Pronounced pain syndrome code according to MCB 10. Pain syndrome. Limited ability to work with lumbodynia

Pain in the pelvic area usually occurs against the background of real pathologies of the pelvic organs, primarily reproductive. There are gynecological and non-gynecological causes of chronic pelvic pain in women. In 75-77% of patients, the morphological basis is the following diseases of the female genital area:
Inflammatory pathologies. Periodic and constant pain syndrome is accompanied by chronic endometritis, salpingitis, adnexitis, oophoritis.
Adhesion processes. Pelvic pain is one of the characteristic signs of plastic pelvioperitonitis and adhesions of the fallopian tubes.
Volumetric neoplasms. Painful sensations arise with sactosalpinx, ovarian cyst, submucous myoma, cancer of the ovary or the body of the uterus, and other benign and malignant neoplasms.
Genital and extragenital endometriosis. Aseptic tissue inflammation due to cyclic rejection of endometrioid growths can provoke pain.
Varicose veins of the pelvic veins. Pathological dilatation of the pelvic vessels and the venous congestion arising on its background have a stimulating effect on the nerve endings located in the pelvic cavity.
Allen's Syndrome. Masters. Typical pelvic pain occurs in women who have suffered an injury during childbirth with rupture of the ligaments of the uterus.
In 21-22% of cases, chronic pain has an organic non-gynecological basis. These reasons include:
Urological pathology. Pain is observed with urolithiasis, prolapse of the kidneys, their dystopia and developmental abnormalities, chronic cystitis.
Pathology of the peripheral nervous system. Chronic pain is characteristic of inflammatory and other lesions of the intrapelvic nerve plexuses.
Diseases of the gastrointestinal tract. Painful sensations are expressed in irritable bowel syndrome, chronic colitis and proctitis, appendicular-genital syndrome, adhesive disease.
Retroperitoneal neoplasia. Pelvic pain occurs with neoplasms of the kidneys, ganglioneuromas and other volumetric processes localized behind the peritoneum.
Diseases of the bone. Joint apparatus. Pain syndrome is manifested by lumbosacral osteochondrosis, damage to the symphysis pubis, tumors and metastases in the pelvic bones, bone tuberculosis, etc.
In 1.1-1.4% of patients, the causes of chronic pain syndrome are inorganic: pain can bother with mental and some other disorders - abdominal epilepsy, depressive conditions, psychogenias, hyperventilation syndrome, spasmophilia. In less than 2% of clinical cases, the specific causes of chronic pelvic pain in women remain unclear.

Lumbodynia is a collective pain syndrome that characterizes most diseases of the spine and is localized in the lumbar region and sacrum. Pathology can be not only vertebrogenic or spondylogenic in nature (associated with the functional characteristics of the spine), but also be the result of disorders in the work of internal organs: the bladder, kidneys, reproductive system and digestive tract. Regardless of the etiological factors, lumbodynia according to the international classification of diseases (ICD 10) refers to vertebral neurological diagnoses and has a universal, single code - M 54.5. Patients with acute or subacute lumbodynia are eligible for sick leave. Its duration depends on the intensity of pain, their effect on a person's mobility and his ability to self-service and the identified degenerative, deformation and dystrophic changes in the osteochondral structures of the spine.

Code M 54.5. in the international classification of diseases, vertebrogenic lumbodynia is designated. This is not an independent disease, therefore this code is used only for the primary designation of pathology, and after the diagnosis, the doctor enters the code of the underlying disease into the card and sick leave sheet, which became the root cause of the pain syndrome (in most cases, it is chronic osteochondrosis).

Lumbodynia is one of the types of dorsopathy (back pain). The terms "dorsopathy" and "dorsalgia" are used in modern medicine to refer to any pain localized in the region of the C3-S1 segment (from the third cervical vertebra to the first sacral vertebra).

Lumbodynia refers to acute, subacute or recurrent (chronic) pain in the lower back segment - in the region of the lumbosacral vertebrae. Pain syndrome can be of moderate or high intensity, one-sided or two-sided course, local or diffuse manifestations.

Local pain on the one hand almost always indicates a focal lesion and occurs against the background of compression of the spinal nerves and their roots. If the patient cannot accurately describe exactly where the pain occurs, that is, the discomfort seizes the entire lumbar region, there can be many reasons: from vertebral neurological pathologies to malignant tumors of the spine and small pelvis.

What symptoms are the basis for diagnosing lumbodynia?

Lumbodynia is a primary diagnosis that cannot be regarded as an independent disease and is used to indicate existing disorders, in particular, pain syndrome. The clinical significance of such a diagnosis is explained by the fact that this symptom is the basis for an X-ray and magnetic resonance examination of the patient in order to identify deformities of the spine and intervertebral discs, inflammatory processes in the paravertebral soft tissues, muscular-tonic status and various tumors.

The diagnosis of "vertebral lumbodynia" can be made by both a local therapist and narrow specialists (neurologist, orthopedic surgeon, vertebrologist) on the basis of the following symptoms:

severe pain (stabbing, cutting, shooting, aching) or burning in the lower back with a transition to the coccyx, located in the area of the intergluteal fold;
violation of sensitivity in the affected segment (feeling of heat in the lower back, tingling, chills, tingling);
reflection of pain in the lower extremities and buttocks (typical for the combined form of lumbodynia - with sciatica);
decreased mobility and muscle stiffness in the lower back;
increased pain syndrome after physical activity or physical activity;
relief of pain after prolonged muscle relaxation (at night).

In most cases, an attack of lumbodynia begins after exposure to any external factors, for example, hypothermia, stress, increased stress, but in an acute course, a sudden onset is possible for no apparent reason. In this case, one of the symptoms of lumbodynia is lumbago - acute lumbago in the lower back, arising spontaneously and always having a high intensity.

Reflex and pain syndromes in lumbodynia, depending on the affected segment

Despite the fact that the term "lumbodynia" can be used as an initial diagnosis in outpatient practice, the clinical course of pathology is of great importance for a comprehensive diagnosis of the condition of the spine and its structures. With lumbarization of various segments of the lumbosacral spine, the patient has a decrease in reflex activity, as well as paresis and reversible paralysis with different localization and manifestations. These features make it possible, even without instrumental and hardware diagnostics, to suggest in which particular part of the spine degenerative-dystrophic changes occurred.

The clinical picture of vertebral lumbodynia depending on the affected segment of the spine

Affected vertebrae	Possible irradiation (reflection) of low back pain	Additional symptoms
Second and third lumbar vertebrae.	The area of the hips and knee joints (along the front wall).	Flexion of the ankles and hip joints is impaired. Reflexes are usually preserved.
Fourth lumbar vertebra.	Popliteal fossa and lower leg area (mainly from the front).	Extension of the ankles is difficult, hip abduction provokes pain and discomfort. Most patients have a pronounced decrease in the knee reflex.
Fifth lumbar vertebra.	The entire surface of the leg, including the legs and feet. In some cases, pain may be reflected in the first toe.	Difficulty bending the foot forward and abducting the big toe.
Sacral vertebrae.	The entire surface of the leg from the inside, including the feet, heel bone and phalanges of the toes.	The Achilles tendon reflex and plantar flexion of the foot are impaired.

Important! In most cases, lumbodynia is manifested not only by reflex symptoms (this also includes neurodystrophic and vegetative-vascular changes), but also by radicular pathology that occurs against the background of pinched nerve endings.

