.) in order to establish the causative agent of the disease.

The temporomandibular joint (TMJ) is a three-way articulation between the mandible and the temporal bone. The TMJ consists of a cartilaginous disc and is surrounded by a capsule that produces a special joint fluid.

Thanks to this fluid, the facial joint moves smoothly, thereby providing a person with articulation and chewing function. Among the existing pathologies of the maxillary joint, arthrosis and arthritis most often occur. Arthritis is manifested by inflammation of the structures of the joint and surrounding tissues.

Arthrosis is dystrophic symptoms TMJ changes.

Causes of inflammation of the temporomandibular joint

Inflammation of the jaw joint usually develops due to the penetration of an infection into it. But often the disease is not infectious, that is, it develops without the participation of microorganisms. Aseptic inflammation may occur due to chronic joint overload or blunt trauma.

Joint overload can be caused by improper prosthetics of missing teeth, or when teeth are missing on one side of the jaw (the other side is doubly stressed).

How does the infection enter the face?

The ways in which infection enters the joint can be very different:

hematogenous with blood from distant tissues and organs;
contact from nearby tissues;
from the outside with open wounds;
lymphogenous with lymph flow.

Contact arthritis and its symptoms

This type of arthritis of the facial joint is the most common. The cause of inflammation of the TMJ in the first place can be:

angina (inflammation of the palatine tonsils);
carbuncles and boils of the temporal region;
phlegmon and abscesses of soft tissues of the facial area;
mastoiditis and otitis media (inflammation of the middle ear);
inflammation of the parotid gland (mumps);
sialadenitis (inflammation salivary glands),
difficult eruption of the wisdom tooth (acute pericoronitis);
osteomyelitis of the temporal bone or mandible.

Note! The root cause of facial arthritis and the source of inflammation can be, for example, a bad tooth. If the treatment of the affected tooth is not started in time, osteomyelitis of the lower jaw may develop.

But often the cause of inflammation of the TMJ is also diseases of the ear and throat.

Causes of development of hematogenous arthritis

If we are talking about the hematogenous path of development of jaw arthritis, the causative agents of infectious inflammation can be:

Rubella, influenza, measles.
Specific diseases (leprosy, tuberculosis, syphilis).
Autoimmune diseases (lupus, rheumatoid arthritis).
Sepsis.
Fungal pathologies.

TMJ Arthritis Symptoms

The inflammatory process of the jaw joint is characterized by the appearance of pulsating pain, which are greatly enhanced by opening the mouth and any attempts to move the jaw.

When pressing on the joint and on the chin, the pain becomes more intense. The area around the TMJ may swell. If nearby soft tissues are involved in the process, hyperemia and swelling of the skin in the ear area may be observed. In this area, it is impossible to take the skin into a fold.

The ability to fully open the mouth is severely limited. The patient cannot open it more than 1 centimeter. The development of an acute inflammatory process is accompanied by the following symptoms:

high body temperature;
dizziness;
chills and others;
symptoms of general intoxication.

As a result of severe edema, the external auditory canal narrows, it seems to the patient that his ear is blocked.

Such symptoms can appear only on one side, for example, with jaw arthritis caused by osteomyelitis of the lower jaw.

Bilateral inflammation of the TMJ is characteristic of hematogenous infections, sepsis, and autoimmune diseases.

Complications of facial arthritis

Complications of arthritis of the jaw joint include phlegmon of the temporal region, sepsis and meningitis. If such a situation arises, pus can break out of the joint cavity and spread beyond it.

First, purulent fluid accumulates in soft tissues, but later it is carried by vessels to other parts of the head, in particular to the dura mater. If the patient has low immunity, this fact contributes to the development of complications. Therefore, in patients with AIDS, such problems occur very often.

Important! Treatment of acute jaw arthritis must be started immediately, otherwise the disease can turn into chronic stage with the development of internal adhesions. First, fibrous ankylosis develops, and then bone ankylosis develops, which occurs against the background of the deposition of calcium salts. Bone ankylosis is dangerous with complete immobility of the joint.

If the lesion is bilateral, a person simply cannot open his mouth, unilateral ankylosis is fraught with significant facial asymmetry.

Establishing diagnosis

To exclude a fracture of the lower jaw in jaw arthritis of traumatic origin, the patient must undergo an X-ray examination. The inflammatory process cannot be detected by this method.

In the picture, you can only notice a slight increase in the joint space, which has developed due to edema. With ankylosis, the joint gap, on the contrary, narrows and can not be detected at all in the picture. In general, diagnostics is clinical symptoms and test results. These measures make it possible to prescribe adequate treatment to the patient.

Treatment of jaw arthritis

Treatment of arthritis of the jaw joint depends entirely on the causes that led to the disease. For example, in arthritis of infectious origin, treatment is based on the use of antibiotics and non-steroidal anti-inflammatory drugs.

If the effect of conservative therapy is minimal and there is a risk of pus getting into the tissues surrounding the joint, the doctor prescribes surgical treatment, which consists in draining the joint.

In traumatic arthritis, the joint must be given maximum rest. A sling-like bandage is applied to the patient, and a plate is placed between the teeth on the side of the lesion, which separates the bite. Thanks to this device, the patient can take liquid food through a tube.

After the disappearance of edema, physiotherapy exercises are recommended to develop the joint. In the case of rheumatoid arthritis of the jaw joint, treatment is prescribed by a rheumatologist. When the acute form of arthritis becomes chronic, physiotherapy is prescribed:

electrophoresis with proteolytic enzymes (ronidase, lidase).
Paraffin therapy.

Many are unaware of the possibility of developing arthritis of the maxillofacial joint, the symptoms and treatment of which have much in common with those of other joint diseases. Pain in the jaw area is most often associated with dental disease. Especially if the pain syndrome was preceded by a visit to the dentist. The temporomandibular joint bears an enormous load. It is almost constantly in motion when a person is awake. With the help of articulation, they chew food, speak and even express emotions. If habitual movements cause difficulty or pain, it may be a sign of arthritis.

Description of the disease

The temporomandibular joint (TMJ) is a paired organ. It unites lower jaw with a skull.

Arthritis of the temporomandibular joint is diagnosed when an inflammatory process appears in the joint. At an early stage of pathology, the focus of inflammation is located in the joint capsule. As the disease progresses, the inflammatory process affects other parts of the joint. If the disease is not treated, the joint may lose its mobility.

The disease often develops after infectious diseases. The infection can spread to the joint from neighboring tissues. Contact arthritis of the TMJ type occurs when:

otitis media;
tonsillitis;
flu
osteomyelitis of the lower jaw;
temporal bone (infectious inflammation of the bone tissue);
angina;
mastoiditis (inflammation of the mucous and bone tissue of the temporal bone);
phlegmon of the parotid-masticatory zone (purulent inflammation of fatty tissue).

