Clinical protocol for the diagnosis and treatment of trigeminal neuralgia. Standard of treatment of trigeminal neuralgia Principles of treatment and management of patients with trigeminal neuralgia

Transcript

1 Recommended by the Expert Council of the Republican Center for Healthcare Development of the Ministry of Healthcare and Social Development of the Republic of Kazakhstan dated December 12, 2014 protocol 9 CLINICAL PROTOCOL FOR DIAGNOSTICS AND TREATMENT TRIPLE NERVE NEURALGY I. INTRODUCTORY PART: 1. Name of the protocol: Trigeminal neuralgia 2. Protocol code: H-NS 10-2 (5) 3. ICD code: G50.0 Trigeminal neuralgia 4. Abbreviations used in the protocol: AD blood pressure ALT alanine aminotransferase AST aspartate aminotransferase HIV human immunodeficiency virus CT computed tomography MRI magnetic resonance tomography NTN trigeminal neuralgia ESR erythrocyte sedimentation rate ECG electrocardiography 5. Date of protocol development: 2014. 6. Patient category: adults. 7. Protocol users: neurosurgeons. II. METHODS, APPROACHES AND PROCEDURES OF DIAGNOSIS AND TREATMENT: 8. Definition: Trigeminal neuralgia (trigeminal neuralgia) paroxysmal stabbing pain lasting several seconds, often caused by secondary sensory stimuli, corresponds to the zone of innervation of one or more branches of the trigeminal nerve on one side of the face, without neurological ... The main cause of the disease

2 is the conflict between the vessel and the root of the trigeminal nerve (neurovascular conflict). In rare cases, facial pain is caused by other pathological conditions (tumor, vascular malformations, herpetic nerve damage). 9. Clinical classification: Distinguish between trigeminal neuralgia type 1 (acute, shooting like electric shock, paroxysmal pain) and trigeminal neuralgia type 2 (aching, throbbing, burning, constant pain\u003e 50%). 10. Indications for hospitalization: Indications for planned hospitalization: Paroxysmal or persistent pain in the innervation of the trigeminal nerve, meeting the criteria for trigeminal neuralgia. Indications for emergency hospitalization: no. 11. The list of basic and additional diagnostic measures: 11.1 Basic (mandatory) diagnostic examinations carried out at the outpatient level: MRI of the brain Additional diagnostic examinations conducted at the outpatient level: CT of the brain general blood analysis; micro-correction; blood chemistry; coagulogram; ELISA for markers of hepatitis B and C; ELISA for HIV; general urine analysis; determination of the blood group; determination of the Rh factor; ECG; fluorography of the chest organs Basic (mandatory) diagnostic examinations conducted at the stationary level: determination of the blood group; determination of the Rh factor. 2

3 11.5 Additional diagnostic examinations carried out at the stationary level: angiography; general blood test (6 parameters: erythrocytes, hemoglobin, leukocytes, platelets, ESR, hematocrit) Diagnostic measures carried out at the stage of emergency emergency care: no. 12. Diagnostic criteria: magnetic resonance imaging of the brain is performed to determine the etiology of trigeminal neuralgia Complaints and anamnesis: Complaints: Paroxysmal attacks of pain in the innervation of one or more branches of the trigeminal nerve. Anamnesis: previous traumatic brain injury; carious teeth; previous herpes infection (neurotropic infection) Physical examination: paroxysmal attacks of pain in the face or forehead, lasting a few seconds to 2 minutes; pain has the following characteristics (at least 4): Localized in the region of one or more branches of the trigeminal nerve; It occurs suddenly, acutely, it is felt as a burning sensation or the passage of an electric current; Pronounced intensity; It can be called from trigger zones, as well as when eating, talking, washing your face, brushing your teeth, etc.; Absent in the interictal period; absence of neurological deficit; the stereotypical nature of pain attacks in each patient; exclusion of other causes of pain during examination Laboratory tests: No specific changes in laboratory parameters for trigeminal neuralgia Instrumental studies: 3

4 MRI is a standard method for detecting neurovascular conflict in the trigeminal nerve zone, and excluding other causes (eg, tumor, vascular malformation, etc.) of the disease. Indications for specialist consultation: consultation of a therapist in the presence of somatic pathology; consultation with a cardiologist if there are changes in the ECG; consultation with a dentist for the purpose of sanitation of the oral cavity Differential diagnosis: The differential diagnosis is carried out with pathological conditions characterized by facial and / or cranial pain. Such diseases (Table 1) include pulpitis, temporomandibular pain, neuropathic trigeminal pain, paroxysmal hemicrania. Table 1. Comparison of signs of trigeminal neuralgia with symptoms of other diseases Symptom Trigeminal neuralgia Character Shooting, stabbing, sharp, like an electric shock Area / spread Intensity Duration of current flow Zone of innervation and trigeminal nerve Moderate to strong Refractory period 1 -60 sec Pulpitis Acute, aching, pulsating Around teeth, intraoral mild to moderate Short, but no refractory period Temporomandibular pain Dull, aching, sometimes sharp Preauricular, radiating down to the lower jaw, temporal region, but postauricu lar neck Weak to strong Non-refractory, last for several hours, mostly continuous, may be 4 Neuropathic kayatriheminal pain Aching, throbbing Around teeth or in the area of \u200b\u200binjury / tooth surgeon or in the area of \u200b\u200bfacial trauma Moderate Continuous, soon after injury Paroxysmal th hemicrania Pulsating, drilling, stabbing Orbit temporal region Strong naya Episodic 2-30 min

5 Frequency Triggering factors Pain relieving factors Disease-related factors Rapid onset and cessation, periods of complete remission from weeks to several months Light touch, non-nociceptive Resting, drugs Local anesthetic reduces pain, severe depression and Weight loss More than 6 months unlikely Contact of hot / cold one to the teeth Do not eat on the sore side Rotten teeth, exposed dentin episodic Tends to grow slowly and gradually decrease, last for many years Teeth clenching, prolonged chewing, yawning Rest, restricted opening mouth Muscle pain on the other side, restriction of opening, clicking when the mouth is opened wide Continuous Light touch Do not touch History of treatment or dental trauma, may have loss of sensation, allodynia near pain, local anesthetic relieves pain 1-40 days, may be periods complete remission None Indomethacin May have a migraine hara cter 13. Treatment goals: Elimination or reduction of pain by microvascular decompression (opcode 04.41) or percutaneous radiofrequency thermocoagulation of the trigeminal nerve (opcode 04.20). The choice of a surgical method of treatment depends on the patient's age and comorbidity, the cause of trigeminal neuralgia, the nature of the pain, and the patient's wishes. 14. Treatment tactics: 14.1 Non-drug treatment: Diet in the absence of concomitant pathology according to the age and needs of the body. Drug treatment: Drug treatment provided on an outpatient basis: List of essential drugs (with 100% probability of use): 5

6 Carbamazepine 200 mg, dose and frequency depend on the frequency and intensity of facial pain, orally. List of additional drugs (less than 100% of the likelihood of use): Pregabalin mg, dose and frequency depends on the frequency and intensity of facial pain, orally Medical treatment provided at the hospital level: In order to reduce facial pain before surgery, patients usually take enteral drug Carbamazepine, dose and the frequency of reception of which depends on the intensity and frequency of attacks of facial pain. Antibiotic prophylaxis: Cefazolin 2 g, intravenously, 1 hour before the incision. Postoperative analgesic therapy: NSAIDs or opioids. Postoperative antiemetic therapy (metoclopramide, ondansetron), intravenously or intramuscularly, according to indications in an age-related dosage. Gastroprotectors in the postoperative period in therapeutic dosages according to indications (omeprazole, famotidine). List of essential drugs (100% likely to be used): analgesics; antibiotics. List of additional drugs (less than 100% probability of use): Fentanyl 0.05mg / ml (0.005% - 2ml), amp Povidone-iodine 1L, Chlorhexidine 0.05% ml bottle, Tramadol 100mg bottle (5% - 2ml ) amp Morphine 10 mg / ml (1% -1 ml), amp Vancomycin 1 g, vial Aluminum oxide, magnesium oxide ml, suspension for oral administration, vial Ondansetron, 2 mg / ml 4 ml, amp Metoclopramide 5 mg / ml 2 ml, amp Omeprazole 20 mg, tab Famotidine 20 mg, vial lyophilized powder for injection Enalapril 1.25 mg / ml - 1 ml, amp Clopidogrel 75 mg, tab Acetylsalicylic acid 100 mg, tab 6

