Inflammation of the trigeminal nerve: causes, symptoms and treatment

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.

Make an appointment

Basic information about the disease

Our two trigeminal nerves provide sensitivity to the face. One nerve passes on the left, the other on the right. Each has three branches.

With neuralgia of the right or left nerve, attacks of intense shooting pain begin in the locations of the branches of the nerve . Pain does not allow you to live an active life: for example, there are difficulties with eating and maintaining hygiene. You can get sick at any age. Women get sick more often.

The disease can occur on its own or be a complication of another disease.

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.

What is the trigeminal nerve and why does it become inflamed?

The trigeminal nerve on the face is the nerve through which we feel the face and can bite and chew. On each side of the face there is a trunk with three branches - the orbital nerve, the maxillary nerve and the mandibular nerve. This nerve is the most complex in the skull.

Inflammation of the trigeminal nerve (or, in other words, neuralgia or neuritis) can be caused by several reasons.

Firstly, this is damage to the fibers by a bacterial infection. Pathology can also be caused by:

• injury or abnormal structure of the skull bones;
• hypothermia of the head;
• high blood pressure;
• stroke;
• intoxication, poisoning;
• tuberculosis;
• infection with herpes or HIV;
• high intracranial pressure due to osteochondrosis;
• inflammatory diseases of the gums, mainly in the area of ​​wisdom teeth;
• changes in hormonal levels, for example, during pregnancy;
• procedures in the dentist's office. Installation of a filling or removal of roots may be accompanied by contact with nearby nerves.

Doctors also identify a complex of psychosomatic causes - stress, strong experiences that affect well-being.

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.

Trigeminal facial pain: systematics of clinical forms, principles of diagnosis and treatment

Facial pain, which includes pain on the surface of the face and/or in the mouth (orofacial pain), is one of the most common types of pain. Most often, orofacial pain manifests itself as acute dental pain, which usually regresses after dental treatment. However, in a number of cases, facial pain itself (prosopalgia) is noted, manifested by chronic or recurrent pain, often resistant to various methods of conservative treatment. A kind of primacy in severity belongs to trigeminal facial pain, especially trigeminal neuralgia and deafferentation trigeminal neuropathy, during exacerbation of which the severity of pain is many times greater than the intensity of acute toothache familiar to most people.

Taxonomy of trigeminal prosopalgia

Trigeminal prosopalgia (Greek prosopon (face) + algos (pain)) includes facial pain caused by damage to the trigeminal nerve. From the point of view of topical diagnosis, the development of any form of trigeminal prosopalgia is associated with damage to the peripheral trigeminal neuron - the peripheral trigeminal branches, the sensory trigeminal ganglion (located at the base of the skull), the sensory root of the trigeminal nerve that follows it in the direction of the brain stem, as well as those entering the brain stem sensory trigeminal fibers and sensory nuclei of the trigeminal nerve (

).

Despite the difference in the symptomatology of the clinical forms of trigeminal prosopalgia, the features of facial pain are of primary importance for their differentiation, in some cases manifested by prolonged (constant) pain, and in others in the form of paroxysms of pain. Paroxysmal forms of trigeminal pain are traditionally referred to as neuralgia, and non-paroxysmal forms - trigeminal neuropathy. However, non-paroxysmal postherpetic facial pain is also called neuralgia. These forms of facial pain—neuralgia and trigeminal neuropathy—fundamentally differ in their approaches to treatment.

Paroxysmal trigeminal prosopalgia

Paroxysmal facial pain, lasting from several seconds to several minutes, is manifested by trigeminal neuralgia (typical trigeminal neuralgia), trigeminal neuralgia due to multiple sclerosis, and symptomatic trigeminal neuralgia arising from a tumor lesion of the trigeminal nerve.

Until recently, trigeminal neuralgia, not associated with multiple sclerosis and tumor lesions of the trigeminal nerve, was called idiopathic, i.e. occurring for no apparent reason. However, as it was established as a result of serial neurosurgical interventions, the main etiological factor of typical trigeminal neuralgia is compression of the sensory root of the trigeminal nerve by an atypically located arterial or venous vessel.

