Types of pain nociceptive neuropathic mixed. Chronic pain syndromes in the clinic of nervous diseases: issues of long-term analgesia. Categories: visceral type

© A. R. Soatov, A. A. Semenikhin, 2013 UDC 616-009.7:615.217.2

Types of pain and major groups of antinociceptives*

N. A. Osipova, V. V. Petrova

Federal State Budgetary Institution "Moscow Research Institute of Oncology named after P. A. Herzen" of the Ministry of Health of the Russian Federation, Moscow

The types of pain and basic groups of antinociceptive agents

N. A. Osipova, V V Petrova Moscow Cancer Institute named after P. A. Hertzen, Moscow

The lecture discusses in detail the various types of pain, their sources and localization, the ways of transmitting pain signals, as well as the appropriate methods of protection and pain control. A critical review of drugs intended for the treatment of pain syndrome of various etiologies is presented. Key words: nociceptive pain, somatic pain, visceral pain, hyperalgesia, pain management, antinociceptives.

The lecture is dedicated to different types of pain, its reasons and localization as well as neural ways of pain signal transmitting and corresponding methods of prevention and pain management. The lecture includes a critical overview of drugs and anesthetic agents applied for treating pain of different etiology. Keywords: nociceptive pain, somatic pain, visceral pain, hyperalgesia, pain management, antinociceptive agents

Types of pain

There are two main types of pain: nociceptive and neuropathic, differing in the pathogenetic mechanisms of their formation. Pain caused by trauma, including surgical, is referred to as nociceptive; it should be assessed taking into account the nature, extent, localization of tissue damage, and the time factor.

Nociceptive pain is pain resulting from stimulation of nociceptors in case of damage to the skin, deep tissues, bone structures, internal organs, according to

the mechanisms of afferent impulses and neurotransmitter processes described above. In an intact organism, such pain appears immediately when a local painful stimulus is applied and disappears when it is quickly stopped. However, in relation to surgery, we are talking about a more or less long-term nociceptive effect and often a significant amount of damage to different types of tissues, which creates conditions for the development of inflammation in them and the persistence of pain, the formation and consolidation of pathological chronic pain.

Nociceptive pain is divided into somatic and visceral pain, depending on

Table 1. Types and sources of pain

Types of pain Sources of pain

Nociceptive activation of nociceptors

Somatic In case of damage, inflammation of the skin, soft tissues, muscles, fascia,

tendons, bones, joints

Visceral In case of damage to the membranes of internal cavities, internal organs

(parenchymal and hollow), overstretching or spasm of hollow organs,

vessels; ischemia, inflammation, organ edema

Neuropathic Damage to peripheral or central nerve structures

Psychological component of pain Fear of upcoming pain, unresolved pain, stress, depression,

sleep disturbance

* The third chapter from the book by N. A. Osipova, V. V. Petrova // “Pain in surgery. Means and methods of protection»

localization of damage: somatic tissues (skin, soft tissues, muscles, tendons, joints, bones) or internal organs and tissues - shells of internal cavities, capsules of internal organs, internal organs, fiber. The neurological mechanisms of somatic and visceral nociceptive pain are not identical, which has not only scientific but also clinical significance (Table 1).

Somatic pain caused by irritation of somatic afferent nociceptors, for example, during mechanical trauma to the skin and underlying tissues, is localized at the site of injury and is well eliminated by traditional analgesics - opioid or non-opioid, depending on the intensity of pain.

Visceral pain has a number of specific differences from somatic pain. The peripheral innervation of different internal organs is functionally different. The receptors of many organs, when activated in response to damage, do not cause conscious perception of the stimulus and a certain sensory sensation, including pain. The central organization of visceral nociceptive mechanisms, compared to the somatic nociceptive system, is characterized by a significantly smaller number of separate sensory pathways. . Visceral receptors are involved in the formation of sensory sensations, including pain, and are interconnected with autonomic regulation. The afferent innervation of the internal organs also contains indifferent ("silent") fibers, which can become active when the organ is damaged and inflamed. This type of receptor is involved in the formation of chronic visceral pain, supports long-term activation of spinal reflexes, impaired autonomic regulation and the function of internal organs. Damage and inflammation of the internal organs disrupts the normal pattern of their motility and secretion, which in turn dramatically changes the environment around

receptors and leads to their activation, the subsequent development of sensitization and visceral hyperalgesia.

In this case, signals can be transmitted from the damaged organ to other organs (the so-called viscero-visceral hyperalgesia) or to the projection zones of somatic tissues (viscerosomatic hyperalgesia). Thus, in different visceral algogenic situations, visceral hyperalgesia can take different forms (Table 2).

Hyperalgesia in the damaged organ is considered as primary, and viscerosomatic and viscero-visceral - as secondary, since it does not occur in the zone of primary damage.

The sources of visceral pain can be: the formation and accumulation of painful substances in the damaged organ (kinins, prostaglandins, hydroxytryptamine, histamine, etc.), abnormal stretching or contraction of the smooth muscles of hollow organs, stretching of the capsule of the parenchymal organ (liver, spleen), anoxia of smooth muscles , traction or compression of ligaments, vessels; zones of organ necrosis (pancreas, myocardium), inflammatory processes. Many of these factors operate during intracavitary surgical interventions, which determines their higher trauma and greater risk of postoperative dysfunctions and complications compared to non-cavitary operations. In order to reduce this risk, research is being conducted to improve the methods of anesthetic protection, and minimally invasive thoraco-, laparoscopic and other endoscopic operations are being actively developed and implemented. Prolonged stimulation of visceral receptors is accompanied by excitation of the corresponding spinal neurons and the involvement of spinal cord somatic neurons in this process (the so-called viscerosomatic interaction). These mechanisms are mediated by IMOL receptors and are responsible for

Table 2. Types of hyperalgesia in visceral pain

Type of hyperalgesia Localization

1. Visceral The organ itself during its nociceptive stimulation or inflammation

2. Viscerosomatic Zones of somatic tissues where visceral hyperalgesia is projected

3. Viscero-visceral Transfer of hyperalgesia from the originally involved internal organ to others whose segmental afferent innervation partially overlaps

development of visceral hyperalgesia and peripheral sensitization.