7 Valsartan 160 mg, tab Amlodipine 10 mg, tab Ketorolac 10 mg / ml, amp Drug treatment provided at the emergency stage: none Other treatments: Other treatments provided on an outpatient level: Nerve exit point blockages Other treatments, Inpatient: Radiosurgery (Gamma Knife) Other treatments provided in the ambulance stage: Not available Surgical intervention: Outpatient surgery: Not available Inpatient surgery: Methods of surgical treatment of trigeminal neuralgia : microvascular decompression; percutaneous selective radio frequency thermocoagulation; The purpose of microvascular decompression is to eliminate the conflict between the vessel and the trigeminal nerve. With radiofrequency thermocoagulation, selective thermal damage to the nerve is performed, thereby interrupting the conduction of pain impulses. Disease Neuralgia of the trigeminal nerve ICD-10 G50.0 Name of medical service Radiofrequency thermal destruction of the trigeminal nerve (percutaneous) Microsurgical microvascular decompression of the trigeminal nerve Operation code according to ICD Destruction of the cranial and peripheral nerves 04.41 Decompression of the nerve root 14.5 limitation of the trigeminal nerve; good nutrition and normalization of the rhythm of sleep and wakefulness; 7

8 avoid hypothermia and overheating (baths, saunas are contraindicated); avoid provoking factors for the development of paroxysms of pain (cold, hot food, etc.) 14.6 Further management: The first stage (early) of medical rehabilitation, provision of MR in the acute and subacute period of trauma or disease in inpatient conditions (intensive care unit or specialized specialized department) from the first hours in the absence of contraindications. MR is performed by MDC specialists directly at the patient's bedside using mobile equipment or in the departments (offices) of the MR hospital. The patient's stay at the first stage ends with an assessment of the severity of the patient's condition and violations of the BSF MDC in accordance with international criteria and the appointment by the doctor as the coordinator of the next stage, volume and medical organization for MR. The subsequent stages of medical rehabilitation are subject to a separate clinical protocol. Observation of a neuropathologist in a polyclinic at the place of residence. 15. Indicators of the effectiveness of treatment and the safety of diagnostic and treatment methods: Absence or decrease in the intensity and frequency of attacks of facial pain in the innervation of the trigeminal nerve. III. ORGANIZATIONAL ASPECTS OF THE PROTOCOL IMPLEMENTATION 16. List of protocol developers: 1) Erbol Targynovich Makhambetov, PhD, JSC National Center of Neurosurgery, Head of the Department of Vascular and Functional Neurosurgery. 2) Shpekov Azat Salimovich JSC "National Center of Neurosurgery", neurosurgeon of the Department of Vascular and Functional Neurosurgery. 3) Bakybaev Didar Yerzhomartovich clinical pharmacologist of JSC "National Center of Neurosurgery". 17. Conflict of interest: none. 18. Reviewer: Sadykov Askar Myrzakhanovich, PhD, Head of the Department of Neurosurgery, FAO ZhGMK "Central Road Hospital", Astana. 19. Indication of the conditions for revision of the protocol: revision of the protocol after 3 years and / or when new methods of diagnosis and / or treatment with a higher level of evidence appear. 8

Trigeminal neuralgia

RCHD (Republican Center for Healthcare Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical Protocols MH RK - 2014

general information

Short description

Trigeminal neuralgia (trigeminal neuralgia) - paroxysmal stabbing pain lasting several seconds, often caused by secondary sensory stimuli, corresponds to the innervation zone of one or more branches of the trigeminal nerve on one side of the face, without neurological deficit. The main cause of the disease is the conflict between the vessel and the root of the trigeminal nerve (neurovascular conflict). In rare cases, facial pain is caused by other pathological conditions (tumor, vascular malformations, herpetic nerve damage).

Classification

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES OF DIAGNOSTICS AND TREATMENT

List of basic and additional diagnostic measures

Basic (mandatory) diagnostic examinations carried out at the outpatient level:

Diagnostic measures carried out at the stage of emergency emergency care: no.

Diagnostic criteria
Magnetic resonance imaging of the brain is performed to determine the etiology of trigeminal neuralgia.

Complaints and anamnesis
Complaints:
Paroxysmal attacks of pain in the innervation area of \u200b\u200bone or more branches of the trigeminal nerve.

Exclusion of other causes of pain during examination;

Instrumental research:
MRI is the standard method for detecting neurovascular conflict in the trigeminal nerve area, and excluding another cause (for example, tumor, vascular malformation, etc.) of the disease.

Indications for specialist consultation:

Differential diagnosis

Differential diagnosis

Differential diagnosis is carried out with pathological conditions characterized by facial and / or cranial pain. Such diseases (Table 1) include pulpitis, temporomandibular pain, neuropathic trigeminal pain, paroxysmal hemicrania.

Table 1. Comparison of signs of trigeminal neuralgia with symptoms of other diseases

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Treatment

Treatment goals
Pain relief or relief by microvascular decompression (opcode 04.41) or transcutaneous radiofrequency thermocoagulation of the trigeminal nerve (opcode 04.20). The choice of a surgical method of treatment depends on the patient's age and comorbidities, the cause of trigeminal neuralgia, the nature of the pain, and the patient's wishes.

Treatment tactics

Non-drug treatment:
Diet in the absence of concomitant pathology - according to the age and needs of the body.

Drug treatment

Outpatient drug treatment

List of essential medicines (having a 100% chance of being applied):
Carbamazepine 200 mg, dose and frequency depend on the frequency and intensity of facial pain, orally.

List of complementary medicines (less than 100% probability of use):
Pregabalin 50-300 mg, dose and frequency depend on the frequency and intensity of facial pain, orally.

In order to reduce facial pain before surgery, patients usually take enterally the drug Carbamazepine, the dose and frequency of administration of which depend on the intensity and frequency of attacks of facial pain.

Antibiotic prophylaxis: Cefazolin 2 g, intravenously, 1 hour before the incision.

Postoperative analgesic therapy: NSAIDs or opioids.

Postoperative antiemetic therapy (metoclopramide, ondansetron), intravenously or intramuscularly, according to indications in an age-related dosage.

Gastroprotectors in the postoperative period in therapeutic dosages according to indications (omeprazole, famotidine).

Medical treatment provided at the stage of ambulance emergency: no.

Other treatments

Other outpatient treatments:
Nerve exit points blockade.

Other types of treatment provided at the inpatient level: radiosurgery (Gamma knife).

Other types of treatment provided during the ambulance stage: Not available.

Surgical intervention

Outpatient surgery: Not performed.

Inpatient surgery
Methods of surgical treatment of trigeminal neuralgia:

The purpose of microvascular decompression is to eliminate the conflict between the vessel and the trigeminal nerve. With radiofrequency thermocoagulation, selective thermal damage to the nerve is performed, thereby interrupting the conduction of pain impulses.

Further management
The first stage (early) of medical rehabilitation is the provision of MR in the acute and subacute period of injury or illness in an inpatient setting (resuscitation and intensive care unit or specialized specialized department) from the first 12-48 hours in the absence of contraindications. MR is performed by MDC specialists directly at the patient's bedside using mobile equipment or in the departments (offices) of the MR hospital. The patient's stay at the first stage ends with an assessment of the severity of the patient's condition and violations of the BSF MDC in accordance with international criteria and the appointment by the coordinating doctor of the next stage, volume and medical organization for MR.
The subsequent stages of medical rehabilitation are topics of a separate clinical protocol.
Observation of a neuropathologist in a polyclinic at the place of residence.

Indicators of the effectiveness of treatment and the safety of diagnostic and treatment methods described in the protocol:
Absence or decrease in the intensity and frequency of attacks of facial pain in the area of \u200b\u200binnervation of the trigeminal nerve.

Principles of treatment and management of patients with trigeminal neuralgia

About article

For citation: Manvelov L.S., Tyurnikov V.M., Kadykov A.V. Principles of treatment and management of patients with trigeminal neuralgia // BC. 2014. No. 16. S. 1198

Trigeminal neuralgia (TN) is a disease manifested by sharp facial pains in the innervation zones of its branches. Painful attacks are often provoked by lightly touching the skin of the so-called trigger zones: areas of the lips, wings of the nose, eyebrows. At the same time, applying strong pressure to these areas makes the attack easier.

The tactics of managing patients with NTN should include:

• diagnosis of the disease, including general clinical, otolaryngological, dental and instrumental examinations;
• identification of etiological factors;
• conservative treatment;
• surgery.

The main goals of HTN treatment are pain relief and prevention of disease recurrence.

Conservative treatment includes medication and physical therapy.

The use of antiepileptic drugs is effective in about 90% of HTN cases. Phenytoin was the first of these to be used, but from 1961 to the present time, a more effective agent, carbamazepine, is widely used, rightly considered the drug of first choice for the treatment of patients with NTN. The initial dose is 200-400 mg / day, it is gradually increased until the pain stops, on average up to 800 mg / day in 4 divided doses, and then reduced to the minimum effective dose. When treating with carbamazepine, pain syndrome can be stopped in 70% of cases.

Second-line drugs are phenytoin, baclofen, valproic acid, tizanidine, antidepressants.

Phenytoin for exacerbations of the disease is prescribed at a dose of 15 mg / kg intravenous drip for 2 hours once.

