Symptoms of trigeminal neuralgia. Inflammation of the trigeminal nerve: symptoms and treatment of trigeminal neuralgia The main symptom of trigeminal neuralgia is

Trigeminal neuralgia or trigeminal neuralgia is the most common cause of facial pain. The disease develops as a result of damage to the peripheral nerves.

The trigeminal nerve consists of three branches and performs the function of providing facial sensitivity. Each branch of the nerve is responsible for the functions of one area of ​​the face - the upper part (eyes, brow ridges), the middle of the face (nose, nasolabial muscles, upper jaw), and the lower part (lower jaw, chin). Symptoms of neuralgia depend on which part of the nerve branch has been damaged.

Trigeminal neuralgia develops due to compression or irritation of the nerve. Often the disease is accompanied by the destruction of the membrane and the exposure of the nerve endings, which causes excruciating pain with such a lesion.

With trigeminal neuralgia, the causes can be divided into two groups - these are age-related changes and infectious causes of the disease.

Trigeminal is often observed in people over 50 years of age and can occur against the background of the following pathologies and disorders:

• atherosclerosis;
• aneurysm;
• tumor;
• age-related elongation of the vessel.

With age, there is a change in the length of blood vessels and a violation of their tone. Often, due to the pressure of the enlarged vessel, irritation of the trigeminal nerve occurs, which provokes the destruction of the myelin sheath and the appearance of an acute pain syndrome.

In the presence of a tumor, the disease is caused by the pressure of the neoplasm on the nerve.

Pathology does not always depend on age and can appear in any person for the following reasons:

• meningitis;
• inflammation of the maxillary sinuses;
• chronic purulent lesions of the mucous membranes of the throat and nose;
• herpes virus;
• advanced caries;
• bacterial infections.

In this case, the infection spreads through the bloodstream and affects the trigeminal nerve. Inflammation of the nerve develops, which is accompanied by pain and dysfunction of the facial muscles.

Age-independent causes of neuralgia include exposure to traumatic factors - trauma, hypothermia, concussions and strokes.

Symptoms of pathology

Trigeminal neuralgia is characterized by the most excruciating pain syndrome that can be felt in the face. Localization of pain depends on the site of damage to the branched nerve. Patients complain of pain in the lower or upper jaw. This is usually associated with caries and the problem is treated by a dentist, which does not bring relief.

The pain is paroxysmal in nature and is aggravated by the following factors:

• face shaving;
• chewing food;
• sneezing
• face washing;
• laughter;
• trying to open the mouth wide.

Distinguish between typical and atypical pain.

A typical pain syndrome in neuralgia is paroxysmal, with a tendency to increase with facial tension. Such a syndrome is cyclical - it either intensifies, then subsides, in order to intensify again after a while. A distinctive feature of this is a clear localization.

With atypical pain, localization is absent and the whole face can hurt. The pain is dull and monotonous, it does not subside during the day.

The disease is accompanied by increased lacrimation, a violation of the motor function of the facial muscles and a violation of sensitivity. The affected area either becomes numb or becomes hypersensitive.

Possible Complications

Trigeminal neuralgia is a serious condition that needs to be treated. If you start the disease, the following complications may develop:

• paresis of mimic muscles;
• the formation of a cerebellar hematoma;
• hearing impairment or total loss;
• development of ataxia.

You should not self-medicate, as this is fraught with the development of negative consequences. Only a neurologist should deal with the diagnosis and treatment of the disease.

Establishing diagnosis

Diagnosis by an experienced doctor is not difficult; to clarify the degree of damage to the trigeminal nerve, it is necessary to undergo some examinations.

The specialist necessarily assesses the intensity of the pain syndrome during palpation. To exclude some concomitant diseases, an MRI and CT examination is performed. It is necessary to examine the conduction of impulses by the damaged nerve.

Medical treatment

Conventional analgesics and opiates usually do not help relieve pain in neuralgia. For treatment apply:

• anticonvulsant drugs;
• muscle relaxants;
• drugs to relieve spasm;
• vitamins;
• medical blocks.

Anticonvulsant drugs are needed in order to stop the pain syndrome. The drugs help to block the conduction of nerve impulses, so the pain quickly passes.

Often the condition is aggravated by spasm of the facial muscles. For this purpose, muscle relaxants and antispasmodics are prescribed.

The therapy must be supplemented with the intake of vitamin preparations that have a positive effect on nerve fibers and strengthen the entire nervous system.

If conservative therapy does not help get rid of pain, it is advisable to use a medical blockade.

Blockade for pain relief

With this form of neuralgia, alcohol blockades are used. The purpose of the method is to create a barrier between the affected nerve and the central nervous system, thus stopping the transmission of pain impulses, which helps to relieve pain.

The blockade is carried out in a hospital and only by an experienced doctor. The injection is made at a point located directly near the affected area of ​​the nerve. This method allows you to instantly relieve pain, however, the duration of the injection is limited and does not exceed two days, after which the pain syndrome returns.

If the procedure is carried out incorrectly, the following complications are possible:

• bleeding;
• hematoma formation;
• nerve damage.

To relieve pain, a layer-by-layer injection with novocaine or lidocaine is made, and alcohol is used as a conductor.

Physiotherapy treatment

Treatment is selected individually, depending on the cause of the pathology. In some cases, physiotherapy procedures are an effective method of getting rid of pain:

• acupuncture;
• massage;
• acupuncture.

The methods help to relieve spasm of the muscles that compress the nerve, but are ineffective for neuralgia provoked by the pressure of an enlarged vessel.

The advantage of such methods of treatment is the safety and absence of contraindications. Physiotherapy should be selected by the attending physician, depending on the characteristics of the disease in a particular patient.

Surgery and radiosurgery

Radiosurgery is a method aimed at destroying the root of the damaged nerve. This allows you to quickly and effectively get rid of the problem. The intervention is carried out using a special gamma knife.

Such an intervention occurs in a non-invasive way, not associated with any risks. Preoperative preparation is not carried out, after the procedure there is no need for hospitalization of the patient. This method is carried out without anesthesia, which makes it completely safe.

Surgical surgery is performed when it is necessary to reduce the pressure of the vessel on the nerve. This operation is called microvascular decompression and requires an incision. The seam left after the operation will be almost invisible, as it is located behind the auricle.

Through the incision, the doctor will push the vessels that are compressing the nerve apart and install a special gasket between them to prevent further nerve compression. The intervention is performed under general anesthesia.

The operative method is associated with a number of risks:

• problems of facial sensitivity;
• hearing loss;
• deterioration of vision.

The operation is not performed if it is necessary to treat older patients, as it is associated with a risk of stroke. General anesthesia is a serious test for the body and it is undesirable to do it in old age.

The safest, most gentle and bloodless method of treatment is the destruction of damaged fibers, which contributes to the rapid removal of pain. Such methods have no contraindications and risks of side effects, which makes them the most popular.

