The first symptoms are often pain. See what “Pain” is in other dictionaries

Pain is an important protective biological phenomenon that mobilizes all the functional systems necessary for the survival of the body, allowing it to overcome or avoid the harmful influences that provoked it.
  About 90% of all diseases are associated with pain. It is the root basis of medical terms: disease, hospital, patient.
  In various regions of the world, from 7 to 64% of the population periodically experience pain, and from 7 to 45% suffer from recurrent or chronic pain.

However, under normal conditions, a person does not feel pain due to the harmonious balance between the nociceptive (conducting pain afferentation) and antinociceptive (suppressing pain afferentation, which does not exceed physiologically acceptable limits in intensity) systems.
  This balance can be disrupted by short-term but intense nociceptive afferentation or moderate but long-term nociceptive afferentation. Less frequently discussed is the possibility of failure of the antinociceptive system, when physiologically normal nociceptive afferentation begins to be perceived as pain.

The temporal aspect of imbalance between the nociceptive and antinociceptive systems distinguishes:

• transient pain
• sharp pain
• chronic pain

Transient pain is provoked by activation of nociceptive receptors in the skin or other body tissues in the absence of significant tissue damage and disappears until it is completely healed. The function of such pain is determined by the speed of occurrence after stimulation and the speed of elimination, which indicates that there is no danger of damaging effects on the body.
  In clinical practice, for example, transient pain is observed during intramuscular or intravenous injection.
  It is assumed that transient pain exists to protect a person from the threat of physical damage from external environmental factors in the form of a kind of training of the antinociceptive system to respond adequately, i.e., acquiring pain experience.

Acute pain

Acute pain– a necessary biological adaptive signal about possible (in the case of pain experience), beginning or already occurring damage. The development of acute pain is associated, as a rule, with well-defined painful irritations of superficial or deep tissues and internal organs or dysfunction of the smooth muscles of internal organs without tissue damage.
  The duration of acute pain is limited by the recovery time of damaged tissues or the duration of smooth muscle dysfunction.
  Neurological reasons acute pain may be:

• traumatic
• infectious
• dismetabolic
• inflammatory
• and other damage to the peripheral and central nervous system, meninges, short-term neural or muscular syndromes.

Acute pain is divided into:

• superficial
• deep
• visceral
• reflected

These types of acute pain differ in subjective sensations, localization, pathogenesis and reasons.

Superficial pain, which occurs when the skin, superficial subcutaneous tissues, and mucous membranes are damaged, is felt as a local sharp, stabbing, burning, pulsating, piercing. It is often accompanied by hyperalgesia and allodynia (a sensation of pain with non-painful stimuli). Deep pain occurs when nociceptors in muscles, tendons, ligaments, joints and bones are irritated. It has a dull, aching character, is less clearly localized than the superficial one.
  This or that localization of pain in case of damage to deep tissues is determined by the corresponding spinal segment innervating tendons, muscles, and ligaments. Structures innervated from the same segment can cause the same localization of pain.
  And on the contrary, closely located structures innervated by nerves originating from different segments cause pain that differs in localization.
  In accordance with the segmental innervation of the damaged tissues, cutaneous hyperalgesia, reflex muscle spasm, and autonomic changes accompanying deep pain are localized.

Visceral pain are caused by involvement in the pathological process of either the internal organs themselves or the parietal peritoneum and pleura covering them. Pain caused by diseases of the internal organs (true visceral pain) is vague, dull, aching in nature.
  They can be diffuse, poorly defined topographically. Often accompanied by parasympathetic manifestations: nausea, vomiting, sweating, decreased blood pressure, bradycardia.

Another type of pain that occurs due to pathology of internal organs is referred pain. Referred pain, or the Ged-Zakharyin phenomenon, is projected into dermatomes innervated by the same segments as the deeply located tissues or internal organs involved in the pathological process.
  In this case, local hyperalgesia, hyperesthesia, muscle tension, local and diffuse vegetative phenomena occur, the severity of which depends on the intensity and duration of the painful effect.

Intense and prolonged muscle tension (“spasm”) can become an independent cause that increases pain, which must be taken into account in the treatment of referred pain.

