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

Inflammation of the facial nerve is an unpleasant ailment that does not go away painlessly. The main complaints of patients are sharp attacks of pain in the face, in the upper and lower jaws.

This inflammation is considered one of the most common among facial pains. Most often, the disease proceeds without a trace, but if treatment is neglected, paralysis may occur.

The disease most often occurs in women over 50 years of age; men are treated with this disease much less frequently. People with a genetic predisposition, such as a narrow bone canal, are also at risk. Due to this anatomical feature, there is an increased risk of pinching due to impaired blood supply and various inflammations.

general information

The trigeminal nerve consists of sensory and motor fibers. It originates in the structures of the brain and is divided into three branches:

• ophthalmic: responsible for the eye, forehead and upper eyelid;
• maxillary: innervates the area from the lower eyelid to the upper lip;
• mandibular: involves the chin, lower jaw, lips and gums.

With neuralgia, one or more branches of the trigeminal nerve are affected, which determines the main symptoms of the pathology. People over 45 years of age are most susceptible to the disease, and women get sick more often than men.

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Chronic course of the disease

Chronic disease of the trigeminal nerve occurs in the absence of treatment or an incorrect rehabilitation plan. If you let the process take its course, many complications may arise that are much more difficult to correct.

• Amyotrophy.
• Decreased sensitivity of the skin, lips, gums and tongue.
• The appearance of facial asymmetry.
• Impaired diction, inability to open the jaw normally.
• Problems with vision and hearing.

Causes

The causes of trigeminal neuralgia can be of different nature:

• compression of the entire trigeminal nerve or its branches against the background of: enlargement of the arteries or veins of the brain (aneurysms, atherosclerosis, strokes, increased intracranial pressure due to osteochondrosis, congenital developmental features);
• tumors of the brain or facial tissues in close proximity to nerve fibers;
• congenital anomalies of bone structure, narrowed openings through which nerve branches pass;
• injuries of the skull, facial area: bone fractures, post-traumatic scars of soft tissues;
• proliferation of scar tissue after injury, surgery, inflammation;

The risk of developing trigeminal neuralgia increases significantly:

• over the age of 50;
• against the background of mental disorders;
• with regular hypothermia;
• with insufficient intake of nutrients and vitamins into the body (anorexia, bulimia, malabsorption, etc.);
• with regular overwork, stress;
• for helminthic infestations and other helminthiases;
• for acute infections: malaria, syphilis, botulism, etc.;
• for chronic inflammation in the oral cavity (caries, gingivitis, abscesses, etc.);
• against the background of autoimmune lesions;
• with excessive exposure to allergies;
• for metabolic disorders.

Causes

Trigeminal neuropathy can be associated with a variety of conditions. Neuropathy can be caused by blood vessel compression on the trigeminal nerve as it exits the brainstem. This compression causes the protective covering around the nerve (myelin sheath) to wear or become damaged. Symptoms of trigeminal neuropathy can also occur in patients with multiple sclerosis, a disease that damages the myelin sheath of the trigeminal nerve. Rarely, symptoms of neuropathy may be due to nerve compression by a tumor or arteriovenous malformation. Damage to the trigeminal nerve (possibly as a result of oral surgery, stroke, or facial trauma) can also lead to neuropathic pain.

Symptoms

The main characteristic symptom of trigeminal neuralgia is paroxysmal pain. It comes suddenly and in its intensity and speed of spread resembles an electric shock. Typically, intense pain forces the patient to freeze in place, waiting for relief. The attack can last from a few seconds to 2-3 minutes, after which there is a period of calm. The next wave of pain may come within hours, days, weeks or months.

Over time, the duration of each attack of neuralgia increases, and periods of calm are reduced until a continuous aching pain develops.

The provoking factor is irritation of trigger points:

• lips;
• wings of the nose;
• eyebrow area;
• middle part of the chin;
• cheeks;
• area of ​​the external auditory canal;
• oral cavity;
• temporomandibular joint.