Folk remedies

Folk remedies in the treatment of neuralgia are based on thermal exposure in order to increase blood flow and relieve spasm. You can use these methods only after consulting a doctor. With severe inflammation, warming up can aggravate the patient's condition and harm health.

In folk medicine, heating with salt is used. Salt should be heated in a metal bowl, and then poured into a tight cloth bag. Thanks to the fabric, a dry indirect effect is carried out, which improves local blood circulation and relieves pain.

Another method is heating with a boiled egg. The egg should be hard-boiled, wait until it cools down a bit, and then apply to the affected area.

Natural fir oil will help to provide a warming effect. A small amount of oil should be gently rubbed into the affected area, without strong pressure with the fingers.

A compress from a mixture of black radish juice and horseradish has a good effect. It is not difficult to prepare the mixture, it is enough to grate the root crops and squeeze out the resulting juice. The compress should be kept on the affected area for half an hour.

Along with symptomatic treatment, it is recommended to take sedatives. It can be homeopathy, special preparations or herbal soothing decoctions of chamomile, mint or lemon balm. This reduces the load on the nervous system. Sedative drugs relieve muscle spasm and improve vascular tone.

It will not be possible to cure the problem with alternative methods, since such treatment is aimed at reducing the symptoms, but not at eliminating the cause. Neuralgia should only be treated by a qualified professional. It is impossible to independently select drug therapy, since drugs used in the treatment of nerve damage have a number of side effects. Incorrectly chosen dosage of the drug can lead to the development of negative consequences.

Treatment of neuralgia can take a long time, so when the first symptoms appear, you should immediately consult a neurologist. Timely started treatment guarantees rapid pain relief and restoration of the normal functioning of the trigeminal nerve.

Among the lesions of the trigeminal nerve system, a significant number are trigeminal odontogenic diseases, which are a heterogeneous group. Examination of patients with lesions of the trigeminal nerve system showed that among them there are groups with different clinical manifestations: odontogenic neuralgia, odontogenic plexalgia, bilateral odontogenic neuralgia, odontogenic neuritis of the alveolar nerves.

The most common odontogenic disease of the trigeminal nerve system is odontogenic trigeminal neuralgia.

It has a number of features, its main clinical symptom is constant pain. The nature of the pain can be throbbing, aching, dull, cutting, pressing, itching. Against the background of constant pain, attacks of increased pain are noted, lasting from tens of minutes to several hours and even days, gradually subsiding. The pain is mainly localized in the area of ​​the affected branches, sometimes there is a spread of pain to the zones of neighboring branches (all three) or irradiation to any area of ​​the head. Patients show changes in the central nervous system. The mood of patients is usually lowered, they are fixed on their painful sensations, conflict. The disease has a chronic relapsing character. There are no trigger zones.

As a rule, odontogenic neuralgia is accompanied by the presence of autonomic disorders in the form of increased salivation, lacrimation, nasal discharge, edema and hyperemia of facial areas, which manifest themselves mainly during increased pain manifestations.

In addition to autonomic disorders of a local nature, a significant number of patients in the acute period of the disease have vegetative changes of a general nature in the form of palpitations, sweating, etc.

In patients with a long course of the disease (several years) and a history of destructive methods of treatment, trophic disorders of facial tissues, as well as sensory disturbances, are found. But usually there are no sensitive disorders.

In these cases, there is pain at the points of Balle. The severity of sensory impairment is directly dependent on the severity of the pain syndrome. In some patients, after the treatment, sensitivity is restored on the face, which proceeds in two stages - hypesthesia is replaced by hyperesthesia, followed by its replacement with normal sensitivity. Apparently, the observed changes are possible with unstable lesions of the trigeminal nerve fibers.

The second place in frequency among odontogenic lesions of the trigeminal nerve system is occupied by odontogenic dental plexalgia. The most common factor in the occurrence of odontogenic dental plexalgia are defects in the filling of teeth and root canals.

Pain in odontogenic plexalgia is permanent and localized in the gums and teeth, in the lips. The nature of the pain is mostly aching, cutting, dull. Against the background of constant pain, their periodic amplifications are noted, lasting for hours. Eating, changing the microclimate (drafts), toileting the face, as a rule, increase pain. The disease has a chronic relapsing character.

For odontogenic dental plexalgia, vegetative disorders are characteristic in the form of swelling of the gums, skin of the buccal region, and their hyperemia.

Unlike odontogenic neuralgia, odontogenic dental plexalgia is not characterized by sensory disturbances in the affected branches, pain during palpation of the points of the Balle on the face, and trophic disorders.

Among the manifestations of odontogenic lesions of the trigeminal nerve system, there is also bilateral odontogenic trigeminal neuralgia.

First, the pain appears on one side, then after a while - on the other. More often, the second and third branches of the trigeminal nerve are affected, both on one and on both sides.

One of the most common causes of bilateral odontogenic neuralgia is poorly made prostheses. As a rule, in such patients, prosthetics were performed on both sides.

The leading symptom in the clinic of bilateral odontogenic neuralgia is pain of a constant nature, localized in the area of ​​the affected branches. The nature of the pain can be aching, throbbing, dull. Against the background of constant attacks, pain intensification is noted, lasting from 20 minutes to 2-3 hours. Provoking moments are physical overwork, mental overstrain, menstruation. Sometimes painful paroxysms occur for no apparent reason.

The disease proceeds with remissions and exacerbations. Many patients have an astheno-neurotic reaction.

Characteristic of bilateral odontogenic neuralgia, as well as unilateral, is the presence of autonomic disorders in the form of hyperemia of the skin, rhinorrhea, swelling of the soft tissues of the face, lacrimation, dry mouth. Many patients also have palpitations and sweating. Especially all these phenomena are manifested during painful paroxysms.

Patients with long-term disease with destructive methods of treatment had a history of sensory disturbances in the area of ​​the affected branches of the trigeminal nerve, pain on palpation at the exit points of the trigeminal nerve, and trophic disorders of facial tissues.

The next most common odontogenic lesions of the trigeminal nerve system are odontogenic neuritis of the alveolar nerves. The course of the disease is chronic, relapsing. The prognosis of the disease is relatively favorable compared with odontogenic neuralgia and odontogenic plexalgia. The inferior alveolar nerve is most often affected due to its anatomical position.

The main odontogenic factor in the occurrence of alveolar nerve neuritis is a complication of conduction anesthesia.

Unlike odontogenic neuralgia and dental plexalgia, the leading in the clinical picture in patients with odontogenic neuritis of the alveolar nerves is a feeling of numbness in the upper and lower teeth. With damage to the lower alveolar nerve, a feeling of numbness is also noted in the corresponding half of the lower lip and chin. Almost half of the patients also complain of constant aching or dull pain.

A characteristic feature of odontogenic neuritis of the alveolar nerves is a violation of sensitivity in the areas of innervation of the alveolar nerves, which is directly dependent on the severity of paresthesia and the intensity of the pain syndrome. Also a characteristic sign of odontogenic neuritis of the alveolar nerves is pain during vertical percussion of the teeth.