Baclofen is taken orally with meals. The initial dose is 5 mg 3 r. / Day, the subsequent dose increase is 5 mg every 3 days until the effect is achieved, but not more than 20-25 mg 3 r. / Day. The maximum dose is 100 mg / day, administered for a short time in a hospital setting. The final dose is set so that when taking the drug, a decrease in muscle tone does not lead to excessive myasthenia gravis and does not impair motor functions. With hypersensitivity, the initial daily dose of baclofen is 6-10 mg, followed by a slow increase. The drug should be discontinued gradually - within 1-2 weeks.

Valproic acid is prescribed as therapy for adults at an initial dose of 3-15 mg / day in 2 divided doses, regardless of food intake. If necessary, the dose of the drug is increased by 5-10 mg / kg / week. The maximum dose is 30 mg / kg / day or 3000 mg / day. For combined treatment, adults are prescribed 10-30 mg / kg / day, followed by an increase of 5-10 mg / kg / week. If a decision is made to switch to intravenous administration of the drug, it is performed 4–6 hours after oral administration at a dose of 0.5–1 mg / kg / h.

Tizanidine is administered orally. The dosage regimen is set individually. The initial daily dose is 6 mg (1 capsule). If necessary, the daily dose can be gradually increased by 6 mg (1 capsule) at intervals of 3–7 days. For most patients, the optimal dose of the drug is 12 mg / day (2 capsules). In rare cases, it may be necessary to increase the daily dose to 24 mg.

Amitriptyline is recommended to be taken orally after meals. The initial dose for adults is 25-50 mg at night, then the dose is increased over 5-6 days to 150-300 mg / day in 3 divided doses. Most of the dose is taken at night. If within 2 weeks. there is no improvement, the daily dose is increased to 300 mg. For elderly patients with mild disorders, the drug is prescribed in a dose of 30-100 mg at night. After reaching the therapeutic effect, they switch to the minimum maintenance dose - 25-50 mg / day. Amitriptyline is administered intramuscularly or intravenously at a dose of 25–40 mg 4 r. / Day, gradually replacing it with oral administration. The duration of treatment is no more than 8-10 months. [RU. Khabriev, A.G. Chuchalin, 2006; A.S. Kadykov, L.S. Manvelov, V.V. Shvedkov, 2011].

Vitamin therapy is shown, mainly the use of B vitamins. Combined preparations have proven themselves well.

Taking analgesics is considered ineffective. In addition, the use of large doses of these drugs, associated with the desire to quickly stop an attack, can lead to the appearance of abusal headaches.

From physiotherapeutic methods in the acute period of the disease and during an attack, a moderate thermal effect is shown: a Sollux lamp, an electric heating pad, ultraviolet irradiation of the sick half of the face. The widely used diadynamic currents have analgesic and anti-inflammatory effects. For the course of treatment, 6-10 procedures are prescribed, which are carried out daily. Recommend 2-3 such courses with a break of 1 week. In addition, this procedure is carried out for 2-3 minutes on the area of \u200b\u200bthe temporal artery and stellate node. With persistent pain, procaine, tetracaine, epinephrine are administered with the help of diadynamic and sinusoidal modulated currents. In this case, the anesthetic effect is more pronounced than when using a galvanic current. With prolonged persistent pain syndrome, chronic course of the disease, the time of exposure to diadynamic currents is increased to 8-10 minutes. 10-18 procedures are prescribed for the course of treatment with a 4-day break after 10 sessions.

With facial pain associated with cervical osteochondrosis, sympathetic-radicular symptom complex, a good effect is given by ultrasound not only paravertebrally, but also at the exit site of the trigeminal nerve for 2 minutes per point every other day. As a result of this effect, facial pain did not recur within 1 year after treatment [N.I. Strelkova, 1991]. Contraindications to ultrasound treatment are a tendency to nosebleeds, retinal detachment, acute inflammatory processes in the sinuses, middle ear, and cerebrovascular accident. During the period of ultrasound treatment, not only pain syndrome decreases, but also regional and general vegetative-vascular disorders.

In the subacute period, in the presence of trigger zones, endonasal electrophoresis of 4% procaine solution and 2% thiamine solution is used, the duration of exposure is from 10 to 30 minutes. In addition, it can be carried out in the form of a half mask and a Bourgogne mask (with 2-sided nerve damage). Electrophoresis of diphenhydramine, pachicarpine hydroiodide, platyphyllin on the affected side of the face is also used. With arthrosis of the temporomandibular joint, electrophoresis of sodium metamizole, hyaluronidase is performed; with rheumatic etiology of the disease - salicylates; with malarial - quinine; with metabolic disorders - iodine and procaine.

The use of an ultrahigh-frequency electric field in an oligothermic dose is also effective.

In chronic forms of NT, cervical osteochondrosis with trigeminal facial pains, face massage is prescribed for 6-7 minutes daily or every other day. Mud applications have a positive effect on the collar area at a temperature of 36–37 ° C for 10 minutes. 10 procedures are prescribed for the course. Ozokerite, paraffin or peat are used. Balneotherapy is successfully used: sulfide, sea, radon baths. The beneficial effects of remedial gymnastics cannot be overestimated. Sanatorium treatment in sanatoriums for patients with diseases of the peripheral nervous system is recommended in the warm season with a chronic course of the disease and rare attacks. Reflexology (acupuncture, moxibustion, laser therapy) has a positive effect.

If conservative therapy is ineffective or severe side effects of drugs are observed, then the need for surgical intervention is discussed.

Surgery. In 1884, the American surgeon D.E. With chronic NTN, Mears first performed the removal of his ganglion. In 1890, the English surgeon W. Ros and the American surgeon E. Enderyus independently developed a special method for removing the Gasser's node, which entered the practice of neurosurgeons in the late 19th and early 20th centuries. Currently, with NTN, the following methods of surgical intervention are used:

• microsurgical decompression of the nerve at the exit from the brainstem;
• partial sensory rhizotomy;
• peripheral block or nerve transection proximal to Gasser's node;
• neuroectomy;
• cryosurgical methods;
• diathermocoagulation;
• high frequency radiation.

The most common modern effective methods of surgical treatment of NTs are microvascular decompression and puncture destructive operations. Among the destructive operations that are part of the arsenal of surgical interventions for NTN, there are percutaneous high-frequency selective rhizotomy (PCRS), balloon microcompression, and glycerol rhizotomy.

The most common destructive method is HRVD, which is a controlled thermal destruction of the Gasser's node, which prevents the transmission of sensory impulses and the development of painful paroxysms. The location of the electrode is controlled in relation to the portions of the assembly. This method is successfully used in leading clinics dealing with the problem of pain [Grigoryan Yu.A., 1989; Broggi G. et al., 1990; Taha J.M. et al., 1995].

The Mayfield Clinik Chincinati M D John Tew has considerable experience in HRCM. In this clinic, more than 3 thousand patients have been operated on using this method. Good results were obtained in 93% of patients. Relapses of pain within 15 years were observed in 25% of patients. Relapses of the disease during the first 5 years were noted in 15% of patients, before 10 years - in 7% and from 10 to 15 years - in 3% of patients. There is a direct relationship between the severity of hypalgesia after percutaneous rhizotomy, the frequency of recurrence of pain and dysesthesia. When mild hypalgesia was achieved after surgery and follow-up for 3 years, the frequency of pain relapses reached 60%, while dysesthesia was observed in 7% of patients. When severe hypalgesia was achieved and patients were observed for 15 years, the frequency of pain relapses was 25%, the probability of dysesthesia increased to 15%. When receiving complete analgesia after percutaneous rhizotomy and observation of patients for 15 years, the frequency of pain relapses was observed in 20% of cases, and the number of dysesthesias increased to 36%. Thus, the most favorable is the second option - the achievement of pronounced hypalgesia.

Unfortunately, patients with advanced forms of NTN often end up in neurosurgical departments, including after numerous destructive procedures. This undoubtedly worsens the functional result of neurosurgical interventions and in some cases requires complex and more dangerous operations at the level of the central nervous system [Ogleznev K.Ya., Grigoryan Yu.A., 1990].

Advantages of HRVD: bloodlessness, speed and safety of intervention, local anesthesia as pain relief, and, finally, a high percentage of positive results. HRVD of the gasser's node in NTN and cluster headaches is a highly effective and safe method of surgical intervention.

Course and forecast. Exacerbations of the disease most often occur in spring and autumn. In the absence of relapses, the prognosis is favorable.

Standard of care for patients with trigeminal neuralgia, clonic hemifacial spasm

MINISTRY OF HEALTH AND SOCIAL DEVELOPMENT OF THE RUSSIAN FEDERATION

ON THE APPROVAL OF THE STANDARD OF MEDICAL CARE FOR PATIENTS WITH TRINAL NERVE NEURALGIA, CLONIC HEMIFACIAL SPASM

In accordance with Art. 40 Fundamentals of the legislation of the Russian Federation on the protection of the health of citizens of July 22, 1993 N 5487-1 (Bulletin of the Congress of People's Deputies of the Russian Federation and the Supreme Council of the Russian Federation, 1993, N 33, Art.1318; Collected Legislation of the Russian Federation, 2003, N 2 , Art. 167; 2004, No. 35, Art. 3607; 2005, No. 10, Art. 763) I order:

1. To approve the attached standard of care for patients with trigeminal neuralgia, clonic hemifacial spasm.

2. Recommend the heads of federal specialized medical institutions to use the standard of medical care for patients with trigeminal neuralgia, clonic hemifacial spasm in the provision of expensive (high-tech) medical care.

from 26.05.2006 N 402

STANDARD OF MEDICAL CARE FOR PATIENTS WITH TRINAL NERVE NEURALGIA, CLONIC HEMIFACIAL SPASM

1. Patient model:

Nosological form: Neuralgia of the trigeminal nerve; clonic hemifacial spasm

Trigeminal neuralgia (NTN) is a disease characterized by paroxysms of severe facial pain in the areas of innervation of one or more branches of the trigeminal nerve.

