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Pain and its consequences

Pain syndrome (pain) is a physical or emotional unpleasant sensation that is accompanied by a certain reaction of the body. With pain, metabolic processes intensify, involuntary movements occur, and work changes. internal organs, activity aimed at getting rid of the damaging factor increases. Prolonged pain causes changes in blood pressure, pulse rate, hormonal levels, as well as dilation of the pupils and paleness of the skin.

Features of acute pain

Pain can be divided into two large groups: acute and chronic. The acute form is short in time and its cause is quite simple to establish - it warns the body about damage to an organ or tissue, about the presence of any disease. This type of pain is concentrated in a specific area of ​​the body and usually responds well to treatment. Severe acute pain, such as from a severe injury, can lead to shock and, if emergency measures are not taken, death. The condition is relieved with drugs from the group of narcotic, non-narcotic analgesics or local anesthetics (novocaine blockade).

There are diseases in which even emergency doctors are not allowed to eliminate pain, as this can make it difficult to make a clinical diagnosis in a hospital. For example, in case of acute appendicitis, often accompanied by severe abdominal pain, the doctor uses an antispasmodic and immediately takes the patient to the hospital.

When is pain considered chronic?

Chronic pain was previously considered a condition that lasted more than six months. It is now defined as pain that persists beyond the expected time, for example, when the cause is eliminated, the disease is cured, but the painful sensations do not leave the patient. In some cases, chronic pain is an integral symptom of the disease (neuritis, some tumors, migraine, etc.). It is difficult to cure and requires special attention doctor

How do people respond to chronic pain?

It should be noted that pain and emotions are inseparable, so patients' reactions to chronic pain syndrome can vary greatly. A person either gets used to it and stops paying attention, switching to everyday activities, or “inflates” himself to an extreme state. In the latter case, the patient's attention is focused on the pain, his face expresses the felt suffering. He often seeks help from doctors and uses a huge variety of medications.

What should you do if you experience acute pain?

In case of acute pain, whether it is paroxysmal or constant, severe or moderate, you should call ambulance. First of all, this concerns pronounced discomfort in the abdomen and in the heart area (behind the sternum). IN emergency care people with a variety of traumatic injuries, chemical and thermal burns need it. Usually, already at the prehospital stage, this group of patients is given painkillers. This is followed by diagnostic measures carried out according to indications. These can be laboratory and instrumental methods, radiography, ultrasound, CT, MRI.

What should people with chronic pain syndrome do?

Most often, the diagnosis of “chronic pain syndrome” is made by exclusion, after consultation with a therapist, neurologist and other specialists. It is better for such patients to contact specialized clinics and pain centers. There, the examination of people with chronic pain syndrome, in addition to the standard diagnosis of physical pathology, includes a questionnaire to assess the emotional and sensory components of pain, as well as psychological tests.

Therapy for chronic pain consists of a whole range of measures: drug pain relief, restoration of biochemical processes in the brain (by taking antidepressants), psychotherapy, physical therapy, massage, physiotherapy, swimming, etc.

Complex regional (CRPS) is a chronic (lasting more than 6 months) condition that most often affects one extremity (arm, leg, foot), usually after injury. CRPS is thought to be caused by damage to or impairment of the peripheral and central nervous systems.

When a person has a heart attack, even if the damaged area is the heart, pain It is more often felt in the shoulder, back and neck area than in the chest area. We have known about it for many centuries, but we still do not know about its origin...

The central nervous system consists of the brain and spinal cord; The peripheral nervous system includes nerve signaling from the brain and spinal cord to the rest of the body. Pain syndrome is characterized by prolonged or excessive pain and changes in skin color, temperature and/or swelling in the affected area.

CRPS is classified into 2 types: CRPS-I and CRPS-II. Patients without documented nerve damage are diagnosed with CRPS-I (formerly known as reflex sympathetic dystrophy syndrome). The diagnosis of CRPS II (formerly known as causalgia) is made when there is associated, documented nerve injury. But some studies have found evidence of nerve damage in CRPS-I. However, the treatment is similar.

Symptoms vary in severity and duration, although some cases are mild and the problems eventually resolve. In more severe cases, patients cannot recover for a long time and suffer from long-term disability.

Although CRPS is more common in women, anyone at any age can experience the problem, with a peak in the 40s. It occurs rarely in older people, and extremely rarely in children under 10 years of age.

Symptoms

The key symptom is prolonged severe pain, which can be constant. It is described as burning, stabbing, pressing. The pain can spread to the entire limb, although only one finger is injured. In rare cases, the pain can sometimes even move to the opposite limb. There is often increased sensitivity in the affected area, known as allodynia, which makes normal skin contact very painful.