Pathogenic microorganisms penetrate the joint cavity, creating a focus of inflammation.

Hematogenous infection of the joint develops against the background of:

syphilis;
gonorrhea;
tuberculosis;
salmonellosis;
measles;
scarlet fever.

Reactive arthritis of the TMJ is found when:

chlamydia;
rubella;
ureaplasmosis;
viral hepatitis;
enteritis.

It develops against the background of meningococcal infection. In such cases, pathogenic organisms do not penetrate into the joint cavity, but are the cause of the disease.

At risk are people who have been diagnosed with rheumatism or rheumatoid arthritis.

Trauma can start the pathological process. Arthritis sometimes begins to disturb a person after a blow or a fall.

Provoke the disease can:

excessive physical activity;
bad habits (nail biting, chewing gum, propping up the cheek or chin);
improperly installed fillings and crowns;
stressful situations;
long open mouth (during a dental procedure);
teeth grinding during sleep (bruxism).

People who are often under stress put excessive strain on their facial muscles, placing an increased strain on the temporomandibular joint.

Signs of exacerbation of arthritis

In acute arthritis of the maxillofacial joint, symptoms can be recognized by dagger pain in the articulation zone, which increases when you try to open your mouth. Sometimes the pain is felt not in the joint itself, but in the ear. It can appear in the temple, in the back of the head and even in the tongue. The nature of the pain syndrome is similar to the signs of neuralgia trigeminal nerve. A feature is the pulsation of pain.

The main symptom of arthritis is a decrease in the range of motion of the joint. The patient has difficulty opening his mouth. The motor function of the jaw is limited.

During an exacerbation of the disease, a swelling is visible in front of the tragus of the ear. The skin in the epicenter of inflammation turns red and becomes very sensitive. When feeling the problem joint, a person feels intense pain.

If maxillofacial arthritis passes into a purulent stage, the person's condition worsens. His body temperature rises to 38°C. From the side of the affected joint, the external auditory canal narrows. The patient partially or completely loses hearing. Ear congestion is observed both on the problematic and healthy sides. A person has severe weakness and dizziness. He loses his appetite and cannot sleep. The patient feels pain during pressure on the chin in an upward and forward direction.

In rheumatic arthritis, both joints become inflamed. During the examination, the patient often reveals heart problems.

In patients rheumatoid arthritis only one TMJ is affected. However, pain is also felt in the hip, knee or shoulder joint.

Chronic form of the disease

If the disease was not cured during acute stage, it gradually becomes chronic. The patient suffers from moderate pain in the joint and around the ear. They may get worse in the morning. When chewing and yawning, the joint clicks, crunches or creaks. It is not possible to open the mouth completely. Articulation movements become limited, they are carried out with effort. It is especially difficult to move the jaw in the morning, after a long rest.

When the jaw drops, it shifts slightly towards the problem joint. If such symptoms appear, arthritis of the maxillofacial joint has become chronic.

With the transition of the disease from an acute form to a chronic one, damage to the auditory canals can disappear on their own. But more often than not, individual hearing problems persist.

Chronic jaw arthritis often causes muscle pain in the back of the head and neck. Painful seals appear in the muscles. In the area of the joint and on the lateral surfaces of the face, discomfort. It is difficult for the patient to talk or chew for a long time. He suffers from headaches.

Over time, asymmetry develops on the patient's face. It becomes skewed towards the affected joint.

Sometimes arthritis of the maxillary joint develops gradually, without an acute stage. In this case, it is difficult to detect it in time. Changes occur slowly and imperceptibly for the patient. Patients often ignore a slight crunch in the joint and aching pain.

When more serious complications develop, it is much more difficult to cure the disease. In the later stages of arthritis, irreversible changes appear. Therefore, it becomes impossible to completely restore the motor function of the joint.

Joint immobilization

If arthritis is diagnosed, the symptoms and treatment depend on the severity. Therapy begins with the appointment of a complete immobilization of the problem joint. If the inflammation appeared as a result of an injury, a fracture is possible. While maintaining motor function, bone fragments can damage nearby tissues. Immobilization will help alleviate the patient's condition until the causes of inflammation are fully clarified.

To fix the jaw, a special sling-like bandage is used. It is a strip of fabric, dissected on both sides in the longitudinal direction. The lower ends of the bandage are placed in front of the ears and tied at the crown of the head. The upper ends are tied at the back at the base of the head. The sling-like bandage keeps the jaw in a closed position. On the side of the affected joint, an interdental plate is placed that separates the jaws. During the acute period (2-3 days), the patient can only eat liquid food. He is not allowed to speak.

Medical therapy

If arthritis of the jaw joint is confirmed, treatment should be prescribed by a doctor. Non-steroidal anti-inflammatory drugs quickly stop pain in TMJ arthritis. The patient is prescribed:

Diclofenac;
Indomethacin;
Nimesil.

Diclofenac is administered intramuscularly, then switched to tablets for oral administration. If the pain is not very strong, Paracetamol is prescribed.

When arthritis is provoked by rheumatic processes, the attending physician prescribes steroid anti-inflammatory drugs:

Prednisolone;
cytostatics (Methotrexate, Leflunomide);
monoclonal antibodies (Adalimumab, Etanercept).

Surgical intervention

If arthritis in the temporomandibular joint is caused by pyogenic pathogens, the surgeon decides whether it is expedient to open the purulent capsule and drain it. Immediately after the operation, broad-spectrum antibiotics (Ceftriaxone) are prescribed intramuscularly. Intramuscular injection of narcotic painkillers (Morphine). Then they switch to non-steroidal anti-inflammatory drugs (Ketorolac, Indomethacin).

The doctor will determine how to treat jaw arthritis after injury. Surgical intervention may be necessary if a fracture of the articular surfaces, rupture of the joint capsule or ligaments has been detected.

Physiotherapy and therapeutic exercises

After the attenuation of the inflammatory process, the patient is prescribed physiotherapy:

electrophoresis;
phonophoresis with hydrocortisone;
diadynamic therapy.

With the rheumatic nature of the disease, there is a high risk of fusion of the articular ends (ankylosis). This complication leads to complete immobility of the joint. To prevent its development, the patient needs to perform a therapeutic set of exercises.

Slightly pressing on the chin, the jaw is slowly lowered, then raised.
During the next exercise, the protruding part of the chin is grasped with fingers. The jaw is gently lowered and raised, pushing it down and back.
The third exercise is performed by pushing the jaw with the fingers, first to the right, then to the left.
During the last exercise, they press their fingers on the chin, pushing the lower jaw forward.
Each exercise should be repeated 2-3 times. If pain occurs, take a break for a few days.