Autonomic disorders are observed in almost half of patients with odontogenic neuritis of the alveolar nerves, usually in the acute period of the disease and manifest themselves as swelling, hyperemia of the gums, and salivation.

Examination of a group of patients with trigeminal neuralgia, predominantly of central origin (classical neuralgia), showed that odontogenic factors in them are only provoking moments, among which the first place is occupied by manipulations in the dentoalveolar system. Most often, the second branch of the trigeminal nerve is involved. The main clinical symptom of trigeminal neuralgia, predominantly of central origin, is pain, which is paroxysmal in nature and localized in the affected area of ​​one or more branches of this nerve, sometimes spreading to adjacent parts of the face and half of the head. The duration of the attack - from. several seconds to several minutes. The provoking moment of seizures is most often any movement of the facial muscles. Unlike odontogenic lesions of the trigeminal nerve system, with neuralgia of predominantly central origin, as a rule, there is no pain in the interictal period.

A characteristic feature of trigeminal neuralgia of predominantly central origin is the presence of trigger zones. Vegetative disorders are also detected, less pronounced than with odontogenic lesions of the trigeminal nerve: involuntary contraction of the facial muscles of a tonic or clonic nature, impaired pain sensitivity and pain on palpation at the exit points of the affected branches of the trigeminal nerve.

With odontogenic neuralgia, the peripheral neurons of the trigeminal nerve are affected, resulting in the formation of groups of neurons with a disturbed mechanism of inhibitory control, which, according to G. N. Kryzhanovsky, become generators of increased excitation. The fact that the peripheral neuron is the primary link in the development of the mechanisms of odontogenic neuralgia indicates that neuralgia is classified as neuralgia of predominantly peripheral origin.

In the development of trigeminal neuralgia of predominantly central origin, central mechanisms are mainly involved. It can be assumed that constant painful pathological impulses, according to A. A. Ukhtomsky, lead to the formation of congestive foci of excitation (pathological dominant) in the region of the brainstem, thalamus and cerebral cortex. Clinically, this is confirmed by an exacerbation of the disease caused by mental trauma, negative emotions, etc.

Despite the fact that the study of rheofasciography in facial pain is of great importance for revealing the pathogenetic mechanisms of the disease, there are no reports in the literature about rheofasciography in odontogenic lesions of the trigeminal nerve.

Comparative analysis of rheofaciograms recorded using the proposed device showed that in odontogenic lesions of the trigeminal nerve, rheographic changes were more stable than in trigeminal neuralgia of predominantly central origin, and changed more slowly. Usually, patients have a change in the blood flow of the face, manifested in a decrease in the rheographic index in the area of ​​pain. In almost all cases, with odontogenic lesions of the trigeminal nerve system, there were rheographic signs of changes in vascular tone. Most of the patients showed an increase.

Studies of the electrical excitability of the points of exit of the branches of the trigeminal nerve and the oral mucosa revealed that in patients with odontogenic lesions of the trigeminal nerve system, in contrast to neuralgia of predominantly central origin, an increase in the threshold of electrical excitability at the points of exit of the affected branches and a distortion of the polar formula AZR>KZR on the mucosa are characteristic membrane of the oral cavity in the affected area, clinically combined (long periods of the disease and destructive methods of treatment in history) with hyperesthesia, hypoesthesia, pain on palpation.

Therefore, the determination of the threshold of electrical excitability of the exit points of the branches of the trigeminal nerve and the oral mucosa in patients with odontogenic lesions of the trigeminal nerve system in combination with clinical data allows us to assess the damage to the terminal structures of this system, monitor the effectiveness of the treatment as a result of a dynamic study, and judge the prognosis of the disease. , and is also a differential diagnostic criterion for recognizing odontogenic lesions of the trigeminal nerve and neuralgia, predominantly of central origin.

Studies of the electrical conductivity of symmetrical facial TA in patients with odontogenic lesions of the trigeminal nerve system showed that the initial indicators of electrical conductivity in them are high (ranging from 21 to 150 μA), while in patients with neuralgia, predominantly of central origin, they are low (from 2 to 16 µA). These indicators confirm the presence of two types of trigeminal neuralgia, predominantly peripheral and predominantly central.

Analyzing the results of the use of auxiliary research methods for odontogenic lesions of the trigeminal nerve system, we came to the conclusion that rheofaciography, electrothermometry, studies of the electrical conductivity of the facial TA, as well as the electrical excitability of the exit points of the trigeminal nerve and the oral mucosa, make it possible to clarify the topical diagnosis, identify the stage of the disease, and conduct observations for the dynamics of the pathological process for the appointment and correction of the appropriate treatment.

In order to increase the efficiency and reduce the duration of treatment, we have developed a method for the treatment of odontogenic lesions of the trigeminal nerve system using reflexology (acupuncture, electropuncture), in which TA electrical conductivity is used to select points.

The nature of the therapeutic effect is determined depending on the values ​​of the studied indications of the electrical conductivity of the selected TA. In patients with odontogenic lesions of the trigeminal nerve system, electropuncture proved to be effective (since the TA electrical conductivity values ​​are high, ranging from 21 to 100 μA). The course of treatment consists of 8-10 procedures.

In patients with a long-term disease and multiple novocaine and alcohol-novocaine blockades in history, the therapeutic effect of electropuncture is significantly reduced. Therefore, these patients, simultaneously with a course of electroacupuncture, should be given a comprehensive course of treatment for each group of odontogenic lesions of the trigeminal nerve system, including medication and physiotherapy. The main drugs in the complex treatment for unilateral and bilateral odontogenic trigeminal neuralgia are analgesics, local anesthetics, vegetotropic drugs, tranquilizers, vitamins, biostimulants, physiotherapeutic treatment (diadynamic currents).

In case of odontogenic plexalgia, the acupuncture method included physiotherapeutic treatment (diadynamic currents with a narcotic mixture), as well as medication, consisting of local anesthetics, vegetotropic agents, tranquilizers, and vitamin therapy, in addition to the acupuncture method. Treatment of odontogenic neuritis of the alveolar nerves is prescribed in combination with physiotherapy (longitudinal gilvanization), as well as with vitamin therapy and biostimulants, tranquilizers, while in trigeminal neuralgia of predominantly central origin, the greatest therapeutic effect was achieved from the use of drugs such as carbamazepine (finlepsin, stazepin) in combination with antihistamines, local anesthetics, vitamin therapy in combination with physiotherapy (diadynamic currents).

Thus, the methods of treatment of odontogenic lesions of the trigeminal system and trigeminal neuralgia, predominantly of central origin, are different. This allows us to confirm the assumptions made that the mechanisms of development of odontogenic lesions of the trigeminal nerve system differ from the mechanisms of the occurrence of trigeminal neuralgia, predominantly of central origin.

The use of complex treatment, which is based on a course of acupuncture, gives a good therapeutic effect. With odontogenic trigeminal neuralgia, improvement was obtained in approximately 93% of cases, with odontogenic dental plexalgia - in 88.9 and with odontogenic neuritis - in 84.9% of cases. Dynamic observation showed the stability of the obtained results.