Chronic pain

Chronic pain in neurological practice, the condition is much more relevant. There is no consensus on what is meant by chronic pain. According to some authors, this is pain that lasts more than three months, according to others – more than 6 months. In our opinion, the most promising is the definition of chronic pain as pain that continues after a period of healing of damaged tissue. In practice, this may take from several weeks to six months or more.

Chronic pain can also include recurring pain conditions (neuralgia, headaches of various origins, etc.). The point, however, is not so much a matter of temporal differences as of qualitatively different neurophysiological, psychological and clinical features.
  The main thing is that acute pain is always a symptom, and chronic pain can essentially become an independent disease. It is clear that therapeutic tactics for eliminating acute and chronic pain have significant features.
  Chronic pain in its pathophysiological basis may have a pathological process in the somatic sphere and/or primary or secondary dysfunction of the peripheral or central nervous system, it can also be caused by psychological factors.

Untimely and inadequate treatment of acute pain can become the basis for its transformation into chronic pain.

Nociceptive afferentation exceeding the physiological threshold is always accompanied by the release of algogenic compounds (hydrogen and potassium ions, serotonin, histamine, prostaglandins, bradykinin, substance P) into the intercellular fluid surrounding the nociceptors.
  These substances play a key role in the formation of pain caused by injury, ischemia and inflammation. In addition to the direct exciting effect on nociceptor membranes, there is an indirect mechanism associated with disruption of local microcirculation.

Increased capillary permeability and venous congestion contribute to the extravasation of active substances such as plasma kinins and serotonin.
  This, in turn, disrupts the physiological and chemical environment around the nociceptors and increases their excitation.
  The ongoing release of inflammatory mediators can cause long-term impulses with the development of sensitization of nociceptive neurons and the formation of “secondary hyperalgesia” of the damaged tissue, contributing to the chronicization of the pathological process.

Any peripheral pain is associated with increased sensitivity of nociceptors due to the release of inflammatory substances. An increase in the sensitivity of the primary nociceptor in the affected peripheral tissue leads to an increase in the activity of neurons sending impulses to the spinal cord and the central nervous system, however, spontaneous electrical activity can be generated at the site of neurogenic inflammation, causing persistent pain.

Such a powerful inducer of pain sensitivity are pro-inflammatory components: bradykins, histamine, neurokinins, nitric oxide, which are usually found at the site of inflammation. Prostaglandins themselves are not pain moderators; they only increase the sensitivity of nociceptors to various stimuli, and their accumulation correlates with the development of the intensity of inflammation and hyperalgesia.
  Prostaglandins seem to mediate the involvement of “sleeping” nociceptors in the process of formation of secondary inflammatory hyperalgesia and peripheral sensitization.

Concepts of secondary hyperalgesia, peripheral and central sensitization essentially reflect the pathophysiological mechanisms of pain syndrome chronicity, behind which there is a whole cascade of neurophysiological and neurochemical transformations that ensure the maintenance of this condition.

Hyperalgesia, which is an exaggerated response to a normal painful stimulus and is often associated with allodynia, has two components: primary and secondary.

  Primary hyperalgesia is associated with the site of tissue damage and occurs mainly in connection with processes occurring locally. Nociceptors become oversensitive due to substances released, accumulated or synthesized at the site of injury (peripheral sensitization). These substances include serotonin and histamine, neurosensory peptides (SR, CGRP), kinins and bradykinins, arachidonic acid metabolic products (prostaglandins and leukotrienes), cytokines, etc.

Secondary hyperalgesia is formed due to the involvement of “sleeping” nociceptors in the pathological process.
  With adequate relationships between the nociceptive and antinociceptive systems, these multimodal receptors are inactive, but become active following tissue damage (under the influence of histamine, serotonin and bradykinin, released as a result of degranulation of mast cells following the release of neurosensory peptides).
  In the central nervous system, increased afferent impulses from sensitized and newly activated “dormant” nociceptors lead to increased release of activating amino acids (glutamate and aspartate) and neuropeptides in the dorsal horn of the spinal cord, which increases the excitability of central neurons.
  As a result, the peripheral zone of hyperalgesia expands. In this regard, initially subthreshold afferentation from tissues adjacent to the lesion now becomes suprathreshold due to increased excitability (i.e., decreased threshold) of central neurons.
  This change in central excitability refers to the concept of “central sensitization” and causes the development of secondary hyperalgesia. Peripheral and central sensitization in chronic pain conditions coexist, are to some extent independent and, from the point of view of therapeutic interventions, can be blocked separately from one another.

