Comparative analysis of the effectiveness of complex pharmacotherapy for pain in trigeminal neuralgia

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

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

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

What is the facial nerve?

The trigeminal nerve, also known as the facial nerve, is the largest of the twelve cranial nerves. It originates in the ear, after which it branches, the first path reaches the frontal part, the second is located at the jaw. The nerve goes around almost the entire surface of the human face; it literally controls it.

Every person has two facial nerves - one on each side of the head. It is in contact with other cranial nerves and has supersensitive fibers.

Doctors divide the disease into two types - primary and secondary. The primary one manifests itself as a complication from a cold, in this case the normal nutrition of the nerve is disrupted. Secondary occurs with severe intoxication against the background of inflammatory or infectious diseases, as well as tumor processes.

How to recognize depression

As already mentioned, the drug helps get rid of depression, but not all of its forms. Grandaxin is taken only for mild to moderate disease with moderately severe symptoms.

During the course of the disease, several syndromes are distinguished:

1. Emotional disorders: low mood, melancholy, anxiety and internal tension, pessimistic attitude; self-flagellation, lack of interest in the world around us, inability to have fun.
2. Behavioral reactions: solitude, reduced activity; bad habits;
3. Cognitive functions: inability to concentrate, slow thinking, decreased memory and perception; pessimistic thoughts, thoughts of suicide, low self-esteem.
4. Autonomic disorders: poor sleep, appetite distortion, weakness and malaise, intestinal dysfunction; discomfort in the heart and other organs, headaches.

A specific indication for the use of the drug is reactive depression. It develops in response to the action of some traumatic factor. The condition is characterized by a consistently reduced emotional background and fixation on the problem.

The patient reproaches and blames himself for what happened, his conversations are aimed only at the problem. And, constantly analyzing it, he seeks support from those around him.

A person is worried about insomnia. And he is fully aware of his condition.

Attacks of despair and demonstrative hysterics are possible. Excitement reaches a state called “melancholic raptus.” At the same time, the person rushes about aimlessly, sobs, screams, and suicide attempts are not ruled out.

This state can be replaced by a depressive stupor, when the patient “freezes” in one position, not reacting to what is happening.

Causes of inflammation of the trigeminal nerve on the face

Usually the disease is caused by infection or bacteria. List of reasons why inflammation of the facial nerve may occur:

• Temporomandibular joint injuries
• Tumors (benign and malignant) of the brain and facial area
• Anomalies of skull development
• Skull injuries - birth, fracture, base, damage to the face or jaw
• Polio
• Pulmonary tuberculosis
• Otitis
• Sinusitis
• Chronic caries
• Inflammation after tooth extraction or treatment
• Hypertension
• HIV and AIDS
• Poisoning
• Inflammation of the middle ear
• Severe hypothermia of the head
• Changes in hormonal levels in women
• Gum inflammation
• Ramsay Hunt syndrome
• Stroke
• Bell's palsy

Causes range from minor to life-threatening illnesses. Each of the reasons determines the further treatment of the patient. In some cases, special tests are performed for diagnosis - auditory, lacrimal, infectious, salivary or gustatory. In this way, the functioning of the receptors and sensory organs is checked.

Interaction

Co-administration of carbamazepine with CYP3A4 inhibitors may lead to an increase in its concentration in the blood plasma and cause adverse reactions. The combined use of CYP3A4 inducers can lead to an acceleration of the metabolism of carbamazepine, a decrease in the concentration of carbamazepine in the blood plasma and a decrease in the therapeutic effect; on the contrary, their withdrawal can reduce the rate of biotransformation of carbamazepine and lead to an increase in its concentration.

The plasma concentration of carbamazepine is increased by verapamil, diltiazem, felodipine, dextropropoxyphene, viloxazine, fluoxetine, fluvoxamine, cimetidine, acetazolamide, danazol, desipramine, nicotinamide (in adults, only in high doses); macrolides (erythromycin, josamycin, clarithromycin, troleandomycin); azoles (itraconazole, ketoconazole, fluconazole), terfenadine, loratadine, isoniazid, propoxyphene, grapefruit juice, viral protease inhibitors used in the treatment of HIV infection (for example, ritonavir) - dosage adjustment or monitoring of carbamazepine plasma concentrations is required.