ICD-10
G50.0 Trigeminal neuralgia.

EPIDEMIOLOGY
The incidence averages 4 cases per 100,000 population per year. NTN is a disease of the elderly, the average age of onset is 60 years. A little more often NTN develops in women.

CLASSIFICATION
It is customary to distinguish idiopathic and symptomatic NTN. Idiopathic NTN is a neuropathy that develops in middle and old age. It is assumed that in most cases it is caused by compression of the root of the trigeminal nerve or its branches (usually II or III) by pathologically altered (dilated, dislocated) blood vessels of the posterior cranial fossa (most often one of the cerebellar arteries). Compression can be associated with narrowing of the bone canals, usually due to a chronic inflammatory process in adjacent areas (sinusitis, periodontitis, etc.). Symptomatic NTN is observed relatively rarely; it develops as one of the manifestations of other diseases of the central nervous system (multiple sclerosis, brainstem glioma, tumors of the cerebellopontine region, stem stroke, etc.).

DIAGNOSTICS
ANAMNESIS AND PHYSICAL EXAMINATION
■ For NTN pain paroxysms lasting from several seconds to 1-2 minutes are characteristic. Pain in HTN can provoke conversation, eating, chewing, and facial movements. The presence of trigger zones is very characteristic, the slight irritation of which (touch, wind, etc.) causes an attack of pain. More prolonged, and even more constant pains are not typical for NTN. Painful paroxysms occur suddenly, more often in the daytime. Their frequency is very variable - from single ones during the day to continuously repeating for several hours (the so-called status neuralgicus).
■ Pain with NTN is unilateral, more often occurs on the right and is usually limited to the area of \u200b\u200binnervation of one, less often two branches of the trigeminal nerve. In some cases, the localization of pain corresponds to the area of \u200b\u200binnervation of one of the terminal branches of the trigeminal nerve - the lingual, upper alveolar, lower alveolar nerves, etc. The pain is very intense, unbearable, patients usually describe them as lumbago or a feeling of electric current.
■ Pain with HTN is controlled by antiepileptic drugs. Non-narcotic analgesics and NSAIDs usually do not significantly affect the severity of pain.
■ A painful attack with NT is often accompanied by a reflex spasm of facial muscles (pain tic) - like facial hemispasm. Sometimes painful paroxysms are accompanied by vegetative symptoms (facial flushing, lacrimation, nasal congestion, etc.).
■ NTN is characterized by a relapsing course - periods of exacerbations are replaced by periods of remission of variable duration.
Neurological examination is primarily aimed at excluding other diseases. With typical NTN, as a rule, they do not reveal any objective symptoms, with the exception of pain in the exit point of the affected branch of the trigeminal nerve and, sometimes, areas of hyperesthesia or hypesthesia in the area of \u200b\u200bits innervation. In the presence of severe symptoms of prolapse from the trigeminal nerve and signs of damage to adjacent cranial nerves and other focal neurological symptoms, it is necessary to exclude secondary NTN.
In case of difficulties in diagnosis, it is permissible to conduct a trial treatment with carbamazepine, which is usually prescribed at a dose of 400-600 mg / day in 2 doses. With NT, such treatment after 24–72 hours causes relief of pain syndrome or a significant decrease in its severity. If carbamazepine is ineffective, the diagnosis of HTN should be questioned.

LABORATORY AND INSTRUMENTAL STUDIES
MANDATORY RESEARCH METHODS
■ General clinical studies (complete blood count, general urine analysis).

ADDITIONAL RESEARCH METHODS
■ Methods of neuroimaging (MRI) are indicated for an atypical course of NTN (presence of focal neurological symptoms, ineffectiveness of drug therapy). MRI allows in most cases to exclude the causes of secondary HTN (multiple sclerosis, tumors, etc.). In addition, MRI can detect vascular compression of the trigeminal root.
■ To detect peripheral compression of the branches of the trigeminal nerve, orthopantomography is performed to assess the width of the bony canals.
■ To detect chronic inflammation and other pathological processes in the sinuses, x-rays of the paranasal sinuses are performed.

DIFFERENTIAL DIAGNOSTICS
■ Secondary NTN.
✧ The most common cause of secondary HTN is multiple sclerosis. The onset of the disease at a relatively young age (up to 45 years) and bilateral symptoms (10–20% versus 3% in primary NT) are suspicious for multiple sclerosis. Neuralgic pain in the area of \u200b\u200binnervation of the trigeminal nerve as the first manifestation of multiple sclerosis is observed in 11–20% of cases, however, they are rarely the only manifestation of the disease - there are other symptoms of brain stem damage (nystagmus, internuclear ophthalmoplegia, etc.). Pi MRI detects foci of demyelination in the area of \u200b\u200bthe nuclei or fibers of the trigeminal nerve.
✧ Approximately 5% of all NTN cases are caused by tumors of the posterior cranial fossa (meningiomas, neuromas VIII or, rarely, V pairs of cranial nerves, etc.). A progressive course is characteristic - constant burning pains, symptoms of prolapse (hyposthesia, absence of a corneal reflex, weakness of the masticatory muscles) join typical neuralgic paroxysms. As a rule, symptoms of damage to adjacent cranial nerves are present (ipsilateral prosoparesis, tinnitus and hearing loss, vestibular disorders, etc.). The diagnosis is confirmed by MRI.
■ With glossopharyngeal nerve neuralgia, pains resemble those with NTN, but they are localized in the area of \u200b\u200bthe tongue root, pharynx, palatine tonsils, and trigger zones are also located there. Pain can provoke talking, swallowing, yawning, laughing, turning the head. The attacks of pain are sometimes accompanied by syncope (see the article "Fainting").
■ Neuralgia of the upper laryngeal nerve is a rare disease characterized by attacks of unilateral neuralgic pain in the larynx, which sometimes radiates to the zygomatic region, lower jaw, and ear. Swallowing and coughing provoke pain. There are no trigger zones, but palpation usually reveals a painful point in the area of \u200b\u200bthe lateral surface of the neck above the thyroid cartilage.
■ Postherpetic neuropathy of the trigeminal nerve usually develops as a consequence of the previous ganglionitis of the Gasser's node of herpetic etiology. It differs from NTN by constant burning pains (against which paroxysmal shooting pains are possible), the presence of pronounced sensitivity disorders (hypo- and anesthesia, dysesthesia, allodynia), and the absence of trigger zones. Sometimes trigeminal neuropathy develops with Lyme disease, collagenoses (systemic lupus erythematosus, Sjogren's syndrome), and in rare cases can be idiopathic.
■ Atypical facial pain is defined as persistent facial pain with no signs of cranial neuralgia and not associated with objective symptoms or organic disease. Atypical facial pains are usually constant, aching in nature, often bilateral, their localization does not correspond to the area of \u200b\u200binnervation of the trigeminal nerve. In some cases, a paroxysmal increase in pain is possible, which can mimic NTN. There are no trigger zones. Characterized by a long-term course and frequent combination with chronic pain of other localization (headache, in the neck, back, etc.). Patients usually present with many complaints, but with careful questioning it is usually possible to find out that pain does not significantly disrupt daily activities. Mostly women are ill, the average age of onset of the disease is 45 years. Most cases of atypical facial pain have psychogenic etiology and are often associated with depression (detected in 72% of patients). Tricyclic antidepressants are usually effective (for example, amitriptyline 30 mg / day for 4 weeks), on the contrary, the effectiveness of carbamazepine does not exceed that of placebo.

INDICATIONS FOR CONSULTATION OF OTHER SPECIALISTS
■ In the case of new-onset neuralgia attacks, it is necessary to consult a neurologist to determine the primary or secondary nature of NTN and to determine the indications for MRI, magnetic resonance angiography.
■ In case of pain in the teeth or gum area, it is necessary to consult a dentist (excluding pulpitis, periodontitis, and other dental pathology).
■ For pain in the pharynx, or for a possible etiologic role for chronic sinusitis, it may be necessary to consult an otorhinolaryngologist.
■ The question of the applicability and expediency of surgical treatment is decided together with a neurosurgeon.
■ In cases of atypical facial pain, consultation with a psychiatrist may be required.

TREATMENT
OBJECTIVES OF TREATMENT
The main goal of treatment is to relieve pain and prevent recurrence of the disease.