Nicotinic acid, known as vitamin PP or niacin, is used to stimulate blood circulation, the metabolism of amino acids, proteins, fats and carbohydrates, and is also indispensable for enhancing brain activity. This vitamin is used to prevent vascular and heart pathologies, helps to lower blood levels of substances that clog blood vessels, such as cholesterol, lipoprotein and triglycerin.

Nicotinic acid is a regulator of biochemical processes, participates in the control of oxidative and reduction reactions, controls tissue respiration.

daily requirement

The daily requirement for nicotinic acid in men is 16-27 mg, in women - 15-20 mg.

The need increases with:

intense neuropsychic and emotional activity;

living in the conditions of the North;

in people whose activities are associated with a long stay at elevated temperatures;

observance of low-protein diets, as well as in people who fast and vegetarians.

Signs of deficiency and overdose

The lack of vitamin PP in the body can be judged by the following symptoms:

roughness skin, especially in winter;
rashes on the skin, which are bubbles of various sizes that appear on swollen skin of a dark red color;
profuse diarrhea;
burning sensation at the tip of the tongue, swelling and roughness of the tongue;
change in the color of the tongue - the organ becomes scarlet or acquires a shiny (comparable to varnished) appearance;
the appearance of small painless ulcers on the oral mucosa;
swelling of the lips;
decrease or lack of appetite;
malaise, general weakness;
muscle hypotension;
weight loss;
emotional disorders (irritability, tearfulness, apathy, etc.);
sleep disorder;
decreased concentration;
slowing down of psychomotor functions;
baldness, including complete.

The following signs indicate an excess of vitamin PP:

severe hyperemia of the upper body, especially the face;
frequent flushes of blood to the face;
nausea and vomiting;
feeling dizzy;
dry skin and mucous eyes;
an increase in blood glucose levels;
change in heart rate;
muscle pain, spasms;
exacerbation chronic diseases digestive organs;
development of fatty degeneration of the liver.

Application in various fields

In addition to the fact that nicotinic acid is used for the prevention and treatment of certain pathological conditions in traditional medicine, the drug has proven itself well in other areas.

So, for example, due to the ability to dilate blood vessels, niacin brings great benefits to hair, namely, it stimulates their growth. To achieve a similar effect, properly rub the substance into the scalp daily for a month. For the procedure, the drug is used in the form injection solution applied to clean, damp hair. In addition to noticeable hair growth, after a month of using nicotinic acid preparations, cleansing of the scalp from dandruff and strengthening of hair roots is noted.

The use of acid for hair is shown in the video

Successfully a nicotinic acid used for weight loss. Vitamin accelerates metabolism, cleanses blood vessels, corrects cholesterol levels, and helps to eliminate toxins and heavy metals. For weight loss, use the drug in the company of tablets.

Pharmacokinetics

After introduction into the body, the drug is rapidly distributed in the tissues. Accumulation occurs mainly in the liver, kidneys and adipose tissue. It can be synthesized by bacteria in the intestine from tryptophan (comes with food), pyridoxine and riboflavin. The half-life is 45 minutes.

Release form, composition

Pharmaceutical companies produce nicotinic acid in 2 dosage forms: tablets and solution.

Injection

additional substances - sodium bicarbonate, distilled water.

Sold in clear glass ampoules (1 ml/10 mg), 10 pieces per carton. Additionally, instructions for the use of the drug and an ampoule scarifier are included in the package.

The average price per pack is 30-45 rubles.

Tablets

The active substance is nicotinic acid;

additional substances - stearic acid, glucose.

They are sold in dark glass bottles of 50 tablets (0.05 g) each and in blister strips of 10 tablets. A bottle or 5 blisters are placed in a cardboard box. Additionally, the packaging of the drug nicotinic acid contains instructions for use.

The average price per pack is 20-30 rubles.

Dosage, scheme of application

Tablets

It is taken orally, after eating, according to the scheme developed by the attending physician.

With a deficiency in the body of vitamin PP, the drug is prescribed for oral administration after meals, 2 tablets every 8-12 hours. The duration of therapy is 2-3 weeks.

Unless otherwise indicated, for the treatment of other diseases, adults are prescribed 1-2 tablets per day. The maximum single dose is 2 tablets, daily - 6 tablets.

In case of circulatory disorders in the brain, vascular spasms, low acidity, neuritis of the facial nerves, etc., the drug is prescribed in a dosage of 1-2 tablets 4-5 times a day. The duration of treatment does not exceed 30 days.

Injections of nicotinic acid

As an antipellagric agent, a solution of nicotinic acid is prescribed at a dosage of 10 mg 2-3 times a day. The drug is administered subcutaneously, intramuscularly or intravenously. The duration of treatment is 10-14 days.

In the treatment of ischemic stroke, the solution is administered intravenously in a jet at a dosage of 10 mg.

The maximum single dose for an adult patient is 100 mg, the daily dose is 300 mg.

In the treatment of Hartnup's disease, 40-200 mg of the drug is administered per day.

Indications for use

osteochondrosis of various parts of the spine;
ischemic strokes;
circulatory disorders in the brain;
tinnitus;
atherosclerosis;
pellagra;
impaired circulation in the limbs;
hemorrhoids;
diseases of the hepatobiliary region;
diabetes mellitus and its complications;
obesity;
neuritis of the facial nerve;
various pathologies of the liver;
alcoholic, drug, chemical intoxication;
trophic ulcers of the lower extremities;
visual disorders.

As prophylactic niacin is used for:

reducing the risk of developing cancer;
rapid breakdown of fats;
increased acidity in gastritis;
preventing the development of symptoms of hemorrhoids;
increase concentration of attention;
vision improvement/

Contraindications

The drug is contraindicated in case of individual intolerance to nicotinic acid or excipients that make up one or another dosage form.

Intravenous administration of the drug is contraindicated in hypertension.

special instructions

Before injecting the drug, it is necessary to conduct a sensitivity test!

Nicotinic acid should be taken with caution in patients with glaucoma, hemorrhages, gout, hyperuricemia, low blood pressure, with a stomach ulcer and / or 12 duodenal ulcer.

Use in children

The use of nicotinic acid in patients under 10 years of age should be strictly limited.

Use in pregnant women

Niacin is prescribed to pregnant and lactating women only in emergency cases.

Side effects

Side effects are observed in the patient in the first days of taking the drug and, as a rule, pass on their own, without the need to cancel treatment. Undesirable reactions include:

flushing of the face and upper body;
tingling and burning in the face;
dizziness;
decrease in blood pressure;
increased secretion of gastric juice;
soreness, redness and itching at the injection site;
diarrhea.