Possible causes of pain

One of the main causes of acute and chronic lumbodynia in patients of various age groups is osteochondrosis. The disease is characterized by dystrophy of the intervertebral discs, which connect the vertebrae to each other in a vertical sequence and act as a shock absorber. A dehydrated nucleus loses its firmness and elasticity, which leads to thinning of the annulus fibrosus and displacement of the pulp outside the end of the cartilaginous plates. This displacement can take two forms:

Neurological symptoms in attacks of lumbodynia are provoked by compression of the nerve endings that extend from the nerve trunks located along the central spinal canal. Irritation of the receptors located in the nerve bundles of the spinal nerves leads to attacks of severe pain, which most often has an aching, burning or shooting character.

Lumbodynia is often confused with radiculopathy, but these are different pathologies. (radicular syndrome) is a complex of pain and neurological syndromes, which are directly caused by compression of the nerve roots of the spinal cord. With lumbodynia, pain can also be caused by myofascial syndromes, circulatory disorders, or mechanical irritation of pain receptors by osteochondral structures (for example, osteophytes).

Other reasons

Other diseases can also be among the causes of chronic low back pain, which include the following pathologies:

diseases of the spine (displacement of the vertebrae, osteoarthritis, osteosclerosis, spondylitis, etc.);
neoplasms of various origins in the spine and pelvic organs;
infectious and inflammatory pathologies of the spine, abdominal and pelvic organs (spondylodiscitis, epiduritis, osteomyelitis, cystitis, pyelonephritis, etc.);
adhesion process in the small pelvis (adhesions are often formed after difficult childbirth and surgical interventions in this area);
injuries and injuries of the lower back (fractures, dislocations, bruises);
Swelling and bruising are the main symptoms of a bruised lower back
pathology of the peripheral nervous system;
myofascial syndrome in myogellosis (the formation of painful seals in the muscles with inadequate physical activity, not appropriate for the age and physical fitness of the patient).

The provoking factors that increase the risk of lumbodynia may be obesity, alcohol and nicotine abuse, increased consumption of caffeinated drinks and foods, and chronic lack of sleep.

The factors for the development of acute shooting pain (lumbago) are usually strong emotional experiences and hypothermia.

Important! Lumbodynia during pregnancy is diagnosed in almost 70% of women. If the expectant mother did not have any abnormalities in the work of internal organs or diseases of the musculoskeletal system that can aggravate under the influence of hormones, the pathology is considered physiologically determined. Lower back pain in pregnant women can occur as a result of irritation of the nerve endings by an enlarging uterus or be the result of edema in the pelvic organs (edematous tissues squeeze the nerves and blood vessels, provoking severe painful sensations). There is no specific treatment for physiological lumbodynia, and all recommendations and appointments are aimed primarily at correcting nutrition, lifestyle and adherence to the daily regimen.

Is it possible to get a sick leave for severe lower back pain?

Disease under the code M 54.5. is the basis for opening a sick leave due to temporary disability. The length of the sick leave depends on various factors and can range from 7 to 14 days. In especially severe cases, when the pain syndrome is combined with severe neurological disorders and interferes with the patient's professional duties (and also temporarily restricts the ability to move and full self-care), the sick leave can be extended up to 30 days.

The main factors affecting the duration of the sick leave for lumbodynia are:

the intensity of the pain. This is the main indicator that a doctor evaluates when deciding on a person's ability to return to work. If the patient cannot move, or the movements cause him severe pain, the sick leave will be extended until these symptoms regress;
working conditions. Office workers usually return to work earlier than those doing hard physical work. This is due not only to the peculiarities of the motor activity of these categories of employees, but also to the possible risk of complications in case of incomplete relief of the causes that caused the onset of pain;
the presence of neurological disorders. If a patient complains of any neurological disorders (poor sensitivity in the legs, fever in the lower back, tingling in the extremities, etc.), the sick leave is usually extended until the possible reasons are fully clarified.

Patients who need hospitalization are issued a sick leave from the moment they are admitted to the hospital. If it is necessary to continue outpatient treatment, the temporary disability certificate is extended for an appropriate period.

Important! If surgical treatment is necessary (for example, with intervertebral hernias larger than 5-6 mm), a sick leave is issued for the entire period of hospitalization, as well as subsequent recovery and rehabilitation. Its duration can be from 1-2 weeks to 2-3 months (depending on the main diagnosis, the chosen method of treatment, the rate of tissue healing).

Limited ability to work with lumbodynia

It is important for patients with chronic lumbodynia to understand that closing a sick leave does not always mean complete recovery (especially if the pathology is provoked by osteochondrosis and other diseases of the spine). In some cases, with vertebral lumbodynia, the doctor may recommend light labor to the patient, if the previous working conditions can complicate the course of the underlying disease and cause new complications. You should not ignore these recommendations, since vertebrogenic pathologies almost always have a chronic course, and hard physical labor is one of the main factors in the exacerbation of pain and neurological symptoms.

Typically, people with disabilities are recognized as representatives of the professions indicated in the table below.

Professions requiring facilitated working conditions in patients with chronic lumbodynia

Professions (positions)	Reasons for limited work ability
	Forced inclined position of the body (disrupts blood circulation in the lumbar region, enhances muscle tension, enhances compression of nerve endings).
	Lifting weights (can provoke an increase in hernia or protrusion, as well as rupture of the fibrous membrane of the intervertebral disc).
	Prolonged sitting (increases the intensity of the pain syndrome due to severe hypodynamic disorders).
	Prolonged stay on the legs (increases tissue swelling, enhances neurological symptoms in lumbodynia).
	High risk of falling back and spinal injury.

Can you serve in the army?

Lumbodynia is not included in the list of restrictions for military service, however, a conscript may be deemed unfit for military service due to an underlying disease, for example, grade 4 osteochondrosis, pathological kyphosis of the lumbar spine, spondylolisthesis, etc.

Treatment: methods and drugs

Treatment of lumbodynia always begins with the relief of inflammatory processes and the elimination of painful sensations. In most cases, anti-inflammatory drugs with analgesic effects from the NSAID group ("Ibuprofen", "Ketoprofen", "Diclofenac", "Nimesulide") are used for this.

The most effective regimen is a combination of oral and local dosage forms, but with moderate lumbodynia, it is better to refuse taking pills, since almost all drugs in this group negatively affect the mucous membranes of the stomach, esophagus and intestines.

Back pain bothers most people, regardless of their age or gender. In case of severe pain, injection therapy can be performed. We recommend that you read, which provides detailed information on injections for back pain: classification, purpose, effectiveness, side effects.

As auxiliary methods for the complex treatment of lumbodynia, the following can also be used:

drugs for normalizing muscle tone, improving blood flow and restoring cartilaginous nutrition of intervertebral discs (microcirculation correctors, muscle relaxants, chondroprotectors, vitamin solutions);
paravertebral blockade with novocaine and glucocorticoid hormones;
massage;
manual therapy (methods of traction traction, relaxation, manipulation and mobilization of the spine;
acupuncture;

In the absence of the effect of conservative therapy, surgical methods of treatment are used.

Video - Exercises for quick treatment of lower back pain

Lumbodynia is one of the most common diagnoses in neurological, surgical and neurosurgical practice. Pathology with strong severity is the basis for issuing a sheet of temporary disability. Despite the fact that vertebrogenic lumbodynia has its own code in the international classification of diseases, treatment is always aimed at correcting the underlying disease and may include medication, physiotherapy, manual therapy, exercise therapy and massage.