A person often provokes an attack when performing hygiene procedures (combing hair, caring for the oral cavity), chewing, laughing, talking, yawning, etc.

Depending on the location of the lesion, the pain takes over:

• the upper half of the head, temple, orbit or nose if the ophthalmic branch of the nerve is affected;
• cheeks, lips, upper jaw – if the maxillary branch is affected;
• chin, lower jaw, as well as the area in front of the ear - with neuralgia of the mandibular branch.

If the lesion affects all three branches or the nerve itself before it is divided, the pain spreads to the entire corresponding half of the face.

Painful sensations are accompanied by other sensory disturbances: numbness, tingling or crawling sensations. Hyperacusis (increased hearing sensitivity) may be observed on the affected side.

Since the trigeminal nerve contains not only sensory, but also motor pathways for the transmission of impulses, with neuralgia the corresponding symptoms are observed:

• twitching of facial muscles;
• spasms of the muscles of the eyelids, masticatory muscles;

The third group of manifestations of neuralgia are trophic disorders. They are associated with a sharp deterioration in blood circulation and lymph outflow. The skin becomes dry, begins to peel, and wrinkles appear. Local graying and even hair loss in the affected area is observed. Not only the scalp suffers, but also the eyebrows and eyelashes. Impaired blood supply to the gums leads to the development of periodontal disease. At the time of the attack, the patient notes lacrimation and drooling, swelling of the facial tissues.

Constant spasms of muscle fibers on the diseased side lead to facial asymmetry: narrowing of the palpebral fissure, drooping of the upper eyelid and eyebrow, upward movement of the corner of the mouth on the healthy side or drooping on the diseased side.

The patient himself gradually becomes nervous and irritable, and often limits himself to food, since chewing can cause another attack.

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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54. Tyler-Kabara EC, Kassam AB, Horowitz MH et al. Predictors of outcome in surgically managed patients with typical and atypical trigeminal neuralgia: Comparison of results following microvascular decompression // J. Neurosurg. 2002. Vol. 96. P. 527–531.
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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

Diagnostics

A neurologist diagnoses trigeminal neuralgia. During the first visit, he carefully interviews the patient to find out:

• complaints: nature of pain, its intensity and localization, conditions and frequency of attacks, their duration;
• medical history: when pain attacks first appeared, how they changed over time, etc.;
• life history: the presence of chronic diseases, previous injuries and operations is clarified, special attention is paid to dental diseases and interventions.

A basic examination includes assessing the condition of the skin and muscles, identifying asymmetry and other characteristic signs, checking the quality of reflexes and skin sensitivity.

To confirm the diagnosis, the following is carried out:

• MRI of the brain and spinal cord with or without contrast: allows you to identify tumors, consequences of injuries, vascular disorders; sometimes the study is replaced by computed tomography (CT), but it is not as informative;
• electroneurography: study of the speed of nerve impulse transmission through fibers; allows you to identify the fact of nerve damage, assess the level of the defect and its features;
• electroneuromyography: not only the speed of impulse passage along the nerve bundle is studied, but also the reaction of muscle fibers to it; allows you to assess nerve damage, as well as determine the sensitivity threshold of trigger zones;
• electroencephalography (EEG): assessment of the bioelectrical activity of the brain.

Laboratory diagnostics includes only general studies to exclude other causes of painful attacks, as well as to assess the condition of the body as a whole (usually a general blood and urine test is prescribed, as well as a standard set of biochemical blood tests). If the infectious nature of the disease is suspected, tests are carried out to identify specific pathogens or antibodies to them.

Additionally, consultations with specialized specialists are prescribed: ENT specialist (if there are signs of nasopharynx pathology), a neurosurgeon (if there are signs of a tumor or injury), and a dentist.

Activities for making a diagnosis

If necessary, the specialist can refer the patient to see a dentist, surgeon or ENT doctor.