For citation: Manvelov L.S., Tyurnikov V.M., Kadykov A.V. Trigeminal neuralgia: epidemiology, etiology, pathomorphology, pathogenesis, clinic, diagnostics // BC. 2013. No. 10. S. 542

Trigeminal neuralgia, or trigeminal neuralgia (TN) is the most severe and common form of facial pain. The disease has been known since ancient times, but M. Andre first described it only in 1756. The author cited 5 cases of suffering, which he called "painful tick". A detailed description of TN was presented by J. Fothergil in the monograph "Painful lesions of the face", which is deservedly considered a fundamental guide. At present, in the conditions of the rapid progress of science, the study of the complex problem of TN involves a multidisciplinary approach using epidemiological, clinical, pathomorphological, neuroimaging, ultrasound, electrophysiological, biochemical, pharmacological and other modern research methods; development and implementation in practical healthcare of new methods of conservative and surgical treatment.

There are primary (idiopathic, essential) and secondary (symptomatic) TN. The first includes TN, which occurs regardless of any disease, existing pathological process. In the vast majority of cases of idiopathic TN, vascular compression of the trigeminal root is found. The second form of TN is a complication of a disease: a viral or bacterial infection, multiple sclerosis, tumors of the cerebellopontine angle. The secondary form of TN predominates in prevalence.
Epidemiology
According to the World Health Organization, the prevalence of TN in various countries is 2-5 people per 100,000 people per year. Women get sick more often than men (in a ratio of 3:2). The disease can begin at any, even childhood, however, in 80-90% of cases it debuts at the age of over 40 years. Moreover, the idiopathic form of TN is most often observed in older people, and symptomatic (for example, with multiple sclerosis, tumors, vascular malformations) - in young people.
Etiology
A large number of studies have been devoted to the study of the etiology of TN, especially in recent years. The relationship between paroxysms of pain and compression of the trigeminal nerve root has been proven. An important role in the occurrence of TN is played by vascular formations (loops, arteriovenous malformations, aneurysms), as well as multiple sclerosis, tumors and cysts of the cerebellopontine angle. According to one hypothesis, TN is a variant of neuropathy.
Until now, the issue of the leading role in the etiology and pathogenesis of trigeminal paroxysms of central or peripheral mechanisms remains debatable.
After the introduction of anticonvulsants into practice, an assumption appeared about epileptiform activity in the stem trigeminal structures as the main cause of pain paroxysms. However, according to modern concepts, the leading cause of TN is vascular compression of the trigeminal root. In 1967, this reason was first named by P. Jannetta. Vascular compression of the trigeminal root is detected in 80-90% of cases of TN. Most often, compression occurs in the proximal part of the trigeminal root at its entrance to the pons. In 80% of cases, the root is compressed by an artery and in 20% by a vein. The latter is considered the most unfavorable for the prognosis. Less commonly, compression is caused by aneurysms of the cerebellopontine angle and arteriovenous malformations.
Compression of the trigeminal nerve root can also be caused by tumors in the middle and posterior cranial fossae, basal meningitis, vestibular schwannomas, meningiomas, epidermoid cysts, and other volumetric formations. A certain role in the development of TN is played by dysplasia of the structures of the posterior cranial fossa.
Familial forms of TN
A number of works describe familial forms of TN. The genetic defect is localized on chromosome 32P. Among hereditary syndromes considered risk factors for TN are autosomal dominant form of hypertension and brachydactyly. Hereditary hypertension is often associated with vascular abnormalities: pathological tortuosity or stenosis of the posterior inferior cerebellar or vertebral arteries. As a result, TN develops due to compression of the ventrolateral medulla oblongata.
Pathomorphology
In 1994, D. Hilton et al. described for the first time ultrastructural changes in the trigeminal nerve root during vascular compression. The authors found local demyelination of axons. Immunohistological examination revealed that the processes of astrocytes were localized mainly on the periphery of the injury. Later, near the demyelinated axons of the damaged trigeminal root, electron microscopy revealed changes in the extracellular space and a large number of collagen fibrils. Increased collagen synthesis and the formation of large aggregates were noted in the center of the area of ​​the trigeminal nerve root damaged by axonopathy.
Pathogenesis
The primary pathogenetic factor in the occurrence of trigeminal pain is considered to be prolonged vascular compression of the trigeminal nerve, which leads to its damage and local demyelination of sensory axons. As a result, a complex of pathophysiological and pathobiochemical disorders is formed, leading to the occurrence of paroxysms of pain. This concept is confirmed by neuroimaging data (detection of microvascular compression of the trigeminal root) and the results of many thousands of microvascular decompression operations, which give a stable and prolonged remission of the neuralgic syndrome. In addition, the results of experimental work show that decompression contributes to the remyelination of the trigeminal root and the normalization of the conduction of excitation.
However, the following conditions are necessary for the occurrence of a neurovascular conflict:
1. dolichoectasia of the superior cerebellar artery;
2. special location of the loop of the superior cerebellar artery;
3. vascular atherosclerosis, leading to a decrease in vascular elasticity and an increase in the mechanical effect of a pulse wave on the trigeminal nerve root.
In addition, it is known that compression of the branches of the trigeminal nerve in the bone canals of the facial skull can serve as an etiological factor. These mechanical effects cause local demyelination of trigeminal neurons, as does multiple sclerosis, which is the most common cause of secondary TN.
Local demyelination is important in the pathogenesis of TN, causing epaptic transmission between damaged and undamaged fibers, forming a generator of pathologically enhanced excitation. However, it is not enough for the development of TN. The appearance of pathological activity in the somatosensory cortex of the brain and its involvement in the pathological algic system is necessary.
Clinical manifestations
The clinical picture of TN is characterized by pronounced bouts of pain - shooting, burning, excruciating, unbearable. It is accompanied by both local (lacrimation, rhinorrhea, salivation) and general (hyperemia, hyperhidrosis) vegetative reactions.
It is noteworthy that during an attack, despite the sharpest pain sensations, patients do not moan, do not scream, do not talk. TN is silent. The patients seem to freeze. However, at the same time, a suffering grimace appears on the face - a “pain tic”. Patients try to strongly squeeze the painful area of ​​the face with their hand "gesture - antagonist". A light touch on this area intensifies the attack or provokes it. The duration of pain paroxysm averages 5-20 s, but not more than 2 minutes. The frequency of attacks can be very different depending on the duration of the disease and the effectiveness of treatment, up to the highest - up to several hundred times a day, completely exhausting the patient. Patients can indicate the area of ​​occurrence of the attack. Clarification of this zone of origin of pain paroxysm is important for determining the affected branch of the trigeminal nerve.
An attack of pain can be provoked by various factors: talking, laughing, chewing, shaving, washing, brushing your teeth, etc. In severe cases, due to pain, patients cannot eat, drink and speak so as not to provoke an attack. This often leads to social isolation of the patient and weight loss.
An important feature of TN is the presence of trigger, or trigger, zones. Although their localization on the face may be different in different people, but for each patient it remains constant and is well known to him. These zones can be located on the lips, wings of the nose, eyebrows, chin, and in some cases - in the area of ​​​​the external auditory canal. Sometimes trigger zones can move from one area of ​​the face to another. However, this is limited to only the branch of the nerve involved in the pain syndrome. A refractory period is characteristic, which consists in the impossibility of causing an attack for a certain period of time (from 30 to 5 minutes) with irritation of the trigger zones immediately after the end of the previous attack.
An interesting fact is that painful stimulation with a sharp needle does not cause a pain attack, while a light touch or feeling of cold does. The localization of trigger zones on the gums, tongue and palate does not allow eating and talking.
In most cases, pain paroxysm occurs against the background of apparent complete health. However, sometimes the disease can begin gradually with unpleasant sensations of twitching, “electricity” of the face, or with a toothache that serves as a reason to visit a dentist. Sometimes in the interictal period there is a non-intense, pressing or burning pain.
Paroxysms of pain are often accompanied by symptoms of damage to the autonomic nervous system. A correlation was established between the severity of pain syndrome and the degree of autonomic dysfunction.
K.Ya. Ogleznev et al. lacrimation and vasodilation of the conjunctiva of the eye were noted in patients with TN only when the ophthalmic branch of the trigeminal nerve was involved in the pain syndrome.
The pain syndrome is always accompanied by contraction of the muscles of the corresponding half of the face and retraction of the corner of the mouth. These muscle contractions are referred to as tonic and clonic convulsions, resulting from the transfer of excitation from the trigeminal nucleus to the facial nerve. These tic-like contractions represent an emotionally reactive response to pain and reflect a behavioral response, and not just a switch of impulses from the trigeminal nucleus to the facial nucleus in the brainstem.
Sensitivity disturbances are usually not detected, however, in some cases mild hypesthesia or hyperpathy is detected.
The clinical picture of TN is in many respects similar to the manifestations of glossopharyngeal neuralgia, idiopathic pain syndrome in the zone of innervation of which is rare and is one case per 60-100 manifestations of TN. A typical picture of neuralgia of the glossopharyngeal nerve is expressed by unilateral sharp pain in the region of the root of the tongue, tonsils and pharynx radiating into the external auditory canal or deep into the ear. In these cases, as in TN, paroxysms of pain are short-lived and provoked by touching the pharynx, the back of the tongue, but most often occur when swallowing. To prevent saliva from getting on the affected part of the pharynx, patients are forced to sleep on the opposite side. Sometimes the disease can debut with unpleasant sensations in the tonsils and pharynx. With neuralgia of the glossopharyngeal nerve, sensory disorders are usually not detected. In the early stages of the disease, long-term remissions are noted, later the pain becomes almost constant and painful. During an attack, there is a sharp opening of the mouth, the expiration of saliva, and sometimes a feeling of strong swelling of the pharynx. Intense paroxysmal pain in the pharynx may be accompanied by cardiac arrest or syncope.
In the literature, there are various names for facial pain associated with damage to the intermediate nerve: atypical facial neuralgia, pterygopalatine neuralgia, erythromelalgia, Horton's syndrome, histamine cephalgia, neuralgia of the large stony nerve, periodic migraine neuralgia. Even such an incomplete enumeration of the names of diseases and syndromes indicates the existing confusion in the interpretation of the problem of facial neuralgia.
E. Sachus cited 4 cases of facial and headache incurable by conservative methods, completely eliminated after transection of the intermediate nerve. The author draws attention to the need to find alternative ways to conduct pain, since in one of the cases he described, the pain disappeared only after transection of the vestibulocochlear nerve. This may be explained by the fact that several thin bundles of the intermediate nerve can run along with the VIII cranial nerve.
J.R. Hunt described two forms of neuralgia of the geniculate node: otological, in which pain is localized deep in the ear with irradiation into the deep structures of the face, and prosopalgic. The first form is a syndrome of severe, often unbearable pain in the depth of the ear or anterior to it. It occurs periodically, at times it is paroxysmal in nature, but more often it is permanent. In this case, trigger zones are sometimes detected anterior to the ear or in the external auditory canal. The disease can occur with remissions, the duration of which decreases as the process progresses.
The prosopalgic form is manifested by bouts of rapidly increasing pain, burning or throbbing in the depths and around the eye. These pains often radiate to the temple, ear, forehead, and upper jaw. Characterized by lacrimation, vasodilation of the conjunctiva of the eye, nasal congestion and rhinorrhea on the side of the pain syndrome. Often there is redness of the face with a feeling of heat. In almost half of the cases of the disease, Bernard Horner's syndrome occurs (ptosis, miosis, enophthalmos).
Patients have several attacks of facial pain during the day, especially at night. Men suffer predominantly - 90% of cases. The disease begins at a young age. The pains are so severe that patients moan, scream, cry (unlike those suffering from TN) and may make a suicidal attempt.