Overdose

In order to reduce the risk of overdose, treatment with nicotinic acid should be carried out while taking methionine and lipotropic drugs.

Interaction with other drugs

Before starting treatment about all medicines that the patient is taking must be reported to the doctor!

Concomitant use of nicotinic acid and antithrombotic drugs or aspirin increases the risk of bleeding.

The intake of vitamin PP together with antihypertensive drugs enhances hypotension, with antidiabetic agents it neutralizes the therapeutic properties of the latter.

Nicotinic acid enhances the effect of antispasmodics.

The toxic effect of nicotinic acid is enhanced when it is taken simultaneously with lipid-lowering drugs.

When nicotinic acid interacts with alpha-blockers, a sharp decrease in blood pressure occurs.

Interaction with alcohol

When nicotinic acid and alcohol interact, the vitamin is neutralized. Even small doses of alcohol make taking the vitamin useless.

Storage and dispensing from pharmacies

The drug is dispensed without a doctor's prescription. The medicine is stored at a temperature not exceeding 22 degrees, in a dry place away from direct sunlight. The shelf life of the drug is 4 years. The date of manufacture is indicated on the packaging.

Analogues

Nikoshpan - average price: 150-170 rubles.

Electrophoresis for osteochondrosis

in osteochondrosis, for the rapid removal of lactic acid from tissues damaged by inflammation, electrophoresis with nicotinic acid is prescribed. This procedure helps to reduce swelling and eliminate pain at the site of injury. In addition, due to increased blood flow, which occurs under the influence of vitamin PP, the procedure with the use of the drug ensures the rapid flow of other medicines to the affected area.

Action on intoxication

Nicotinic acid has a positive effect on the body with various intoxications. Under influence active substance toxic substances, heavy metals and other toxic substances are very quickly excreted from the body. Nicotinic acid binds free radicals and "neutralizes" toxic substances, neutralizing their effect.

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Symptoms and course of the disease

Clinical manifestations of damage to the facial nerve largely depend on the level of damage.
Usually, neuritis of the facial nerve develops gradually. At the beginning, there is pain behind the ear, after 1-2 days, facial asymmetry becomes noticeable. The development of paralysis of the affected side of the face begins, that is, the patient cannot make any voluntary facial movements. Paresis of facial muscles may develop. During the conversation of the patient, facial asymmetry is clearly visible. The doctor notes the unequal width of the palpebral fissures, the different severity of the nasolabial and frontal folds, the skewed corner of the mouth towards the healthy side of the face. A striking symptom of inflammation of the facial nerve is also the impossibility or obvious limitation of movements of the eyebrows, eyes, cheeks. On the side of the affected nerve, the nasolabial fold is smoothed out, the corner of the mouth is lowered and the face is warped to the healthy side. The patient cannot close his eyelids. When he tries to do this, his eye turns upward (Bell's symptom).

Weakness of facial muscles is manifested by the inability to move them: smile, grin, frown or raise an eyebrow, stretch lips with a tube.

In a patient with neuritis of the facial nerve, 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 taste sensations on the front of the tongue, also innervated by the facial nerve. Dry eyes or watery eyes may occur. In some cases, a symptom of "crocodile tears" develops - against the background of constant dryness of the eye, the patient lacrimation occurs during meals. There is salivation.

On the side of neuritis of the facial nerve, auditory sensitivity (hyperacusia) may increase and ordinary sounds seem louder to the patient.
With a pathology of the nucleus of the facial nerve (for example, with the stem form of poliomyelitis), only weakness of the facial muscles is observed in patients. When the process is localized in the pons of the brain (for example, a stem stroke), not only the facial nerve root is involved in it, but also the nucleus of the abducens nerve that innervates the external muscle of the eye, which is manifested by a combination of paresis of the facial muscles with converging strabismus. Hearing impairment in combination with symptoms of facial neuritis are observed when the facial nerve is damaged at the exit from the brain stem, since there is a concomitant lesion auditory nerve. This picture is often observed with neurinoma in the area of the internal auditory input. If the pathological process is located in the bone canal of the pyramid of the temporal bone to the exit point of the superficial stony nerve, then mimic paralysis is combined with dry eyes, impaired taste and salivation, and hyperacusis. When neuritis occurs in the area from the place of origin of the petrosal nerve to the origin of the stirrup nerve, instead of dryness of the eye, lacrimation is observed. Neuritis of the facial nerve at the level of its exit from the stylomastoid foramen of the skull to the face is manifested only by motor disorders in the muscles of the face.
Allocate Hunt's syndrome - a herpetic lesion of the geniculate ganglion, through which the innervation of the external auditory canal, tympanic cavity, auricle, palate and tonsils passes. Nearby motor fibers of the facial nerve are also involved in the process. The disease starts with severe pain in the ear, extending to the face, neck and back of the head. There are rashes of herpes on the auricle, in the outer ear canal, on the mucous membrane of the pharynx and in the anterior part of the tongue. Characterized by paresis of facial muscles on the side of the lesion and a violation of the perception of taste in the anterior third of the tongue. Perhaps the appearance of ringing in the ears, hearing loss, the occurrence of dizziness and horizontal nystagmus.
Neuritis of the facial nerve mumps accompanied by symptoms of general intoxication (weakness, headache, aching limbs), fever and an increase in salivary glands (the appearance of swelling behind the ear).
Neuritis of the facial nerve 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 neuritis of the facial nerve, a characteristic wrinkled tongue and dense swelling of the face.
Bilateral neuritis of the facial nerve occurs only in 2% of cases. Perhaps a recurrent course of neuritis.