Neuropathic pain (NPP) is a specific and most severe manifestation of pain associated with damage and disease of the peripheral or central somatosensory nervous system. It develops as a result of traumatic, toxic, ischemic damage to nerve formations and is characterized by abnormal sensory sensations that exacerbate this pathological pain. NPB can be burning, stabbing, spontaneous, paroxysmal, can be provoked by non-painful stimuli, such as movement, touch (the so-called allodynia), spreads radially from the area of ​​nerve damage. The main pathophysiological mechanisms of NPB include peripheral and central sensitization (increased excitability of peripheral and spinal nociceptive structures), spontaneous ectopic activity of damaged nerves, sympathetically enhanced pain due to the release of norepinephrine, which stimulates nerve endings with involvement of neighboring neurons in the process of excitation, while reducing the descending inhibitory control of these processes with a variety of severe sensory disorders. The most severe manifestation of NPB is a phantom pain syndrome after amputation of the limbs, associated with the intersection of all the nerves of the limb (deafferentation) and the formation of overexcitation of nociceptive structures. NPB is often resistant to conventional analgesic therapy, persists for a long time, and does not decrease over time. The mechanisms of NPB are being refined in experimental studies. It is clear that there is a violation of the processes of sensory information, an increase in excitability (sensitization) of nociceptive structures, and inhibitory control suffers.

The development of special approaches to the prevention and treatment of NPB, aimed at reducing the overexcitation of the peripheral and central structures of the sensory nervous system, continues. Depending on the etiology of clinical manifestations, NSAIDs, local applications of ointments and patches with local anesthetics, glucocorticoids or NSAIDs are used; muscle relaxants

central action, serotonin and norepinephrine reuptake inhibitors, antidepressants, anticonvulsants. The latter seem to be the most promising in relation to severe neuropathic pain syndromes associated with trauma to nerve structures.

Persistent/inflammatory pain in the area of ​​surgical or other invasive impact develops with continued stimulation of nociceptors by mediators of pain and inflammation, if these processes are not controlled by preventive and therapeutic agents. Unresolved persistent postoperative pain is the basis of chronic postoperative pain syndrome. Its different types are described: postthoracotomy, postmastectomy, posthysterectomy, postherniotomy, etc. . Such persistent pain, according to these authors, can last days, weeks, months, years. The research conducted in the world indicates the high importance of the problem of persistent postoperative pain and its prevention. The development of such pain can contribute to many factors acting before, during and after surgery. Among the preoperative factors - the psychosocial status of the patient, the initial pain at the site of the upcoming intervention, other concomitant pain syndromes; among intraoperative - surgical access, the degree of invasiveness of the intervention and damage to the nervous structures; among postoperative ones - unresolved postoperative pain, means of its treatment and doses, relapse of the disease (malignant tumor, hernia, etc.), quality of patient management (observation, consultations with the attending physician or in the pain clinic, the use of special testing methods, etc.).

The frequent combination of different types of pain should be taken into account. In surgery during intracavitary operations, activation of the mechanisms of both somatic and visceral pain is inevitable. During noncavitary and intracavitary operations accompanied by trauma, intersection of nerves, plexuses, conditions are created for the development of manifestations of neuropathic pain against the background of somatic and visceral pain, followed by its chronicity.

The importance of the psychological component associated with pain or

expected pain, which is especially important for surgical clinics. The psychological state of the patient significantly affects his pain reactivity and, conversely, the presence of pain is accompanied by negative emotional reactions, violates the stability of the psychological status. There is an objective justification for this. For example, in patients entering the operating table without premedication (i.e., in a state of psycho-emotional stress), a sensory study recorded a significant change in reactions to an electrocutaneous stimulus compared to the initial ones: the pain threshold is significantly reduced (pain is aggravated), or, on the contrary , increases (i.e., pain reactivity decreases). At the same time, important patterns were revealed when comparing the analgesic effect of a standard dose of fentanyl 0.005 mg/kg in people with reduced and increased emotional pain response. In patients with emotional stress analgesia, fentanyl caused a significant increase in pain thresholds - 4 times, and in patients with high emotional pain reactivity, pain thresholds did not change significantly, remaining low. The same study established the leading role of benzodiazepines in eliminating preoperative emotional stress and achieving an optimal background for the manifestation of the analgesic effect of the opioid.

Along with this, the so-called. psychosomatic pain syndromes associated with psycho-emotional overloads of various kinds, as well as somatopsychological ones that develop against the background of organic diseases (for example, oncological ones), when the psychological component makes a significant contribution to the processing and modulation of pain information, intensifying pain, so that a mixed picture is ultimately formed. somatic, somatopsychological and psychosomatic pain.

