Trigeminal neuralgia (facial or trigeminal neuralgia, painful tic, Fothergill's disease, tic douloureux)

Neurologist (algologist)

Vasilenko

Marina Gennadievna

Experience 26 years

Head of the Pain Treatment Center, neurologist-algologist, member of the Society of Neurologists and Neurosurgeons, Russian Society for the Study of Pain, Association of Interdisciplinary Medicine, International Association for the Study of Pain (IASP)

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The trigeminal nerve is the largest of the 12 cranial nerves, specifically their fifth pair. It belongs to the nerves of a mixed type and includes very sensitive fibers. This name is due to the fact that the nerve is divided into three branches, providing mobility and sensitivity of the face, mucous membranes of the mouth and teeth. These are the ophthalmic, maxillary and mandibular branches.

Inflammation of the trigeminal nerve is a serious pathology that causes severe pain in the facial area. Otherwise it is called neuritis. In turn, neuralgia is pain along the trigeminal nerve. It can act as an independent sensitivity disorder, but it often accompanies inflammation, i.e. neuritis.

Symptoms and signs

Acute trigeminal neuralgia causes sudden and very severe pain along the nerve fiber. It manifests itself in attacks and is shooting and burning in nature. On average, the duration of an attack is up to 3 minutes; in approximately 7% of patients it lasts up to 3 days. Their number can reach 200 per day.

Pain from trigeminal neuralgia can be observed in different parts of the face. It all depends on which branch of the nerve was affected:

• if maxillary - in the area of ​​​​the facial muscles, upper jaw and nose.
• mandibular – the pain will resemble a toothache.
• ophthalmic – in the area of ​​the temples, forehead and above the eyebrows.

Against the background of pain, the patient develops increased anxiety and even phobias. A person strives to avoid those poses and movements that provoke unpleasant sensations in him. Other characteristic symptoms of inflammation of the trigeminal nerve:

• facial muscle spasms;
• increased salivation;
• increased or decreased sensitivity of facial skin;
• moderate increase in temperature;
• weakness and muscle pain.

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Causes and risk factors

Neuralgia of the trigeminal nerve branch is a disease with many possible causes. First of all, this is compression by vessels: displaced arteries or veins. Inflammation can also be provoked by metabolic disorders and diseases that are associated with them. These are diabetes mellitus, gout and other similar pathologies.

There are other possible causes of trigeminal neuralgia:

• inflammations that occur during dental treatment;
• hypothermia (general or facial area);
• mental disorders;
• purulent diseases of the jaw bones or skull;
• infection of the body with worms;
• chronic caries or sinusitis;
• infectious and viral diseases (herpes, adenoviruses, mumps, pulmonary tuberculosis, herpes zoster);
• very severe allergies;
• brain tumors;
• inflammation of the outer, middle or inner ear;
• multiple sclerosis;
• too narrow canal of the facial nerve from birth;
• injuries or operations on the temporal bone.

Causes

Facial neuritis occurs under the influence of the following etiological factors:

• in 15% of patients this is damage to the branches of the nerve during surgical interventions on the middle ear, mastoid process, and also associated with otitis media and other lesions of the hearing organ, for example, cholesteatoma;
• in rare cases, the disease is caused by infection - herpes virus (Hunt syndrome), mumps, polio, influenza, as well as Lyme disease, transmitted through tick bites;
• in 75% of cases, the cause of neuritis of the facial nerve cannot be determined; in this case, they speak of Bell's palsy, which worsens after hypothermia and colds.

Other causes include head trauma, surgery on the salivary gland, and removal of an acoustic neuroma.

Possible complications

Over time, symptoms of inflammation of the trigeminal nerve can give rise to neuropathic complications and lead to the development of secondary pain syndrome in the head. In the chronic form of the disease, the auditory and facial nerves are irritated. Without treatment, trigeminal neuralgia can lead to more serious complications:

• dystrophy of masticatory muscles;
• decreased sensitivity of the affected area;
• Sykinesia (cooperative movements in which one nerve controls many muscles);
• contracture and spontaneous contraction of the facial muscles;
• conjunctivitis.

Location and functions of the facial nerve

The facial nerve controls muscle movements in this anatomical region. This gives a person the opportunity to smile, express emotions with facial expressions, cry, and wink. Facial neuritis can lead to severe physical disability that is poorly tolerated psychologically. Although in most cases the symptoms of the disease gradually disappear, this requires long-term rehabilitation.