Patients also experience changes in temperature, skin color, or swelling of the affected limb. This occurs due to microcirculatory disorders caused by damage to the nerves that control blood flow and temperature. As a result, the affected arm or leg may feel warmer or colder compared to the opposite limb. The skin on the affected limb may change color and become mottled, bluish, purple, pale, or red.

Other common signs of pain:

  • changes in skin texture in the affected area - it may appear shiny and thinner;
  • profuse sweating in the affected area or surrounding areas;
  • slowing or accelerating the growth of nails and hair;
  • stiffness of the affected joints;
  • impaired motor coordination, with reduced ability to move the affected part of the body;
  • disturbances in movement of the affected limb, most often a fixed abnormal posture (dystonia), as well as trembling or twitching.

Video about pain syndrome

Causes

It is not clear why some people develop pain while others with a similar injury do not. In more than 90% of cases, the condition is caused by a clear history of trauma. Most common triggers:

  • fractures;
  • stretching/deformation;
  • soft tissue damage (such as burns, cuts, or bruises);
  • immobilization of limbs (for example, casting);
  • surgery or even minor medical procedures such as a needle stick.

Pain syndrome is an abnormal reaction in which the consequences become more pronounced. Some people overreact to a trigger that does not cause problems in others, as with a food allergy.

Peripheral nerve abnormalities found in people with CRPS typically involve small unmyelinated and thinly myelinated sensory nerve fibers (axons) that carry pain messages. Myelin is a mixture of proteins and fat-like substances that surround and insulate some nerve fibers. Because small fibers in nerves communicate with blood vessels, injuries to the fibers can cause many different symptoms. Molecules released from the ends of overactive small nerve fibers are thought to promote inflammation and damage to blood vessels. These abnormalities, in turn, cause damage to the spinal cord and brain.

Blood vessels in the affected limb may dilate or leak fluid into surrounding tissue, causing redness and swelling of the skin. The dilation and constriction of small blood vessels is controlled by small axons of nerve fibers as well as chemical messengers in the blood. Muscles and underlying tissues lose oxygen and nutrients, causing muscle and joint pain. Due to severe vasoconstriction, the skin becomes pale or bluish.

Pain also affects the immune system. An increase in inflammatory chemicals (cytokines) has been found in the tissues of such patients. They promote redness, swelling and warmth. CRPS is more common in people with other inflammatory and autoimmune conditions, such as asthma.

Limited evidence suggests that CRPS may also be influenced by genetics. Familial pain syndrome may be more severe, characterized by early onset, severe dystonia, and involvement of two or all limbs.

Sometimes CRPS develops without any known trauma. In these cases, an infection, a blood vessel problem, or a nerve injury may have caused internal injury. The doctor will conduct a thorough examination to determine the cause.

In many cases, pain occurs for a number of reasons. In such cases, treatment is aimed at all contributing factors.

Diagnostics

There is currently no specific test that can confirm the condition. Its diagnosis is based on the person's medical history and the signs and symptoms that meet the definition. Because other health problems can cause similar symptoms, a thorough examination is especially important. As the condition gradually improves over time in most people, making a diagnosis may be more difficult later in the course of the disorder.

Diagnostic tests are used to rule out other diseases such as arthritis, Lyme disease, generalized muscle disorders, and minor polyneuropathies.

Magnetic resonance imaging or a three-phase bone scan may be required to confirm the diagnosis. While pain is often associated with excess bone resorption, the process by which certain cells break down bone and release calcium into the blood can occur in other diseases.

Forecast

The outcome of CRPS varies greatly. Young people and children have better results. The elderly can also expect a good prognosis, but in some cases suffer severe pain and disability despite treatment. There is some suggestion that early treatment, especially rehabilitation, is beneficial, but this has not yet been proven in clinical trials. More research is needed to understand the causes of CRPS, how it progresses, and the role of early treatment.

Treatment of pain syndrome

The following treatment methods are often used:

  • Rehabilitation and physiotherapy. An exercise program can help improve blood flow and reduce symptoms. Additionally, the exercises help improve flexibility, strength, and function of the affected area. Rehabilitation of the affected limb may also help prevent or reverse secondary brain changes associated with chronic pain. Occupational therapy can help a person learn new ways of working and performing daily tasks.
  • Psychotherapy. CRPS and other painful conditions are often associated with deep psychological symptoms. The patient may develop depression, anxiety, or post-traumatic stress disorder, which will only increase the perception of pain and complicate rehabilitation efforts. Treatment of these secondary conditions is important to help people cope and recover from pain.
  • Medications. Several different classes of drugs have been reported to be effective, especially when used on early stage diseases. However, no single drug or combination of drugs guarantees a complete cure for every person. Drugs to treat CRPS include:
  • Bisphosphonates, such as high-dose adendronate or intravenous pamidronate.
  • Nonsteroidal anti-inflammatory drugs for the treatment of moderate pain, including aspirin, ibuprofen, and naproxen.
  • Corticosteroids, which treat inflammation and swelling, such as prednisolone and methylprednisolone (mostly in the early stages).
  • Drugs originally developed to treat seizures or depression but now shown to be effective for neuropathic pain, such as gabapentin, pregabalin, amitriptyline, nortriptyline and duloxetine.
  • Botulinum toxin injections.
  • Opioids such as oxycodone, morphine, hydrocodone, and fentanyl. These drugs must be prescribed and administered under close medical supervision as they may be addictive.
  • N-methyl-D-aspartate (NMDA) receptor antagonists such as dextromethorphan and ketamine.
  • Local anesthetic creams and patches, such as lidocaine.
    All medications or a combination of medications may have different side effects such as drowsiness, dizziness, increased heart rate and memory impairment. The patient must inform the doctor about any changes after starting drug therapy.
  • Sympathetic nerve blockade. Some people report temporary pain relief after the block, but there is no published evidence of long-term benefit. The procedure involves injecting an anesthetic near the spine to block sympathetic nerve activity and improve blood flow.
  • Surgical sympathectomy. The use of this surgery, which destroys some nerves, is controversial. Some experts believe that it is unnecessary and worsens the condition, while others report favorable results. Sympathectomy should only be used in people whose pain is significantly relieved (albeit temporarily) by the block.
  • Spinal cord stimulation. Placing stimulating electrodes through a needle into the spine near the spinal cord produces a tingling sensation in the painful area. Electrodes may be temporarily placed for a few days to assess whether stimulation may be beneficial. Minor surgery is necessary to implant all parts of the stimulator, battery and electrodes under the skin on the torso. Once implanted, the stimulator can be turned on and off and adjusted using an external controller. About 25% of people experience hardware problems that may require additional surgery.
  • Other types of neural stimulation. Neurostimulation can be performed at other locations along the pain pathway, not just at the spinal cord. These are nearby damaged nerves (peripheral nerve stimulators), outside the membranes of the brain (motor cortex stimulation with dural electrodes), and inside parts of the brain that control pain (deep brain stimulation). Recently, the use of magnetic currents applied externally to the brain (known as repetitive transcranial magnetic stimulation or rTMS) has been developed. A similar method that uses transcranial direct electrical stimulation is also being explored. These methods are non-invasive but require repeated treatment sessions.
  • Intrathecal narcotic pumps. These devices pump pain medications directly into the cerebrospinal fluid, typically opioids, local anesthetics, clonidine and baclofen. This makes it possible to reach targets in the spinal cord using lower doses compared to oral administration, which reduces side effects and increases the effectiveness of the drug.

New treatments for CRPS:

  • Intravenous immunoglobulin. Researchers in the UK reported reduced pain intensity in a small study of 13 patients with CRPS after receiving intravenous immune globulin for 6 to 30 months.
  • Ketamine. Researchers used low doses of ketamine, administered intravenously over several days, to significantly reduce or eliminate chronic pain. Ketamine has been shown to be useful in treating pain that does not respond well to other treatments.

Several alternative treatments have been used to treat other disease conditions. Options include behavior modification, acupuncture, relaxation techniques (biofeedback, progressive muscle relaxation, and guided movement therapy), and chiropractic.

Research

Previous research has shown that inflammation associated with pain is caused by the body's own immune response. Researchers hope to better understand how CRPS develops by studying immune system activation and peripheral nerve signaling using animal models. The model was designed to mimic some of the symptoms following fracture or limb surgery by activating certain molecules involved in the immune system.

Trauma to a limb, such as a fracture, followed by immobilization in a cast, is the most common cause of CRPS. By studying the model, the researchers hope to better understand the neuroinflammatory basis of the syndrome in order to identify the relevant inflammatory signaling pathways that lead to the development of post-traumatic CRPS.

They are also studying the inflammatory effects of immobilization and exercise on pain development. Peripheral nerve damage and subsequent regeneration often lead to various sensory changes. Researchers hope to identify specific cellular and molecular changes in sensory neurons after peripheral nerve injury to better understand the processes underlying neuroplasticity (the ability of the brain to reorganize or form new neural connections and pathways after injury or nerve cell death). Identifying these mechanisms would provide an opportunity to develop new drugs that could improve recovery from regeneration.

Children and adolescents with CRPS generally have a better prognosis than adults, which may provide insight into the mechanisms that help prevent chronic pain. Scientists study sick children because their brains adapt more quickly through a mechanism known as neuroplasticity. Scientists hope to use these discoveries to develop more effective treatments.