A correct assessment of the type of pain and its intensity, depending on the nature, location and extent of the surgical intervention, underlies the appointment of means for its adequate therapy. Even more important is the preventive pathogenetic approach to the planned selection of specific antinociceptive agents for various types of surgical interventions in order to avoid inadequate anesthetic protection (AP), the formation of a strong

postoperative pain syndrome and its chronicity.

The main groups of means of protection against pain associated with tissue injury

In the surgical clinic, specialists have to deal with acute pain of various types of intensity and duration, which affect the definition of tactics not only for pain relief, but also for the management of the patient as a whole. So, in the case of unexpected, sudden onset of acute pain associated with the underlying (surgical) or concomitant disease (perforation of a hollow abdominal organ, acute attack of hepatic / renal colic, angina pectoris, etc.), anesthesia is started by establishing the cause of the pain and tactics for its elimination ( surgical treatment or drug therapy for the disease that caused the pain).

In elective surgery, we are talking about predictable pain, when the time of the surgical injury, the location of the intervention, the estimated zones and extent of damage to tissues and nerve structures are known. At the same time, the approach to protecting the patient from pain, in contrast to pain relief in case of actually developed acute pain, should be preventive, aimed at inhibiting the processes of triggering nociceptive mechanisms before the onset of surgical trauma.

The construction of an adequate AZ of a patient in surgery is based on the multilevel neurotransmitter mechanisms of nociception discussed above. Research on the improvement of AZ in various areas of surgery is actively conducted in the world, and, along with the well-known traditional means of systemic and regional anesthesia and analgesia, in recent years the significance of a number of special antinociceptive agents that increase the effectiveness and reduce the disadvantages of traditional agents has been substantiated.

Means, the use of which is advisable to protect the patient from pain at all stages of surgical treatment, are divided primarily into 2 main groups:

Systemic antinociceptives

actions;

local antinociceptives

(regional) action.

Systemic antinociceptives

These drugs suppress one or another pain mechanism by entering the systemic circulation through various routes of administration (intravenous, intramuscular, subcutaneous, inhaled, orally, rectally, transdermally, transmucosally) and acting on the appropriate targets. Numerous systemic drugs include drugs of various pharmacological groups that differ in certain antinociceptive mechanisms and properties. Their targets can be peripheral receptors, segmental or central nociceptive structures, including the cerebral cortex.

There are different classifications of systemic antinociceptives based on their chemical structure, mechanism of action, clinical effects, and taking into account the rules for their medical use (controlled and uncontrolled). These classifications include different groups of analgesic drugs, the main pharmacological property of which is the elimination or reduction of pain. However, in anesthesiology, in addition to analgesics proper, other systemic agents with antinociceptive properties are used, which belong to other pharmacological groups and play an equally important role in the patient's anesthetic protection.

Their action is focused on different parts of the nociceptive system and the mechanisms of the formation of acute pain associated with surgery.

Antinociceptive agents of local (regional) action (local anesthetics)

Unlike systemic agents, local anesthetics have their effect when they are applied directly to the nervous structures of different levels (terminal endings, nerve fibers, trunks, plexuses, structures of the spinal cord). Depending on this, local anesthesia can be superficial, infiltration, conduction, regional or neuraxial (spinal, epidural). Local anesthetics block the generation and propagation of action potentials in nerve tissues mainly by inhibiting the function of Na+ channels in axonal membranes. Na+ channels are specific receptors for local anesthetic molecules. Different sensitivity of nerves to local anesthetics can be manifested by a clinically significant difference in the blockade of somatic sensory innervation, motor and preganglionic sympathetic fibers, which, along with the desired sensory blockade, may be accompanied by additional side effects.

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Dear Colleagues!

At the beginning of this year, the publishing house "Medical Information Agency" published a monograph by the famous specialist in the field of treatment of postoperative pain, long-term head of the department of anesthesiology and resuscitation of the Research Institute of Oncology named after P. A. Herzen, Honored Scientist of the Russian Federation, Professor N. A. Osipova " Pain in surgery. Means and methods of protection, co-authored with a senior researcher, Ph.D. V. V. Petrova.

The lack of specialized literature on postoperative pain relief makes this event particularly significant. We can say that since the appearance in Russia of M. Ferrante's monograph "Postoperative Pain", Russian anesthesiologists have not received such a complete guide to combat pain in patients who have undergone various surgical interventions. The authors present the most up-to-date data on the anatomical and physiological basis of pain, molecular genetic and neurotransmitter mechanisms of its formation.

The book provides a critical analysis of various non-opioid and opioid analgesics, non-analgesics that affect IMEL receptors. Particular attention is paid to the neuropathic component of postoperative pain, the significance of which is rarely taken into account by practitioners. Of great interest is the chapter devoted to the prevention of phantom pain syndrome, an issue that is considered unresolved all over the world, but is successfully solved within the walls of the Research Institute of Oncology. P. A. Herzen. Separate chapters are devoted to the issues of perioperative analgesia in the orthopedic clinic, anesthetic protection of patients during intracavitary operations, interventions on the head and neck. In this issue of the journal, we present one of the chapters of the monograph by N. A. Osipova and V. V. Petrova, which presents the types of pain and the main groups of means of protection against pain in surgery.

We hope that it will interest you, and you will want to read the monograph as a whole.

Chief editor, prof. A. M. Ovechkin

Pain, or nociceptive sensitivity, is the perception of stimuli that cause the sensation of pain in the body.

Currently, there is no generally accepted concept of pain. In a narrow sense pain is an unpleasant sensation that occurs under the action of superstrong stimuli that cause structural and functional changes in the body.