The facial nerve is the seventh of 12 paired cranial nerves. Each person has 2 facial nerves, corresponding to the right and left halves of the face. This nerve is adjacent to the eighth nerve, the auditory nerve, and passes through the structures of the middle ear, the mastoid process, and the parotid salivary gland, where it splits into many small branches.

When to see a doctor

If you experience symptoms of trigeminal neuralgia, you should immediately consult a doctor, as it may be a sign of another serious disease. In the treatment of neurological pathologies, accurate and timely diagnosis is extremely important. This is done by a neurologist, with whom you can make an appointment at our clinic in the center of Moscow. The specialist knows not only how to relieve trigeminal neuralgia, but also how to correctly diagnose it in order to prescribe effective treatment in the future.

Diagnosis of the disease

Modern medicine has in its arsenal many diagnostic techniques that make it possible to determine the type of neuralgia and the cause of its occurrence:

• visual examination and questioning of the patient;
• X-ray of the jaw;
• MRI of the brain and blood vessels;
• laboratory analysis of urine and blood;
• electromyography.

Diagnosis is carried out by a neurologist, but additional examinations by other specialists are often required: dentist, ophthalmologist, otolaryngologist. Particular attention is paid to differential diagnosis, since neuralgia may resemble other diseases in its symptoms, in particular glaucoma, otitis media, ethmoiditis, Slader syndrome, etc.

Diagnosis of trigeminal neuralgia

A preliminary diagnosis can be made by a neurologist based on the patient’s complaints, studying the history of his disease and an objective examination of the face with an assessment of symmetry at rest and when trying to smile. Also, during the consultation, the doctor may conduct additional tests, asking the patient to close his eyes, purse his lips, frown, etc.

Laboratory and instrumental diagnostics of trigeminal neuralgia include the following examinations:

• general blood and urine tests;
• computed tomography (CT) and magnetic resonance imaging (MRI);
• radiography of the paranasal sinuses;
• panoramic radiography of the oral cavity;
• electroneuromyography to determine the localization of inflammation.

Treatment

Treatment of inflammation of the trigeminal nerve is carried out depending on the severity of symptoms. First, conservative therapy is prescribed. If this does not help, doctors resort to surgical methods. Their essence is to eliminate the cause of neuralgia. This may be compression of the nerve by the vessel. Surgical treatment is carried out using radiofrequency destruction, microvascular decompression or percutaneous surgery.

What drugs are most effective for the treatment of trigeminal neuralgia:

• antibiotics. Prescribed for infectious nature of the disease;
• glucocorticosteroids. Relieves severe inflammation in the body;
• non-steroidal anti-inflammatory drugs (NSAIDs). Helps suppress inflammatory processes;
• painkillers. Relieves soreness in the facial muscles;
• muscle relaxants.

To improve metabolic processes in the nervous tissue, the patient is prescribed B vitamins. How to relieve acute pain with trigeminal neuralgia:

• use anticonvulsants;
• provide physical rest, preferably bed rest;
• Apply an anti-inflammatory ointment or a warm compress to the site of pain.

Modern approach to the treatment of trigeminal neuralgia

Trigeminal neuralgia (TN) (synonyms: tic douloureux, or Fothergill's disease) is one of the most common facial pain (prosopalgia) and is one of the most persistent pain syndromes in clinical neurology [1]. TN is a typical example of neuropathic pain (NP) of a paroxysmal nature and is considered the most painful type of prosopalgia. TN most often has a chronic or recurrent course, is accompanied by a large number of comorbid disorders, is much more difficult to treat than many other types of chronic pain and leads to temporary or permanent disability, which makes it a major economic and social problem [2]. Chronic NP has a significant negative impact on the quality of life of patients, causing sleep disturbances, increased anxiety, depression, and decreased daily activity [3]. The high intensity and persistence of TN, its special, often painful nature, and resistance to traditional methods of pain relief give this problem exceptional relevance. Trigeminal neuralgia is a disease characterized by the occurrence of paroxysmal, usually unilateral, short-term, acute, sharp, intense, electric shock-like pain in the area of ​​innervation of one or more branches of the trigeminal nerve [4, 5]. Most often, the lesion occurs in the zone of the II and/or III branch and extremely rarely - in the I branch n. trigeminus [6].

According to WHO, the prevalence of TN is up to 30–50 patients per 100,000 population, and the incidence is 2–4 people per 100,000 population. TN is more common in women than in men, debuts in the fifth decade of life and in 60% of cases has a right-sided localization [7, 8].