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Treatment of the disease

Treatment should be started as early as possible, because this is the possibility of preventing complications and the occurrence of residual phenomena. In the absence of timely and proper treatment, neuritis of the facial nerve can lead to permanent paralysis (skew) of the face.
With the diagnosis of neuritis of the facial nerve, the treatment is the more successful, the more timely it is started. In this case, it is possible to achieve complete elimination of the symptoms of the disease in 75-80% of cases. The best results in neuritis of the facial nerve are shown by a complex technique, including the use of acupuncture, acupressure faces, special warm-ups and herbal medicine. Together, these therapeutic measures can eliminate the inflammatory process, stimulate regeneration nerve fibers, restore normal functions of the facial nerve and the mobility of facial muscles, improve blood circulation nervous system and enhance local immunity.
In the initial period of neuritis of the facial nerve, glucocorticoids (prednisone), decongestants (furosemide, triampur, glycerol), vasodilators (nicotinic acid, coplamine, theonicol), vitamins of group B are prescribed. Analgesics are indicated for pain relief. With 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. Physiotherapy in the form of non-contact heat (solux) can be used from the first days of the disease. From the 5-6th day - UHF (course of 8-10 procedures) and contact heat in the form of paraffin therapy or ozocerite applications.
Massage and physiotherapy exercises for the affected muscles begin from the second week of the disease. The load is gradually increased. To improve conductivity, anticholinesterase drugs (prozerin, galantamine) and dibazol are prescribed from the end of the second week. Ultrasound or hydrocortisone phonophoresis is used. With a slow recovery of the nerve, drugs are prescribed that improve metabolic processes in the nervous tissue (nerobol). In some cases, it is possible to conduct electrical nerve stimulation.
If the complete recovery of the facial nerve did not occur during the first 2-3 months, lidase and biostimulants (aloe, FIBS) are prescribed. When contractures appear, anticholinesterase drugs are canceled, medocalm, tegretol are prescribed.
Surgical treatment is indicated in case of congenital neuritis of the facial nerve or complete rupture of the facial nerve as a result of trauma. It consists in suturing the nerve or carrying out neurolysis. In the absence of the effect of conservative therapy after 8-10 months and the identification of electrophysiological data on the degeneration of the nerve, it is also necessary to decide on the operation. Surgical treatment of neuritis of the facial nerve makes sense only during the first year, since in the future there comes an irreversible atrophy of the mimic muscles left without innervation, and it will be impossible to restore them.
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 from the healthy side are sutured to the muscles on the affected half of the face. Thus, the 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. Form loading..." data-toggle="modal" data-form-id="42" data-slogan-idbgd="7310" data-slogan-id-popup="10616" data-slogan-on-click= "Price request AB_Slogan2 ID_GDB_7310 http://prntscr.com/mergwb" class="center-block btn btn-lg btn-primary gf-button-form" id="gf_button_get_form_671299">Price request

Diagnosis of the disease

The clinical picture of neuritis of the facial nerve is so bright that the diagnosis does not cause difficulties for the neurologist.

Analysis of complaints and anamnesis of the disease:

how long ago there was weakness of the muscles of the face, dry eyes or watery eyes, a violation of the taste sensitivity of the tongue;
whether any injuries of the face or head were received in the period preceding the development of these complaints;
whether there have been previous episodes of a similar disorder;
whether the patient was ill before the occurrence of these complaints with any ENT pathology (especially inflammation of the inner and middle ear, salivary gland);
whether there were bubbling painful rashes on the skin of the face and torso before the appearance of these complaints.

Neurological examination: assessment of the strength of facial muscles, the presence of lacrimation disorders (dry eyes or, conversely, lacrimation).
Consultation with an otolaryngologist: hearing assessment, examination and palpation of the parotid salivary gland.
To confirm the diagnosis of neuritis of the facial nerve, the symptoms of which bother the patient, as well as to establish the degree of general damage to the facial muscles, electromyography (or EMG) is performed, and appropriate studies are carried out aimed at determining the conductivity characteristic of the facial nerve at this particular stage.
To exclude another type of disease, magnetic resonance or computed tomography may also be prescribed for brain examination.
Electroneurography, electromyography and evoked potentials of the facial nerve are used to determine the location of the pathological process, the degree of nerve damage and the dynamics of its recovery during treatment.

Neuritis of the facial nerve occupies the first place in children among diseases of the peripheral nervous system. Such frequent damage to the nerve is due to the complexity of its anatomical relationships and the location of the nerve - on one of the segments of its path - in the narrow facial (fallopian) canal.

A cosmetic defect arising in connection with paralysis of the facial muscles creates an inferiority complex in patients and limits the range of their activities; a number of professions are not available to them.

Etiology. The disease affects people of all ages. Children make up about 30% of the total number of patients with neuritis of the facial nerve; the vast majority of them are of school age. The causes of damage to the facial nerve in children are varied. The nucleus of the nerve and its intracerebral root are affected during inflammatory processes in the brain stem (encephalitis, poliomyelitis, etc.). In the cerebellopontine angle, the nerve is affected in meningitis and arachnoiditis of various etiologies, fractures of the base of the skull, extending to the pyramid of the temporal bone. With all these diseases, in addition to the facial nerve, other formations are also involved in the pathological process. Along with other nerves, the facial nerve is affected in polyneuritis.

The etiology of solitary (isolated) neuritis of the facial nerve is also varied. In the upper part of the facial canal, this nerve is affected in otitis, and after exiting the skull, in complicated mumps. Damage to the facial nerve can be caused by trauma to the face, and in newborns - when applying obstetric forceps and childbirth in the facial presentation [Bondarenko E. S. et al., 1982]. But the vast majority are patients in whom neuritis of the facial nerve is caused by cooling, general infections, or they are of unknown etiology. Such neuritis is called "Bell's palsy", or "prosopplegia".

Bell's cold paralysis is caused by exposure in some cases to general cooling (prolonged exposure to cold, rain, in a cool room); in others - by predominant cooling of the face (the effect of a through wind in the room, in transport, when working in the field). Bell's paralysis of infectious etiology in the vast majority of cases is caused by the influenza virus, sometimes by the herpes virus, entero- and adenoviruses [Umansky KG, 1978; Bondarenko E. S., Freidkov V. I., 1982]. In a significant proportion of patients, it is not possible to determine the etiology of Bell's palsy. Idiopathic neuritis occurs against the background of complete health. There is reason to believe that in some cases they are due to a latent infection; in others - allergic factors. Bell's paralysis often occurs in the cold season - about 60% of diseases fall in autumn and winter [Alperovich P. M. et al., 1978].

Pathogenesis. The mechanism of damage to the facial nerve during inflammation of the brain and its membranes, as well as organs adjacent to the nerve, does not require special explanation. In all these cases, nerve damage is associated with the spread of the inflammatory process to it. In fractures of the pyramid of the temporal bone, the nerve is usually compressed in the facial canal by hemorrhage or bone fragments.

The pathogenesis of Bell's palsy is less clear. According to modern theories, various etiological factors (cooling, infections) cause damage to the facial nerve in the facial canal, affecting its neurovascular apparatus.

In Bell's paralysis, exposure to cold in the vast majority of cases causes dysfunction of the facial nerve, not so much due to spasm of the vessels that feed it, but due to their subsequent vasodilation with the development of nerve edema and compression. In infectious and idiopathic Bell's palsy, the leading role also belongs to nerve edema. This is also indicated by the location of the nerve lesion: it is usually affected in the distal part of the facial canal, where, due to the peculiarities anatomical structure epineural membrane (at the level of the stylomastoid opening it is thickened and has increased elasticity), conditions are created for nerve compression during its edema [Alperovich P. M. et al., 1978].