Mechanisms of chronic pain, depending on the predominant role in its genesis of different parts of the nervous system, are divided into:

• peripheral
• central
• combined peripheral-central
• psychological

By peripheral mechanisms we mean constant irritation of nociceptors of internal organs, blood vessels, the musculoskeletal system, the nerves themselves (nociceptors nervi nervorum), etc.
  In these cases, eliminating the cause - effective therapy for the ischemic and inflammatory process, arthropathic syndrome, etc., as well as local anesthesia, leads to relief from pain.
  The peripheral-central mechanism, along with the participation of the peripheral component, suggests dysfunction of the central nociceptive and antinociceptive systems of the spinal and cerebral level associated with it (and/or caused by it). At the same time, long-lasting pain of peripheral origin can be the cause of dysfunction of central mechanisms, which necessitates the need for the most effective elimination of peripheral pain.

Principles of pain treatment

Therapy for pain syndromes involves identifying and eliminating the source or cause that caused pain, determining the degree of involvement of various parts of the nervous system in the formation of pain and relieving or suppressing acute pain.
  Therefore, based on the general principles of pain therapy, first of all the impact is on its source, receptors and peripheral fibers, and then on the dorsal horns of the spinal cord, the pain conducting systems, the motivational-affective sphere and the regulation of behavior, i.e. on everything levels of organization of the pain system.

Treatment of acute pain involves the use of several main classes of drugs:

• simple and combined analgesics
• nonsteroidal or steroidal anti-inflammatory drugs

An alternative to outdated analgesics, for example, can be considered new generation combined analgesics, such as Caffetin ® - one of the drugs that optimally meets these requirements and is intended for the relief of acute pain of moderate and moderate intensity.
  The drug contains caffeine, codeine, paracetamol and propyphenazone, which have analgesic, antipyretic and mild anti-inflammatory effects.
  The mechanism of their action is associated with the ability to inhibit the synthesis of prostaglandins with an effect on the thermoregulation center in the hypothalamus.
  Caffeine stimulates excitation processes in the cerebral cortex (like codeine) and increases the analgesic effect of other components of the drug. The effectiveness of this kind of drugs is confirmed by practice: it is possible to overcome pain, you just need to choose the right medicine.

In addition, it should be noted that Caffetin® is approved for use as an over-the-counter drug, but the simultaneous use of analgesics with sleeping pills and alcohol is not recommended.

Treatment of chronic pain syndromes is a more complex task, requiring an integrated approach. First-line drugs in this case are tricyclic antidepressants, among which both non-selective and selective serotonin and norepinephrine reuptake inhibitors are used. The next class of drugs are anticonvulsants.
  The experience available today has proven the need to treat patients with chronic pain in specialized inpatient or outpatient centers with the involvement of neurologists, therapists, anesthesiologists, psychologists, clinical electrophysiologists, physiotherapists, etc.

The basic principle of the treatment of acute pain involves a clinical assessment of the state of the neurophysiological and psychological components of the nociceptive and antinociceptive systems and influence on all levels of organization of this system in order to prevent the chronicization of the pain syndrome, when the dominant clinical component becomes the psychological aspects of the experience of social maladjustment, leading to a deterioration in the quality of life.

Neuropathic pain - diagnosis, rule - “Three Cs”

Pain is assessed in terms of etiology (trauma, burn, disease), duration (acute, chronic), localization (local, diffuse), intensity (strong, moderate, weak)...

Pain - types of pain, choice of drugs to treat pain

One of the most common symptoms in patients of any profile is pain, since it is often its presence that forces a person to seek medical help....