According to the International Classification of Headache Disorders (2nd edition), proposed by the International Headache Society (2003), TN is divided into classical, caused by compression of the trigeminal root by tortuous or pathologically altered vessels, without signs of obvious neurological deficit, and symptomatic, caused by proven structural damage to the trigeminal nerve, different from vascular compression [9].

The most common cause of TN is compression of the proximal part of the trigeminal root within a few millimeters of the entrance of the root into the pons (the so-called “root entry zone”). In approximately 80% of cases, compression occurs by an arterial vessel (most often a pathologically tortuous loop of the superior cerebellar artery). This explains the fact that TN occurs in old and senile age and practically does not occur in children. In other cases, such compression is caused by an aneurysm of the basilar artery, space-occupying processes in the posterior cranial fossa, tumors of the cerebellopontine angle and multiple sclerosis plaques [1, 8, 10, 11].

At the extracranial level, the main factors leading to the occurrence of TN are: tunnel syndrome - compression in the bone canal through which the nerve passes (usually in the infraorbital foramen and mandible), associated with its congenital narrowness, the addition of vascular diseases in old age, as well as as a result of a chronic inflammatory process in adjacent areas (caries, sinusitis); local odontogenic or rhinogenic inflammatory processes. The development of TN can be provoked by infectious processes, neuroendocrine and allergic diseases, demyelination of the trigeminal nerve root in multiple sclerosis [7, 12].

Depending on the impact of the pathological process on the corresponding part of the trigeminal system, TN is divided into predominantly central and peripheral genesis. In the occurrence of TN of central origin, neuroendocrine, immunological and vascular factors play an important role, which lead to impaired reactivity of cortical-subcortical structures and the formation of a focus of pathological activity in the central nervous system. In the pathogenesis of peripheral TN, a large role is played by the compression factor, infections, injuries, allergic reactions, and odontogenic processes [7, 8, 12].

Despite the large number of literature reviews and meta-analyses that have appeared in recent years on the problem of treating NB [13], which includes TN, there is no consensus among researchers regarding the basic principles of drug therapy for this disease [14]. Treatment of neuropathic pain is still insufficiently effective: less than half of patients experience significant improvement as a result of pharmacological treatment [15, 16].

The problem of treating trigeminal neuralgia today remains not fully resolved, which is associated with the heterogeneity of this disease in terms of etiology, pathogenetic mechanisms and symptoms, as well as the low effectiveness of conventional analgesics and the development of pharmacoresistant forms of TN that require surgical treatment. In modern conditions, treatment tactics for this disease include medicinal and surgical methods.

The main directions of drug therapy are: eliminating the cause of TN, if it is known (treatment of diseased teeth, inflammatory processes in adjacent areas, etc.), and carrying out symptomatic treatment (relief of pain).