Diagnostics
The criteria for diagnosing TN are:
1. Paroxysms of attacks of facial or head (frontal) localization lasting an average of 5-20 seconds, but not more than 2 minutes.
2. Pain is characterized by at least 4 of the following symptoms:
- sharp expression, cruelty;
- Occurrence mainly when exposed to trigger points or when performing a number of household activities: eating, talking, washing your face, shaving, brushing your teeth;
- during an attack, "pain behavior" is observed (patients try not to move, freeze, do not speak);
- in the interictal period, neurological symptoms are absent.
3. Each patient's seizures are stereotyped, but individual.
4. The diagnosis is established by excluding other causes of facial pain by clarifying the anamnestic data, a thorough neurological examination, and, if necessary, using additional special research methods, incl. computer and magnetic resonance imaging, electrophysiological, ultrasound, biochemical and others.

Literature
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Trigeminal neuralgia is one of the most common diseases of the peripheral nervous system. It has been known to mankind since the beginning of our era for its excruciating, maddening pains.

Trigeminia (Fozergil's disease, Trousseau's pain tic) was tried to be treated by physicians of the Middle Ages of the last century, and the first description of trigeminal neuralgia was recorded in the writings of the ancient Chinese healer Hua-Toa.

The prevalence of trigeminal neuralgia is 40 to 60 cases for every 10,000 people. The maximum risk of trigeminia is noted in the middle age group - in persons from 45 to 60 years. Another feature of the disease is related to the gender of patients - it is known that women suffer from pain tics much more often than men.

What it is?

Trigeminal neuralgia (trigeminal neuralgia) is a chronic disease manifested by bouts of intense, shooting, burning pain in the zones of innervation of the trigeminal nerve.

The International Association for the Study of Pain (IASP-International Association for the Study of Pain) defines trigeminal neuralgia as a syndrome characterized by sudden, short-term, intense, recurring pain in the zone of innervation of one or more branches of the trigeminal nerve, usually on one side of the face.

There is a primary (idiopathic) form of trigeminal neuralgia that occurs in the absence of other diseases or pathological processes due to compression of the trigeminal nerve root, and a secondary (symptomatic) form caused by a complication of another disease (infection, tumors, multiple sclerosis).