INDICATIONS FOR HOSPITALIZATION
Treatment for HTN is usually carried out on an outpatient basis. Hospitalization may be required in diagnostically difficult cases for a comprehensive examination. In addition, hospitalization is indicated for extremely severe NTN with intractable pain syndrome that interferes with oral nutrition and drug intake, and in cases when surgical treatment is planned (in a neurosurgical hospital).

NON-MEDICINAL TREATMENT METHODS
It is important to identify and, if possible, eliminate the factors that provoke the onset of pain (see below).

DRUG THERAPY
■ The drugs of choice are carbamazepine, oxcarbazepine, and gabapentin.
✧ Treatment begins with a dose of 200 mg / day in 2–3 doses, which is gradually increased (by 200 mg / day) until a clinical effect is achieved (usually 400–1000 mg / day). The maximum daily dose is 1200 mg. Monotherapy with carbamazepine has an effect in more than 70% of cases. The most common side effects are drowsiness, dizziness, nausea, and vomiting. A gradual increase in the dose of the drug usually minimizes the side effects.
✧ Oxcarbazepine is prescribed at a dose of 600 mg / day in 2 divided doses, followed by an increase to 2400 mg / day.
✧ Gabapentin is prescribed 300 mg 3 times a day with a gradual increase in the dose by 300 mg / day (but not more than 3600 mg / day).
■ Topiramate and lamotrigine are also used.
After achieving the clinical effect, the dosage of drugs is slowly reduced to the minimum maintenance, the treatment with which is carried out for a long period of time. Cancellation of drug therapy is decided on an individual basis.

SURGERY
In rare cases, with the ineffectiveness of drug therapy, as well as in cases of the development of pronounced side effects that significantly complicate its implementation, the question of surgical treatment (for example, microvascular decompression) is raised.

FURTHER INTRODUCTION
The observation plan is made on an individual basis. The severity of pain syndrome is monitored (for this purpose it is convenient to use one of the pain scales, for example, a short version of the McGill questionnaire), the effectiveness and tolerability of drug therapy, the presence and severity of side effects. In patients taking carbamazepine, it is necessary to monitor the content of erythrocytes, leukocytes and platelets, the activity of hepatic aminotransferases and the concentration of electrolytes in the blood serum. During the first 2 months, analyzes are carried out every 2 weeks, then 1 time in 2-3 months (for at least 6 months). In patients after partial denervation surgery with hypo- or anesthesia in the region of the I branch of the trigeminal nerve, it is necessary to carefully monitor the state of the cornea, if signs of keratitis appear (pain in the eye, its hyperemia, visual impairment, etc.), you should immediately consult an ophthalmologist.

PATIENT TRAINING
The patient is advised to identify the factors that provoke the onset of pain, and, if possible, eliminate them.
■ Avoid exposure to cold air currents (for example, from a running air conditioner); in cold windy weather, cover your face with a soft cloth.
■ You should eat semi-liquid or soft foods, avoid very cold or very hot drinks, foods that require careful chewing.
■ In case of localization of trigger zones in the oral cavity, taking liquid through a straw sometimes prevents the occurrence of painful paroxysms.
■ When localizing trigger zones in the gum or palate, in some cases, the use of local anesthetics is effective.
■ Intense kneading or pressure on the soft tissues of the face can sometimes prevent or control the onset of pain.

FORECAST
With regard to life, the prognosis is favorable - the disease does not affect the overall life expectancy. In terms of cure, the prognosis is uncertain. NTN is characterized by a chronic recurrent course. Sometimes periods of remission can be very long (months or years), but in most cases, over time, the frequency and duration of exacerbations increase, and the effectiveness of drug therapy decreases.
See also Standard of Care for Trigeminal Disorders, p. 1145; “The standard of sanatorium-resort care for patients with lesions of individual nerves, nerve roots and plexuses, polyneuropathies and other lesions of the peripheral nervous system”, p. 1329.

Nerve Root and Plexus Disorders

Profile: neurological.
Stage of treatment: polyclinic (outpatient).

Stage goal: restoration of the function of the affected nerve roots and plexuses. Duration of treatment: depending on the severity of clinical manifestations from 7 days to 14 days.

ICD codes:
G50- G59 Lesion of individual nerves, nerve roots and plexuses
M50.1 Disorder of cervical intervertebral disc with radiculopathy
M51.1 Lumbar and other intervertebral disc disorders with radiculopathy
M54.1 Radiculopathy

Definition: Mononeuropathy is a lesion of one, multiple mononeuropathy, a lesion of several large nerves. Pathomorphologically, with mononeuropathy and multiple mononeuropathy, damage to the vasa nervorum is detected. Many lesions of the nerve roots and plexuses develop as compression neuropathies caused by external compression, single or recurrent. The most common causes are trauma, external compression (pinching), or volume compression. Nerves and roots that are not surrounded by soft tissues are most susceptible to compression damage. After the removal of external pressure, the restoration of the functions of the root, nerve and plexus usually occurs independently.

Tunnel Syndrome - compression of the peripheral nerve by the surrounding anatomical structures (very often of metabolic origin). Compression of a nerve, root, plexus is usually constant, but its severity may vary depending on tissue edema and muscle tension in the limb. In clinical practice, neuropathy of the ulnar nerve due to its compression in the ulnar groove or cubital tunnel and neuropathy of the median nerve as a result of its compression in the carpal tunnel are common. Neuralgia of the lateral cutaneous nerve of the thigh is the most common cause - trauma, wearing a corset, wearing a bandage. Compression of the tibial nerve is the cause of the tunnel syndrome in metabolic disorders, arthropathies, trauma. Usually neuropathy is accompanied by pain. Sometimes the cranial nerves are involved, more often the VII pair; V pair; oculomotor nerves.

Bell's palsy- Acute unilateral paralysis or paresis of facial muscles as a result of peripheral damage to the facial nerve. With Bell's palsy, there may be pain in or behind the ear, loss of sensitivity on the affected side of the face, hyperacusis, and a violation of taste on the front of the tongue on the corresponding side.

Trigeminal neuralgia (NTN) is a characteristic pain syndrome that occurs along one or more branches of the V cranial nerve. The diagnosis is made only from the history and is based on the characteristic signs of pain. It appears suddenly and lasts from a few seconds to 2 minutes. The frequency of pain attacks varies widely, from hundreds of attacks per day to very rare attacks, where periods of remission can last for years.
The pain with HTN is very intense and is described as intense, sharp, superficial, piercing, burning, or similar to an electrical shock. In a particular patient, the characteristics of pain during attacks are always the same. Often the trigger for a pain attack can be touching a specific trigger zone, eating, talking, washing your face, or brushing your teeth. In the periods between paroxysms of pain, the disease is asymptomatic. When making a diagnosis, other causes of facial pain should be ruled out.

Classification:
The lesions of the nerve roots and plexuses are divided according to the etiological principle into:
1. Infectious: viral, microbial (with scarlet fever, brucellosis, syphilis, leptospirosis, etc.).
2. Infectious-allergic (for childhood infections: measles, rubella, vaccine, multiple sclerosis, serum, etc.)
3. Toxic (with chronic intoxication (alcoholism, lead, etc.);
4. Dysmetabolic: with a deficiency of vitamins, with endocrine diseases (diabetes mellitus), etc.
5. Dyscirculatory: with nodular periarteritis, rheumatic and other vasculitis.
6. Idiopathic and hereditary (neural amyotrophy of Charcot-Marie, etc.).
7. Traumatic lesions of the nerve roots and plexuses
8. Compression-ischemic lesions of individual peripheral nerves (carpal tunnel syndrome, tarsal canal syndrome, etc.).
9. Vertebral lesions.

According to the topographic and anatomical principle, there are:
radiculitis - lesions of the spinal roots;
plexitis - damage to the plexuses (cervical, brachial, lumbosacral);
mononeuritis - peripheral nerves of the cranial nerves, intercostal, limb nerves;
polyneuropathy multiple lesions of peripheral nerves;
multi-neuropathies or multiple mononeuropathies in which multiple peripheral nerves are affected, often asymmetrically.

Risk factors: compression of the roots of the spinal nerves, due to a herniated disc.

Diagnostic criteria:
1. Pain;
2. Positive symptoms of tension, Tinnel's symptom;
3. Motor and sensory disorders.

List of main diagnostic measures:
1. Complete blood count
2. General urine analysis
3. Radiography
4. Biochemical blood test.

List of additional diagnostic measures:
1. Computed tomography and / or magnetic resonance imaging
2. Consultation of a therapist
5. Consultation with an ophthalmologist
6. Consultation of a traumatologist
7. Consultation of an infectious disease specialist
8. Consultation of an endocrinologist
9. Consultation with a neurosurgeon.