Pathogenetic treatment of patients with TN includes the use of drugs with neurometabolic, neurotrophic, antioxidant, and antihypoxic effects. In recent years, the high effectiveness of the use of metabolic drugs in the complex treatment of NB has been discovered [8, 17]. In the treatment of patients with TN, the high effectiveness of the metabolic drug Actovegin, a deproteinized derivative from the blood of young calves, has been shown. The main effect of this drug is to stabilize the energy potential of cells by increasing intracellular transport and utilization of glucose and oxygen. Actovegin also has an antihypoxic effect, being an indirect antioxidant. In addition, the effect of Actovegin is manifested by indirect vasoactive and rheological effects by increasing capillary blood flow, reducing peripheral vascular resistance and improving the perfusion of organs and tissues [17]. Such a wide spectrum of pharmacological action of Actovegin allows its use in the treatment of TN. During an attack, it is advisable to use Actovegin intravenously in a slow stream or drip for 10 days at a dose of 400–600 mg/day. In the interictal period, the drug is prescribed orally at a dose of 200 mg 3 times a day for 1–3 months [8]. The pathogenetic treatment of patients with TN includes the use of high doses of B vitamins as part of multicomponent preparations, which is due to their multimodal neurotropic effect (impact on metabolism, metabolism of mediators, transmission of excitation in the nervous system), as well as the ability to significantly improve nerve regeneration. In addition, B vitamins have analgesic activity. Such drugs, in particular, include Milgamma, Neuromultivit, Neurobion, containing a balanced combination of thiamine (B1), pyridoxine (B6), cyanocobalamin (B12). Vitamin B1 eliminates acidosis, which reduces the pain threshold; activates ion channels in neuronal membranes, improves endoneurial blood flow, increases the energy supply of neurons and supports axoplasmic transport of proteins. These effects of thiamine promote nerve fiber regeneration [18–20]. Vitamin B6, by activating the synthesis of the myelin sheath of nerve fiber and transport proteins in axons, accelerates the process of regeneration of peripheral nerves, thereby exhibiting a neurotropic effect. Restoration of the synthesis of a number of mediators (serotonin, norepinephrine, dopamine, gamma-aminobutyric acid (GABA) and activation of descending inhibitory serotonergic pathways included in the antinociceptive system leads to a decrease in pain sensitivity (antinociceptive effect of pyridoxine) [18, 21]. Vitamin B12 is involved in processes of regeneration of nervous tissue, activating the synthesis of lipoproteins necessary for the construction of cell membranes and the myelin sheath; reduces the release of excitatory neurotransmitters (glutamate); has an antianemic, hematopoietic and metabolic effect [18, 22]. For rapid relief of pain and pathogenetic neurotropic effects in TN, it is advisable use of the parenteral form of the drug Neurobion - a combined preparation of B vitamins containing the optimal amount of vitamin B12 in both ampoule and tablet form. Neurobion is used in a dose of 3 ml per day intramuscularly 2-3 times a week - 10 injections (for severe pain syndrome can be used daily in the same dosage for 10–15 days). Then, to enhance and prolong the therapeutic effect and prevent relapse of the disease, Neurobion is prescribed in tablet form at a dosage of 1 tablet orally 3 times a day for 1–2 months [8].

Anticonvulsants are also the drugs of choice for the treatment of TN, and carbamazepine was one of the first drugs officially registered for the treatment of this condition [24].

In the early 90s of the last century, a new generation of antiepileptic drugs appeared, and now anticonvulsants are usually divided into first and second generation drugs.

First generation anticonvulsants include phenytoin, phenobarbital, primidone, ethosuximide, carbamazepine, valproic acid, diazepam, lorazepam, clonazepam. First-generation drugs are practically not considered as the first line of treatment for NB (with the exception of carbamazepine for TN) due to the insufficient level of analgesic effect and the high risk of adverse reactions. The most common side effects of first-generation anticonvulsants include: central nervous system reactions (drowsiness, dizziness, ataxia, sedation or increased excitability, diplopia, dysarthria, cognitive impairment, memory and mood impairment), hematological disorders (agranulocytosis, aplastic anemia, thrombocytopenia, leukopenia), hepatotoxicity, decreased bone mineral density, skin rashes, gingival hyperplasia, gastrointestinal symptoms (vomiting, anorexia). Second generation anticonvulsants include pregabalin (Lyrica), gabapentin (Neurontin, Gabagamma, Tebantin), lamotrigine (Lamictal), oxcarbazepine (Trileptal), topiramate (Topamax), levetiracetam (Keppra), tiagabine (Gabitril), zonisamide (Zonegran), vigabatrin (Sabril), felbamate (Taloxa). These drugs have more favorable pharmacokinetic characteristics and safety profiles, as well as a low risk of drug interactions compared to first-generation anticonvulsants [24, 25].

The main mechanisms of action of 1st and 2nd generation anticonvulsants are presented in table [26].

The first anticonvulsant successfully used to treat TN was phenytoin (Difenin) [27]. Diphenin, a derivative of hydantoin, similar in chemical structure to barbituric acid, is contraindicated in severe diseases of the kidneys, liver, and heart failure.

According to the recommendations of the European Federation of Neurological Societies (2009), pharmacotherapy for TN is based primarily on the use of carbamazepine (Finlepsin, Tegretol) proposed by S. Blum in 1962 (200–1200 mg/day), which is the drug of first choice (level of evidence A) [27, 28]. The analgesic effect of this drug is mainly due to its ability to reduce the permeability to sodium of the membranes of neurons involved in nociceptive reactions. The following treatment regimen with carbamazepine is usually prescribed. In the first two days, the daily dose is 200 mg (1/2 tablet in the morning and evening), then within two days the daily dose is increased to 400 mg (morning and evening), and after that - to 600 mg (1 tablet in the morning, at lunchtime and in the evening). If the effect is insufficient, then the total amount of the drug per day can be increased to 800–1000 mg. In some patients with TN (about 15% of the population), carbamazepine does not have an analgesic effect, so in such cases another anticonvulsant, phenytoin, is used.