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Sharp pain.
Acute pain is defined as pain that is short in duration with an easily identifiable cause. Acute pain is a warning to the body about the current danger of organic damage or disease. Often persistent and sharp pain is also accompanied by aching pain. Acute pain usually concentrates in a specific area before it somehow spreads more widely. This type of pain usually responds well to treatment.
Chronic pain.
Chronic pain was originally defined as pain that lasts about 6 months or more. It is now defined as pain that persists for longer than the appropriate length of time during which it should normally be completed. It is often more difficult to heal than acute pain. Particular attention is required when addressing any pain that has become chronic. In exceptional cases, neurosurgeons can perform a complex operation to remove parts of the patient's brain to cope with chronic pain. Such an intervention can relieve the patient of the subjective sensation of pain, but since the signals from the painful focus will still be transmitted through neurons, the body will continue to respond to them.
Skin pain.
Skin pain occurs when the skin or subcutaneous tissue is damaged. Cutaneous nociceptors terminate just below the skin and, due to the high concentration of nerve endings, provide a highly precise, localized sensation of pain of short duration.
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Somatic pain.
Somatic pain occurs in ligaments, tendons, joints, bones, blood vessels, and even in the nerves themselves. It is determined by somatic nociceptors. Due to the lack of pain receptors in these areas, they produce dull, poorly localized, more prolonged pain than skin pain. This includes, for example, joint sprains and broken bones.
Internal pain.
Internal pain arises from the internal organs of the body. Internal nociceptors are located in organs and internal cavities. An even greater lack of pain receptors in these parts of the body leads to the appearance of more nagging and prolonged pain compared to somatic pain. Internal pain is particularly difficult to localize, and some internal organic lesions are "attributed" pains where pain is ascribed to an area of the body that has nothing to do with the site of the injury itself. Cardiac ischemia (insufficient blood in the heart muscle) is perhaps the best-known example of attributed pain; the sensation may be located as a separate sensation of pain just above the rib cage, in the left shoulder, arm, or even in the palm. The pain attributed may be attributed to the discovery that pain receptors in internal organs also excite spinal neurons, which are fired when skin lesions occur. After the brain begins to associate the excitation of these spinal neurons with the stimulation of somatic tissues in the skin or muscles, pain signals coming from the internal organs are interpreted by the brain as coming from the skin.
Phantom pain.
Phantom limb pain is a sensation of pain that occurs in a missing limb or limb that is not felt through normal sensations. This phenomenon is almost always associated with cases of amputation and paralysis.
Neuropathic pain.
Neuropathic pain ("neuralgia") can result from damage or disease to the nerve tissues themselves (eg, toothache). This can disrupt the ability of the sensory nerves to transmit correct information to the thalamus (a section of the diencephalon), and hence the brain misinterprets pain stimuli, even if there are no obvious physiological causes of pain.
Psychogenic pain.
Psychogenic pain is diagnosed in the absence of an organic disease or in the case when the latter cannot explain the nature and severity of the pain syndrome. Psychogenic pain is always chronic and occurs against the background of mental disorders: depression, anxiety, hypochondria, hysteria, phobia. In a significant part of patients, psychosocial factors play an important role (dissatisfaction with work, the desire to obtain moral or material benefits). There are especially strong links between chronic pain and depression.

Spontaneous attacks of pain in the tooth associated with inflammation of the pulp. Constant pain localized in the area of one tooth, often pulsating, aggravated by touching the tooth, is associated with inflammation of the periapical tissues. Acute toothache can also be caused by periodontitis, exacerbations of which are accompanied by the formation of periodontal abscesses.

The projection zones of toothache are irradiated on the skin and zones up to 4 minutes on the field. The total irradiation time is up to 15 minutes.

Modes of action of the crown of the tooth in the treatment of acute pain The duration of treatment is determined by the onset of positive dynamics. It should be noted that even after effective relief of pain syndrome, it is imperative to go to the dentist for specialized help.

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Description of dental lesions in relation to the classification of caries according to ICD 10

The caries grading system is designed to rank the extent of the lesion. She helps to choose a technique for further treatment.

Caries is one of the most famous and common dental diseases in the world. If tissue damage is found, compulsory dental treatment is required to prevent further destruction of the elements of the dentition.

General information

Doctors have repeatedly attempted to create a unified, universal system for classifying human diseases.

As a result, in the XX century, the "International Classification - ICD" was developed. Since the creation of a unified system (in 1948), it has been constantly revised and supplemented with new information.

The final, 10th revision was carried out in 1989 (hence the name - ICD-10). Already in 1994, the International Classification began to be used in countries that are members of the World Health Organization.

In the system, all diseases are divided into sections and marked with a special code. Diseases of the oral cavity, salivary glands and jaws K00-K14 belong to the category of diseases of the digestive system K00-K93. It describes all dental pathologies, not just caries.

K00-K14 includes the following list of pathologies related to dental lesions:

Item K00. Developmental and teething problems. Adentia, the presence of extra teeth, anomalies in the appearance of teeth, mottling (fluorosis and other darkening of the enamel), abnormalities in the formation of teeth, hereditary underdevelopment of teeth, problems with teething.
Item K01. Retained (immersed) teeth, i.e. changed position during eruption, with or without an obstacle.
Paragraph K02. All types of caries. Enamels, dentine, cement. Suspended caries. Pulp exposure. Odontoclasia. Other types.
Paragraph K03. Various lesions of hard tissues of teeth. Abrasion, grinding of enamel, erosion, granuloma, cement hyperplasia.
Paragraph K04. Lesion of the pulp and periapical tissues. Pulpitis, pulpal degeneration and gangrene, secondary dentin, periodontitis (acute and chronic apical), periapical abscess with and without cavity, various cysts.
Paragraph K06. Pathology of the gums and the edge of the alveolar ridge. Recession and hypertrophy, trauma to the alveolar margin and gums, epulis, atrophic ridge, various granulomas.

Paragraph K07. Changes in the bite and various anomalies of the jaw. Hyperplasia and hypopalsia, macrognathia and micrognathia of the upper and lower jaws, asymmetry, prognathia, retrognathia, all types of malocclusion, torsion, diastema, tremes, displacement and rotation of teeth, transposition.

Improper closure of the jaws and acquired malocclusion. Diseases of the temporomandibular joint: laxity, clicking when opening the mouth, pain dysfunction of the TMJ.

Paragraph K08. Functional problems with the supporting apparatus and changes in the number of teeth due to external factors. Loss of teeth due to trauma, extraction, or illness. Atrophy of the alveolar ridge due to the long absence of a tooth. Pathology of the alveolar ridge.

Let's take a closer look at section K02 Dental caries. If the patient wants to find out what the dentist made in the card after the tooth treatment, you need to find the code among the subsections and study the description.

K02.0 Enamels

Initial caries or chalk stain is the primary form of the disease. At this stage, there is still no damage to hard tissues, but demineralization and a high susceptibility of enamel to irritation are already diagnosed.

In dentistry, 2 forms of initial caries are determined:

Active (white spot);
Stable (brown spot).

Caries in an active form during treatment can become stable or disappear completely.

The brown spot is irreversible, you can get rid of the problem only by preparation with filling.

Symptoms:

Pain - toothache is not typical for the initial stage. However, due to the fact that enamel demineralization occurs (its protective function decreases), a strong susceptibility to influences may be felt in the affected area.
External violations - visible when caries is located on one of the teeth of the outer row. Looks like an inconspicuous patch of white or brown.

Treatment directly depends on the specific stage of the disease.

When the stain is chalky, remineralizing treatment and fluoridation are prescribed. When the caries is pigmented, preparation and filling are performed. With timely treatment and oral hygiene, a positive prognosis is expected.

K02.1 Dentin

A huge number of bacteria live in the mouth. As a result of their vital activity, organic acids are released. They are responsible for the destruction of the basic mineral components that make up the enamel crystal lattice.