Types of neuralgia

Conventionally, all types of trigeminal neuralgia can be divided into primary (true) and secondary neuralgia.

• Primary (true) neuralgia is considered a separate pathology resulting from nerve compression or impaired blood supply in this area.
• Secondary neuralgia is the result of other pathologies. These include tumor processes, severe infectious diseases.

Neuralgia can affect both all nerve branches at once, and manifest itself as inflammation of one or two branches.

Causes of neuralgia

According to the mechanism of occurrence of trigeminal neuralgia, this pathology can be primary or true (isolated lesion of only the trigeminal nerve) or secondary (manifestation of neuralgia as a symptom of systemic diseases of the nervous system).

The exact cause of the development of trigeminal neuralgia has not been clarified, as mentioned above, it refers to idiopathic diseases. But there are factors that most often lead to the development of this disease.

Factors that contribute to the development of trigeminal neuralgia:

1) Compression of the trigeminal nerve in the skull or its branches after leaving the skull:

• injuries and post-traumatic scars;
• injuries in the area of ​​the maxillotemporal joint;
• congenital anomalies in the development of the bone structures of the skull;
• tumor formations of the brain or facial area along the branches of the trigeminal nerve;
• proliferation of connective tissue (adhesions) as a result of an infectious inflammatory process, sclerosis with damage to the myelin sheath of nerve fibers;
• expansion of cerebral vessels: aneurysms (pathological expansion of blood vessels), atherosclerosis, hemorrhagic and ischemic strokes, increased intracranial pressure as a result of osteochondrosis of the cervical spine, congenital anomalies in the development of blood vessels, and so on - the most common cause of trigeminal neuralgia.

2) Odontogenic causes (associated with teeth):

• reaction to anesthesia of the canals of the teeth;
• jaw injury with damage to the teeth;
• dental flux;
• "failed" filling or extraction of teeth or other surgical interventions in the face and oral cavity.

3) Diseases of the nervous system:

• multiple sclerosis;
• children's central paralysis (ICP);
• meningitis, meningoencephalitis (viral, tuberculosis);
• epilepsy;
• brain tumors and circulatory disorders in the nuclei and fibers of the trigeminal nerve, and so on;
• encephalopathy due to head injuries, infectious processes, hypoxia (lack of oxygen in the brain), lack of nutrients;

4) Viral nerve lesions: herpes infection, poliomyelitis, neuro-AIDS.

Symptoms of trigeminal neuralgia

Neuralgia of the facial nerve is divided into the following groups according to the nature of the symptoms: reflex and movement disorders, pain syndrome, vegetative-trophic symptoms.

Intense, paroxysmal, burning, sharp, excruciating pain. At the moment of an attack, patients sometimes freeze, describe the sensation as a backache, the passage of an electric current. The duration of the spasm is from 3 seconds to several minutes, in some cases the frequency of repetitions reaches 300 per day. Localization of the pain syndrome:

• Mandibular nerve: Chin, lower cheek, lower lip, neck, occiput, teeth, and mandibular surface.
• Maxillary: lower eyelid, upper jaw and teeth, upper cheek, nasal mucosa, upper lip, maxillary sinus.
• Optic nerve: bridge of the nose, forehead, upper eyelid, anterior scalp, inner corner of the eye, ethmoid sinus.

Motor and reflex disorders:

• Muscle spasms of the face (pain tic). During an attack, an involuntary muscle contraction occurs in the circular muscles of the eye, which is called blepharospasm. The symptom affects the chewing and other muscles of the face, often spread to the entire half of the face.
• There are changes in corneal, superciliary, mandibular reflexes, which is determined upon examination by a doctor.

Vegetative-trophic symptoms appear during an attack, in the first stages they are mild, but with the progression of the pathology they become more noticeable:

• runny nose, salivation, lacrimation;
• there is local redness or pallor of the skin color;
• in the later stages, dryness / greasiness of the skin, swelling of the face, loss of eyelashes develops.

If the disease is not treated in time, a point of painful pathological activity is formed in the thalamus. This causes a change in the localization, nature of the pain. At this stage, the elimination of the treatment of the disease does not lead to recovery.

This stage is characterized by the following symptoms:

• extends to the entire half of the face;
• any touch to the face causes pain;
• loud sound, bright light become irritants and a provoking factor of pain;
• in some cases, even the memory of the disease leads to a paroxysm;
• pain syndrome from paroxysmal develops into permanent (chronic);
• vegetative-trophic disorders are intensifying.

The disease is more typical for middle-aged people. The signs of trigeminal neuralgia are diagnosed at the age of 40-50. In most cases, the right side of the face is affected (70%). Rarely, trigeminal neuralgia can be bilateral, the disease has a cyclical nature: exacerbation is replaced by remission and worsening occurs again, exacerbations occur in the autumn-spring period.

Diagnostics

Drug therapy can eliminate the pain syndrome, but with neuralgia it is necessary to identify and eliminate the main cause of the disease. Otherwise, the attacks of pain will become more acute, appear more often.

Basic diagnostic methods:

• Dental examination. Neuralgia often occurs against the background of dental diseases, low-quality prostheses.
• Consultation of a neurologist. Based on the results of the initial examination, the doctor determines further types of examination.
• MRI. The study helps to see the structure of the nerves, the presence and localization of vascular pathologies, various types of tumors.
• Panoramic x-ray of the skull and teeth. Helps to see formations that could pinch the nerve.
• Blood test - allows you to exclude the viral origin of pathological changes in the trigeminal nerve.
• Electromyography - designed to study the characteristics of the passage of impulses along the nerve.

How to treat trigeminal neuralgia?

The method of treatment is selected depending on the cause that provoked the disease.

The main drug for the treatment of trigeminal neuralgia is carbamazepine. It develops inhibitory processes in nerve cells that are prone to paroxysmal activity (painful excitation). The dosage of the drug is selected by the doctor, so we will not dwell on the dosage regimens used. Let's just say that carbamazepine is taken for a long time, up to 8 weeks.

In addition, the drug is quite toxic. Affects the liver, urinary, bronchial system. Among the side effects from taking carbamazepine, various mental disorders, memory impairment, and drowsiness were noted. Carbamazepine is contraindicated in pregnant women. The drug has a teratogenic effect - it has a toxic effect on the embryo. Also, you can not take carbamazepine to people with glaucoma, heart block, blood diseases.

During treatment with carbamazepine, grapefruits should not be consumed, since the fruit enhances the manifestation of adverse reactions of the drug. To enhance the effect, it is recommended to take Carbamazepine together with Pipolfen. The duration of treatment rarely exceeds 30 days.

Other types of drugs:

• anticonvulsants - Phenibut, Baclofen;
• tranquilizers - Dizepam;
• neuroleptics - pimozide;
• Vasotonics are prescribed for damage to the vessels of the brain - Trental, Nicotinic acid.