Clinic. With otogenic neuritis, damage to the facial nerve develops against the background of acute or chronic purulent otitis media. The clinical picture of inflammation of the parotid gland usually precedes the defeat of the facial nerve with mumps. The development of the disease in Bell's palsy is largely determined by its etiology. In Bell's palsy, the clinical picture usually develops acutely a few hours (often at night, during sleep) after exposure to cold and only sometimes immediately after cooling. In infectious Bell's palsy, the clinical picture develops acutely or subacutely (over 2–3 days), usually after the end of the acute period. infectious disease. Acute or subacute develop and idiopathic neuritis of the facial nerve, and in these cases, paralysis of the mimic muscles especially often develops at night.

Bilateral (isolated) neuritis of the facial nerve are rare. Usually one of the facial nerves is affected, and paralysis or paresis of the facial muscles occurs on the side of the lesion. With paralysis at rest, asymmetry of the face is noted: horizontal folds on the corresponding half of the forehead are smoothed, the eyebrow is lowered; palpebral fissure on the affected side is wider than on the healthy side, blinking is weakened or absent. The tip of the nose is turned to the healthy side, the wing of the nose does not participate in breathing. The nasolabial fold on the side of the lesion is smoothed, the corner of the mouth is lowered and pointed, the mouth is drawn to the healthy side.

Due to paralysis of the frontal muscle, the patient cannot wrinkle his forehead, and therefore horizontal folds are not formed. Due to paralysis of the circular muscle of the eye, the patient is not able to completely close the eyelids; when you try to close your eyes, the palpebral fissure remains open, the eyeball turns outward and upward (Bell's phenomenon). When showing the teeth, the corner of the mouth on the affected side is not pulled back and up, it is pointed due to paralysis of the perioral muscles. Due to paralysis of the circular muscle of the mouth, the patient cannot protrude his lips, fold them into a tube. Paralysis of this muscle also makes it difficult to pronounce labial sounds. The act of chewing is disturbed, because due to paralysis of the buccal muscle, food gets stuck between the cheek and the teeth. On the side of the lesion, the nasopalpebral and superciliary reflexes fade, the corneal and conjunctival reflexes decrease.

With paresis of the facial muscles, the violations described above are less pronounced. In connection with some preservation of the tone of mimic muscles, the asymmetry of the face in patients is absent or slightly expressed; lagophthalmos is expressed unsharply; the nasolabial fold does not completely disappear; preserved, but to a lesser extent than on the healthy side, folds in the forehead. Contractions of facial muscles are possible, but weakened. In infants, paresis of the facial muscles is well detected when crying and determining a number of unconditioned reflexes - nasopalpebral, sucking, proboscis [Bondarenko E. S. et al., 1982].

With diplegia of the facial nerve, the patient's face is mask-like, more noticeable in comparison with a unilateral lesion, chewing and speech disorders. In some cases, the depth of damage to the facial nerves is not the same on both sides.

In addition to motor disorders, patients often complain of pain in the behind-the-ear region and the affected half of the face. Objectively, there is pain when pressing on the mastoid process, in the maxillary fossa, in front of the tragus of the ear, on the trigeminal points, with compression of the skin fold of the cheek. Along with spontaneous and reactive pain in some patients, hyper- or hypoesthesia of the affected half of the face is determined. Pain precedes (for 1 - 3 days) motor disorders or occurs simultaneously with them. These sensory disturbances are mainly associated with damage to the intermediate (Wrisberg) nerve, which is the sensitive part of the facial nerve, but to some extent they may be due to the involvement of the trigeminal nerve and its anastomoses.

Much less often, compared with motor and sensory disorders, there are hearing and taste disorders. The essence of the emerging hearing disorders is reduced to an increased perception of sounds, especially low tones (hyperacusia). However, it should be noted that patients often define this not as an exacerbation of hearing, but as noise in the corresponding ear. Hyperacusia occurs due to paralysis of the stapedius muscle, which pulls the stirrup in the oval window.

Taste disorders are manifested by a decrease or perversion of taste sensations in the anterior two-thirds of the corresponding half of the tongue. They usually occur 1-2 days before the onset of movement disorders and soon disappear. These taste disorders are caused by damage to the tympanic string, which runs for a considerable distance as part of the facial nerve.

The vast majority of patients complain of lacrimation and only a few of dry eyes. Increased tearing occurs when the facial nerve is damaged below the branch of the large stony

Rice. 14. Scheme of the relationship between the facial and intermediate nerves (according to V. A. Smirnov. 1976).

1 - drum string; 2 - stirrup nerve; 3 - large stony nerve; 4 - knee of the facial nerve; 5 - facial nerve; 6 - the nucleus of the facial nerve; 7 - upper salivary nucleus; 8 - the nucleus of a single nerve; 9-exit of the facial nerve from the stylomastoid foramen; 10 - crankshaft; 11 - intermediate nerve; 12 - sensitive descending nucleus of the trigeminal nerve.

nerve. It is caused by constant irritation of the cornea and conjunctiva with dust particles due to paralysis of the circular muscle of the eye. In addition, due to a decrease in the tone of this muscle, the lower eyelid does not fit snugly against eyeball and the tear does not enter the lacrimal canaliculus; the suction action of the lacrimal duct is also lost. A decrease in lacrimation is observed when the facial nerve is damaged above the origin of the large stony nerve to the lacrimal gland. Dryness of the eye and the inability to close it lead to the fact that dust particles and foreign bodies that enter the conjunctival sac are not removed by tears and blinking, causing conjunctivitis and keratitis.

Patients with unilateral neuritis of the facial nerve do not complain about dryness of the mucous membranes of the mouth, since the insufficiency of the function of the submandibular and sublingual glands on the side of the lesion is compensated by the activity of other salivary glands.

Diagnosis. When establishing a diagnosis, it is necessary to find out the etiology of neuritis of the facial nerve and the level of its damage. Nosological diagnosis is established on the basis of clinical picture disease that caused damage to the facial nerve, and laboratory research. To establish the topic of the lesion of the facial nerve, use the scheme proposed by W. Erb (1875) and then supplemented by other researchers (Fig. 14). This scheme is based on two prerequisites: 1) when the facial nerve is damaged, anatomical structures located in the neighborhood are simultaneously affected; 2) fibers of different functional significance, which are part of the facial nerve, leave it for various levels. When the nucleus of the facial nerve or the intracerebral root is damaged, the pyramidal path is involved in the pathological process, as a result of which paralysis of the mimic muscles develops on the side of the lesion, and hemiplegia (Miyar-Gubler syndrome) on the opposite side.

In the cerebellopontine angle, the facial nerve is affected together with the auditory nerve. Sometimes the trigeminal and abducens nerves are also damaged. The clinical picture of damage to the facial nerve at this level is expressed by paralysis of the facial muscles, dry eyes, taste disturbance in the anterior two-thirds of the tongue. In the affected half of the face, spontaneous and reactive pains, an increase or decrease in superficial types of sensitivity are noted. Hyperacusia is usually absent due to damage to the cochlear nerve.