Dentin caries is the second stage of the disease. It is accompanied by a violation of the structure of the tooth with the appearance of a cavity.

However, the hole is not always visible. Often, violations can be noticed only at the dentist's appointment when a probe is inserted for diagnosis. Sometimes you can notice caries on your own.

Symptoms:

the patient is uncomfortable to chew;
pain from temperatures (cold or hot food, sugary foods);
external disorders that are especially visible on the front teeth.

Painful sensations can be triggered by one or several foci of the disease at once, but quickly disappear after the problem is eliminated.

There are only several types of dentin diagnostics - instrumental, subjective, objective. Sometimes it is difficult to detect a disease solely by the symptomatology described by the patient.

At this stage, you can no longer do without a drill. The doctor drills the aching teeth and places a filling. In the course of treatment, the specialist not only tries to preserve the tissues, but also the nerve.

K02.2 Cement

In comparison with damage to enamel (initial stage) and dentin, caries of the cement (root) is diagnosed much less often, but it is considered aggressive and harmful to the tooth.

The root is characterized by relatively thin walls, which means that the disease does not take much time for the complete destruction of tissues. All this can develop into pulpitis or periodontitis, which sometimes leads to tooth extraction.

Clinical symptoms depend on the location of the concentration of the focus of the disease. For example, when placing the cause in the periodontal region, when the swollen gum protects the root from other influences, we can talk about the closed form.

With this outcome, vivid symptoms are not observed. Usually, when the caries of the cement is closed, there is no pain or they are not expressed.

Photo of an extracted tooth with cement caries

With an open form, in addition to the root, the cervical region can also undergo destruction. The patient may be accompanied by:

External disturbances (especially pronounced in the front);
Inconvenience while eating;
Painful sensations from irritants (sweet, temperature, when food gets under the gum).

Modern medicine allows you to get rid of caries in several, and sometimes in one, dentist's appointment. Everything will depend on the form of the disease. If the gum closes the focus, bleeds or strongly interferes with the filling, then the gum correction is performed first.

After getting rid of soft tissues, the affected area (after or without exposure) is temporarily filled with cement and oily dentin. After the tissue has healed, the patient comes back for re-filling.

K02.3 Suspended

Suspended caries is a stable form of the initial stage of the disease. It manifests itself as a dense pigmentation spot.

Usually, such caries is asymptomatic, patients do not complain about anything. It is possible to detect the stain during a dental examination.

Caries is dark brown, sometimes black. The surface of the tissues is studied by probing.

Most often, the focus of stalled caries is located in the cervical part and natural cavities (fossae, etc.).

The method of treatment depends on various factors:

Spot sizes - too large formations are prepared and filled;
From the wishes of the patient - if the stain is on the outer teeth, then the damage is eliminated with photopolymer fillings so that the color matches the enamel.

Small dense foci of demineralization are usually found during a period of time with a frequency of several months.

If the teeth are properly cleaned, and the amount of carbohydrates consumed by the patient decreases, then there may be a halt in the future progressive development of the disease.

When the stain grows and becomes soft, it is dissected and filled.

K02.4 Odontoclasia

Odontoclasia is a severe form of damage to dental tissues. The disease affects the enamel, thinning it and leading to the formation of caries. No one is immune from odontoclasia.

The appearance and development of damage is influenced by a huge number of factors. Such prerequisites even include poor heredity, regularity of oral hygiene, chronic diseases, metabolic rate, and bad habits.

The main visible symptom of odontoclasia is toothache. In some cases, due to a non-standard clinical form or an increased pain threshold, the patient does not even feel this.

Then only the dentist will be able to make the correct diagnosis during the examination. The main visual sign of enamel problems is tooth damage.

This form of the disease, like other forms of tooth decay, is treatable. The doctor first cleans the affected area, then fills the painful area.

Only high-quality oral prophylaxis and regular examinations at the dentist will help to avoid the development of odontoclasia.

K02.5 Exposed pulp

All tooth tissues are destroyed, including the pulp chamber - the septum that separates dentin from the pulp (nerve). If the wall of the pulp chamber is rotten, then the infection penetrates into the soft tissues of the tooth and causes inflammation.

The patient feels severe pain when food and water gets into the carious cavity. After cleansing it, the pain recedes. In addition, in advanced cases, a specific odor from the mouth appears.

This condition is considered a deep caries and requires a long and expensive treatment: the obligatory removal of the "nerve", cleaning the canals, filling with gutta-percha. Several visits to the dentist are required.

Details of the treatment of all types of deep caries are described in a separate article.

Item added in January 2013.

K02.8 Another view

Another caries is a moderate or deep form of the disease that develops in a previously treated tooth (relapse or re-development near the filling).

Medium caries is the destruction of enamel elements on the teeth, accompanied by paroxysmal or persistent pain in the area of the focus. They are explained by the fact that the disease has already passed to the upper layers of dentin.

The form requires mandatory dental care, in which the doctor removes the affected areas, followed by their restoration and filling.

Deep caries is a form characterized by extensive damage to the internal dental tissues. It affects a large area of dentin.

The disease cannot be ignored at this stage, and failure to treat can lead to nerve (pulp) damage. In the future, if you do not use medical help, pulpitis or periodontitis develops.

The affected area is completely removed with subsequent restorative filling.

K02.9 Unspecified

Unspecified caries is a disease that develops not on living, but on pulped teeth (those from which a nerve has been removed). The reasons for the formation of this form do not differ from standard factors. Usually, unspecified caries occurs at the junction of the filling and the infected tooth. Its appearance in other places of the oral cavity is observed much less often.

The fact that a tooth is dead does not protect it from the development of caries. Teeth depend on the presence of sugar to enter the oral cavity along with food and bacteria. After the bacteria are saturated with glucose, the formation of acid begins, leading to the formation of dental plaque.

Caries of a pulped tooth is treated according to the standard scheme. However, in this case, there is no need to use pain relief. The nerve responsible for pain is no longer in the tooth.

Prophylaxis

The condition of the dental tissue is strongly influenced by the human diet. To prevent tooth decay, you need to follow some guidelines:

eat less sweet, starchy foods;
balance the diet;
monitor vitamins;
chew food well;
rinse your mouth after eating;
brush your teeth regularly and correctly;
avoid the simultaneous intake of cold and hot food;
periodically inspect and sanitize the oral cavity.

The video provides additional information on the topic of the article.

Timely treatment will help you get rid of caries quickly and painlessly. Preventive measures prevent damage to the enamel. It is always better not to cause illness than to cure it.

If you find an error, please select a piece of text and press Ctrl + Enter.

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Other changes in teeth and their supporting apparatus

ICD-10 → K00-K93 → K00-K14 → K08.0

Exfoliation of teeth due to systemic disorders

Loss of teeth due to accident, extraction, or local periodontal disease

Atrophy of the edentulous alveolar ridge

Retaining dental root [retention root]

K08.8 was last modified: January 2011

Unspecified changes in teeth and their supporting structures

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International Statistical Classification of Diseases and Related Health Problems. 10th revision.

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Acute toothache - Dolor dentalis acutus

Acute toothache is understood as a sudden sharp painful sensation in the teeth or alveolar processes.

ETIOLOGY AND PATHOGENESIS

Pain syndrome is a constant companion of most diseases of the maxillofacial region, which is determined by the rich mixed (somatic and vegetative) innervation of this area, leading to the intensity of pain and the possibility of its irradiation to various parts of the maxillofacial region. Some somatic diseases (neuralgia and neuritis of the trigeminal nerve, otitis media, sinusitis, myocardial infarction and other diseases) can simulate toothache, which makes it difficult to diagnose the existing pathology.