Attention! the information on the site does not constitute a medical diagnosis or a guide to action and is intended for informational purposes only.

The vast majority of diseases are accompanied by pain. Pain is an unpleasant painful feeling associated with one or another tissue damage. Pain is one of the main, most common and leading symptoms that force the patient to seek medical help from various medical specialists.

Pain is not just a symptom of a disease, it is a complex complex of pathological reactions and sensations of the patient.

Having arisen as a defensive reaction to pathological stimuli, pain is a signal of trouble and makes us understand that the body is in some kind of danger. When experiencing pain, a person immediately tries to find a way to overcome these negative sensations and stop the pain. Thus, pain as a symptom is always a marker of some health problem. Pain, even minor pain, cannot be ignored and its symptoms cannot be ignored. Unfortunately, there are diseases that do not always manifest as pain at an early stage. But in this case, you can almost always look for other, equally important signs of the disease and consult a doctor.

For an objective assessment of pain, specially developed scales are used, with the help of which, when interviewing a patient, the intensity and severity of the pain syndrome can be clarified. The degree of pain is not always directly proportional to the severity of the sufferer’s condition, although such a dependence certainly exists.

To assess the intensity of pain, there is a visual technique based on the patient’s assessment of the pain scale using a ten-point system. Numbers from 0 to 10 sequentially represent the transition from mild, to moderate, and finally to severe pain. Moreover, the number “10” on the scale means unbearable pain that is impossible to endure. The patient is asked to show on the scale the number that corresponds to his sensations of pain. The patient's assessment of pain intensity may vary depending on the effectiveness of treatment after taking an analgesic drug.

Another method for assessing pain uses the “pain tolerance” scale. Thus, “mild pain” is assessed as pain that can be ignored. “Severe pain” impairs a person’s basic needs, “unbearable pain” forces the patient to be on bed rest. Pain sensations may vary significantly among different patients.

Causes and types of pain syndrome

Throughout life, a person encounters pain. There are many reasons for the occurrence of pain, since the vast majority of ailments, among other symptoms, are accompanied by pain.

The pain can be acute or chronic. Acute pain is a pain syndrome that lasts less than three months. Accordingly, the pain syndrome becomes chronic if its duration extends beyond this time interval. Acute pain can be relieved after the cause of it is eliminated, or it can become chronic.

An acute, difficult situation is not always accompanied by acute, severe pain, so the manifestations of pain should always be assessed simultaneously with other complaints and symptoms of the disease.

Chronic pain is accompanied by anxiety, depressive symptoms, hypochondria, restlessness, indifference to other problems, and a person’s personality changes. Chronic pain syndrome often occurs with cancer (acute pain is also possible), chronic rheumatic processes in the joints and connective tissue, in the spine and other diseases. In patients with chronic pain, sleep and appetite are disturbed, the range of interests is narrowed, and everything becomes subordinate to pain. There is a dependence of a person with pain syndrome on others, on pain and taking medications.

Acute and chronic pain can vary in intensity (from mild pain to unbearable excruciating pain). Pain syndrome may differ in origin and have a different mechanism of development.

Acute and chronic pain can accompany and be a symptom of diseases of the joints and internal organs. Pain can occur with painful spasms and inflammatory processes of any localization, with increased pressure and spasm in a hollow organ, with tissue swelling, the impact of a pathological process directly on a sensitive nerve fiber, and so on. There are many causes of pain, but all types of pain can be divided into the following several types.

Nociceptive pain

Nociceptive pain is a pain syndrome that occurs when exposed to painful stimuli that affect pain receptors. For example, this type of pain is observed in various inflammatory processes, traumatic injuries, bruises, swelling of tissues and organs, sprains and tissue ruptures.

With decreased blood circulation in the organ, hypoxia, and dysmetabolic changes in surrounding tissues, nociceptive pain also occurs. As a rule, nociceptive pain can be clearly localized. The pain can radiate, that is, go to other places.

Nociceptive pain is observed in various inflammatory diseases of the joints (arthritis, arthrosis), muscles, ligaments, muscle spasms, and in the postoperative period. The listed types of pain are classified as somatic pain.