The physiological role of pain is as follows:

1. It acts as a signal about the threat or damage to body tissues and warns them.
2. It is a factor in the mobilization of protective and adaptive reactions in case of damage to its organs and tissues
3. It has a cognitive function: through pain, a person from early childhood learns to avoid possible dangers of the external environment.
4. The emotional component of pain performs the function of reinforcement in the formation of conditioned reflexes even with a single combination of conditioned and unconditioned stimuli.

Causes of pain. Pain occurs when, firstly, the integrity of the protective integumentary membranes of the body (skin, mucous membranes) and internal cavities of the body (meninges, pleura, peritoneum, etc.) is violated, and, secondly, the oxygen regime of organs and tissues to a level that causes structural and functional damage.

Pain classification. There are two types of pain:

1. Somatic, arising from damage to the skin and the musculoskeletal system. Somatic pain is divided into superficial and deep. Superficial pain is called pain of skin origin, and if its source is localized in the muscles, bones and joints, it is called deep pain. Superficial pain is manifested in tingling, tingling. Deep pain, as a rule, is dull, poorly localized, has a tendency to radiate to surrounding structures, is accompanied by discomfort, nausea, severe sweating, and a drop in blood pressure.

2. Visceral, arising from damage to internal organs and having a similar picture with deep pain.

Projection and reflected pain. There are special types of pain - projection and reflected.

As an example projection pain you can cause a sharp blow to the ulnar nerve. Such a blow causes an unpleasant, hard to describe sensation that spreads to those parts of the hand that are innervated by this nerve. Their occurrence is based on the law of pain projection: no matter what part of the afferent pathway is irritated, pain is felt in the region of the receptors of this sensory pathway. One of the common causes of projection pain is compression of the spinal nerves at the points of their entry into the spinal cord as a result of damage to the intervertebral cartilage discs. Afferent impulses in nociceptive fibers in such a pathology cause pain sensations that are projected into the area associated with the injured spinal nerve. Projection (phantom) pain also includes pain that patients feel in the area of ​​the remote part of the limb.

Reflected pains pain sensations are called not in the internal organs, from which pain signals are received, but in certain parts of the skin surface (Zakharyin-Ged zones). So, with angina pectoris, in addition to pain in the region of the heart, pain is felt in the left arm and shoulder blade. Reflected pain differs from projection pain in that it is not caused by direct stimulation of nerve fibers, but by irritation of some receptive endings. The occurrence of these pains is due to the fact that the neurons that conduct pain impulses from the receptors of the affected organ and the receptors of the corresponding skin area converge on the same neuron of the spinothalamic pathway. Irritation of this neuron from the receptors of the affected organ, in accordance with the law of pain projection, leads to the fact that pain is also felt in the area of ​​skin receptors.

Anti-pain (antinociceptive) system. In the second half of the twentieth century, data were obtained on the existence of a physiological system that limits the conduction and perception of pain sensitivity. Its important component is the “gate control” of the spinal cord. It is carried out in the posterior columns by inhibitory neurons, which, through presynaptic inhibition, limit the transmission of pain impulses along the spinothalamic pathway.

A number of brain structures exert a downward activating effect on the inhibitory neurons of the spinal cord. These include the central gray matter, the raphe nuclei, the locus coeruleus, the lateral reticular nucleus, the paraventricular and preoptic nuclei of the hypothalamus. The somatosensory area of ​​the cortex integrates and controls the activity of the structures of the analgesic system. Violation of this function can cause unbearable pain.

The most important role in the mechanisms of the analgesic function of the CNS is played by the endogenous opiate system (opiate receptors and endogenous stimulants).

Endogenous stimulants of opiate receptors are enkephalins and endorphins. Some hormones, such as corticoliberin, can stimulate their formation. Endorphins act mainly through morphine receptors, which are especially abundant in the brain: in the central gray matter, raphe nuclei, and the middle thalamus. Enkephalins act through receptors located predominantly in the spinal cord.

Theories of pain. There are three theories of pain:

1.intensity theory . According to this theory, pain is not a specific feeling and does not have its own special receptors, but arises under the action of superstrong stimuli on the receptors of the five sense organs. Convergence and summation of impulses in the spinal cord and brain are involved in the formation of pain.

2.Specificity theory . According to this theory, pain is a specific (sixth) sense that has its own receptor apparatus, afferent pathways and brain structures that process pain information.

3.Modern theory pain is based primarily on the theory of specificity. The existence of specific pain receptors has been proven.

At the same time, in the modern theory of pain, the position on the role of central summation and convergence in the mechanisms of pain is used. The most important achievement in the development of modern pain theory is the study of the mechanisms of the central perception of pain and the analgesic system of the body.

pain receptors (nociceptors)

Pain receptors are free endings of sensitive myelinated and non-myelinated nerve fibers located in the skin, mucous membranes, periosteum, teeth, muscles, organs of the chest and abdominal cavity and other organs and tissues. The number of nocireceptors in human skin is approximately 100-200 per 1 sq. see skin surface. The total number of such receptors reaches 2-4 million. The following main types of pain receptors are distinguished:

1. Mechanociceptors: respond to strong mechanical stimuli, conduct rapid pain and quickly adapt.

2. Mechanothermic nociceptors: they react to strong mechanical and thermal (more than 40 degrees) stimuli, conduct rapid mechanical and thermal pain, quickly adapt.

3. Polymodal nociceptors: respond to mechanical, thermal and chemical stimuli, conduct poorly localized pain, adapt slowly.