Treatment tactics:Treatment is specific, depending on the cause of the disease, and begins with the cessation of exposure to the harmful factor. But vitamin therapy is always carried out, if necessary, massage, physiotherapy exercises and physiotherapy, which constitute the so-called non-specific treatment. With radiculopathy, in most cases, especially in the case of a herniated disc, conservative treatment is effective: bed rest, tranquilizers (at night), traction. For radicular pain, along with conservative therapy, non-steroidal anti-inflammatory drugs (NSAIDs), lornoxicam from 8 to 16 mg / day, diclofenac from 25 to 75 mg / day are prescribed.

Pathogenetically important in diseases of the peripheral nervous system is the appointment of vitamins of the "B" group, since they are necessary for the activity of oxidative energy mechanisms and the maintenance of the normal structure and function of nerves. Recently, along with injectable forms, a complex of B vitamins has been used for oral administration.
Topical preparations: diclofenac ointment, chondroxide, etc.
Physiotherapeutic procedures and acupuncture are effective.
Therapeutic drug blockade is carried out with corticosteroids.
The most effective are ready-made syringes from Ambene (Germany) with a combined preparation that causes a rapid anti-inflammatory, antipyretic and analgesic effect.

Active ingredients:
dexametosan (glucocorticosteroid) has a local anti-inflammatory, dehydrating, analgesic effect; phenylbutazone (NSAIDs); sodium salicylamide (analgesic effect); cyanocobalamide (vitamin B) has a beneficial effect on nerve function: lidocaine has a local analgesic effect.

Treatment of tunnel syndrome in mild cases is limited to rest. The introduction of corticosteroids (prolonged forms) into the canal is effective.

With idiopathic paralysis of facial muscles, it is necessary to prescribe courses of corticosteroid therapy of 30-60 mg of prednisolone every other day, in the morning gradually reducing the dosage by 5 mg. Prescribe drugs that improve microcirculation - dextrans from 200 to 400 ml intravenously drip for a course of treatment 3 to 5 times.
To carry out decompression, dehydrating therapy is necessary. Mannitol 10-20% intravenously at a dose of 0.5-1.5 g / kg is more effective.
Then, in terms of rehabilitation therapy, neuroprotective therapy is recommended - deproteinized hemoderivat from calf blood (dragees from 200 to 600 mg or 40 mg intramuscularly), vitamins of group "B" (neuromultivitis, magnesium lactate in combination with pyridoxine). that proserin causes contracture.) With the right tactics and timely treatment started, contracture does not happen.

For trigeminal neuralgia, carbamazepine is prescribed up to 600 mg / day to relieve pain. The use of lamotrigine (400 mg / day) compared with placebo increased the proportion of patients who improved after 4 weeks.

With herpes zoster, antiviral drugs are prescribed acyclovir is prescribed orally at a dose of 400 mg 5 times a day for 7-10 days, immunomodulators, aspirin, nonsteroidal anti-inflammatory drugs, analgesics. Lornoxicam 8-16 mg is effective.
Percutaneous electrical stimulation is performed, antidepressants and B vitamins are prescribed at the same time.
For burning pain, carbamazepine is effective, an initial dose of 100 mg orally 2 times a day, then the dose is gradually increased to 200 mg orally 2 times a day.
Topically applied 0.025% capsaicin cream, it is applied to the affected areas 4 times a day. To avoid burning, a cream with a local anesthetic is applied to the affected areas 20 minutes before.
The bubbles are also treated with 1% -2% brilliant green. Also used are injections of corticosteroids and local anesthetics into the affected areas, nerve blocks. The most formidable complications of herpes with lesions of cranial nerves are meningoencephalitis, blepharitis, keratitis, uveitis, postherpetic neuralgia, peripheral muscle paresis.

List of essential medicines:
1. Lornoxicam 4 mg, 8 mg, table
2. Diclofenac 100 mg, ointment
3. Chondroitin sulfate 30 g, ointment
4. Vitamins of group B (neuromultivitis).

List of additional medicines:
1. Prednisolone 5 mg, table
2. Mannitol, solution 10%, 20% in a bottle of 100 ml, 500 ml
3. Deproteinized hemoderivat from calf blood 200 mg, pills
4. Carbamazepine 100 mg, 200 mg, table
5. Dextran, solution for infusion in a bottle of 200 ml, 400 ml
6. Lamotrigine 25 mg, 50 mg, table
7. Acetylsalicylic acid 100 mg, table
8. Acyclovir 400 mg, tab.

Transfer criteria for the next stage:
1. Examination to clarify the cause (volumetric process, inflammation, trauma);
2. Severe pain syndrome;
3. Complications.

The well-known term "neuralgia" is interpreted only as a lesion of the peripheral nerve bundles, characterized by acute attacks of burning pain in the innervation zone. In medical practice, neuralgias of the cranial, spinal, and femoral nerves are distinguished.

Spinal intercostal neuralgia (thoracalgia) is a condition in which the peripheral nerves extending from the spine are compressed in the chest area.

Most often, such an ailment can occur in older people against the background of age-related changes. Meanwhile, the occurrence of characteristic pain is also possible in children with intensive formation of the skeleton.

In men, pain is localized in the lower part of the ribs, while in women it is mainly in the region of the heart.

The main causes and prerequisites for the development of the disease

The cause of the onset of constant and periodic (paroxysmal) pain is a thin intercostal nerve, reflexively compressed / squeezed between muscle fibers.

A sharp pain, accompanied by burning, numbness or tingling, spreads throughout the chest at the moment when impulses run along the nerves in the spinal column.

The prerequisites for the development of intercostal neuralgia are:

• severe stress and hypothermia;
• intoxication;
• rib injuries resulting from sudden physical overload;
• inflammatory diseases (including malignant ones);
• pathological changes in the spine (for example, osteochondrosis).

Despite some similarity of symptoms, the disease should be distinguished from neuritis, since with intercostal neuralgia, inflammatory processes do not occur, the sensitivity of the skin is not impaired while maintaining muscle activity.

An increase in pain in the chest can be caused by excessive tone of certain muscles - the shoulder, scapula, or back extensors.

Symptoms and manifestations of intercostal thoracalgia

The main symptom of thoracalgia is a sharp pain in the intercostal space, which is easily detected by palpation. The pain is localized, usually on the right or left.

The patient is irritated, and sneezing and coughing cause acute pain.

With the onset of atrophic changes in the nerve root, the pain goes away, gradually giving way to a feeling of heaviness in the chest, which indicates the neglect of the disease.

In addition, the patient's lung capacity decreases and shallow breathing appears.

In most cases, the onset of neuralgia is preceded by a short muscle spasm, which leads to immediate irritation of the nerve endings and the appearance of severe pain syndrome.

What does the correct diagnosis of the disease include?

Diagnosis of the disease begins with a simple neurological examination.

Based on typical complaints from the patient, the neurologist performs a differential examination of the chest in order to identify (exclude) respiratory diseases.

Left-sided localization of pain indicates the need to examine the work of the heart using an ECG (electrocardiogram) to exclude pathologies (angina pectoris, ischemia).

In addition, x-rays of the thoracic spine are performed.

As additional measures, electroneurography, MRI, computed tomography and other examinations may be required.

Modern approach to the treatment of intercostal thoracalgia (neuralgia)

According to statistics, the method of treating neuralgia depends on the nature of the nerve damage and the degree of neglect of this disease.

In this regard, the treatment of intercostal neuralgia can take many months, especially if the disease is neglected.

After diagnosing and identifying the causes of the disease, the neurologist prescribes a comprehensive treatment.

If neuralgia is characterized by secondary signs, then its treatment should be carried out taking into account the underlying disease or upon reaching its remission.

As the main methods of drug treatment, the patient is prescribed:

1. local pain relievers (ointments);
2. non-steroidal anti-inflammatory drugs (in the form of tablets or injections);
3. vitamin therapy - B vitamins are prescribed;
4. antidepressants and relaxants.

In the case of the complete absence of any result with the use of drugs, the neurologist may recommend surgical intervention, the purpose of which is to remove tissues that clamp the nerve process or narrow the nerve canal.

Traditional methods of healing intercostal thoracalgia (neuralgia)

In alternative traditional medicine, there are many recipes that produce anesthetic effect.

Here are some of them:

1. Recipe number 1. Rub freshly squeezed radish juice in a circular motion into the skin in the area of \u200b\u200bthe squeezed nerve.
2. Recipe number 2. Brew 1-2 tbsp. l. sandy immortelle flowers in 0.5 liters of boiling water. Strain the broth, drink in small doses.
3. Recipe number 3. Make a decoction of chamomile pharmacy, taking 4 tbsp. l. flowers for 1 tbsp. hot water. Strain and drink 3 r. a day, but always after a meal.
4. Recipe number 4. Insist 4 tbsp. l. Pour sage in a glass of warm water for 1 hour, then strain. Pour the resulting infusion into a bath (37 ° C) and add 4 tbsp. l. mineral-rich sea salt. Take a therapeutic bath at night, the course of treatment is 10 procedures.
5. Recipe number 5. Prepare a decoction of peppermint from 1 tbsp. l. leaves in 200 ml of boiling water. Ingestion of 100 ml (in the morning on an empty stomach and at night).
6. Recipe number 6. ½ tsp. orange peel and ½ tsp. Mix lemon balm and steam in boiling water (200 ml), then insist for 30 minutes. and strain. The course of procedures - within 1 month, take at least 3 times a day for a third of the glass, after adding 1 tsp. honey and valerian tincture.