Trigeminal neuralgia

Trigeminal neuralgia is the most common form of paroxysmal (paroxysmal) facial pain. It is also considered the most excruciating type of facial pain. It manifests itself as attacks of sharp, high-intensity pain in the area of ​​innervation of the trigeminal nerve. The cessation of an attack of facial pain within a few tens of minutes after taking the anticonvulsant carbamazepine radically distinguishes trigeminal neuralgia from most other types of chronic pain. The symptoms of trigeminal neuralgia undergo significant changes as the pain syndrome increases and regresses, reaching its greatest severity at the height of the exacerbation period.

In secondary (symptomatic) forms of trigeminal neuralgia, which arise from tumor damage to the trigeminal nerve, already at the first stage of the disease symptoms may be observed that differ from the typical clinical picture.

Non-paroxysmal trigeminal prosopalgia

Non-paroxysmal trigeminal prosopalgia, manifested by prolonged facial pain, as well as sensitivity deficit (hypesthesia, anesthesia) in the facial area, includes various clinical forms of trigeminal neuropathy, including postherpetic neuralgia (). Most often, the development of trigeminal neuropathy is associated with obvious etiological factors - trigeminal herpes zoster and traumatic injury to the trigeminal nerve. In some cases, trigeminal neuropathy is one of the early manifestations of systemic diseases, in particular systemic scleroderma, systemic lupus erythematosus, sarcoidosis and Lyme disease.

Traumatic trigeminal neuropathy

It is the main form of trigeminal neuropathy, the clinical signs of which are non-paroxysmal facial pain, sensory impairment (numbness) and, very rarely, motor impairment. As a rule, the acute development of these symptoms has an obvious relationship with local pathological processes and iatrogenic effects in the maxillofacial area.

The first sign of traumatic trigeminal neuropathy is acutely developed sensory insufficiency - from mild hypoesthesia to anesthesia, limited to the innervation zone of the affected sensory branch. Subsequently, paresthesia (a feeling of “pins and needles”) and/or non-paroxysmal pain occurs in the same area of ​​the face. Symptoms of sensory loss that accompany facial pain may persist significantly longer than facial pain. In the affected area, hyperesthesia is often detected, as well as pain on palpation of limited areas of facial skin.

Postherpetic trigeminal neuralgia

Trigeminal postherpetic neuralgia is persistent facial pain and/or burning and itching that persists from the time herpetic lesions develop or occurs several weeks after the lesions resolve (delayed postherpetic neuralgia).

Trigeminal postherpetic neuralgia most often develops in patients over 60 years of age. Its occurrence is usually facilitated by:

• late seeking medical help during the period of acute herpes zoster;
• presence of concomitant pathology;
• complicated resolution of rashes - rashes with a hemorrhagic component and secondary pyoderma;
• pronounced residual sensory deficit (“numbness” of the skin after resolution of the rash).

Deafferentation trigeminal neuropathy (prosopalgia)

Deafferentation facial pain (prosopalgia) is the most severe form of trigeminal lesion, manifested by highly intense facial pain, often resistant to conservative therapy, and severe sensory impairment. Develops as a result of significant damage (destruction) of the peripheral or central structures of the trigeminal system.

The concept of “deafferentation trigeminal prosopalgia”, as a general syndromological definition, was proposed by Yu. V. Grachev and Yu. A. Grigoryan (1995) to designate a special form of facial pain that develops as a result of deafferentation in the sensory system of the trigeminal nerve. The pathophysiological term “deafferentation” (de- + lat. afferentis bringing), literally means the separation of the receptor zones of peripheral nerves from the central sensory structures, due to a violation of the integrity or conductivity of nerve fibers.

Typical peripheral forms of deafferentation trigeminal prosopalgia are postherpetic, tumor and iatrogenically caused facial pain (caused by destruction of the ganglion and trigeminal nerve root), and central are two quite rare forms caused by syringobulbia and medulla oblongata infarction.

Diagnosis of trigeminal prosopalgia

The examination of a patient experiencing facial pain should begin with a systematic medical interview, including clarification of the clinical characteristics of the pain and analysis of anamnestic data (

).

The presence of facial pain requires a detailed study of the function of the cranial nerves, and also makes certain additions to the traditional neurological examination. Objective signs of damage to the nervous system of the face are sensory disturbances in the orofacial region - trigger zones, areas of increased and/or decreased sensitivity (Fig. 2, 3), local autonomic disorders, as well as the presence of local palpation pain.