In some cases, complaints about characteristic symptoms are sufficient to confirm the diagnosis. In difficult situations, a set of measures is prescribed for a thorough examination:

• CBC and blood test for biochemistry;
• magnetic resonance imaging of the head;
• computed tomography of the head;
• electroneurography;
• X-ray of the half of the face where the pain is localized.

After conducting an external examination and establishing the cause of the patient’s complaints, the doctor selects a treatment regimen, which includes medications, physical therapy or surgery.

Treatment of trigeminal neuralgia

Treatment is aimed at:

• to eliminate the cause of damage;
• to alleviate the patient's condition;
• to stimulate the restoration of nerve structures;
• to reduce the excitability of trigger zones.

Properly selected treatment can reduce the frequency, intensity and duration of pain waves, and ideally achieve stable remission.

Drug treatment

Trigeminal neuralgia requires complex treatment using drugs from several groups:

• anticonvulsants (carbamazepine and analogues): reduce the excitability of nerve fibers;
• muscle relaxants (baclofen, mydocalm): reduce muscle spasms, improve blood circulation, reduce pain;
• B vitamins (neuromultivit, milgamma): stimulate the restoration of nerve fibers, have an antidepressant effect;
• antihistamines (diphenhydramine): enhance the effect of anticonvulsants;
• sedatives and antidepressants (glycine, aminazine): stabilize the patient’s emotional state.

For severe pain, narcotic analgesics may be prescribed. Previously, drug blockades (injecting the problem area with anesthetics) were actively used, but today this method of treatment is almost never used. It contributes to additional damage to nerve fibers.

Treatment of the root cause of the disease is mandatory: elimination of dental problems, taking medications to improve cerebral circulation, etc.

Physiotherapy and other non-drug methods

Non-drug methods complement drug therapy well and help stabilize patients’ condition. Depending on the condition and concomitant diseases, the following may be prescribed:

• ultraviolet irradiation: inhibits the passage of impulses along nerve fibers, providing an analgesic effect;
• laser therapy: reduces pain;
• UHF therapy: improves microcirculation and prevents muscle atrophy;
• electrophoresis with analgesics or antispasmodics to relieve pain and relax muscles;
• diadynamic currents: reduce the conductivity of nerve fibers, significantly increase the intervals between attacks;
• massage of the face, head, cervical-collar area: improves blood circulation and lymph outflow, improving tissue nutrition; must be carried out with caution so as not to touch trigger zones and provoke an attack; the course is carried out only during the period of remission;
• acupuncture: helps relieve pain.

Surgery

The help of surgeons is indispensable when it is necessary to eliminate nerve compression. If indicated, the following is carried out:

• removal of tumors;
• displacement or removal of dilated vessels pressing on the nerve (microvascular decompression);
• expansion of the bone canals in which the branches of the nerve pass.

A number of operations are aimed at reducing nerve fiber conductivity:

• exposure to a gamma knife or cyber knife;
• balloon compression of the trigeminal node: compression of the node using an air-filled balloon installed in close proximity to it, followed by death of the nerve fibers; surgery often leads to partial loss of sensation and decreased muscle movement;
• resection of the trigeminal node: rarely performed due to the complexity and large number of complications.

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Treatment for inflammation of the facial nerve

Drug treatment

Treatment of trigeminal neuritis is complex. The disease is first treated with medication - the patient is prescribed drugs that will alleviate the situation. These include painkillers, decongestants, vasodilators and B vitamins. Most often, the recommended medications are tablets, but you can speed up the recovery process by using ointments and gels. Sometimes doctors prescribe intramuscular injections.

In special cases, the recovery process of the facial nerve may be slowed down. Then the patient is prescribed glucocorticosteroids, which improve the metabolic processes of nervous tissue. Various biostimulants and hyaluronidases also contribute to a speedy recovery.