How to prevent the development of intercostal neuralgia?

As a prophylaxis for intercostal neuralgia, hypothermia of the body should be avoided in every possible way, as well as seek medical help in time in case of colds.

The following measures are considered the most effective measures to prevent the disease:

• acupuncture acupuncture - it is necessary to carry out 3 courses with a break of 2 months;
• manual therapy - allows you to restore the position of the cervical and thoracic vertebrae, which relieves pain in this area of \u200b\u200bthe spine;
• therapeutic massage using warming creams and ointments;
• "Shiatsu" - Japanese "pressing" massage, the object of which is the active points associated with the affected area of \u200b\u200bthe intercostal space;
• osteopathy - a method of anatomical reconstruction of the chest, which improves blood flow and lymph circulation, etc.;
• medical and physical training.

From the foregoing it follows that intercostal neuralgia is an insidious disease, often "disguised" as symptoms of other diseases.

The neglected form of the disease will require maximum energy during the treatment process.

Treatment of sciatica with medication and folk remedies

Literally translated from Latin, sciatica is pain due to the pathology of the sciatic nerve (ischion - pelvis, seat, algus - pain). Sciatica is often identified with sciatica. Although sciatica is a broader concept that includes not only pain, but also the causes and pathological factors that led to its appearance. In this article, these concepts, sciatica and sciatica, will also be used interchangeably, although there are some differences between them.

Causes

Because of the pain intensity, sciatica is an extremely unpleasant process, and sometimes even painful for the patient. It is quite logical that patients want to get rid of this ailment by any available means. Everything is in demand - from the latest medicines to “grandmother's” recipes. But, before discussing the treatment of sciatica, it is worth understanding the essence of the negative processes that led to its appearance.

As everyone who is at least a little familiar with anatomy knows, the sciatic nerve is the longest and thickest nerve in the human body. This is the nerve of the lumbosacral plexus. It is formed by the roots of 5 pairs of spinal nerves - 2 lower lumbar and 3 upper sacral. Descending along the back surface of the buttocks and thighs, it gives branches to the muscles located here. In the popliteal fossa, it divides into 2 nerves, the fibers of which go to the back of the foot.

Sciatica, sciatica are not independent diseases, but syndromes, symptom complexes of a number of other diseases and pathological conditions. There are the following diseases and conditions in which sciatica syndrome develops:

• Osteochondrosis with protrusion (displacement) of the intervertebral disc and disc hernia
• Rachiocampsis
• Bechterew's disease (ankylosing spondylitis)
• Spine injury
• Spine tumors
• Spinal tuberculosis
• Pregnancy.

With all these diseases (many doctors also consider pregnancy a disease), in one way or another, the roots of the lumbar and sacral spinal nerves are involved in the pathological process. They are compressed by the vertebral bodies, infringed in the intervertebral foramen, and are under pressure from the outside by a tumor, a pregnant uterus. Reactive inflammation develops in the nervous tissue with the appearance of corresponding symptoms.

Symptoms

Pain is the leading symptom of sciatica. Typical pain in sciatic nerve neuritis corresponds to the anatomical location of this nerve and goes from the lower back to the gluteal region, then along the back of the thigh and lower leg to the back of the foot. One-sided pain with varying degrees of intensity - from dull and aching to severe and burning.

Sometimes the appearance of the above-described pain is preceded by back pain in the type of lumbago (lumbago). In this case, they speak of lumboischialgia. Sometimes the pain does not affect the entire lower extremity, but some one anatomical area, for example, the knee joint. And the person heals the knee, unaware of the existing disorders in the spine.

In addition to pain, the following signs of sciatica are noted:

• Pathological muscle tension in the lower back, pelvis and lower extremities.
• Unpleasant sensations in the form of burning, tingling
• Decreased sensitivity in the affected area
• Movement disorders from mild lameness to complete inability to move
• In especially severe forms of the disease - dysfunction of the pelvic organs (urinary and fecal incontinence).

Diagnostics

Sciatica is diagnosed by a neuropathologist or vertebrologist. It is these specialists who should be contacted when the above symptoms appear. The diagnosis can already be made on the basis of characteristic complaints, the patient's appearance and neurological symptoms. In order to clarify the causes of the disease, an X-ray of the lumbar spine is performed.

You can also resort to more informative methods - computed and magnetic resonance imaging. The severity of neuritis can be judged by a routine blood test. In order to differentiate sciatica from kidney disease, the patient's urine is taken for analysis. For successful treatment, it is important that these diagnostic tests, as well as an appointment with a doctor, are carried out in a timely manner.

Traditional treatment

Sciatica treatment is aimed at eliminating pain, suppressing inflammatory processes in the nervous and muscle tissues, normalizing muscle tone, expanding the range of motion. In this regard, they use:

• Drug treatment
• Massage and remedial gymnastics
• Physiotherapy procedures
• Folk remedies.

Drug treatment can be general (injections, pills) and local. Taking pills (analgin, renalgan) for the purpose of anesthesia is practically not used due to low effectiveness. More effective ointments with non-steroidal anti-inflammatory drugs - diclofenac, indomethacin, ibuprofen.

Paravertebral blockade using local anesthetics does not eliminate the cause of the disease and does not affect the course of pathological processes in sciatica. Nevertheless, pain relief in the treatment of lumbago with sciatica contributes to the expansion of motor activity and the normalization of the patient's emotional background.

The non-drug methods of treating sciatica include physiotherapy, various types of massage and physiotherapy exercises (LFK). All of them are aimed at strengthening and relaxing muscles, increasing local blood flow and metabolic processes in the affected area. Among physical procedures, diadynamic therapy, UHF, phonophoresis, amplipulse therapy are effective.

Exercise therapy for sciatica is recommended to be carried out in a horizontal position, which is the most gentle. At the beginning, the exercises are minimal in terms of load and range of motion. Subsequently, the range of motion with the involvement of the muscles of the lower back and lower extremities increases. During the massage, tense muscles are stretched, the ligamentous apparatus is strengthened. Massage for sciatica can be acupressure and segmental. Duration - about half an hour every other day. It is important that non-drug methods are not carried out during an exacerbation of sciatica. They are also contraindicated in pregnant women, children, in the presence of tuberculosis, tumors, skin diseases.

Folk remedies

Can sciatica be treated at home? Can. At home, they are treated with folk remedies. At the same time, herbal decoctions, minerals, food products (honey, eggs, vegetable oil) are used. Below, for clarity, some effective folk remedies will be given:

1. The egg white is mixed with 15 ml of pure turpentine. The resulting mixture is shaken. Natural fabric is impregnated with it. The fabric is applied to the lower back, covered with paper on top and wrapped in a woolen scarf. It turns out something like a compress. Keep until intense pain appears. After that, remove the compress, remove the rest of the mixture with a clean towel. After 6 hours, repeat the procedure
2. Grate 30 g of laundry soap. Mix soap with 1 tbsp. a spoonful of honey and 1 egg white. The resulting mixture is used in the form of a compress according to the above method. Duration - 1-2 hours, frequency - daily.
3. Mix 200 g of grated horseradish with the same amount of grated radish. Add 10 ml. kerosene, 15 ml. table vinegar and 1 tbsp. a spoonful of salt. The resulting mixture is infused for 10 days, after which it is used as a compress. The duration of the compress is 1 hour, the frequency is twice a day.

Although sciatica and lumbago can be treated at home, a visit to the hospital is essential. After all, traditional medicine is an assistant to traditional treatment. All necessary diagnostic studies and treatment procedures are feasible only within the walls of the hospital.

Trigeminal neuralgia (TN) (synonyms: tic douloureux, or Fothergill's disease) is one of the most common facial pains (prosopalgia) and is one of the most persistent pain syndromes in clinical neurology. TN is a typical example of neuropathic pain (ND) of a paroxysmal nature and is considered the most distressing 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. Chronic NB has a significant negative effect on the quality of life of patients, causing sleep disturbances, increased anxiety, depression, and decreased daily activity. The high intensity and persistence of TN, its special, often painful character, and resistance to traditional methods of anesthesia make this problem extremely urgent. Trigeminal neuralgia is a disease characterized by the occurrence of paroxysmal, usually unilateral, short-term, acute, sharp, intense, resembling an electric shock, pain in the innervation area of \u200b\u200bone or more branches of the trigeminal nerve. Most often, the lesion occurs in the zone II and / or III branches and extremely rarely - I branch n. trigeminus.

According to the 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; it debuts in the fifth decade of life, and in 60% of cases has a right-sided localization.

According to the International Classification of Headaches (2nd Edition), proposed by the International Headache Society (2003), TN is subdivided into classical TN, 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 a nerve other than vascular compression.