If pain impulses come from the internal organs (heart, gastrointestinal tract), then such pain is called visceral. In this case, the nerve fiber itself is not damaged, and pain is perceived by a sensitive neuron, which is affected by damaging factors. Examples of visceral nociceptive pain can be sore throat, pain during exacerbation of a peptic ulcer, pain during biliary and renal colic, pain due to insufficient blood circulation in the affected limb.

The mechanism of development of nociceptive pain is due to the fact that due to damage to cells and tissues, a large number of special substances (pain mediators) are formed, which cause a painful unpleasant sensation called pain. These biological substances include bradykinin, prostaglandins, histamine and acetylcholine. In addition, during inflammation, protective blood cells of the leukocyte series (leukocytes, lymphocytes) rush to the pathological focus, additionally releasing inflammatory factors into the surrounding tissues. This contributes to an even greater pain response and degree of pain.

Complaints of patients with nociceptive pain are of the nature of cutting, pressing, shooting pain. Often this pain is perceived as throbbing, squeezing, stabbing, aching, sawing. After the cessation of the pathological effect that led to pain, pain tends to quickly fade and stop. The intensity of pain may increase with movements, turns, and changes in body position. And vice versa, as a rule, the pain syndrome (with nociceptive pain) decreases somewhat at rest (not always).

Another type of pain syndrome is neuropathic pain.

Neuropathic pain

Neuropathic pain is mediated by the damaging effects of various factors directly on the functional units of the peripheral and central (spinal cord and brain) nervous systems. At the same time, the possibility of pathological excitation of nerve cells sharply increases, which can lead to the fact that various non-painful stimuli are perceived as pain. This type of pain is not protective, but at the same time, it brings numerous suffering to patients and sharply reduces the level of quality of life of the sick person. As a rule, this pain is long-lasting and chronic.

Neuropathic pain is perceived by patients as a feeling of painful tingling, burning unbearable pain, or a sensation of needles or injections, “as if struck by an electric shock.” In some patients, neuropathic pain is of a drilling, shooting, burning nature, and can disturb during the day and at night. Often the pain is accompanied by a crawling sensation, paresthesia, numbness, and burning. Often, neuropathic pain is accompanied by a feeling of cold or heat; there may be sensations like being struck by nettles. Neuropathic pain syndrome may occur after herpes zoster ( depriving), due to compression of an area of ​​the spinal cord, with neuropathy as a result of chronic hyperglycemia (diabetes mellitus of both types). Postherpetic neuropathic pain (after suffering from herpes zoster) can bother the patient for several months or more, when the blistering rash is no longer detectable.

Neuropathic pain is often combined with impaired sensory functions and an increased pain threshold.

Neuropathic pain is classified into two types.

Neuropathic pain of the peripheral type is formed with various neuralgia, polyneuropathies, neuritis, damage to nerve trunks due to tunnel syndromes (compression of the nerve trunk in natural anatomical formations), neuropathies of various origins, herpes zoster.

Neuropathic pain that develops after an acute cerebrovascular accident, with multiple sclerosis, myelopathy and traumatic lesions of the spinal cord, is called central.

Another type of pain is dysfunctional pain- pain symptoms associated with impaired sensitivity to pain due to an imbalance between the level of painful stimulus and response to it. In this case, control over pain by the nervous system is disrupted. With this type of pain, “dysfunction” of the central nervous system occurs.

Principles of treatment and diagnosis of pain syndrome

Often, a patient may have pain of both neuropathic and nociceptive origin, since the same person, especially in old age, may have several diseases. It can be quite difficult to understand what type of pain prevails in this case. Therefore, pain treatment should be carried out by a doctor or a team of doctors.

If pain occurs, you should not self-medicate; you must contact a specialist of the appropriate profile. There is no universal medicine that would have the same analgesic effect in all patients.

In addition, approaches to the treatment of acute and chronic pain, therapies and medications used can be completely different.

Both doctors providing emergency care (traumatologists, surgeons, resuscitators) and other specialists (therapists, neurologists, endocrinologists and others) can take part in the treatment of pain syndrome.