Pathways of pain sensitivity.Pain sensitivity of the trunk and limbs, internal organs, from the receptors of which the fibers of the first neurons depart, are located in the spinal nodes. The axons of these neurons enter the spinal cord and switch to second neurons located in the posterior horns. Part of the pain impulses of the first neurons switches to flexor motor neurons and participates in the formation of protective pain reflexes. The main part of pain impulses (after switching in the posterior horns) enters the ascending pathways, among which the main ones are the lateral spinothalamic and spinal-reticular ones.

Pain sensitivity of the face and oral cavity is transmitted through the fibers of the first neurons of the trigeminal ganglion, which switch to the second neurons located mainly in the spinal nucleus (from skin receptors) and the pontine nucleus (from muscle and joint receptors) of the trigeminal nerve. From these nuclei, pain impulses are carried out along the bulbo-thalamic pathways. Along these pathways, part of the pain sensitivity is also carried from the internal organs along the afferent fibers of the vagus and glossopharyngeal nerves to the nucleus of the solitary pathway.

Thus, pain sensations are transmitted to the brain using two systems - medial and lateral.

The medial system runs through the central regions of the brain. She is responsible for persistent pain, transmits signals to the limbic system involved in emotional behavior. It is this medial system that provides the emotional component of pain, which is expressed in its characteristics such as “terrible”, “unbearable”, etc. The medial system consists predominantly of small fibers and terminates in the thalamus. This system transmits signals slowly, not adapted for accurate and fast transmission of information about strong stimuli in critical situations. It conveys diffuse discomfort.

The lateral pain system consists of nerve tracts projecting into the somatosensory cortex. It is most active with sudden, sharp (phasic) pain, pain with a clearly defined localization. The lateral pathways are responsible for the sensory quality of pain, i.e. the nature of the sensation - throbbing pain, prick, burning, etc. The activity of the lateral system quickly fades, so phasic pain is short-lived, it is subjected to powerful inhibition by other structures.

Nociceptive pain is a syndrome that every person has encountered at least once in their life. This term refers to pain caused by a damaging factor. It is formed when there is an influence on some tissue. Sensations are acute, in medicine they are called epicritical. Accompanied by the excitation of peripheral receptors responsible for the perception of pain. Signals are sent to the central nervous system. This transmission of impulse explains the localization of the onset of pain.

Physiology

Nociceptive pain appears if a person is injured, if an inflammatory focus develops, or ischemic processes occur in the body. This syndrome accompanies degenerative tissue changes. The area of ​​localization of the pain syndrome is precisely defined, obvious. When the damaging factor is removed, the soreness (usually) disappears. To weaken it, you can use classic anesthetics. The short-term effect of drugs is enough to stop the nociceptive phenomenon.

Nociceptive pain is physiologically necessary for the body to receive a warning about the unfavorable state of a certain area in time. This phenomenon is considered protective. If pain is observed for a long time, if an aggressive factor is excluded, but the pain still worries a person, it cannot be regarded as a signal. This phenomenon is no longer a symptom. It must be regarded as a disease.

It is known from statistics that most often the pain syndrome of this type in the form of a chronicle is formed when a person has arthritis. Muscular and skeletal pains of this nature are not uncommon.

What happens?

There are two main types of pain: nociceptive and neuropathic. The division into these categories is due to the pathogenesis of the phenomenon, the specific mechanisms by which the syndromes are formed. To assess the nociceptive phenomenon, it is necessary to analyze the nature of the pain and assess the scale, determine which tissues, where and how badly damaged. No less important for the analysis of the condition of patients is the time factor.

Nociceptive pain is associated with stimulation of nociceptors. These can be activated if the skin is deeply damaged, the integrity of bones, deeply located tissues, and internal organs is violated. Studies of intact organisms have shown the formation of the considered type of pain immediately upon the appearance of a local stimulus. If the stimulus is quickly removed, the syndrome immediately disappears. If we consider nociceptive pain in relation to surgical practices, we must recognize a relatively long-term effect on the receptors, accompanied in most cases by a large-scale working area. These aspects explain why the risk of persistent pain and the formation of an inflammatory focus is increased. Perhaps the appearance of an area of ​​chronic pain syndrome with the consolidation of this phenomenon.

About categories

There is pain: nociceptive somatic, visceral. The first is detected if a skin inflammatory area is formed, the skin or muscles are damaged, if the integrity of the fascial tissues, soft ones is violated. Somatic cases include the situation of damage and inflammation in the articular and bone zone, tendons. The second type of phenomenon is formed when damage is done to the internal cavity membranes and hollow, parenchymal organic structures. The hollow elements of the body may stretch excessively, and a spasmodic phenomenon may form. Such processes can affect the vascular system. Visceral pain appears with an ischemic process, an inflammatory focus and swelling of a certain organ.

The second category of pain is neuropathic. To more accurately understand the essence of nociceptive pain syndrome, you need to describe this class in order to know the differences. Neuropathic appears if the peripheral or central blocks of the National Assembly suffer.

Morbidity has an additional psychological aspect. It is human nature to fear the approach of pain. It is a source of stress and a factor that can provoke depression. There is a possibility of a psychological phenomenon of unresolved pain. Pain syndrome provokes sleep disorders.

Nuances of phenomena

As can be seen from the above, the types of nociceptive pain (somatic, visceral) have different neurological mechanisms. This fact is explained scientifically and is important for researchers. The differences in the mechanisms of pain formation are of particular importance for clinical practice. The somatic phenomenon, caused by irritation of nociceptors of the afferent somatic type, is localized clearly in the tissue area that is damaged due to some factor. The use of a classic anesthetic allows you to quickly alleviate the patient's condition. The intensity of the syndrome dictates the choice of an opioid analgesic or non-opioid.