In addition to tablets, vitamin injections of ascorbic acid, vitamins of group B are used in therapy. Non-steroidal anti-inflammatory drugs in the form of injections or tablets are used as painkillers - Neurodiclovit, Milgama, Diclofenac. Antidepressants for neuralgia - Amitriptyline, help eliminate nervous tension and stress in the patient. To improve metabolic processes, prevent the formation of cholesterol plaques, Atoris is prescribed.

Equally useful is physiotherapy. It can enhance the effect of any drug, as well as its effectiveness. Treatment of inflammation of the trigeminal nerve is carried out using the following physiotherapy procedures:

• electrophoresis
• Phonophoresis
• Ultrasound.
• Acupuncture.
• laser therapy. It relieves pain, as it slows down the passage of a nerve impulse through the fibers.
• The impact of the electromagnetic field.
• Irradiation with ultraviolet or infrared rays. Provides relief from pain.

Drug therapy is selected for each patient individually, depending on the severity of the pathology, as well as the characteristics of his body.

Surgery

In the absence of the effect of conservative treatment at home, as well as in cases where trigeminal neuralgia is caused by compression of the root by an anatomical formation, surgical methods are used:

• if the cause of compression is a pathologically altered vessel, then microvascular decompression is performed. The essence of the operation is to separate the vessel and nerve using microsurgical techniques. This operation is highly effective, but very traumatic;
• percutaneous balloon compression: cessation of pain impulses along the nerve by squeezing its fibers with a balloon brought to the nerve with a catheter;
• percutaneous stereotaxic rhizotomy: the nerve root is destroyed using an electric current supplied to the nerve with a needle in the form of an electrode;
• nerve destruction using ionizing radiation: a non-invasive technique using radiation;
• glycerin injections: destroying the nerve by injecting glycerin into the branching of the nerve;
• if the tumor process became the cause, then, of course, the removal of the tumor comes to the fore;
• radiofrequency ablation: the destruction of nerve fibers with the help of high temperature.

A characteristic feature of all surgical methods is a more pronounced effect when they are performed early. Those. the earlier this or that operation is carried out, the higher the likelihood of a cure. It should also be borne in mind that the disappearance of pain attacks does not occur immediately after surgical treatment, but somewhat remotely (the timing depends on the duration of the disease, the extent of the process and the type of surgical intervention). Therefore, all patients with trigeminal neuralgia need to see a doctor in a timely manner.

Gymnastics

Movements and contractions of the facial muscles cause not only relief during the next attack of the disease, but also help to reduce the compression of the nerve branches in the future. Additional positive effects of gymnastics:

• improvement of blood circulation;
• optimization of lymph outflow;
• restoration of the conductivity of nerve impulses (if it is disturbed);
• prevention of the development of stagnation in the muscles.

• Tilts and circular rotations of the head (2 minutes).
• Stretching the neck and head as far as possible towards each shoulder (4 times).
• Stretching the lips in a smile, bringing them into a "tube" (6 times).
• Drawing air into the cheeks, exhaling it through a narrow gap in the lips (4 times).
• Cheek retraction (6 times).
• Closing and opening of the eyes with strong contraction of the eyelids (6 times).
• Raising the eyebrows up while fixing the forehead with the hand (6 times).

New developments

The most modern and effective methods of treating trigeminal neuralgia can be called radiosurgical operations using CyberKnife. This device uses a photon stream for treatment, which penetrates exactly into the area of ​​​​inflammation and eliminates it. Cyber ​​Knife treatment provides high accuracy of radiation doses, comfortable and fast healing. In addition, the procedure is absolutely safe for the patient.

Modern treatment with the help of Cyber ​​Knife can be considered the most effective. This technique is used not only abroad, but also in the expanses of the former USSR: in Russia, Ukraine, Belarus. For your information, treatment in Moscow will cost 180,000 rubles.

Preventive measures

Prevention of the disease are:

• Try to eat a balanced diet and take multivitamins.
• In the event of the occurrence and detection of infectious diseases, especially of the oral cavity and nasopharynx, try to cure them in a timely and complete manner.
• Avoiding hypothermia of both the face and the whole organism as a whole. Dressing for the weather is much wiser than treating (sometimes to no avail) severe pain.
• A systematic visit to the dentist to identify an infection that can later become the cause of the disease.
• Atherosclerosis (the appearance of plaques in the vessels of the body, the brain is no exception), to which people of the older age group are more susceptible, is among the causes of trigeminal neuralgia.

Any disease is easier to prevent than to treat, so the emphasis should be on the prevention of trigeminal neuralgia in order to avoid its consequences. If it so happened that the disease has taken over, do not self-medicate, do not prescribe yourself painkillers that relieve pain for a couple of hours, but contact an experienced specialist for a rational and complete course of treatment.

Forecast

Neuralgia does not pose a direct threat to life. Trigeminal neuralgia is no exception. However, the human psyche can be severely affected by this disease. Frequent and very intense pain syndromes quickly drive the patient into a state of depression. He begins to avoid communication, begins to lead an asocial lifestyle. The development of a wide variety of mental pathologies can begin.

Timely treatment will minimize the damage to a person's mental health. Even in the most difficult situations, you should not endure pain. It is better to decide on an operation, since the disease can be effectively treated even in the most difficult situations.

Recurrent lesion of the trigeminal cranial nerve, characterized by shooting paroxysmal prosopalgia. The clinical picture consists of repeated paroxysms of unilateral intense facial pain. Typically, the alternation of phases of exacerbation and remission. Diagnosis is based on clinical data, the results of a neurological examination, additional studies (CT, MRI). The basis of conservative therapy is anticonvulsant pharmaceuticals. According to indications, surgical treatment is carried out: root decompression, destruction of the trunk and individual branches.

ICD-10

G50.0

General information

The first description of trigeminal neuralgia dates back to 1671. In 1756, the disease was separated into a separate nosology. In 1773, the British physician J. Fothergill made a detailed report on the pain syndrome characteristic of the disease. In honor of the author of the report, neuralgia was named Fothergill's disease. In modern neurology, the term "trigeminal (trigeminal) neuralgia" is more often used. According to the World Health Organization, the incidence is 2-4 people per 10 thousand people. Pathologies are more susceptible to persons over 50 years of age. Women get sick more often than men.

Causes

Over the entire period of research into the etiology of this disease, various authors have mentioned about 50 causative factors. It has been established that in 95% of cases the etiofactor is compression of the trunk and branches of the trigeminal nerve. The main causes of compression are the following:

• Vascular pathology. Expansion, tortuosity, aneurysm of the vessel lying next to the nerve trunk leads to irritation and compression of the latter. The result is pain. Predisposing factors are cerebral atherosclerosis, arterial hypertension.
• Volumetric formations. Cerebral tumors, neoplasms of the bones of the skull, localized in the area of ​​​​the exit of the trigeminal nerve from the cerebral trunk or along its branches, as they grow, they begin to compress the nerve fibers. Compression provokes the development of neuralgia.
• Changes in the structures of the skull. Of etiological significance is the narrowing of the bone canals and holes, which occurs as a result of head injuries, chronic sinusitis, otitis media. Changing the relative position of the cranial structures is possible with the pathology of the bite, deformation of the dentition.