Acute toothache can occur with damage to the tissues of the tooth, oral mucosa, periodontal, bone.

■ Hyperesthesia of hard tissues of the tooth is often associated with defects in hard tissues (increased tooth wear, erosion of hard tissues, wedge-shaped defects, chemical damage to the enamel, gum recession, etc.).

■ Caries is a pathological process manifested by damage to the hard tissues of the tooth, their demineralization and softening with the formation of a cavity.

■ Pulpitis is an inflammation of the tooth pulp that occurs when microorganisms or their toxins, chemical irritants enter the tooth pulp (through the carious cavity, the apical opening of the tooth root, from the periodontal pocket, hematogenous), as well as with trauma to the tooth pulp.

■ Periodontitis - inflammation of the periodontium, which develops when microorganisms, their toxins, and pulp decay products enter the periodontium, as well as when a tooth is injured (contusion, dislocation, fracture).

■ Neuralgia of the trigeminal nerve is a polyetiological disease, in the genesis of which disturbances in the peripheral and central mechanisms of regulation of pain sensitivity are of great importance. With molar pathology, pain can spread to the temporal region, lower jaw, radiate to the larynx and ear, parietal region. With the defeat of the incisors and premolars, the pain can spread to the forehead, nose, and chin.

CLASSIFICATION

Acute toothache is classified by the nature of the pathological process that caused it.

■ Acute toothache caused by damage to hard tissues, tooth pulp and periodontal tissues, which requires outpatient treatment by a dentist.

■ Acute toothache caused by involvement of bone and bone marrow in the process, which requires urgent hospitalization in a dental surgery or maxillofacial surgery department.

CLINICAL PICTURE

Acute toothache can be of a different nature and occur in different situations, depending on which tissues and how much affected.

The nature of pain in the defeat of hard tissues depends on the depth of the pathological process.

■ With hyperesthesia of the enamel and superficial caries, the pain is acute, but short-term. It occurs when exposed to exogenous (temperature and chemical) irritants and stops after the source of irritation is eliminated. Examination of teeth with superficial caries reveals a shallow carious cavity within the enamel, with uneven edges. Probing can be painful.

■ With medium caries, enamel and dentin are affected, when probing, the cavity is deeper, pain arises not only from thermal and chemical, but also from mechanical stimuli, and disappears after they are eliminated.

■ With deep caries, when food enters the carious cavity, a short-term, acute toothache occurs, which disappears when the irritant is eliminated. Since with deep caries a thin layer of dentin remains, covering the dental pulp, the phenomena of focal pulpitis may develop.

■ Pulpitis is characterized by more intense pain than with caries, which can occur for no apparent reason.

□ In acute focal pulpitis, acute toothache is localized, paroxysmal, short-term (lasts a few seconds), occurs for no apparent reason, but can be prolonged when exposed to temperature stimuli, increases at night. The intervals between pain attacks are long.

Over time, the pain gets longer. The carious cavity is deep, the sounding of the bottom is painful.

□ In acute diffuse pulpitis, prolonged bouts of acute widespread toothache are noted, intensifying at night, radiating along the branches of the trigeminal nerve, with short periods of remission. The carious cavity is deep, the sounding of the bottom is painful.

□ With the development of a chronic process (chronic fibrous pulpitis, chronic hypertrophic pulpitis, chronic gangrenous pulpitis), the intensity of the pain syndrome decreases, the pain becomes aching chronic, often occurs only when eating and brushing teeth.

■ In acute periodontal disease and exacerbation of chronic periodontitis, the patient complains of constant localized pain of varying intensity, aggravated by eating and percussion, the feeling that the tooth has "grown" has become, as it were, higher. Examination of the oral cavity reveals hyperemia and swelling of the gums, its pain on palpation. With an exacerbation of chronic periodontitis, there may be a fistulous course with purulent discharge.

Percussion of the affected tooth is painful; probing can reveal an opened tooth cavity. In the future, the general condition worsens, collateral edema of the soft tissues of the face appears, sometimes enlarged, painful submandibular lymph nodes are palpable. With chronic periodontitis, the pain is less severe. Constant breaking pain in the area of the affected tooth may be troubling, but in some patients it is absent.

■ With trigeminal neuralgia, paroxysmal twitching, cutting, burning pains appear in a specific area of the face, corresponding to the innervation zone of one or more branches of the trigeminal nerve.

Severe pain does not allow the patient to talk, wash, eat for fear of provoking a new attack. The attacks come on suddenly and also stop. They can be accompanied by vegetative manifestations (hyperemia in the innervation area of the affected branch of the trigeminal nerve, dilated pupil on the affected side, increased saliva, lacrimation) and contraction of facial muscles. With neuralgia of the second branch of the trigeminal nerve, pain syndrome can spread to the teeth of the upper jaw, and with neuralgia of the third branch of the trigeminal nerve, to the teeth of the lower jaw.

When palpating the innervation zone of the corresponding branch of the trigeminal nerve, hyperesthesia of the facial skin can be detected, and when pressing on the pain points, an attack of neuralgia is provoked. A characteristic feature of trigeminal neuralgia is the absence of pain during sleep.

Characteristics and localization of pain in diseases of the maxillofacial region are given below.

■ Superficial caries. Pain sensations can be of varying intensity and have a paroxysmal nature: short-term localized (in the area of the causative tooth) pain occurs under the action of chemical, thermal, less often mechanical stimuli and disappears after the stimulus is removed.

■ Medium caries. The pain is usually dull, short-term, localized in the area of the causative tooth, arises under the action of chemical, thermal, less often mechanical stimuli and disappears after the stimulus is removed.

■ Deep caries is characterized by the occurrence of acute localized (in the area of the causative tooth) intense pain when food enters the carious cavity, which disappears after the stimulus is removed.

■ Acute focal pulpitis. Disturbed by a short-term localized (in the area of the causative tooth) intense acute pain, which has a spontaneous paroxysmal nature. The pain is worse at night.

■ Acute diffuse pulpitis. The pain is intense, prolonged, has an acute spontaneous character. The pain is not localized, radiates along the branches of the trigeminal nerve and intensifies at night.

■ Acute periodontitis and exacerbation of chronic periodontitis are characterized by acute paroxysmal, pulsating prolonged (with rare intervals of remission) pain. The pain is localized in the area of the causative tooth, has a different intensity, increases with food and percussion of the affected tooth. The patient notes the feeling that the tooth has "grown".

■ Neuralgia of the trigeminal nerve. The pain is acute, paroxysmal, often occurs when talking and when touching the skin of the face. The pain is not localized, radiates along the branches of the trigeminal nerve. Painful sensations are intense, weaken or stop at night, are usually short-term.

DIFFERENTIAL DIAGNOSTICS

Differential diagnosis of lesions of hard tissues and dental pulp is not indicated in the provision of emergency medical care.

To resolve the issue of hospitalization of a patient at the prehospital stage, differential diagnosis of acute osteomyelitis with acute purulent periostitis and exacerbation of chronic periodontitis is important.

■ Acute periodontitis. Characterized by constant localized pain of varying intensity, aggravated by eating and percussion of the affected tooth. The patient complains of the feeling that the tooth has "grown", sleep disturbance. With an objective examination, a deterioration in the general condition of the patient is noted, an increase in body temperature, an increase in regional lymph nodes are possible. Examination of the oral cavity reveals hyperemia and swelling of the gingival mucosa, its pain on palpation; the presence of a fistulous tract with purulent discharge is possible.