Felbamate reduces the plasma concentration of carbamazepine and increases the concentration of carbamazepine-10,11-epoxide, and a simultaneous decrease in the serum concentration of felbamate is possible.

The concentration of carbamazepine is reduced by phenobarbital, phenytoin, primidone, methsuximide, fensuximide, theophylline, rifampicin, cisplatin, doxorubicin, possibly clonazepam, valpromide, valproic acid, oxcarbazepine and herbal preparations containing St. John's wort (Hypericum perforatum). There is a possibility of valproic acid and primidone displacing carbamazepine from binding to plasma proteins and increasing the concentration of the pharmacologically active metabolite (carbamazepine-10,11-epoxide). When finlepsin is used in combination with valproic acid, in exceptional cases, coma and confusion may occur. Isotretinoin alters the bioavailability and/or clearance of carbamazepine and carbamazepine-10,11-epoxide (monitoring of carbamazepine plasma concentrations is necessary).

Carbamazepine may reduce plasma concentrations (reduce or even completely eliminate the effects) and require dose adjustment of the following drugs: clobazam, clonazepam, digoxin, ethosuximide, primidone, valproic acid, alprazolam, corticosteroids (prednisolone, dexamethasone), cyclosporine, tetracyclines (doxycycline), haloperidol, methadone, oral medications containing estrogens and/or progesterone (selection of alternative methods of contraception is necessary), theophylline, oral anticoagulants (warfarin, phenprocoumon, dicumarol), lamotrigine, topiramate, tricyclic antidepressants (imipramine, amitriptyline, nortriptyline, clomipramine), clozapine , фелбамата, тиагабина, окскарбазепина, ингибиторов протеаз, применяемых при терапии ВИЧ-инфекции (индинавира, ритонавира, саквинавира), БКК (группа дигидропиридина, например фелодипин), итраконазола, левотироксина, мидазолама, оланзапина, празиквантела, рисперидона, трамадола, зипрасидона.

There is a possibility of an increase or decrease in phenytoin plasma levels in the presence of carbamazepine and an increase in mephenytoin levels. With the simultaneous use of carbamazepine and lithium preparations, the neurotoxic effects of both active substances may be enhanced.

Tetracyclines may weaken the therapeutic effect of carbamazepine. When used together with paracetamol, the risk of its toxic effect on the liver increases and therapeutic effectiveness decreases (acceleration of paracetamol metabolism).

The simultaneous administration of carbamazepine with phenothiazine, pimozide, thioxanthenes, molindone, haloperidol, maprotiline, clozapine and tricyclic antidepressants leads to an increased inhibitory effect on the central nervous system and a weakening of the anticonvulsant effect of carbamazepine.

MAO inhibitors increase the risk of developing hyperpyretic crises, hypertensive crises, convulsions, and death (before prescribing carbamazepine, MAO inhibitors should be discontinued at least 2 weeks in advance or, if the clinical situation allows, even longer).

Concomitant administration with diuretics (hydrochlorothiazide, furosemide) can lead to hyponatremia, accompanied by clinical manifestations.

Weakens the effects of non-depolarizing muscle relaxants (pancuronium). If this combination is used, it may be necessary to increase the dose of muscle relaxants, and careful monitoring of the patient's condition is necessary due to the possibility of faster cessation of the effect of muscle relaxants.

Carbamazepine reduces ethanol tolerance.

Myelotoxic drugs increase the manifestations of hematotoxicity of the drug.

Accelerates the metabolism of indirect anticoagulants, hormonal contraceptives, folic acid, praziquantel, and may enhance the elimination of thyroid hormones.

Accelerates the metabolism of anesthetics (enflurane, halothane, fluorothane) and increases the risk of developing hepatotoxic effects; enhances the formation of nephrotoxic metabolites of methoxyflurane. Strengthens the hepatotoxic effect of isoniazid.

Symptoms of inflammation of the trigeminal nerve

Experts include short-term, but acute and intense pain in different parts of the head as the main symptoms of facial neuralgia. Shooting attacks spread over the entire surface of the face - lips, eyes, nose, upper and lower jaw, gums and tongue.

