The clinical picture is typical for paroxysmal neuralgia. During the period of exacerbation of the disease, the patient usually has such a peculiar appearance that it is often possible to suspect trigeminal neuralgia only at one glance at him. On the face there is a pronounced mask of suffering, fear and even horror before the resumption of attacks of pain.

As a rule, such patients answer questions in monosyllables, barely opening their mouths, since the slightest movement of the facial muscles can provoke a painful paroxysm. Sometimes patients do not speak and communicate with others only in writing.. During an attack, they do not rush, do not moan, but freeze, stunned by terrifying pain. Thus, trigeminal neuralgia is "

Often, the patient's face is distorted due to the occurrence of twitching of the facial muscles (pain tic). In this case, patients try to squeeze the painful area with their hand or rub it roughly (antagonist gesture), while a light, insignificant touch on the trigger area usually causes painful paroxysm. During the period of exacerbation of trigeminal neuralgia, patients do not wash, almost do not eat, do not brush their teeth, men do not shave.

The exit points of the trigeminal nerve are not always painful in an objective examination. Curve zones are localized mainly in the medial parts of the face: with neuralgia of the 1st branch - at the inner corner of the eye, root of the nose, in the eyebrow, 2nd branch - at the wing of the nose, nasolabial fold, above the upper lip, on the mucous membrane of the upper jaw. Revealed hyperesthesia predominantly pain sensitivity in the area of \u200b\u200bthe affected branch, in patients treated with alcoholism - hypesthesia and even anesthesia in the central parts of the affected area. Hypesthesia can also be observed with prolonged course of neuralgia, etc..

In stage 1 of the disease, there are no changes in sensitivity without exacerbation.. In stage 2, they often appear and often persist without exacerbation in the form of hyperesthesia.. The third stage of trigeminal neuralgia is characterized by constant, relatively low-intensity pain.

Usually they have a sympathetic character, against their background there are paroxysms of acute pain, there is a violation of sensitivity in the form of hyper- and hypesthesia. With neuralgia of the 1st and 2nd branches, a corneal or conjunctival reflex may fall out, with neuralgia of the 3rd branch in the acute period, trismus is sometimes observed.

As a rule, as the disease progresses, the pain spreads to the adjacent branches of the trigeminal nerve.. If the disease usually begins with a lesion of one branch of the trigeminal nerve (2nd, less often the 3rd and only in exceptional cases 1st), then in the 2nd and 3rd stages of the disease, the 2nd and 3rd branches are captured, less often the 2nd.

Cardiac manifestations of trigeminal neuralgia during an exacerbation of the disease appear quite clearly: there are short-term paroxysms of pain like electric shocks and trigger zones. During the period of remission, as the pain subsides, the trigger zones disappear (Karlov V.

With a longer duration of the disease (usually more than 2 years), trophic disorders are noted (especially in patients who have been repeatedly treated with destructive methods) in the areas of the affected branches, which are manifested by dryness, peeling of the skin of the face, early graying and hair loss on the anterior scalp, facial atrophy.

Most patients with trigeminal neuralgia suffer from various neurotic disorders - from neurotic reactions to asthenoneurotic syndrome. Depressive syndrome develops more often, less often - anxiety-phobic and hypochondriacal (B. Grechko).

Differential diagnosis.

From neuralgia of the glossopharyngeal and superior laryngeal nerves, trigeminal neuralgia is distinguished by a different area of \u200b\u200blocalization of the trigger zones. Difficulty may represent the recognition of the most severe manifestation of trigeminal neuralgia in the form of a neuralgic status (status neuralgicus), in which there is a prolonged attack of paroxysmal pain.

With a detailed questioning of the patient, it is possible to establish that the indicated painful paroxysm is the status of painful attacks following almost continuously one after another by the type of electric shocks, the trigger zones are necessarily identified. Patients avoid movement, conversation.

Differentiation from pterygopalatine neuralgia and migraine neuralgia may pose a known difficulty in some cases..

Treatment.

With a long duration of the disease, the anticonvulsant drug carbamazepine (finlepsin, stazepine, tegretol, amizepine, mezatol) is prescribed in individually selected doses.. If the patient has not previously received this drug, then carbamazepine is administered orally, starting with 1 tablet (0.2 g) 1-2 times a day, the dose is gradually increased by 1/2 tablet or tablet, but not more than 2 tablets (0,.