Therapeutic or surgical outpatient treatment is indicated.

■ In acute purulent periostitis, severe, sometimes pulsating pain occurs. On physical examination, an increase in body temperature, collateral edema of the surrounding tissues, and an increase in regional lymph nodes are noted. Examination of the oral cavity reveals swelling and hyperemia of the mucous membrane of the gum edge, smoothness and hyperemia of the transitional fold. Outpatient emergency surgical treatment is indicated.

■ In acute osteomyelitis, the patient complains of pain in the area of the causative tooth, which quickly spreads and intensifies. On physical examination, marked intoxication, increased body temperature, chills, weakness, collateral edema of the surrounding tissues, an increase in regional lymph nodes; in severe cases, pus can spread into the surrounding soft tissues with the development of phlegmon. Examination of the oral cavity reveals hyperemia and swelling of the mucous membrane in the area of the gum edge. Urgent hospitalization and surgical treatment in a hospital with subsequent conservative therapy are shown.

CALLER TIPS

■ At normal body temperature and the absence of collateral edema, the patient should be given NSAIDs (ketoprofen, ketorolac, lornoxicam, paracetamol, revalgin, solpadein, ibuprofen, indomethacin, etc.) to alleviate the condition, then consult a dentist.

■ In case of elevated body temperature and the presence of collateral tissue edema, an urgent need to consult a dental surgeon.

■ In case of high body temperature, severe intoxication, chills, collateral edema, enlargement of regional lymph nodes, urgent hospitalization of the patient in a specialized surgical department is necessary.

CALL ACTIONS

Diagnostics

MANDATORY QUESTIONS

■ How does the patient feel?

■ What is your body temperature?

■ How long has the tooth hurt?

■ Have you had bouts of acute tooth pain before?

■ Is there swelling of the gums or face?

■ What pain is felt: in a particular tooth or is the pain radiating?

■ Does the pain occur spontaneously or under the influence of any irritants (food, cold air, cold or hot water)?

■ Does the pain stop when the stimulus stops?

■ What is the nature of the pain (acute, dull, aching, paroxysmal or persistent, long-term or short-term)?

■ Is it difficult to eat?

■ Does the nature of pain change at night?

■ Are there functional disorders of the dentition (mouth opening, talking, etc.)?

In cases where there is diffuse pain and collateral tissue edema, it is necessary to find out the following points.

■ Are there soft tissue swelling, infiltrates, or pus?

■ Are you worried about general weakness?

■ Did your body temperature rise?

■ Are you worried about the chills?

■ How does the mouth open?

■ Is swallowing difficult?

■ Has the patient taken any drugs?

■ Is the pain relieved by the used drugs (NSAIDs)?

INSPECTION AND PHYSICAL EXAMINATION

Examination of a patient with acute toothache includes several stages.

■ External examination of the patient (facial expression and symmetry, teeth closing, skin coloration).

■ Examination of the oral cavity.

□ Condition of teeth (carious teeth, enamel hypoplasia, wedge-shaped defect, fluorosis, increased enamel abrasion).

□ The condition of the gum edge (hyperemia, swelling, bleeding, the presence of a periodontal pocket, fistulous passage, etc.).

□ Condition of the oral mucosa.

■ Palpation of soft tissues and bones of the maxillofacial region, regional submandibular and submental lymph nodes, as well as lymph nodes in the neck and supraclavicular regions.

■ Identification of specific symptoms of neuralgia.

Determination of facial skin hyperesthesia.

Provoking an attack of trigeminal neuralgia by pressing on the pain points (the first in the infraorbital region, 1 cm below the edge of the orbit along the pupillary line, the second on the lower jaw, below 4-5 teeth, in the projection of the chin foramen).

INSTRUMENTAL STUDIES

It is not performed at the prehospital stage.

The main task in the provision of emergency medical care to a patient with acute toothache at the prehospital stage is the identification of patients with acute osteomyelitis and their urgent hospitalization. To relieve acute toothache, NSAIDs are prescribed.

INDICATIONS FOR HOSPITALIZATION

Patients with severe symptoms of intoxication, an increase in body temperature up to 38 ° C and above, chills, weakness, collateral edema of surrounding tissues, an increase in regional lymph nodes are shown urgent hospitalization in a surgical dental hospital or the department of maxillofacial surgery.

■ Patients with acute purulent periostitis are shown the appointment of NSAIDs for pain relief and antibacterial drugs and a recommendation to urgently consult a dental surgeon for outpatient care.

COMMON ERRORS

■ Insufficiently complete collection of anamnesis.

■ Incorrect assessment of the prevalence and severity of the inflammatory process.

■ Incorrectly carried out differential diagnostics, leading to errors in the diagnosis and treatment tactics.

■ Prescribing drugs without taking into account the somatic condition and the drug therapy used by the patient.

■ Unreasonable prescription of antibacterial drugs and glucocorticoids.

METHOD OF APPLICATION AND DOSES OF MEDICINES The method of administration and doses of drugs are given below. ■ Diclofenac is administered orally at a dose of 25-50 mg (for pain syndrome up to 75 mg once) 2-3 times a day. The maximum daily dose is 150 mg. ■ Ibuprofen is prescribed by mouth at a dose of 200-400 mg 3-4 times a day. The maximum daily dose is 3 g. ■ Indomethacin is administered orally at a dose of 25 mg 3-4 times a day. The maximum daily dose is 200 mg. ■ Ketoprofen is prescribed orally at a dose of 30-50 mg 3-4 times a day, rectally 100 mg 2-3 times a day, i / m 100 mg 1-2 times a day and i / v 100-200 mg / days The maximum daily dose is 300 mg. ■ Ketorolac: to relieve severe pain, the first dose of 10-30 mg is injected intramuscularly, then 10 mg orally 4-6 times a day. The maximum daily dose is 90 mg. ■ Lornoxicam is prescribed orally, intramuscularly and intravenously at a dose of 8 mg 2 times a day. The maximum daily dose is 16 mg. ■ Paracetamol is prescribed by mouth 500 mg 4 times a day. The maximum daily dose is 4 g. ■ Revalgin * is prescribed by mouth in a dose of 1-2 tablets 2-3 times a day. The maximum daily dose is 6 tablets.

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By its biological origin, pain is a signal of danger and trouble in the body, and in medical practice such pain is often considered as a symptom of any disease that occurs when tissue is damaged due to trauma, inflammation or ischemia. The formation of pain is mediated by the structures of the nociceptive system. Without the normal functioning of systems that ensure the perception of pain, the existence of humans and animals is impossible. The sensation of pain forms a whole complex of protective reactions aimed at eliminating damage.

Pain is the most frequent and subjectively difficult complaint of patients. It causes suffering to many millions of people around the world, significantly worsening the conditions for human existence. To date, it has been proven that the nature, duration and intensity of pain sensations depend not only on the damage itself, but also largely determined by unfavorable life situations, social and economic problems. Within the framework of the biopsychosocial model, pain is considered as the result of a two-way dynamic interaction of biological (neurophysiological), psychological, social, religious and other factors. The result of this interaction will be the individual nature of the pain sensation and the form of the patient's response to pain. In accordance with this model, behavior, emotions and even simple physiological reactions change depending on the person's attitude to the events taking place. Pain is the result of simultaneous dynamic processing of impulses from nociceptors and a large number of other incoming exteroceptive (auditory, visual, olfactory) and interoceptive (visceral) signals. Therefore, pain is always subjective and each person experiences it in his own way. The same irritation can be perceived by our consciousness in different ways. The perception of pain depends not only on the place and nature of the injury, but also on the conditions or circumstances under which the injury occurred, on the psychological state of a person, his individual life experience, culture, and national traditions.