Patients also report the following symptoms:

• Metallic taste in the mouth
• Muscle weakness
• 2-3 days before facial expressions are affected, pain occurs behind the outer ear, spreading to the face, back of the head and eyes
• Facial asymmetry
• Inability to close the eye on the affected side
• Drooping corner of the mouth
• Dry mouth
• Slurred speech
• Cross-eyed strabismus
• Uncontrollable tearing
• Disorders of taste buds
• Increased drooling
• Facial muscle spasms
• Increased or decreased facial sensitivity
• Temperature increase

Due to discomfort and pain, the patient begins to develop a phobia and increased anxiety. He tries to avoid poses and movements that provoke discomfort.

Compound

Diagnosis of inflammation of the trigeminal nerve

Depending on the affected area and the set of symptoms, the strategy for diagnosing the disease is determined. To determine the location of nerve damage, the severity and dynamics of recovery, doctors prescribe a hardware diagnostic method, for example, electromyography. MRI and CT scans are used to determine the presence of tumors in the brain.

The patient may also be referred for a general or biochemical blood test, x-ray of the lungs, ultrasound of soft tissues or ophthalmoscopy.

You can be confident in the quality of the procedures performed in the clinic and the high accuracy of the results of MRI, CT and other methods of diagnosing various diseases. Medunion performs magnetic resonance imaging of all types: head, spine, abdominal cavity and joints using modern equipment.

Impact of Grandaxin

The main effect of the drug is manifested in the anxiolytic effect. It helps eliminate feelings of anxiety and fear, reduce emotional stress, anxiety and agitation, both mental and motor.

Tofizopam exhibits vegetative stabilizing properties to a high degree. With him it is expressed to the greatest extent compared to other tranquilizers:

• normalizes sleep - eliminates insomnia, promotes rapid falling asleep;
• restores blood pressure;
• stabilizes heart rate;
• reduces sweating;
• improves the functioning of the gastrointestinal tract, eliminates constipation.

The vegetative stabilizing effect is achieved by establishing a balance between the sympathetic and parasympathetic systems.

The stress-protective effect of Grandaxin protects the central nervous system from the effects of a destructive factor. It gives the patient a state of psychological comfort and provides an adequate assessment of what is happening. Protects against the development of unwanted vegetative-vascular reactions: tachycardia, vascular spasms, destruction of the gastrointestinal mucosa. Eliminates excitement.

Tofizopam has a coronary effect to some extent:

• improves coronary circulation;
• reduces the need for oxygen in the heart muscle;
• normalizes metabolism in cardiac tissues;
• increases the amount of oxygen delivered to the heart.

This ability of Tofizopam is widely used in the treatment of coronary heart disease. The drug stabilizes the functioning of both parts of the autonomic nervous system, and thereby improves the electrical conductivity of the heart muscle.

The psychostimulating effect of the drug helps restore the patient’s mental and physical activity. Helps improve cognitive functions, restores thinking abilities, improves mood. Strengthens the ability to resist the effects of unwanted environmental factors.

Grandaxin is recommended to be included in complex therapy as:

• enhancing the effect of antidepressants;
• to eliminate anxiety and panic attacks that can be triggered by starting to take antidepressant medications;
• in cases where the dosage of antidepressants is insufficient, and increasing it is impossible due to the risk of adverse reactions.

The use of the drug as monotherapy is undesirable.

Treatment for inflammation of the facial nerve

Drug treatment

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

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

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

Surgery

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

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

Massage

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

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

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

Physiotherapy

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

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

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

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

Alternative Methods

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

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

Gymnastics for the face

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

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

Gymnastics for inflammation of the trigeminal nerve:

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

Pharmacokinetics

Absorption is slow but complete (food intake does not significantly affect the speed and extent of absorption). After a single dose of the tablet, Cmax is reached after 32 hours. The average Cmax of unchanged active substance after a single dose of 400 mg of carbamazepine is about 2.5 μg/ml. Css of the drug in plasma are achieved in 1–2 weeks (the speed of achievement depends on the individual characteristics of metabolism: autoinduction of liver enzyme systems, heteroinduction by other simultaneously used drugs), as well as on the patient’s condition, the dose of the drug and the duration of treatment. There are significant individual differences in Css values ​​in the therapeutic range: in most patients these values ​​range from 4 to 12 μg/ml (17–50 μmol/l). Concentrations of carbamazepine-10,11-epoxide (a pharmacologically active metabolite) are approximately 30% of those of carbamazepine. Communication with plasma proteins in children is 55–59%, in adults – 70–80%. Apparent Vd - 0.8–1.9 l/kg. In the cerebrospinal fluid and saliva, concentrations are created that are proportional to the amount of active substance not bound to proteins (20–30%). Penetrates through the placental barrier. The concentration in breast milk is 25–60% of that in plasma. Metabolized in the liver, mainly along the epoxide pathway with the formation of the main metabolites - active carbamazepine-10,11-epoxide and an inactive conjugate with glucuronic acid. The main isoenzyme that ensures the biotransformation of carbamazepine into carbamazepine-10,11-epoxide is cytochrome P450 (CYPZA4). As a result of these metabolic reactions, a metabolite, 9-hydroxymethyl-10-carbamoylacridan, is also formed, which has weak pharmacological activity. Carbamazepine can induce its own metabolism. T1/2 after oral administration of a single dose is 60–100 hours (on average about 70 hours); with prolonged use, T1/2 decreases due to autoinduction of liver enzyme systems. After a single oral dose of carbamazepine, 72% of the dose taken is excreted in the urine and 28% in the feces; in this case, about 2% of the dose taken is excreted in the urine in the form of unchanged carbamazepine, about 1% - in the form of a 10,11-epoxide metabolite.

There is no data indicating that the pharmacokinetics of carbamazepine changes in elderly patients.

Disease prevention

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

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

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

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

Grandaxin and other tranquilizers

Due to its mild and selective effect, the drug has a minimum of side effects, unlike other anxiolytics. It does not cause the negative consequences inherent in most representatives of this group. The main ones are:

1. "Behavioral Toxicity." Manifested by increased sleepiness during the day, weakness and malaise. Characterized by decreased reaction speed and inability to concentrate. Coordination of movements is impaired, and confusion may occur.
2. Addiction. A common problem when taking tranquilizers. There is a possibility that it will worsen even to substance abuse. But more often, addiction develops with long-term treatment with such drugs, with an unauthorized increase in dose or concurrent use of alcohol.
3. Withdrawal syndrome occurs when you suddenly stop using a tranquilizer. In this case, the symptoms of the disease return to the patient in a more pronounced or even complicated form.

Grandaxin does not exhibit such complications. It is low-toxic and resistance to it is not developed upon repeated use. Therefore, it is taken during the daytime.

The drug does not reduce physical and mental activity and does not lead to drowsiness. It does not suppress the efficiency of perception, the speed of reactions, and does not interfere with professional activities.

Limitations and adverse reactions

Contraindications to the use of the drug are:

• severe forms of depression - with them there is a high probability of suicidal thoughts and actions;
• phobias, obsessions - possible increase in aggression;
• allergic reactions;
• uncompensated respiratory failure.

The drug is prescribed with caution to elderly people due to their increased susceptibility to it. It is not recommended to use it at this age for too long a time.

The drug is contraindicated for children under 18 years of age. It can be taken only in rare cases after carefully weighing the need and risks. In this case, therapy should be short-term.

Taking the drug in the 1st trimester of pregnancy is contraindicated. It easily crosses the placental barrier and can cause developmental defects in the child. Grandaxin can pass into breast milk, so you should avoid breastfeeding while treating with the drug.

Otherwise, when it enters the child’s body, it accumulates and causes a sedative effect. The newborn's sucking reflex decreases, he cannot suck out milk fully, and loses weight.

Despite the mild effect of the drug, it still exhibits some side effects:

• headaches, agitation and aggressiveness;
• sleep problems;
• confusion;
• increased frequency of seizures in epileptic patients;
• breathing disorders;
• poor appetite, thirst, digestive problems;
• jaundice;
• muscle hypertonicity, muscle pain;
• allergic manifestations.

In such cases, taking the drug is canceled.