When conducting palpation examination of the facial area, it is necessary to distinguish between “neuralgic” and “myofascial trigger” (English trigger).

1. Neuralgic trigger points or zones (in patients with trigeminal neuralgia) are hyperexcitable areas of the skin and mucous membrane, with mechanical irritation, including light touch, causing a painful attack. At the same time, strong pressure, usually applied by the patient himself, not only does not cause pain, but in some cases leads to a decrease or disappearance of pain.
2. Myofascial trigger points (essentially pain points) are located in the soft tissues of the face in the projection of the masticatory muscles. “Pressing” on them is accompanied by localized or radiating pain.

Establishing a specific form of trigeminal facial pain, which usually requires an interdisciplinary clinical examination, involves excluding a number of forms of orofacial pain not associated with damage to the trigeminal nerve, in particular temporomandibular (arthrogenic and myofascial), symptomatic (ophthalmo-, rhino- and odontogenic) and psychogenic prosopalgia.

Treatment of trigeminal prosopalgia

The complexity of treating patients with trigeminal facial pain is due to the need to determine differentiated treatment approaches due to the ineffectiveness of the use of conventional analgesics for certain forms of trigeminal prosopalgia, the frequent need to change standard treatment regimens and, in some cases, the development of “pharmacoresistant” forms of facial pain that require surgical treatment.

The ineffectiveness of traditional analgesics (for example, NSAIDs) prescribed in connection with the development of trigeminal facial pain is an indication for the use of drugs from other groups, in particular carbamazepine, gabapentin or amitriptyline, which have analgesic activity in a number of forms of prosopalgia (scheme of differentiated therapeutic approaches for paroxysmal and non-paroxysmal trigeminal prosopalgia is presented in

).

Over the past few decades, carbamazepine has remained the most effective and affordable drug in the treatment of patients with trigeminal neuralgia. At the same time, the maximum effectiveness of carbamazepine (as a “monotherapy”) appears in the initial period of the disease. The main indication for the use of carbamazepine is paroxysmal pain, covering the area of ​​innervation of the trigeminal nerve. The daily dose of carbamazepine during an exacerbation of trigeminal neuralgia is usually 600–1200 mg (with a 3–4-time dose of the usual dosage form or 2 times of the retard form), but with uncontrolled use by a doctor it often exceeds 2000 mg/day. As neuralgia regresses, a transition is made to maintenance doses of carbamazepine and its gradual withdrawal when facial pain disappears. If there are contraindications for the prescription of carbamazepine or its forced withdrawal, gabapentin is used as an alternative remedy for the elimination of paroxysmal trigeminal pain.

Gabapentin (Gabagamma) is an anticonvulsant that has an analgesic (GABAergic-like) effect. Obviously, this explains its effectiveness in the treatment of patients with neuropathic pain, including paroxysmal and non-paroxysmal trigeminal prosopalgia. Indications for the use of gabapentin (Gabagamma) are paroxysmal facial pain in trigeminal neuralgia and trigeminal neuralgia caused by multiple sclerosis, as well as subacute and chronic non-paroxysmal pain (including deafferentation) in herpetic and traumatic trigeminal neuropathy. The daily dose of Gabagamma in patients with trigeminal prosopalgia can range from 300 to 1500 mg, with a dosage frequency of at least 3 times a day. Gabagamma is used for a long time and is gradually withdrawn. In general, the use of gabapentin (Gabagamma) is considered safer than carbamazepine and especially amitriptyline.

Amitriptyline is a tricyclic antidepressant that is a norepinephrine and serotonin reuptake inhibitor. This drug is widely used for the treatment of postherpetic neuralgia, especially accompanied by a burning sensation. The analgesic effect of amitriptyline usually develops within 1–2 weeks. To reduce the sedative and anticholinergic effects of amitriptyline, treatment begins with small doses of the drug - 10 mg 2-3 times a day (especially at night), gradually increasing the daily dose (due to evening administration) to 75-100 mg. If amitriptyline is insufficiently effective and facial pain persists, gabapentin (Gabagamma) is indicated.