Visceral nociceptive pain is due to specific features of the structure of internal organs, and a particularly important aspect is the innervation of such systems. It is known that the provision of performance due to nerve fibers for different internal structures is different. Many internal organs have receptors whose activation due to damage does not lead to awareness of the stimulus. Sensory perception is not formed. The patient does not identify pain. The organization of the mechanisms of such morbidity (against the background of somatic pain) has fewer separation mechanisms of sensory transmission.

Receptors and their features

Studying what is characteristic of nociceptive pain of the visceral type, it was found that the receptors, whose activity is necessary for sensory perception, are interconnected. There is a phenomenon of autonomous adjustment. Innervation of the afferent type, available in the internal organic structures of the body, is partially provided by indifferent structures. Such are able to go into an active state if the integrity of the organ is violated. Their activation is observed during the inflammatory process. Receptors of this class are one of the elements of the body responsible for chronic pain syndrome of the visceral format. Due to it, spinal reflexes are active for a long time. At the same time, autonomous adjustment is lost. The functionality of the organs is impaired.

Violation of the integrity of the organ, the inflammatory process are the reasons due to which the classic secretory and motor patterns of activity go astray. The environment in which receptors exist is changing unpredictably and dramatically. These changes will activate the silent elements. The sensitivity of the zone develops, visceral soreness appears.

Pain and its sources

An important characteristic of nociceptive pain is whether it belongs to a somatic or visceral type. It is possible to transmit a signal from one internal structure that has received damage to others. There is a possibility of projection of somatic tissues. Hyperalgesia in the area where the injury is localized is considered primary tenderness, other types are classified as secondary, since they are not localized in the area where there is damage.

Visceral nociceptive pain occurs when mediators, substances that provoke pain, appear in the area where the damage is localized. Perhaps inadequate stretching of muscle tissue or excessive contraction of this part of the hollow organ. In the parenchymal structure, the capsule in which the organ is enclosed can stretch. Smooth muscle tissues are subject to anoxia, vascular and ligamentous apparatus - traction, compression. Visceral pain syndrome of nociceptive type is formed during necrotic processes and the appearance of a focus of inflammation.

These factors are often encountered when operating on the intracavitary type. Operations of this class are particularly traumatic and are more likely to lead to dysfunctions and complications. Nociceptive pain, studied in neurology, is an important aspect, the study of which should provide new ways to improve methods and approaches to surgical intervention and anesthesia.

Categories: visceral type

Visceral hyperalgesia is observed directly in the affected organ. This is possible in the case of an inflammatory focus or stimulation of nociceptors. The viscerosomatic form is fixed in the area of ​​somatic tissues, which are affected by the projection of pain. Viscero-visceral is a format in which the pain syndrome spreads from one organ to another. The phenomenon is explained by the specific innervation provision of tissues. If it overlaps in some areas, the soreness spreads to new parts of the body.

About drugs

Treatment of nociceptive pain involves the use of specialized drugs developed for this purpose. If the syndrome is unforeseen, appears suddenly, the sensations are acute, due to surgical measures or the disease due to which surgery is prescribed, an analgesic should be chosen, taking into account the root cause of the condition. The doctor should immediately think over a system of measures to eliminate the cause of the pathology.

If a person is to be operated on, the situation is planned, it is important to predict the pain syndrome in advance and develop measures to prevent it. They take into account where the operation will be performed, how large the intervention is, how many tissues will be damaged, what elements of the nervous system will have to be affected. Preventive protection against pain is required, realized through a slowdown in the launch of nociceptors. Measures for anesthesia are carried out before the intervention of the surgeon.

Science and practice

Nociceptive somatic pain is known to result from the activation of nociceptors. Such elements of the body were first identified in 1969. Information about them appeared in scientific papers published by scientists Iggo and Pearl. Studies have shown that such elements are non-encapsulated endings. There are three types of elements. The excitation of a particular is explained by the stimulus affecting the body. There are: mechano-, thermo-, polymodal nociceptors. The first block of the chain of such structures is located in the ganglion. Affirents mainly find themselves in the spinal structures through the posterior roots.

Scientists, identifying the characteristics of nociceptive somatic pain, discovered the fact of transmission of nociceptive data. The main task of such information is the recognition of a damaging effect with an accurate definition of the site. Due to such information, an attempt to avoid exposure is activated. The transmission of information about the pain syndrome from the face, head is realized through the trigeminal nerve.

Syndromes: what are they?

To characterize nociceptive somatic pain, it is necessary to determine which pain syndrome has formed in a particular case. It can be psychogenic, somatogenic, neurogenic. The nociceptive syndrome is clinically divided into the following after surgery or trauma, due to oncology. There is also a syndrome associated with muscle, joint inflammation, gallstones.

Possibly psychogenic. Such pain is not due to somatic damage, but is associated with social influence and psychological influence. In practice, doctors are most often forced to deal with cases of a combined phenomenon, in which several forms of the syndrome are combined at once. In order to correctly formulate treatment tactics, it is necessary to identify all types and fix them in the patient's personal card.

Pain: sharp or not?