You cannot prescribe medications for yourself. Be sure to see a neurologist or neuropathologist at the first symptoms to determine the diagnosis and treatment strategy. Recovery medications are recommended to patients on a case-by-case basis, paying attention to the presence of chronic diseases, symptoms, and so on.

Surgery

Another way to treat the facial nerve is surgery. However, doctors turn to this option quite rarely - only when the trigeminal nerve is ruptured. Surgery is also required if there is no effect from the conservative method after six months or a year. Surgical intervention is only relevant during the first year of the presence of the disease; later, the muscles on the face irreversibly atrophy.

The surgical process involves suturing the damaged area of ​​the facial nerve to restore its motor function.

Massage

The next treatment method is massage for the treatment of the facial nerve. The purpose of this method is to remove swelling, improve blood circulation, restore sensitivity and conduction of nerve impulses. Massage is contraindicated for tuberculosis, oncology, atherosclerosis and elevated temperature.

Initially, the massage therapist works only with the healthy side of the face, collar area, neck and area above the shoulders. Basically, the master uses rubbing, stroking, kneading and vibration.

For noticeable desired changes, it is necessary to conduct ten to twenty massage sessions from five to fifteen minutes. The duration is determined based on the degree of inflammation of the trigeminal nerve, the goals of therapy and the dynamics of recovery.

Physiotherapy

The next treatment method is physical therapy. It alleviates the severity of symptoms, helps to activate metabolic processes in tissues and restore the functions of the facial nerve.

Doctors prescribe this course of treatment from the first days of the onset of neuritis. The list of physical procedures includes:

• Ultrasound
• Laser irradiation of blood
• Electrophoresis of drugs
• Microwave therapy
• Exposure to ultra-high frequency electricity
• Ozocerite treatment
• Myoelectrostimulation
• Darsonvalization

This complex is indicated for the first week of treatment. Doctors prescribe it together with medication. This tandem helps speed up the process of restoration of the facial nerve. And its most important advantages are the absence of side effects and painlessness.

Alternative Methods

There are also alternative treatment methods. These are procedures aimed at restoring facial muscles and eliminating the symptoms of facial neuritis. Such procedures include:

• Clay or paraffin masks
• Acupuncture
• Reflexology
• Injections to eliminate muscle disorders
• Therapeutic baths
• Taping – stretching the face using adhesive plasters
• Immunosorption – purification of blood from antigens and antibodies
• Biofeedback – facial muscle training

Gymnastics for the face

Also, in conjunction with complex treatment, you can do facial exercises. Before this, you need to consult with a specialist; the doctor will draw up an individual list of exercises based on the severity of the process, location of the lesion and symptoms. Typically, such gymnastics takes about ten minutes a day.

A standard set of exercises includes relaxing and tensing individual facial muscles. For example, to restore articulation, it is recommended to pronounce the sounds “u”, “o”, “and”. Afterwards, you need to bring your lower lip under your upper teeth and reproduce the sounds “v” and “a”.

Gymnastics for inflammation of the trigeminal nerve:

1. Close eyes
2. Raise your eyebrows
3. Frown
4. Squint
5. Smile with your mouth closed
6. Smile with your mouth open
7. Puff up your cheeks
8. Pull them back
9. Whistle
10. Widen your nostrils
11. Curl your lips
12. Raise your upper lip and return to the starting position
13. Lower your lower lip and return to the starting position
14. Take water into your mouth
15. Rinse your mouth
16. Close your mouth
17. Run the tip of your tongue along your gums
18. Move your tongue right and left

Complications

Without treatment, trigeminal neuralgia gradually progresses. Over time, a pathological pain focus forms in one of the parts of the brain. As a result, the pain covers the entire face, is provoked by any minor irritant and even the memory of an attack, and subsequently becomes permanent. Vegetative-trophic disorders progress:

• irreversible atrophy of the facial muscles is formed;
• teeth become loose and begin to fall out due to advanced periodontal disease;
• baldness is increasing.