Psychological and social problems can have a significant impact on a person's experience of pain. In these cases, the intensity and duration of pain may exceed its signaling function and may not correspond to the degree of damage. This pain becomes pathological. Pathological pain (pain syndrome), depending on the duration, is divided into acute and chronic pain. Acute pain is new, recent pain that is inextricably linked to the injury that caused it and is usually a symptom of a medical condition. Acute pain usually disappears when the injury is repaired. Treatment of such pain is usually symptomatic, and, depending on its intensity, either non-narcotic or narcotic analgesics are used. The course of pain in the form of a symptom accompanying the underlying disease is favorable. When the function of damaged tissues is restored, pain symptoms also disappear. However, in some patients, the duration of pain may exceed the duration of the underlying disease. In these cases, pain becomes the leading pathogenic factor, causing serious disturbances in many body functions and shortening the life expectancy of patients. According to the European Epidemiological Study, the incidence of chronic non-cancer pain syndromes in Western Europe is about 20%, that is, every fifth European adult suffers from chronic pain syndrome.

Among chronic pain syndromes, the most widespread are pains associated with joint diseases, back pain, headaches, musculoskeletal pains, neuropathic pains. Doctors are faced with a situation in which the identification and elimination of damage is not accompanied by the disappearance of the pain syndrome. In conditions of chronic pain syndrome, as a rule, there is no direct connection with organic pathology, or this connection has an unclear, indefinite character. According to the definition of experts of the International Association for the Study of Pain, chronic pain refers to pain lasting more than three months and continuing beyond the normal period of tissue healing. Chronic pain began to be considered not as a symptom of any disease, but as an independent disease requiring special attention and complex etiopathogenetic treatment. The problem of chronic pain, due to the high prevalence and variety of forms, is so important and significant that in many countries specialized analgesic centers and clinics have been created to treat patients with pain syndromes.

What underlies the chronicity of pain and why is chronic pain resistant to the action of classic analgesics? The search for answers to these questions is of extreme interest for researchers and doctors and largely determines the current trends in the study of the problem of pain.

All pain syndromes, depending on the etiopathogenesis, can be conditionally divided into three main groups: nociceptive, neuropathic and psychogenic (pain of a psychological nature). In real life, these pathophysiological variants of pain syndromes often coexist.

Nociceptive pain syndromes

Nociceptive pains are considered as arising from tissue damage followed by activation of nociceptors - free nerve endings that are activated by various damaging stimuli. Examples of such pain are postoperative pain, pain in trauma, angina pectoris in patients with coronary heart disease, epigastric pain in gastric ulcer, pain in patients with arthritis and myositis. In the clinical picture of nociceptive pain syndromes, zones of primary and secondary hyperalgesia (areas with increased pain sensitivity) are always found.

Primary hyperalgesia develops in the area of tissue damage, the area of secondary hyperalgesia extends to healthy (intact) areas of the body. The development of primary hyperalgesia is based on the phenomenon of sensitization of nociceptors (an increase in the sensitivity of nociceptors to the action of damaging stimuli). Sensitization of nociceptors occurs due to the action of substances with a pro-inflammatory effect (prostaglandins, cytokines, biogenic amines, neurokinins, etc.) and coming from blood plasma, released from damaged tissue, as well as secreted from peripheral terminals of C-nociceptors. These chemical compounds, interacting with the corresponding receptors located on the membrane of nociceptors, make the nerve fiber more excitable and more sensitive to external stimuli. The presented mechanisms of sensitization are characteristic of all types of nociceptors localized in any tissue, and the development of primary hyperalgesia is noted not only in the skin, but also in muscles, joints, bones and internal organs.

Secondary hyperalgesia occurs as a result of central sensitization (increased excitability of nociceptive neurons in the structures of the central nervous system). The pathophysiological basis of sensitization of central nociceptive neurons is the long-term depolarizing effect of glutamate and neurokinins released from the central terminals of nociceptive afferents due to intense constant impulses coming from the area of damaged tissues. The resulting increased excitability of nociceptive neurons can persist for a long time, contributing to the expansion of the area of hyperalgesia and its spread to healthy tissues. The severity and duration of sensitization of peripheral and central nociceptive neurons directly depend on the nature of tissue damage, and in the case of tissue healing, the phenomenon of peripheral and central sensitization disappears. In other words, nociceptive pain is a symptom that occurs when tissue is damaged.

Neuropathic pain syndromes

Neuropathic pain, as defined by the International Association for the Study of Pain experts, is a consequence of primary damage or dysfunction of the nervous system, however, at the 2nd International Congress on Neuropathic Pain (2007), the definition was changed. According to the new definition, neuropathic pain refers to pain arising from direct injury or disease of the somatosensory system. Clinically, neuropathic pain is manifested by a combination of negative and positive symptoms in the form of partial or complete loss of sensitivity (including pain) with the simultaneous occurrence in the affected area of unpleasant, often pronounced pain sensations in the form of allodynia, hyperalgesia, dysesthesia, hyperpathy. Neuropathic pain can occur both with damage to the peripheral nervous system and the central structures of the somatosensory analyzer.

The pathophysiological basis of neuropathic pain syndromes is a violation of the mechanisms of generation and conduction of nociceptive signals in nerve fibers and the processes of control of the excitability of nociceptive neurons in the structures of the spinal cord and brain. Nerve damage leads to structural and functional transformations in the nerve fiber: the number of sodium channels on the membrane of the nerve fiber increases, new atypical receptors and zones of ectopic impulse generation appear, mechanosensitivity occurs, conditions are created for cross-excitation of dorsal ganglion neurons. All of the above forms an inadequate response of the nerve fiber to stimulation, contributing to a significant change in the pattern of the transmitted signal. Enhanced impulses from the periphery disorganize the work of central structures: sensitization of nociceptive neurons occurs, death of inhibitory interneurons, neuroplastic processes are initiated, leading to new interneuronal contacts of tactile and nociceptive afferents, and the efficiency of synaptic transmission increases. In these conditions, the formation of pain is facilitated.

However, damage to the peripheral and central structures of the somatosensory system, in our opinion, cannot be considered as a direct independent cause of neuropathic pain, but is only a predisposing factor. The basis for such reasoning is the data indicating that neuropathic pain does not always occur, even in the presence of clinically confirmed damage to the structures of the somatosensory analyzer. Thus, transection of the sciatic nerve leads to pain behavior in only 40-70% of rats. Spinal cord injury with symptoms of hypalgesia and thermal hypesthesia is accompanied by central pain in 30% of patients. No more than 8% of patients who have suffered a cerebral stroke with a deficiency of somatosensory sensitivity experience neuropathic pain. Postherpetic neuralgia, depending on the age of patients, develops in 27-70% of patients who have undergone shingles.

Neuropathic pain in patients with clinically verified sensory diabetic polyneuropathy is observed in 18-35% of cases. Conversely, in 8% of cases, patients with diabetes mellitus present with clinical symptoms of neuropathic pain in the absence of signs of sensory polyneuropathy. Considering also that the severity of pain symptoms and the degree of sensitivity disorders in the vast majority of patients with neuropathies are not interrelated, it can be assumed that damage to the somatosensory nervous system is not enough for the development of neuropathic pain, and a number of conditions are required that lead to a violation of integrative processes in the field of systemic regulation of pain. sensitivity. That is why in the definition of neuropathic pain, along with an indication of the root cause (damage to the somatosensory nervous system), either the term "dysfunction" or "dysregulation" should be present, reflecting the importance of neuroplastic reactions that affect the stability of the pain sensitivity regulation system to the action of damaging factors. In other words, a number of individuals initially have a predisposition to the development of stable pathological conditions, including in the form of chronic and neuropathic pain.