The same symptoms occur when the facial nerve is damaged in the labyrinth of the facial canal (up to the knee of the facial nerve), but instead of hearing loss, hyperacusis appears.

With the localization of the pathological process at the level of the geniculate ganglion, a clinical picture occurs, called Hunt's syndrome. Patients complain of intense pain in the area of the mastoid process, auricle and in the corresponding half of the face. Movement disorders are pronounced. In the external auditory canal, on the auricle, lips, less often - on the mucous membrane of the soft palate and the anterior two-thirds of the tongue, a herpetic rash is observed. Along with these symptoms, a decrease in surface sensitivity on the affected half of the face, a decrease in lacrimation, hyperacusis, and a violation of taste are determined.

With damage to the facial nerve tympanic department of the facial canal, below the origin of the large stony nerve, but above the branch of the stapedial nerve, paralysis of the facial muscles, taste disorder, hyperacusis, and lacrimation occur. Along with this, there are pains and objective disorders of sensitivity in the face. The same symptoms, but without hearing impairment, occur when the facial nerve is damaged in the mastoid facial canal, below the origin of the stapedial nerve and above the branch of the tympanic string. The defeat of the facial nerve in the same section of the canal, but below the branch of the drum string, causes paralysis of the mimic muscles and lacrimation. However, in these cases, pain in the mastoid process and the affected half of the face is often noted.

Laboratory diagnostic methods help to find out the etiology of neuritis and determine the depth of nerve damage. To solve the first problem, in addition to the usual laboratory tests, virological and serological studies. The depth of damage to the facial nerve is characterized by the data of classical electrodiagnostics and electromyography. The state of electrical excitability of the facial nerve and the muscles innervated by it, determined by the first method of research, usually corresponds to the clinical severity of motor disorders: qualitative changes in electrical excitability (complete or partial reaction of degeneration) correspond to paralysis or deep paresis of facial muscles; quantitative changes in electrical excitability - moderate paresis. In an electromyographic study, a global or needle method of diverting biocurrents is used. The absence of bioelectrical signals indicates the depth of damage to the facial nerve with the global method. But to a greater extent, this is evidenced by the appearance of fibrillation potentials on the electromyogram with the needle method.

Forecast and outcomes. The duration of neuritis and its outcome depend on whether the pathological process causes functional (parabiotic) changes in the affected facial nerve or degeneration of its fibers. The development time of the latter ranges from several hours to several days. There are no reliable clinical criteria to predict the outcome of neuritis in the first days. Relative indicators of the severity of neuritis at this stage are paralysis of mimic muscles, intense pain, taste disturbance. More reliable information is provided by electrophysiological methods. The degeneration of the fibers of the facial nerve in classical electrodiagnostics is indicated by the reaction of degeneration; at electromyography - potentials of fibrillations of mimic muscles. However, these indicators can be established not earlier than the 12-14th day of illness.

In the absence of electrophysiological signs of denervation of the facial muscles, the function of the facial nerve is usually fully restored within 3-6 weeks. In the presence of these signs, there is usually an incomplete restoration of nerve function in terms of 2-4 to 6-8 months.

Neuritis of the facial nerve is often complicated by contracture of facial muscles. The conditions that determine the formation of contractures are the severity of motor disorders, their relative stability, the presence of prolonged and intense pain. Contracture occurs against the background of partial regression of mimic muscle paralysis, usually after 3-6 months from the onset of the disease. Contracture of the mimic muscles often accompanies a peculiar symptom known as "crocodile tears". It lies in the fact that in patients on the side of the lesion, a tear reaction occurs during meals. Both the contracture of facial muscles and the symptom of "crocodile tears" are due to irritation of the sensory fibers of the facial nerve. Its source is scars and adhesions formed in the nerve trunk.

Neuritis of the facial nerve recurs in 15% of cases. This primarily applies to Bell's palsy. Repeated neuritis occurs on the same or opposite side and is caused by the same etiological factors as single ones. They are sometimes combined with swelling of the soft tissues of the face on the side of the lesion and a peculiar striation of the tongue ("folded tongue"). This clinical picture was called the Melkersson-Rosenthal syndrome (Fig. 15). The prognosis of repeated neuritis is worse than single; in most cases, they do not end with a complete restoration of nerve function [Starinets G. A., 1975].

Treatment. The effectiveness of the treatment of neuritis of the facial nerve is determined by the extent to which it is able to prevent the degeneration of the fibers of the affected nerve and restore their function. In this regard, with Bell's palsy in the first days of the disease, it is necessary to eliminate ischemia and edema, which cause nerve compression in the facial canal. It is also necessary to eliminate the causes that caused these pathological processes. Given this, traditional therapeutic measures (etiotropic, restorative and resolving agents) have been supplemented in the last 20 years by a number of new methods of treatment. They were the early appointment of vasodilators (eufillin and nicotinic acid intravenously), dehydrating agents, antihistamines and oral corticosteroids, as well as novocaine blockades of the stellate ganglion and acupuncture.

Clinical experience, however, has shown that therapeutic effect vasodilators and dehydrators, as well as oral corticosteroids, does not differ significantly (60% of recovered patients) from the results of traditional methods of treatment [Alperovich P. M. et al., 1981]. This is due to the fact that with these methods of introducing funds into the body pharmachologic effect due to their low concentration, they are insufficient on the affected nerve. Novocaine blockades of the stellate ganglion are somewhat more effective, but their use due to a number of negative properties is hardly advisable. Acupuncture renders healing effect only in milder cases of Well's palsy.

Rice. 15. Recurrent neuritis of the facial nerve. There are swelling of the lips, "folded" tongue.

Pathogenetically justified local (perineural) use of corticosteroids. Possessing anti-inflammatory, decongestant and desensitizing effects, they cause pharmacological decompression of the affected facial nerve. With this method of treatment, there is no side effect of corticosteroids on the patient's body. Perineural hydrocortisone injections are prescribed in the first week of illness. The procedure for their implementation is as follows. After treating the skin of the maxillary fossa with alcohol and iodine at the level of the apex of the mastoid process, an injection is made with a needle connected to a syringe containing 3 ml of a 2% solution of novocaine. Moving the needle anteriorly and upwards, novocaine is simultaneously injected. Depending on the severity of the subcutaneous fat layer, the needle is immersed by 1-1.5 cm and verified by gently pulling the plunger that there is no blood in the syringe. Then fill the syringe with 0.5 - 1 ml of hydrocortisone acetate and inject it into the region of the stylomastoid foramen. Injections are made with an interval of 2-3 days, the course of treatment is 6-12 injections. Any serious complications not visible. Sometimes, with some change in the direction of the needle towards the mandibular joint, patients notice pain during chewing, which soon disappears. Perineural hydrocortisone-vocaine injections give a higher therapeutic effect compared to the methods listed above - 72% of recovered patients. The pain syndrome also regresses faster [Alperovich P. M. et al., 1981].