The most common cause of TN is compression of the proximal part of the trigeminal root within a few millimeters from the root entrance to the pons of the brain (the so-called “root entrance zone”). In about 80% of cases, compression occurs by an arterial vessel (most often a pathologically twisted 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, volumetric processes in the posterior cranial fossa, tumors of the cerebellopontine angle and plaques of multiple sclerosis.

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 (more often in the infraorbital foramen and lower jaw), associated with its congenital narrowness, the addition of vascular diseases in old age, and 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.

Depending on the impact of the pathological process on the corresponding section of the trigeminal system, TN are isolated mainly of central and peripheral genesis. In the emergence of TN of central genesis, neuroendocrine, immunological and vascular factors play an important role, which lead to a violation of the reactivity of the cortical-subcortical structures and the formation of a focus of pathological activity in the central nervous system. In the pathogenesis of TN of the peripheral level, the compression factor, infections, trauma, allergic reactions, odontogenic processes play an important role.

Despite the large number of literature reviews and meta-analyzes that have appeared in recent years on the problem of treating NB, which includes TN, there is no consensus among researchers regarding the basic principles of drug therapy for this disease. Treatment of neuropathic pain is still not effective enough: less than half of patients show significant improvement as a result of pharmacological treatment.

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

The main directions of drug therapy are: elimination of the cause of TN, if known (treatment of diseased teeth, inflammatory processes of adjacent zones, etc.), and symptomatic treatment (relief of pain syndrome).

Pathogenetic treatment of patients with TN includes the use of drugs of neurometabolic, neurotrophic, antioxidant, antihypoxant action. In recent years, a high efficiency of the use of metabolic drugs in the complex treatment of NB was found. In the treatment of patients with TN, the high efficacy 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 action of Actovegin is manifested by indirect vasoactive and rheological effects due to an increase in capillary blood flow, a decrease in peripheral vascular resistance, and an improvement in organ and tissue perfusion. Such a wide spectrum of pharmacological action of Actovegin allows its use in therapy of TN. During an attack, it is advisable to use Actovegin intravenously, slowly, in a stream or drip for 10 days at a dose of 400-600 mg / day. In the interictal period, the drug is administered orally at a dose of 200 mg 3 times a day for 1-3 months. The pathogenetic treatment of patients with TN can be attributed to the use of high doses of B vitamins in the composition of multicomponent drugs, which is due to their polymodal neurotropic effect (influence 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 (B 1), pyridoxine (B 6), cyanocobalamin (B 12). Vitamin B 1 eliminates acidosis, which lowers the pain threshold; activates ion channels in neuronal membranes, improves endoneural blood flow, increases the energy supply of neurons and supports axoplasmic protein transport. These effects of thiamine contribute to the regeneration of nerve fibers. Vitamin B 6, activating the synthesis of the myelin sheath of the nerve fiber and transport proteins in the axons, accelerates the 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 (the antinociceptive effect of pyridoxine). Vitamin B 12 participates in the 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 antianemic, hematopoietic and metabolic effects. For rapid relief of pain and pathogenetic neurotropic effects in TN, it is advisable to use the parenteral form of Neurobion - a combined preparation of B vitamins containing the optimal amount of vitamin B 12 both in ampouled and in tablet form. Neurobion is applied at a dose of 3 ml per day intramuscularly 2-3 times a week - 10 injections (with severe pain syndrome, it can be used daily at the same dosage for 10-15 days). Then, to enhance, prolong the therapeutic effect and prevent relapse of the disease, Neurobion is prescribed in tablet form in a dosage of 1 tablet inside 3 times a day for 1-2 months.

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

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.

The 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 therapy 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: CNS reactions (drowsiness, dizziness, ataxia, sedation or hyperexcitability, diplopia, dysarthria, cognitive impairment, memory and mood impairment), hematological disorders (agranulocytosis, aplastic anemia, thrombocytopenia, leukopenia), hepatotoxicity, decreased bone mineral density, skin rashes, gingival hyperplasia, symptoms from the gastrointestinal tract (vomiting, anorexia). Second-generation anticonvulsants include pregabalin (Lyrica), gabapentin (Neurontin, Gabagamma, Tebantin), lamotrigine (Lamictal), oxcarbazepine (Trileptal), topiramate (Topamax), levetiracetam (Keppra), tiagabine (zonis), Gabitril (v) (Sabril), felbamat (Taloxa). These drugs have more favorable pharmacokinetic characteristics and safety profiles, as well as a lower risk of drug interactions compared to first generation anticonvulsants.

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

Phenytoin (Diphenin) was the first anticonvulsant successfully used to treat TN. Diphenin, a derivative of hydantoin, which is close in chemical structure to barbituric acid, is contraindicated in severe diseases of the kidneys, liver, heart failure.

According to the recommendations of the European Federation of Neurological Communities (2009), TN pharmacotherapy is based primarily on the use of carbamazepine (Finlepsin, Tegretol) (200-1200 mg / day), proposed by S. Blum in 1962, which is the drug of the first choice ( Evidence level A). The analgesic effect of this drug is mainly due to its ability to reduce the sodium permeability of neuronal membranes involved in nociceptive reactions. The following carbamazepine regimen is usually prescribed. In the first two days, the daily dose is 200 mg (1/2 tablet in the morning and in the evening), then within two days the daily dose is increased to 400 mg (in the morning and in the evening), and after that - up 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% in the population), carbamazepine does not have an analgesic effect, therefore, in such cases, another anticonvulsant is used - phenytoin.

Conducted about 40 years ago, three placebo-controlled studies, which included a total of 150 patients with malnutrition, showed the effectiveness of carbamazepine in terms of both the frequency and intensity of paroxysms. A number of authors have shown that carbamazepine can reduce pain symptoms in about 70% of cases. ... However, the use of carbamazepine is limited by pharmacokinetic factors and in some cases, 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 start of TH treatment at a dose of 600-1800 mg / day (level of evidence B).

Lamotrigine (Lamiktal) at a dose of 400 mg / day and baclofen at a dose of 40-80 mg / day, which are second-line drugs, have been shown as additional therapy for TN (Evidence level C). Small open studies (class IV) indicate the effectiveness of the use of clonazepam, valproate, phenytoin. This therapy is most effective in the classical form of TN. In TN of peripheral genesis, it is preferable to include non-narcotic analgesics in treatment regimens, and in the case of chronic pain syndrome (more than three months), antidepressants (amitriptyline) are indicated.

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 efficacy of gabapentin in patients with TN who do not respond to treatment with other drugs (carbamazepine, phenytoin, valproate, amitriptyline); however, in most cases, there was a complete relief of the pain syndrome. The therapeutic dose ranges from 1800 to 3600 mg / day. The drug is taken 3 times a day according to the following scheme: 1st week - 900 mg / day, 2nd week - 1800 mg / day, 3rd week - 2400 mg / day, 4th week - 3600 mg / day.

Recently, the results of an open-label prospective 12-month study of 53 patients with TN were published, which evaluated the efficacy 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. In another multicenter prospective 12-week study of 65 patients refractory to previous analgesic therapy, treatment with pregabalin at an average dose of 196 mg / day (in the monotherapy subgroup) and 234 mg / day (in the polytherapy subgroup) resulted in a decrease in pain intensity of ≥ 50% in on average in 60% of patients, and also reduced the severity of anxiety, depression and sleep disorders. In the treatment of TN, the initial dose of pregabalin may 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 K. R. Edwards et al. ... The mechanism of action of levetiracetam is unknown; there is evidence from animal experiments that it is a selective blocker of N-type calcium channels. The properties of this drug are especially suitable for the treatment of TN patients with severe pain who require a quick response to therapy. The pharmacokinetics of levetiracetam are linear and predictable; the concentration in blood plasma increases in proportion to the dose within the clinically reasonable range from 500 to 5000 mg. 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. In addition, this drug has a favorable therapeutic index and few adverse side effects (which is the main problem when using drugs for the treatment of TH). The most 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, 3000-5000 mg / day (50-60 mg / kg / day), were required for the treatment of TN compared with the treatment of epilepsy, which, however, did not have caused significant side effects. This circumstance indicates the prospect of using this drug for the treatment of TN.

In one Russian study, positive results were noted with the combination of carbamazepine and gabapentin.

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

Until now, the selection of analgesic therapy for NB is more an art than a science, since the choice of drugs is mainly empirical. There are often situations when the use of one drug is not effective enough and there is a need for a combination of drugs. The appointment of "rational polypharmacotherapy" (the simultaneous use of drugs with neurotropic, neurometabolic and analgesic mechanisms of action) allows you to increase the effectiveness of treatment with lower dosages of drugs and fewer side effects.

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

1) surgical microvascular decompression;
2) stereotactic radiation therapy, gamma knife;
3) percutaneous balloon microcompression;
4) percutaneous glycerol rhizolysis;
5) percutaneous radiofrequency treatment of the Gasser's node.

The most effective method for surgical treatment of TN is the P. Janetta method, which consists in placing a special pad between the trigeminal nerve and the irritating vessel; in the long term, the effectiveness of treatment is 80%.

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

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