This is indicated by data on the existence in rats of various genetic lines of high and low resistance to the development of neuropathic pain syndrome after transection of the sciatic nerve. In addition, the analysis of diseases comorbid with neuropathic pain also indicates the initial failure of the regulatory systems of the body in these patients. In patients with neuropathic pain, the incidence of migraine, fibromyalgia, and anxiety-depressive disorders is significantly higher than in patients without neuropathic pain. In turn, in patients with migraine, the following diseases are comorbid: epilepsy, irritable bowel syndrome, stomach ulcer, bronchial asthma, allergies, anxiety and depressive disorders. Patients with fibromyalgia are more likely to suffer from hypertension, irritable bowel syndrome, osteoarthritis, anxiety and depressive disorders. The listed diseases, despite the variety of clinical symptoms, can be attributed to the so-called "regulation diseases", the essence of which is largely determined by the dysfunction of the body's neuroimmuno-humoral systems, which are unable to provide adequate adaptation to stress.

The study of the features of the bioelectrical activity of the brain in patients with neuropathic, chronic and idiopathic pain syndromes indicates the presence of similar changes in the background EEG rhythm, reflecting the dysfunction of the cortical-subcortical relations. The presented facts suggest that for the occurrence of neuropathic pain, a dramatic combination of two main events is necessary - damage to the structures of the somatosensory nervous system and dysfunction in the cortical-subcortical relations of the brain. It is the presence of dysfunction of the brain stem structures that will largely determine the brain's response to damage, contribute to the existence of a long-lasting hyperexcitability of the nociceptive system and persistence of pain symptoms.

Psychogenic pain syndromes

According to the classification of the International Association for the Study of Pain, psychogenic pain syndromes include:

Pain provoked by emotional factors and caused by muscle tension;

Pain like delirium or hallucination in patients with psychosis, disappearing with treatment of the underlying disease;

Pain in hysteria and hypochondria, not having a somatic basis;

Pain associated with depression that does not precede it and does not have any other cause.

In the clinic, psychogenic pain syndromes are characterized by the presence of pain in patients that cannot be explained by any known somatic diseases or damage to the structures of the nervous system. The localization of this pain usually does not correspond to the anatomical features of tissues or areas of innervation, the lesion of which could be suspected as the cause of the pain. Situations are possible in which somatic injuries, including disturbances in the structures of the somatosensory nervous system, can be detected, but the intensity of pain in this case greatly exceeds the degree of damage. In other words, the leading triggering factor in the genesis of psychogenic pain is a psychological conflict, and not damage to somatic or visceral organs or structures of the somatosensory nervous system.

Identifying psychogenic pain is difficult enough. Psychogenic pain syndromes often occur in the form of somatoform pain disorder, in which pain symptoms cannot be explained by the existing somatic pathology and they are not intentional. Patients prone to somatoform disorders are characterized by a history of multiple somatic complaints that appear before the age of 30 and last for many years. According to ICD-10, chronic somatoform pain disorder is characterized by a combination of pain with emotional conflict or psychosocial problems; therefore, it is necessary to identify a psychogenic etiological factor, which can be judged by the presence of temporary connections between pain symptoms and psychological problems. For the correct diagnosis of somatoform pain disorder, it is necessary to consult a psychiatrist to differentiate this condition from depression, schizophrenia and other mental disorders, in the structure of which pain syndromes can also be noted. The concept of somatoform pain disorder was introduced into the classification of mental disorders relatively recently, and to this day it causes a lot of discussion.

At the same time, it must be remembered that the onset of pain, including psychogenic pain, is possible only if the nociceptive system is activated. If, when nociceptive or neuropathic pain occurs, the structures of the nociceptive system are directly activated (due to tissue injury or damage to the structures of the somatosensory nervous system), then in patients with psychogenic pain, indirect excitation of nociceptors is possible - either by the mechanism of retrograde activation by sympathetic efferents and / or through reflex muscle tension ... Prolonged muscle tension in psychoemotional disorders is accompanied by an increase in the synthesis of algogens in muscle tissue and sensitization of the terminals of nociceptors localized in the muscles.

Psychological conflict is almost always also accompanied by the activation of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis, which can, through alpha2-adrenergic receptors localized on the nociceptor membrane, contribute to the retrograde excitation of nociceptors and their subsequent sensitization through the mechanisms of neurogenic inflammation. Under conditions of neurogenic inflammation, neurokinins (substance P, neurokinin A, etc.) are secreted from the peripheral terminals of nociceptors in the tissue, which have a pro-inflammatory effect, causing an increase in vascular permeability and the release of prostaglandins, cytokines and biogenic amines from mast cells and leukocytes. In turn, inflammatory mediators, acting on the membrane of nociceptors, increase their excitability. The clinical manifestation of sensitization of nociceptors in psychoemotional disorders will be zones of hyperalgesia, which are easily diagnosed, for example, in patients with fibromyalgia or tension headaches.

Conclusion

The presented data indicate that pain syndrome, regardless of the etiology of its occurrence, is the result of not only functional, but also structural changes affecting the entire nociceptive system - from tissue receptors to cortical neurons. In nociceptive and psychogenic pain, functional and structural changes in the pain sensitivity system are manifested by sensitization of peripheral and central nociceptive neurons, as a result of which the efficiency of synaptic transmission increases and persistent hyperexcitability of nociceptive neurons occurs. In patients with neuropathic pain, structural changes in the nociceptive system are more significant and include the formation of loci of ectopic activity in damaged nerves and pronounced changes in the integration of nociceptive, temperature and tactile signals in the central nervous system. It should also be emphasized that the pathological processes observed in the nociceptive structures of the peripheral and central nervous systems are closely interrelated in the dynamics of the development of any pain syndrome. Damage to tissues or peripheral nerves, increasing the flow of nociceptive signals, leads to the development of central sensitization (a long-term increase in the efficiency of synaptic transmission and hyperactivity of nociceptive neurons in the spinal cord and brain).

In turn, an increase in the activity of central nociceptive structures is reflected in the excitability of nociceptors, for example, through the mechanisms of neurogenic inflammation, as a result of which a vicious circle is formed that maintains the long-lasting hyperexcitability of the nociceptive system. Obviously, the stability of such a vicious circle and, consequently, the duration of pain will depend either on the duration of the inflammatory process in damaged tissues, which provide a constant influx of nociceptive signals into the structures of the central nervous system, or on the initially existing cortical-subcortical dysfunction in the central nervous system, due to which central sensitization will be maintained. and retrograde activation of nociceptors. This is also indicated by the analysis of the dependence of the occurrence of long-term pain on age. It has been proven that the onset of chronic pain in old age is most often due to degenerative diseases of the joints (nociceptive pain), while idiopathic chronic pain syndromes (fibromyalgia, irritable bowel syndrome) and neuropathic pain rarely begin in old age.

Thus, in the formation of chronic pain syndrome, the determining factor is the genetically determined reactivity of the body (primarily the structures of the central nervous system), which, as a rule, is excessive, inadequate to damage, as a result of which a vicious circle arises that maintains the long-lasting hyperexcitability of the nociceptive system.

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M. L. Kukushkin, Doctor of Medical Sciences, Professor

Institution of the Russian Academy of Medical Sciences Research Institute of General Pathology and Pathophysiology of the Russian Academy of Medical Sciences, Moscow