When treating pain, it is necessary to find the cause of the disease, and along with correcting the pain syndrome, treat the disease that caused the pain. By taking painkillers without a doctor’s prescription, without affecting the cause of the pain, the disease can progress to a stage that will be difficult, and sometimes impossible, to influence.

Diagnosis of the causes of pain syndrome includes the entire range of necessary tests and studies required in this case, which are prescribed only by a doctor.

Therefore, it is very important to seek the help of a doctor as soon as possible at the first manifestations of pain. Considering the nature and mechanism of development of pain in a given patient, the doctor may prescribe various drugs that have analgesic activity. Currently, painkillers are represented by several groups that affect various parts of the pathogenesis of pain. At the same time, analgesics, which are successfully used in the treatment of nociceptive pain, may be ineffective in neuropathic pain. In some cases, it is possible to use various drugs simultaneously, as prescribed by a doctor.

Thus, the treatment of pain and pain syndrome appears to be a complex task, in the treatment of which doctors of various profiles may be involved. It is important to prevent the transition of acute pain syndrome to chronic, when, despite the possibilities of pharmacotherapy, the patient must constantly take painkillers.

Pain I

In the description of patients, pain sensations by their nature can be sharp, dull, cutting, stabbing, burning, pressing (squeezing), aching, pulsating. In duration and frequency they can be constant, paroxysmal, associated with the time of day, seasons of the year, physical activity , body posture, with certain movements (for example, breathing, walking), eating, acts of defecation or urination, etc., which makes it possible to suspect the location and pathology causing pain. The characteristics of the emotional reactions accompanying pain are also of diagnostic importance, for example, the feeling of fear of death that accompanies retrosternal pain in angina pectoris, myocardial infarction, and pulmonary embolism.

A certain diagnostic orientation is provided by the differentiation of somatalgia, i.e. pain caused by irritation of somatic nerve fibers, and vegetalgia (sympathalgia) that occurs when autonomic innervation is involved in sensory fibers. Somatalgia (constant or paroxysmal) is localized in the zone of innervation of peripheral nerves or roots and is usually not accompanied by autonomic disorders, or the latter (with very intense pain) are of a nature (general, increased blood pressure, increased heart rate, etc.).

With vegetalgia, disorders of autonomic functions are observed as a rule and are often local in nature, expressed by local spasms of peripheral vessels, changes in skin temperature, goose bumps, impaired sweating, trophic disorders, etc. Sometimes vegetalgia reaches the level of causalgia (Causalgia) , often with referred pain of the repercussion type (Repercussion) with the appearance of pain in the Zakharyin-Ged zones. Pain may appear in one half of the body (), which is observed, in particular, with damage to the thalamus. The high frequency of repercussion with the appearance of pain in areas remote from the affected organ should be kept in mind in the differential diagnosis of diseases of internal organs, blood vessels, bones, and joints. for example, with myocardial infarction (myocardial infarction), B. is possible not only in the sternum area with irradiation to the left arm, but also B. in the thoracic spine, B. in the lower, in the forehead, in the right arm, in the abdominal area (abdominal form), etc. With all the variety of manifestations of pain repercussion, B.’s summary characteristics help to highlight features that are typical or atypical for any process in the area of ​​internal organs. for example, dissecting aortic aneurysm is similar to myocardial infarction in many of its characteristics, but the spread of dissection along the spine with irradiation to the legs, characteristic of a dissecting aneurysm, is not typical for myocardial infarction.

The patient's behavior during painful paroxysms also has diagnostic significance. for example, during a myocardial infarction, a patient tries to lie still, a patient with an attack of renal colic rushes about, takes various positions, which is not observed with a similar localization of pain in a patient with lumbar radiculitis.