With the appearance of side effects (loss of appetite, nausea, vomiting, headaches, drowsiness, ataxia, impaired accommodation), the dose is reduced. Patients who have previously received the drug can be immediately prescribed carbamazepine, 2-3 tablets (0.4-0. 6 d) 2-3 times a day.

To enhance the effect of the anticonvulsant, antihistamines are prescribed - intramuscularly 2 ml of a 2.5% solution of diprazine (pipolfen) or 1 ml of a 1% solution of diphenhydramine at night.

Elderly people who have symptoms of chronic cerebrovascular insufficiency (even in the stage of compensation) should be prescribed antispasmodic and vasodilators (aminophylline, diaphyllin, synthophyllin, etc..

It is more expedient to immediately inject 10-20 ml of a 40% glucose solution into the vein. At the same time, sedatives and vitamins are prescribed, the most effective of which are B vitamins: B, 2 - 500-1000 mcg intramuscularly daily, for a course of 10 injections, then vitamin Bf 2 ml of a 5% solution intramuscularly daily, for a course of 15-20.

If an exacerbation occurs during treatment with carbamazepine, it should be replaced with a drug from another company or even another anticonsulsant that gives a therapeutic effect for trigeminal neuralgia. Among the recently proposed drugs, the effectiveness of ethosuximide (suxilep, ronton, asamide) is noted.

In severe forms of neuralgia, sodium oxybutyrate is recommended (except for patients with glaucoma). You can use a ready-made 20% aqueous solution in 10 ml ampoules. The drug is injected intravenously (1-2 ml per minute), 1-2 times a day.

Mild attacks of pain can be relieved by transcutaneous electrical stimulation of the affected branches of the trigeminal nerve. The following devices have been serially produced by the domestic industry: an electrostimulator for pain relief "

The psychotherapeutic effect on the patient should not be underestimated.. Often, a convincing conversation with a doctor or hospitalization of the patient can stop the recurrence of painful paroxysms..

In the acute period of the disease, physiotherapy is prescribed: irradiation with a Solux lamp, UFO, UHF therapy, electrophoresis of novocaine, diphenhydramine, platifillin on the affected area of \u200b\u200bthe face. Diadynamic currents have an analgesic effect.

With severe pain, diadynamic electrophoresis is recommended with a mixture: codeine, dicain, sovkain but 0.1 g, 6 drops of adrenaline solution 1: 1000, 100 g of distilled water. Sinusoidal modulated currents are also prescribed: current strength 2-10 mA, procedure duration 5-10 minutes daily, can also be combined with medicinal substances.

In case of exacerbation of neuralgia, ultrasound or phonophoresis of analgin is applied to the area of \u200b\u200bthe affected branches of the trigeminal nerve in a pulsed mode using a labile technique (small head of the \; intensity 0.005-0.2 W / cm2, 2-3 minutes on the field, for a course of treatment 10-15 procedures (Popova E. , 1972).

It is possible to recommend a course of treatment with nicotinic acid in combination with antihistamines and vitamin therapy. Nicotinic acid is administered intravenously as a 1% solution (starting with 1 ml daily for 10 days, increasing the dose to 10 ml, and then also gradually decreasing it).

During the period of exacerbation subsiding, patients can be recommended a very light massage of the face, first only the skin and muscles, and after 4-5 days - along the branches of the trigeminal nerve (15-20 procedures).

Patients with trigeminal neuralgia are shown a course of treatment with aloe extract - 1 ml intramuscularly daily, for a course of 15 injections.

Patients with bilateral neuralgia should be treated for a month in a hospital setting. In the future, patients should be under the supervision of a neurologist.. Preventive treatment of patients with mild and moderate severity of the disease is carried out once a year, with severe - twice a year. In all cases, an examination by a dentist is required before prescribing a course of treatment..

For some patients with trigeminal neuralgia, commonly used drugs are ineffective.. In these cases, neuroexeresis is prescribed, which is carried out by surgeons and neurosurgeons.. The method of treating the nerve stump with liquid nitrogen is especially effective (Grechko V. , Kornienko A. , Nesterenko G. , 1986).

One of the methods of treating trigeminal neuralgia is tissue therapy by replanting a preserved nerve. The trigeminal nerve, the gasser knot are used, but more often the sciatic nerve, which is more easily retrievable (Munteanu I. In our clinic, alcoholization of the Gasser knot is very successfully used (Nazarov V. , 1999). Experience in treating 400 patients.

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