One of the key characteristics of nociceptive somatic pain is temporary. Any pain syndrome can be formed in the form of a chronicle or be acute. Acute is formed as a result of nociceptive influence: trauma, illness, muscle dysfunction. Influence is possible due to a violation of the functionality of some internal organ. In most cases, this type of pain is accompanied by endocrine stress, neuronal. Its strength is directly determined by the aggressiveness of the influence on the body. Nociceptive pain of this type is observed during the period of childbirth and against the background of an acute illness covering internal structures. Its task is to identify which tissue is damaged, to determine and limit the aggressive influence.

Considering what characteristics nociceptive somatic pain has, it should be recognized that most cases are characterized by the ability to resolve themselves. If this does not happen with a certain variant of the course, the syndrome disappears due to treatment. The duration of preservation is a matter of days, although less often the time frame stretches for weeks.

About the chronicle

Speaking about the characteristics of nociceptive somatic pain, one of the first to be mentioned is temporary. It is formed on the basis of acute. This usually happens if regenerative abilities are impaired or the patient received an incorrectly selected therapeutic program. A feature of chronic pain of the nociceptive type is the ability to persist if the acute stage of the disease has resolved. It is customary to talk about the chronicle, if enough time has passed, the person should have already been cured, but the pain syndrome is still bothering. The period of formation of the chronicle is from a month to six months.

Finding out what is characteristic of nociceptive somatic pain of the chronic type, it was found that the phenomenon is often formed due to the peripheral influence of nociceptors. There is a possibility of dysfunction of the PNS, CNS. In humans, the neuroendocrine response to stress factors is weakened, sleep disorders and an affective state are formed.

Kryzhanovsky's theory

This scientist published two papers on the features of pain. The first saw the light in the 97th, the second - in 2005. Determining what is characteristic of nociceptive somatic pain, he proposed to divide all cases of pain into pathological, physiological. Normally, pain is a physiological defense of the body, an adaptation reaction designed to exclude an aggressive factor. Pathological, however, has no protective functionality, hinders adaptation. Such a phenomenon cannot be overcome, it is difficult for the body, leads to a violation of the psychological status and disorders of the emotional sphere. CNS activity is disintegrated. People suffering from such pain are suicidal. The internal organs undergo changes, deformations, damage to the structure, functionality, vegetative work are disturbed, secondary immunity suffers.

Frequent myological pain. This accompanies somatic pathologies and diseases of the nervous system.

About treatment

If the pain syndrome is characterized as nociceptive, the therapeutic program should include three aspects. It is important to limit the flow of information from the area of ​​damage to the nervous system, slow down the production of algogens, their release into the body, and also activate antinociception.

Control of impulses from the area of ​​violation is provided by painkillers with a local effect. At the moment, lidocaine, novocaine are most often used. Studies have shown that such active compounds block sodium channels present in neuronal membranes and processes. Activation of the sodium system is a prerequisite for the presence of an action potential and an impulse.

Inhibition of afferentation requires the use of blockade approaches that affect the spinal structures and the peripheral nervous system. In some cases, superficial anesthesia is recommended, sometimes infiltration. For control, central or regional blockade can be used. The latter involves stopping the activity of peripheral elements of the NS.

About subtleties

Superficial anesthesia is necessary to prevent the activity of nociceptors. It is effective if the factor that provoked the pain is located in the skin, that is, superficial. General therapeutic, neurological practice allows infiltration with novocaine solution at a concentration of 0.25% to twice as high. Local anesthesia with ointments, gel-like substances is allowed.

Infiltration anesthesia allows you to deliver the analgesic to the deep skin layers and muscles that support the skeleton. More often for such purposes, "Procaine" is used.

The regional format is implemented by strictly highly qualified specialists who have been trained in this area. An incorrectly performed event with a high degree of probability initiates apnea, an epileptic seizure, and oppression of blood flow. In order to exclude and eliminate the complication in time, it is necessary to monitor the patient's condition, as defined by the standard of general anesthesia. In medicine, the nerves between the ribs, skin, radial, median, which ensure the work of the elbow, are actively used. Sometimes intravenous anesthesia of the arm is indicated. For this event, they resort to the technology developed by Beer.

Based on pathophysiological mechanisms, it is proposed to distinguish between nociceptive and neuropathic pain.

Nociceptive pain occurs when a tissue-damaging stimulus acts on peripheral pain receptors. The causes of this pain can be a variety of traumatic, infectious, dysmetabolic and other injuries (carcinomatosis, metastases, retroperitoneal neoplasms) that cause activation of peripheral pain receptors.

nociceptive pain- this is most often acute pain, with all its inherent characteristics. As a rule, the pain stimulus is obvious, the pain is usually well localized and easily described by patients. However, visceral pain, less clearly localized and described, as well as referred pain, is also classified as nociceptive. The appearance of nociceptive pain as a result of a new injury or disease is usually familiar to the patient and is described by him in the context of previous pain sensations. Characteristic of this type of pain is their rapid regression after the cessation of the damaging factor and a short course of treatment with adequate painkillers. However, it should be emphasized that prolonged peripheral irritation can lead to dysfunction of the central nociceptive and antinociceptive systems at the spinal and cerebral levels, which necessitates the fastest and most effective elimination of peripheral pain.

Pain resulting from damage or changes in the somatosensory (peripheral and (or) central) nervous system is referred to as neuropathic. Despite some, in our opinion, the failure of the term "neuropathic", it should be emphasized that we are talking about pain that can occur when there is a violation not only in the peripheral sensory nerves (for example, with neuropathies), but also in the pathology of somatosensory systems in all of its levels from the peripheral nerve to the cerebral cortex.