Three placebo-controlled studies conducted about 40 years ago, which included a total of 150 patients with TN, showed the effectiveness of carbamazepine on both the frequency and intensity of paroxysms [24]. A number of authors have shown that carbamazepine can reduce pain symptoms in approximately 70% of cases. [29]. However, the use of carbamazepine is limited by pharmacokinetic factors and occasional severe side effects (for example, Stevens-Johnson syndrome), especially in elderly patients.

Oxcarbazepine (Trileptal) is structurally similar to carbamazepine, but is much better tolerated by patients and has far fewer side effects. Typically, oxcarbazepine is used at the beginning of treatment for TN at a dose of 600–1800 mg/day (Evidence Level B) [30].

As additional therapy for TN, the effectiveness of lamotrigine (Lamictal) at a dose of 400 mg/day [31] and baclofen at a dose of 40–80 mg/day [32], which are second-line drugs, has been shown (level of evidence: C). Small open studies (class IV) indicate the effectiveness of clonazepam, valproate, and phenytoin [33, 34]. This therapy is most effective in the classical form of TN. For TN of peripheral origin, it is preferable to include non-narcotic analgesics in treatment regimens, and in the case of the development of chronic pain syndrome (more than three months), the prescription of antidepressants (amitriptyline) is indicated [7, 12].

Gabapentin (Neurontin) is the first drug in the world to be registered for the treatment of all types of neuropathic pain. Many studies have shown the effectiveness of gabapentin in patients with TN who do not respond to treatment with other drugs (carbamazepine, phenytoin, valproate, amitriptyline); in most cases, complete relief of pain was observed [35]. The therapeutic dose ranges from 1800 to 3600 mg/day. The drug is taken 3 times a day according to the following regimen: 1st week - 900 mg/day, 2nd week - 1800 mg/day, 3rd week - 2400 mg/day, 4th week - 3600 mg/day.

The results of an open-label, prospective, 12-month study of 53 patients with TN were recently published, evaluating the effectiveness of pregabalin (Lyrica) at a dose of 150–600 mg/day. Treatment with pregabalin resulted in pain relief or at least a 50% reduction in pain intensity in 25% and 49% of patients, respectively [36]. In another multicenter, prospective, 12-week study of 65 patients refractory to prior analgesic therapy, treatment with pregabalin at a mean dose of 196 mg/day (monotherapy subgroup) and 234 mg/day (polytherapy subgroup) resulted in a ≥50% reduction in pain intensity in on average in 60% of patients, and also reduced the severity of anxiety, depression and sleep disorders [37]. When treating TN, the initial dose of pregabalin can be 150 mg/day in 2 divided doses. Depending on the effect and tolerability, the dose can be increased to 300 mg/day after 3–7 days. If necessary, you can increase the dose to the maximum (600 mg/day) after a 7-day interval.

The use of levetiracetam (Keppra) in the treatment of TN was first reported in 2004 by KR Edwards et al. [38]. The mechanism of action of levetiracetam is unknown; There is evidence obtained from animal experiments that it is a selective blocker of N-type calcium channels [39]. The properties of this drug are particularly suitable for the treatment of TN patients with severe pain who require a rapid response to therapy. The pharmacokinetics of levetiracetam are linear and predictable; Plasma concentrations increase proportionally to the dose within the clinically reasonable range of 500 to 5000 mg [40]. Unlike other anticonvulsants, especially carbamazepine, the hepatic cytochrome P450 system is not involved in the metabolism of levetiracetam and the drug is excreted through the kidneys [41]. In addition, this drug is characterized by a favorable therapeutic index and has a small number of adverse side effects (which is the main problem when using drugs to treat TN) [42]. Commonly reported side effects of levetiracetam are asthenia, dizziness, drowsiness, headache and depression. A 10-week, prospective, open-label study showed that higher doses of levetiracetam, ranging from 3000–5000 mg/day (50–60 mg/kg/day), were required for the treatment of TN compared with the treatment of epilepsy, but did not caused significant side effects. This circumstance indicates the prospect of using this drug for the treatment of TN [43].

One domestic study reported positive results with a combination of carbamazepine and gabapentin [44].

Since the 1970s, antidepressants have been used to treat TN [45]. Currently, the effectiveness of the use of tricyclic antidepressants (TCAs) in the treatment of TN has been proven [46].