Due to constant pain, the patient's sleep is disturbed and severe depression develops. In severe cases, patients may commit suicide.

Neuropathy of the buccal nerve.

The causes of the disease can be periostitis, inflammatory diseases of the teeth and gums, traumatic removal of teeth in the lower jaw.

Clinic.

The pain occurs subacutely, is constant, and its intensity gradually increases. First it occurs on the front surface of the gum, transitional fold, and then spreads to the entire front surface of the teeth of the lower jaw and covers the entire area of ​​innervation of the buccal nerve. Numbness is uncharacteristic; an objective examination reveals a decrease in all types of sensitivity in the area of ​​innervation of the mucous membrane of the cheek and vestibular surface of the gums, as well as the skin of the corner of the mouth.

Prevention

Prevention of trigeminal neuralgia is a set of simple measures that significantly reduce the risk of developing pathology. Doctors recommend:

• undergo regular preventive examinations;
• at the first signs of the disease, seek help (the sooner treatment is started, the greater its effect will be);
• eat right, get the required amount of vitamins, minerals, unsaturated fatty acids;
• regularly engage in light sports and gymnastics;
• get enough sleep and rest;
• minimize stress and physical overload;
• avoid hypothermia and harden yourself;
• to refuse from bad habits.

Disease prevention

Doctors recommend eliminating effects on the body that cause inflammation of the trigeminal nerve. Here are some recommendations to help avoid illness:

• Avoid drafts and hypothermia
• Keep your head warm during the cold season
• Monitor your blood pressure
• Timely treatment of infectious and bacterial diseases
• Have a routine check-up with an oncologist
• Avoid skull and head injuries

You can sign up for an individual consultation, take tests or undergo treatment at the Medunion private clinic. You can easily make an appointment with us by calling 202-95-54 or online, directly on the website, by clicking on the “Online booking” button.

We have been working in Krasnoyarsk since 2006 and provide high-quality medical services to the population. The staff consists of highly qualified doctors of broad and narrow specialization.

Treatment at the Energy of Health clinic

If you or your relative are bothered by severe pain in one or another part of the face, the neurologists of the Health Energy clinic will come to the rescue. We will conduct a full diagnosis to identify the causes of the pathology and prescribe comprehensive treatment. At your service:

• modern drug regimens to reduce the frequency and intensity of attacks;
• physiotherapeutic procedures: magnetotherapy, laser therapy, electrophoresis, phonophoresis, etc.;
• delicate therapeutic massage;
• acupuncture;
• help from a psychologist if necessary.

Neuropathy of the superior alveolar nerve.

The causes of the disease may be chronic pulpitis and periodontitis, nerve damage in case of complex tooth extraction, sinusitis, and surgical intervention for sinusitis.

It manifests itself as pain and a feeling of numbness in the teeth of the upper jaw. Objectively, there is a decrease or absence of sensitivity in the gum area of ​​the upper jaw, as well as the adjacent area of ​​the buccal mucosa. The electrical excitability of the pulp in the corresponding teeth of the upper jaw is reduced or absent.

If the cause of the disease is stenosis of the infraorbital canal, then patients will complain of pain and numbness of the skin in the area of ​​innervation of the infraorbital nerve (wing of the nose, area above the canine fossa, upper lip).

Advantages of the Health Energy Clinic

The Health Energy Clinic is a multidisciplinary medical center where every patient has access to:

• screening diagnostic programs aimed at early detection of diseases and pathologies;
• targeted diagnostics using modern equipment and laboratory tests;
• consultations with experienced specialists, including foreign ones;
• modern and effective comprehensive treatment;
• necessary certificates and extracts;
• documents and appointments for spa treatment.

Trigeminal neuralgia is a serious pathology that can seriously disrupt a person’s normal lifestyle. Don't let pain and fear take over your thoughts, get treatment at Health Energy.

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.