The following is a short list of causes of neuropathic pain, depending on the level of the lesion. Among these diseases, it should be noted the forms for which the pain syndrome is the most characteristic and occurs more often. These are trigeminal and postherpetic neuralgia, diabetic and alcoholic polyneuropathy, tunnel syndromes, syringobulbia.

"Pain syndromes in neurological practice", A.M. Vein

The possibility of habituation (habituation) with repeated stimuli in epicritical pain and the phenomenon of pain intensification (sensitization) in protopathic pain suggest different involvement of two afferent nociceptive systems in the formation of acute and chronic pain. Different emotional-affective and somatovegetative accompaniment in these types of pain also indicates the different involvement of pain afferentation systems in the formation of acute and chronic pain: ...

The fundamental aspect in the problem of pain is its division into two types: acute and chronic. Acute pain is a sensory reaction followed by activation of emotional motivational vegetative and other factors in violation of the integrity of the organism. The development of acute pain is associated, as a rule, with well-defined painful irritations of superficial or deep tissues, skeletal muscles and internal organs, dysfunction of the smooth ...

Pain Receptors and Peripheral Nerves Traditionally, there are two main theories of pain perception. According to the first, put forward by M. Frey, there are pain receptors in the skin, from which specific afferent pathways to the brain begin. It was shown that when human skin was irritated through metal electrodes, the touch of which was not even felt, “points” were detected, the threshold stimulation of which was perceived as a sharp unbearable pain. Second…

There are several hypotheses. According to one of them, pathological impulses from the internal organs, entering the posterior horn of the spinal cord, excite the conductors of pain sensitivity of the corresponding dermatomes, where the pain spreads. In accordance with another hypothesis, afferentation from visceral tissues on the way to the spinal cord switches to the cutaneous branch and antidromically causes an increase in the sensitivity of skin pain receptors, which ...

Various types of pain sensations are associated with the activation of afferent fibers of a certain caliber: the so-called primary - short-latency, well-localized and qualitatively determined pain and secondary - long-latency, poorly localized, painful, dull pain. It was experimentally shown that "primary" pain is associated with afferent impulses in A-delta fibers, and "secondary" - with C-fibers. However, A-delta and C-fibers are not exclusively ...

Nociceptive pain syndromes result from the activation of nociceptors in damaged tissues. Characterized by the appearance of areas of constant pain and increased pain sensitivity (decrease in thresholds) at the site of injury (hyperalgesia). Over time, the zone of increased pain sensitivity can expand and cover healthy tissue areas. There are primary and secondary hyperalgesia. Primary hyperalgesia develops in the area of ​​tissue damage, secondary hyperalgesia develops outside the damage zone, spreading to healthy tissues. The zone of primary hyperalgesia is characterized by a decrease in pain threshold (PT) and pain tolerance threshold (PT) to mechanical and thermal stimuli. Zones of secondary hyperalgesia have a normal pain threshold reduced by PPB only to mechanical stimuli.

The cause of primary hyperalgesia is the sensitization of nociceptors - non-encapsulated endings of A8 and C-afferents.

Sesitization of nociceptors occurs as a result of the action of pathogens released from damaged cells (histamine, serotonin, ATP, leukotrienes, interleukin 1, tumor necrosis factor a, endothelins, prostaglandins, etc.), formed in our blood (bradykinin), released from C-terminals. afferents (substance P, neurokinin A).

The appearance of zones of secondary hyperalgesia after tissue damage is due to sensitization of central nociceptive neurons, mainly the posterior horns of the spinal cord.

The zone of secondary hyperalgesia can be significantly removed from the injury site, or even located on the opposite side of the body.

As a rule, sensitization of nociceptive neurons caused by tissue damage persists for several hours and even days. This is largely due to the mechanisms of neuronal plasticity. A massive entry of calcium into cells through NMDA-regulated channels activates early response genes, which, in turn, change both the metabolism of neurons and the receptor potential on their membrane through effector genes, as a result of which neurons become hyperexcitable for a long time. Activation of early response genes and neuroplastic changes occur as early as 15 minutes after tissue damage.

Subsequently, sensitization of neurons can also occur in structures located above the dorsal horn, including the nuclei of the thalamus and the sensorimotor cortex of the cerebral hemispheres, forming the morphological substrate of the pathological algic system.

Clinical and experimental evidence suggests that the cerebral cortex plays a significant role in pain perception and the functioning of the antinociceptive system. The opioidergic and serotonergic systems play a significant role in this, and corticofugal control is one of the components in the mechanisms of the analgesic action of a number of drugs.

Experimental studies have shown that the removal of the somatosensory cortex responsible for the perception of pain delays the development of pain syndrome caused by damage to the sciatic nerve, but does not prevent its development at a later date. Removal of the frontal cortex, which is responsible for the emotional coloring of pain, not only delays development, but also stops the onset of pain in a significant number of animals. Different zones of the somatosensory cortex ambiguously relate to the development of the pathological algic system (PAS). Removal of the primary cortex (S1) delays the development of PAS, removal of the secondary cortex (S2), on the contrary, promotes the development of PAS.

Visceral pain occurs as a result of diseases and dysfunctions of the internal organs and their membranes. Four subtypes of visceral pain have been described: true localized visceral pain; localized parietal pain; radiating visceral pain; radiating parietal pain. Visceral pain is often accompanied by autonomic dysfunction (nausea, vomiting, hyperhidrosis, instability of blood pressure and cardiac activity). The phenomenon of irradiation of visceral pain (Zakharyin-Ged zone) is due to the convergence of visceral and somatic impulses on neurons of a wide dynamic range of the spinal cord.