Our experience allows us to recommend a certain tactic for the treatment of Bell's palsy [Alperovich P. M. et al., 1981], which takes into account their etiology and pathogenesis, the level of damage to the facial nerve, the features of the clinical picture, the stage of the disease. Patients with Bell's palsy need emergency treatment. It should, especially in the early stages of the disease, be carried out in a hospital. In the first week of the disease, etiotropic agents (antibiotics, hexamethylenetetramine, anti-influenza y-globulin, with herpetic infection- interferon, DNase), with catarrhal and idiopathic paralysis - salicylates. All patients, regardless of etiology, are given antihistamines (diphenhydramine, pipolfen) and perineural hydrocortisone-novocaine injections; Sollux is prescribed to the affected half of the face or to the area of the mastoid process - UHF.

From the 2nd week of the disease, all patients with Bell's palsy are prescribed absorbable (iodine preparations) and restorative agents, electrotherapy, massage and gymnastics of the affected half of the face. For patients with a long-term disease, restorative agents are prescribed in 2 stages: first, a course of prozerin and a vitamin B complex (25-30 injections), then the same course of galantamine. In order to increase the reactivity of the body, biostimulants are prescribed (aloe extract - 25-30 injections). In 2 stages, in such cases, electroprocedures are also prescribed: first, stable (15-20 sessions), and then rhythmic galvanization or electrical stimulation of the nerve and facial muscles of the affected half of the face. M. M. Antropova (1971), A. B. Grinshtein (1980) recommend using ultrasound for Bell's palsy.

With otogenic neuritis, in addition to treating the ear, anti-inflammatory, restorative and resolving agents are used, described in the treatment of Bell's palsy. Chronic purulent otitis media complicated by damage to the facial nerve is an indication for surgical intervention. Indications for surgery also occur with some injuries of the facial nerve.

Neuritis of the facial nerve, as already mentioned, is often complicated by contracture of the facial muscles. Treatment methods for neuritis do not play a significant role in its formation. However, when the first signs of contracture appear (friendly movements, fascicular twitches, an increase in mechanical and a decrease in the threshold of electrical excitability of facial muscles), anticholinesterase drugs and stimulating types of physiotherapy should be discontinued, since they can increase the resulting contracture; instead, sedatives (bromides, calcium chloride), diathermy of the affected half of the face or thermal applications are prescribed.

Patients discharged from the hospital with incomplete restoration of nerve function should continue drug treatment (dibazole, glutamic acid) and therapeutic gymnastics. With significant residual effects, mud applications on the affected half of the face may be recommended. In recent decades positive results achieved with surgical treatment Bell's palsy, not amenable to conservative treatment. The essence of the operation is to open the facial canal and decompress the nerve [Kalina V. O., Shuster M. A., 1970; Kettel K., 1959].

Prevention of neuritis of the facial nerve comes down to general measures aimed at preventing many diseases (hardening of the body, prevention of infections and their vigorous treatment). A specific embodiment receives the prevention of recurrent neuritis. In cases where damage to the facial nerve was caused by the presence of an infection in the body (otitis media, chronic tonsillitis, etc.), careful sanitation is necessary. Patients who have suffered Bell's palsy should not hypothermia. In the case of common infections, especially influenza and tonsillitis, special care and careful treatment are necessary. It must be remembered that Bell's paralysis of infectious etiology usually develops not at the height of the febrile period, but after it, and hypothermia contributes to their occurrence. Patients who have undergone Bell's palsy are shown measures aimed at increasing the overall resistance of the body (morning exercises, in the cold season - courses of treatment with multivitamins, antihistamines, exposure to ultraviolet rays). Importance for the prevention of Bell's palsy has the elimination of such adverse factors as drafts, dampness, and sudden changes in temperature in industrial and educational premises.

With neuritis of the facial nerve, inflammation of some part of this nerve occurs, which causes a violation of the transmission of impulses to the muscles of the face. The muscles stop contracting, and the main reflexes also disappear: chewing, blinking, sucking and other reflexes that form facial expressions.
The reason for the formation can be hypothermia, the presence of inflammatory processes, swelling, trauma, as a result of which the nerve canal is infringed. This disease can be primary and secondary.

The emergence of the primary form neuritis of the facial nerve in children occurs under the influence of some thermal or mechanical causes. In this case, the nerve becomes inflamed against the background of the general health of the child. In the presence of certain diseases in children, a secondary form often develops. this disease.

Diseases that provoke the appearance neuritis of the facial nerve in children:
1. Otitis media. In the absence of treatment for otitis media (here you can read), the inflammation gradually spreads over a wider area and can reach the area through which the canal with the corresponding nerve passes;
2. Mumps. At the same time, against the background of a viral infection, intoxication and swelling of facial tissues develop. This, in turn, can lead to infringement of the channel in which the corresponding nerve is located;
3. Shingles(here you can read about), in which the area may be affected auricles and neck, as well as the oral mucosa. As a result of this, the inflammatory process can spread to the region of the facial nerve;
4. Melkerson-Rosenthal syndrome. it congenital disease, which causes periodic episodes of neuritis.

Symptoms that characterize this disease:
1. Pain behind the ear;
2. Facial asymmetry;
3. Violation of mimic movements of the muscles of the face;
4. Loss of taste sensations;
5. Lachrymation;
6. Salivation;
7. Sound distortion in one ear.

That is, with this disease, when you try to close your eyes, the eyelid on the diseased side remains open, a hare eye syndrome appears, when a white stripe of sclera is visible between the iris and the lower eyelid. When children try to close their eyes, fold their lips in a tube, raise an eyebrow, the face is skewed in a healthy direction. With this disease, changes occur both in muscle movement and in the sensory organs from the side of the affected nerve.
Treatment of this disease in children involves an integrated approach. Medical treatment involves the use of dehydrating, vasodilating and vitamin preparations. With very clear inflammatory process anti-inflammatory and analgesic drugs are used. Physiotherapy treatment involves thermal procedures, microwave therapy, UHF, paraffin applications. In some cases, electrical stimulation is indicated.
Therapeutic exercises with a slowly increasing load and massage are also used in the treatment neuritis of the facial nerve in children. Sometimes biostimulants and reflexology are prescribed during the recovery period. With inefficiency conservative treatment resort to surgery.