Until now, the selection of analgesic therapy for NB is more an art than a science, since the choice of drugs is carried out mainly empirically. There are often situations when the use of one drug is not effective enough and there is a need for a combination of drugs. Prescribing “rational polypharmacotherapy” (simultaneous use of drugs with neurotropic, neurometabolic and analgesic mechanisms of action) allows increasing the effectiveness of treatment with lower dosages of drugs and fewer side effects [47].

For patients suffering from unbearable pain for a long time, and if conservative therapy is ineffective in the case of classical TN, surgical treatment is recommended. The following approaches are currently used:

1) surgical microvascular decompression [48]; 2) stereotactic radiation therapy, gamma knife [49]; 3) percutaneous balloon microcompression [50]; 4) percutaneous glycerol rhizolysis [51]; 5) percutaneous radiofrequency treatment of the Gasserian node [52].

The most effective method of surgical treatment of TN is the P. Janetta method, which consists of placing a special gasket between the trigeminal nerve and the irritating vessel; in the long-term period, the effectiveness of treatment is 80% [53–55].

In conclusion, we note that the treatment of TN should be multidisciplinary in nature, and the choice of various treatment methods and the risks of possible complications should be discussed with the patient.

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S. A. Gordeev*, Doctor of Medical Sciences L. G. Turbina**, Doctor of Medical Sciences, Professor A. A. Zusman**, Candidate of Medical Sciences *First Moscow State Medical University named after. I. M. Sechenov, **MONIKI im. M. F. Vladimirsky, Moscow

Contact information for authors for correspondence

Home remedies

Before treating trigeminal neuralgia at home, you should consult a doctor, since many remedies can only worsen the situation. If the specialist allows it, it is also possible to use various home recipes.

According to recommendations for trigeminal neuralgia, it is worth consuming orally or lubricating the affected side with birch sap. You need to drink 4-5 glasses per day. Heated buckwheat folded in cotton cloth will help relieve pain. The compress is made 2 times a day, keeping it at the site of inflammation until it cools down. At home, it is useful to massage the sore area: rub, stroke and lightly knead the area of ​​inflammation.

Myths and dangerous misconceptions in treatment

Due to the fact that neuralgia does not affect the general condition of the body, many patients postpone visiting a doctor and treating the trigeminal nerve. In fact, this is the wrong approach, since the disease can lead to paralysis and muscle paresis. In addition, it has a significant impact on psychological and social aspects of life.

No less important is the fact that painkillers for trigeminal neuralgia provide only a temporary effect. Over time, anticonvulsant medications may also stop working as they become addictive. Therefore, you should not abuse medications. They only relieve the symptoms of neuralgia, and its cause can only be identified by a qualified specialist.

Prevention

There is no specific prevention against neuralgia. Doctors only recommend eliminating as much as possible exposure to the body of those risk factors that can lead to nerve inflammation. To avoid this, it is necessary to prevent hypothermia of the face, especially in the summer when using fans and air conditioners. It is important to harden yourself and worry less in order to reduce the impact of stress. It is also imperative to treat underlying diseases that are risk factors for neuralgia.

Otogenic neuritis of the facial nerve

Neuritis of the facial nerve, which occurs secondary to serious diseases of the middle ear, requires urgent surgery. During the intervention, the doctor relieves excess pressure on the nerve (decompresses it) by removing part of the bone wall of the nerve canal that runs in the middle ear. Subsequently, treatment of the underlying disease is prescribed, as a result of which the function of the affected facial nerve is also restored.

If the pathology develops at an early stage of acute otitis media, a decision may be made on conservative treatment of facial neuritis:

• vitamin therapy with ascorbic acid and group B preparations (Milgamma);
• decongestants (furosemide);
• glucocorticoids for rapid relief of inflammation and pain;
• after acute manifestations subside, actovegin, solcoseryl, and other drugs that affect the metabolism of nervous tissue are prescribed;
• If conservative treatment is ineffective, different types of surgical interventions are prescribed.

Physiotherapeutic methods are included in the complex of restorative treatment measures:

• therapy with UHF, quartz radiation, laser;
• electrophoresis with B vitamins, lidase;
• acupuncture and massage, especially performed on the inside of the cheek;
• applications of therapeutic mud, ozokerite, paraffin;
• physical therapy aimed at restoring the activity of the muscles of the lower part of the face.