Treatment of patients with damage to the trigeminal nerve also includes the use of high doses of B vitamins in the form of multicomponent preparations “Milgamma” and “Milgamma compositum”. The composition of the drug "Milgamma" (solution for intramuscular administration) includes 100 mg of thiamine and pyridoxine, 1000 mcg of cyanocobalamin and 20 mg of lidocaine. Milgamma compositum is available in the form of tablets containing 100 mg of benfotiamine and pyridoxine. The effectiveness of Milgamma in the treatment of patients with neuropathic pain is associated with inhibition (probably serotonergic) of nociceptive impulses, as well as acceleration of the regeneration of axons and the myelin sheath of peripheral nerves. The regimen for using Milgamma for trigeminal facial pain includes: prescribing Milgamma in the form of a solution for intramuscular administration - 2 ml daily, for 10 or 15 days, then Milgamma compositum - orally, 1 tablet 3 times a day, for 6 weeks.

Yu. V. Grachev , Doctor of Medical Sciences, V. I. Shmyrev, Doctor of Medical Sciences, Professor, Scientific Research Institute of Advanced Promotion of the Russian Academy of Medical Sciences, State Medical University of the Administration of the President of the Russian Federation, Moscow

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.

Symptoms of the disease

The most striking symptom of inflammation of the trigeminal nerve is unbearable pain, which is felt in a certain area of ​​the head, on the face. The sensations are shooting and burning in nature, and with minimal movements or touches they intensify and pass through the muscle fibers.

Regardless of the causes of neuritis, the gender of the patient and the pairing of the organ, pain in the vast majority of cases is felt on the right.

Inflammation may also be indicated by:

• increased frequency of sharp attacks of pain up to once every fifteen minutes;
• metallic taste in the mouth;
• discomfort when pressing on the gums;
• twitching of muscles responsible for facial expressions;
• a feeling of hyperthermia at the suspected site of the inflammatory process.

If you do not start therapy, the pain will become stronger and attacks will occur more often. As a result, the fibers will die, and the affected areas will lose sensitivity and paralysis will occur.

It is important to consult a neurologist to eliminate the cause of the pathology, because taking painkillers and NSAIDs only relieves symptoms, but does not affect the disease itself.

The disease usually worsens during the cold season. Sharp pain occurs mainly during the daytime, when the facial muscles are actively used.

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.

Make an appointment

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.

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.

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.

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.

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.

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.

Clinical researches

At the Department of Therapeutic Dentistry of St. Petersburg State Medical University named after. acad. I.P. Pavlova, it was proven that the joint use of Asepta series products can achieve a positive effect. The products can be used either independently in the initial stages of diseases or in combination with medications for severe forms of chronic periodontal diseases.

Considering the therapeutic and prophylactic properties of the Asepta line, experts recommend using them for inflammatory diseases of the oral mucosa, such as catarrhal stomatitis, glossitis and cheilitis.

Sources:

1. The use of new anti-inflammatory drugs in the complex of therapeutic and preventive measures for periodontal diseases (E.D. Kuchumova, A.A. Leontyev, O.V. Kalinina, L.Yu. Orekhova, S.B. Ulitovsky) E.D. Kuchumova, Ph.D., Associate Professor, A.A. Leontyev, dentist, O.V. Kalinina, dentist, L.Yu. Orekhova, Doctor of Medical Sciences, Professor, Head of Department, S.B. Ulitovsky, Doctor of Medical Sciences, Prof. Department of Therapeutic Dentistry of St. Petersburg State Medical University named after. acad. I.P. Pavlova
2. The use of drugs from the Asepta line in the complex treatment of inflammatory periodontal diseases (N.V. Berezina E.N. Silantyeva S.M. Krivonos, Kazan State Medical Academy. Kazan.) N.V. BEREZINA, E.N. SILANTIEVA, S.M. KRIVONOS Kazan State Medical Academy
3. Study of the clinical effectiveness of treatment and prophylactic agents of the Asepta line in the treatment of inflammatory periodontal diseases (A.I. Grudyanov, I.Yu. Aleksandrovskaya, V.Yu. Korzunina) A.I. GRUDYANOV, Doctor of Medical Sciences, Prof., Head of Department I.Yu. ALEXANDROVSKAYA, Ph.D. V.Yu. KORZUNINA, asp. Department of Periodontology, Central Research Institute of Dentistry and Maxillofacial Surgery, Rosmedtekhnologii, Moscow