In diseases of the internal organs, B. occurs as a consequence of blood flow disturbances (thrombosis of the mesenteric or renal artery, atherosclerotic stenosis of the abdominal aorta, etc.); spasm of smooth muscles of internal organs (stomach); stretching of the walls of hollow organs (gallbladder, renal pelvis, ureter); spread of the inflammatory process to areas equipped with sensitive innervation (parietal pleura, peritoneum, etc.). brain substance is not accompanied by B., it occurs when the membranes, venous sinuses, and intracranial vessels are irritated. Pathological processes in the lung are accompanied by B. only when they spread to the parietal pleura. Severe B. occurs with spasm of the heart vessels. B. in the esophagus, stomach and intestines often occurs when they are spastic or stretched. Pathological processes in the parenchyma of the liver, spleen, and kidneys do not cause pain unless they are accompanied by acute stretching of the capsule of these organs. Muscle pain occurs with bruises, myositis, convulsions, and arterial circulation disorders (in the latter cases, pain occurs as sympathalgia). When the periosteum and bone processes are affected, B. are extremely painful.

It must be borne in mind that pain in diseases of internal organs may not occur for a long time and may increase like an avalanche only during the incurable stage of the process (for example, with malignant neoplasms). After treatment of a somatic disease, persistent pain is possible, associated with the consequences of damage to the nerve trunks, their ischemic changes, adhesions, changes in the functional state of the nodes of preganglionic autonomic innervation, as well as with psychogenic fixation of pain.

Elimination of pain as one of the most painful manifestations of the disease for the patient is one of the primary tasks solved by the doctor in the process of determining treatment tactics. The best option is to eliminate the cause of the pain, for example, removing a foreign body or a compressive object, reducing a dislocation, etc. If this is not possible, preference is given to influencing those links of pathogenesis with which pain is associated, for example, taking alkalis to relieve pain in duodenal ulcers, nitroglycerin for angina, antispasmodics (see Antispasmodics) and anticholinergics (see Anticholinergics) - for hepatic and renal colic, etc. If causal and pathogenetic therapy is ineffective or impossible, they resort to symptomatic treatment of pain with the help of analgesics (Analgesics) , the effect of which can be enhanced by the simultaneous use of neuroleptic drugs (neuroleptic drugs) or tranquilizers (tranquilizers) . However, if the nature of the somatic disease is unspecified, especially with unclear abdominal pain, the use of analgesics is contraindicated due to a possible modification of the clinical picture, which complicates the diagnosis of the disease, in which urgent surgical intervention may be indicated (see Acute abdomen) . For local pain, incl. for some neuralgia, local anesthesia is sometimes advisable . For persistent debilitating pain in patients with chronic diseases and low effectiveness of analgesics, symptomatic surgical treatment is used - radicotomy, cordotomy, tractotomy and other methods.

Bibliography: Valdman A.V. and Ignatov Yu.D. Central mechanisms of pain, L., 1976, bibliogr.; Grinshtein A.M. and Popova N.A. Vegetative syndromes, M., 1971; Erokhina L.G. Facial pain, M., 1973; Kalyuzhny L.V. Physiological mechanisms of regulation of pain sensitivity, M., 1984, bibliogr.; Karpov V.D. nervous diseases, M., 1987; Kassil G.N. Science of pain, M., 1975; Kryzhanovsky G.N. Determinant structures in the pathology of the nervous system, M., 1980; Nordemar R. Back pain, . from Swedish, M., 1988; Shtok V.N. , M., 1987, bibliogr.

Rice. 1. Scheme of the occurrence of projected pain. Nerve impulses caused by direct stimulation (indicated by the arrow) travel along afferent fibers in the spinothalamic tract to the corresponding zone of the cerebral cortex, causing a sensation of pain in that part of the body (arms) that is usually caused by irritation of nerve endings: 1 - part of the body with pain receptors; 2 - sensation of pain at the location of the corresponding pain receptors; 3 - brain; 4 - lateral spinothalamic tract; 5 - spinal cord; 6 - afferent nerve fiber.

Rice. 2. Scheme of the occurrence of referred pain. Painful sensations from the internal ones come to the spinal cord, individual structures of which synaptically contact the nerve cells of the spinothalamic tract, on which the nerve fibers that innervate a certain segment of the skin end: 1 - skin; 2 - trunk of the sympathetic nervous system; 3 - posterior root; 4 - lateral spinothalamic tract; 5 - spinal cord; 6 - anterior root; 7 - internal organ; 8 - visceral nerve.