In some cases, damage to the nerve sheath and fibers is caused by a herpes infection, a chronic infectious process of the dentition (periodontitis, stomatitis, gingivitis). In some patients, trigeminal neuralgia is formed against the background of a demyelinating disease. The factors provoking the occurrence of pathology include hypothermia, dental procedures, increased chewing load, in the case of an infectious genesis, a decrease in immunity.

Pathogenesis

The above etiofactors potentiate morphological changes in the sheath of the trigeminal nerve. Studies have shown that structural changes in the myelin sheath and axial cylinders develop 3-6 months after the onset of the disease. Local microstructural disorders provoke the formation of a peripheral generator of pathologically enhanced excitation. Excessive impulsation, constantly coming from the periphery, causes the formation of a central focus of hyperexcitation. There are several theories explaining the relationship between local demyelination and the occurrence of a focus of hyperexcitation. Some authors point to the possibility of transverse interaxonal transmission of impulses. According to another theory, pathological afferent impulses cause damage to the trigeminal nuclei of the cerebral trunk. According to the third theory, at the site of injury, axon regeneration proceeds in the opposite direction.

Classification

Of practical importance is the systematization of the disease in accordance with the etiology. This principle underlies the determination of the most appropriate treatment tactics (conservative or surgical). According to the etiological aspect, trigeminal neuralgia is divided into two main forms:

• Idiopathic (primary). It is caused by vascular compression of the trigeminal root, more often in the region of the brain stem. Due to the difficulties in diagnosing pathological vessel-nerve relationships, idiopathic neuralgia is assumed after the exclusion of other causes of trigeminal pain syndrome.
• Secondary (symptomatic). It becomes the result of neoplasms, infections, demyelinating pathology, bone changes. It is diagnosed according to neuroimaging data, tomography of the skull.

Symptoms

The clinical picture consists of paroxysms of prosopalgia (facial pain), characterized by a series of intense pain impulses coming from the side of the face to the center. Patients describe the pain syndrome as "electric shock", "lumbago", "electric discharge". The attack lasts up to two minutes, repeats many times. Localization of pain depends on the location of the lesion. With the pathology of individual branches, pain impulses occur in the supraorbital region, along the zygomatic arch, and the lower jaw. Damage to the trunk leads to the spread of pain to the entire half of the face. Characteristic is the behavior of patients at the time of paroxysm: they freeze in place, afraid to move, speak. Despite the high intensity of pain, patients do not scream.

Trigeminal paroxysm is potentiated by various external influences: wind, cold air and water, shaving. Since the load on the facial and chewing muscles can act as a provoking factor, patients avoid opening their mouths wide, talking, laughing, and eating hard food. Trigeminal neuralgia is characterized by a recurrent course. There are no paroxysms during the period of remission. Subsequently, symptoms of loss of the function of the trigeminal nerve appear - a decrease in the sensitivity of the skin of the face. The symptomatic form proceeds with a combination of typical pain attacks and other neurological symptoms. Possible nystagmus, symptoms of damage to other cranial nerves, vestibular syndrome, cerebellar ataxia.

Complications

The fear of provoking a neuralgic paroxysm forces patients to chew only with the healthy half of the mouth, which leads to the formation of seals in the muscles of the contralateral part of the face. Frequent paroxysms reduce the quality of life of patients, negatively affect their emotional background, and impair their performance. Intense excruciating pain, constant fear of another paroxysm can cause the development of neurotic disorders: neurosis, depression, hypochondria. Progressive morphological changes (demyelinization, degenerative processes) cause a deterioration in the functioning of the nerve, which is clinically manifested by sensory deficit, some atrophy of the masticatory muscles.

Diagnostics

In typical cases, trigeminal neuralgia is easily diagnosed by a neurologist. The diagnosis is established on the basis of clinical data and the results of a neurological examination. The main diagnostic criterion is the presence of trigger points corresponding to the exit of the nerve branches into the facial region. The presence of a neurological deficit testifies in favor of the symptomatic nature of the pathology. To clarify the etiology of the lesion, the following instrumental studies are used:

• CT scan of the skull. Allows you to identify changes in the size and relative position of bone structures. Helps to diagnose the narrowing of the holes and channels through which the trigeminal nerve passes.
• MRI of the brain. It is performed to exclude volumetric formation as a cause of compression of the nerve trunk. Visualizes tumors, brain cysts, foci of demyelination.
• MR angiography. It is used for targeted verification of the vascular genesis of compression. Informative with a sufficiently large size of the vascular loop or aneurysm.

Trigeminal neuralgia differentiates with prosopalgia of a vascular, myogenic, psychogenic nature. The presence of a pronounced vegetative component (lacrimation, swelling, redness) indicates the vascular nature of the paroxysm, typical for cluster headache, paroxysmal hemicrania. Psychogenic facial pain is characterized by variability in the duration and pattern of pain paroxysm. To exclude ophthalmogenic, odontogenic and rhinogenic pain syndromes, consultation with an ophthalmologist, dentist, otorhinolaryngologist is required.

Treatment of trigeminal neuralgia

Basic therapy is aimed at stopping peripheral and central focal hyperexcitation. First line drugs are anticonvulsants (carbamazepine). Treatment begins with a gradual increase in dose until the optimal clinical effect is achieved. Maintenance therapy is carried out for a long time for several months, followed by a gradual decrease in dosages. In the absence of paroxysms, it is possible to cancel the pharmaceutical preparation. To increase the effectiveness of treatment with anticonvulsants, additional medications are used. Complementary therapies include:

• Means that potentiate the effect of anticonvulsants. Antihistamines can help reduce swelling. Antispasmodics contribute to the relief of pain paroxysm. Microcirculation correctors (nicotinic acid, pentoxifylline) provide increased oxygenation and nutrition of the nerve trunk.
. It is carried out in the area of ​​​​the exit of the nerve from the brain stem. It is necessary to remember about the high risk of using the technique in elderly patients, patients with aggravated premorbid background.
• Percutaneous radiofrequency destruction. A modern alternative to open interventions with the intersection of trigeminal branches. A significant disadvantage of the method is the relatively high percentage of relapses.
• Stereotactic radiosurgery. The operation consists in the destruction of the sensory root by directed local gamma radiation. Side effects include loss of sensitivity in the zone of innervation of the destroyed root.

Forecast and prevention

Trigeminal neuralgia does not pose a threat to life, but the attacks of the disease are excruciatingly debilitating. The outcome is determined by the etiology, premorbid background, the duration of the disease. For the first time, trigeminal neuralgia in young patients with adequate treatment has a favorable prognosis. Relapses after surgery are 3-15%. Primary prevention consists in the timely treatment of inflammatory pathologies of the dentition, ear, and paranasal sinuses. Measures of secondary prevention are regular monitoring by a neurologist, the exclusion of exposure to trigger factors, the prophylactic use of anticonvulsants for colds.