M.L. Kukushkin, G.R. Tabeeva, E.V. Podchufarova

PAIN SYNDROME:

pathogenesis, clinic, treatment

Edited by acad. RAMS N.N. Yakhno

IMA-PRESS, Moscow, 2011

UDC 616-009.7-07 BBK 52.5

Clinical recommendations. Pain syndrome: pathophysiology, clinical picture, treatment. M.L. Kukushkin, G.R. Tabeeva, E.V. Podchufarova. Ed. acad. RAMS N.N. Yakhno. - M.: IMA-PRESS, 2011. - 72 p.

The book outlines modern ideas about the physiology of pain, pathophysiological mechanisms of pain syndromes, diagnostic methods, clinical features and treatment of the most common forms of pain - headaches and back pain.

The book is intended for therapists, general practitioners, and neurologists.

Yakhno Nikolay Nikolaevich- Doctor of Medical Sciences, Professor, Academician of the Russian Academy of Medical Sciences, Head. Department of Nervous Diseases of the First Moscow State Medical University named after. THEM. Sechenov

Kukushkin Mikhail Lvovich- Doctor of Medical Sciences, Professor, Head. Laboratory of Pathophysiology of Pain Institutions of the Russian Academy of Medical Sciences Research Institute of General Pathology and Pathophysiology of the Russian Academy of Medical Sciences Tabeeva Gyuzal Rafkatovna- Doctor of Medical Sciences, Professor, Head. Department of Neurology and Clinical Neurophysiology, Professor of the Department of Nervous Diseases, Faculty of Medicine, First Moscow State Medical University named after. THEM. Sechenov

Podchufarova Ekaterina Vladimirovna - Candidate of Medical Sciences, Assistant at the Department of Nervous Diseases of the First Moscow State Medical University named after. THEM. Sechenov

Russian Interregional Society for the Study of Pain, 2011 IMA-PRESS, 2011

Content

Chapter 1 . PHYSIOLOGY AND PATHOPHYSIOLOGY OF PAIN

1.1. Nociceptive system................................................... ..........

1.2. Antinociceptive system................................................... ....

1.3. Pathophysiology of nociceptive pain....................................................

1.4. Pathophysiology of neuropathic pain.................................................

1.5. Pathophysiology of psychogenic pain....................................................

Chapter 2. HEADACHE ................................................ ........................

2.1. Migraine................................................. ........................................

2.2. Tension headache................................................................... ......

2.3. Trigeminal vegetative

(autonomous) cephalgia.................................................... ............

2.4. Secondary headache........................................................

Chapter 3. BACKACHE ............................................... ............................

3.1. Epidemiology, risk factors,

sources and classification of back pain...................................

3.2. Examination of patients........................................................ ........

3.3. Compression radiculopathy............................................................

3.4. Musculoskeletal back pain....................................................

3.5. Treatment................................................. ...................................

LIST OF USED ABBREVIATIONS

TTH - tension headache

GK – glucocorticoids

Gastrointestinal tract - gastrointestinal tract

IHD – coronary heart disease

CONX – short-term unilateral neuralgic headache with conjunctival injection and lacrimation

CT – computed tomography

MA – migraine with aura

MbA - migraine without aura

ICHD – International Classification of Headaches

MRI – magnetic resonance imaging

MFPS – myofascial pain syndrome

NSAIDs – non-steroidal anti-inflammatory drugs

PG – paroxysmal hemicrania

PHB – cluster headache

PIR – post-isometric relaxation

RFD – radiofrequency denervation

TVC – trigeminal vegetative (autonomous) cephalgia

TZ – trigger zones

CGTH – chronic tension headache

CNS - central nervous system

COX - cyclooxygenase

EGTH – episodic tension headache

EchoCG – echocardiography

EEG – electroencephalography

COMT – gene encoding the synthesis of the enzyme catecholamine-O-methyltransferase

Pain is the most common and subjectively difficult complaint of patients. It causes suffering to millions of people around the world, significantly reducing the quality of life. Bad influence pain affects not only the patients themselves, but also their immediate environment. The problem of pain, due to the high prevalence and diversity of its forms, is so important that in many countries specialized pain centers and clinics have been created to treat patients with acute and chronic pain syndromes.

By biological origin, pain is a signal of danger and trouble in the body and in medical practice it is often considered as a symptom of any disease that occurs when tissue is damaged due to injury, inflammation or ischemia. Without the feeling of pain, the existence of humans and animals is impossible. This sensation forms a whole complex of defensive reactions aimed at eliminating damage.

Pain is always subjective and each person experiences it differently. The same irritation can be perceived by our consciousness in different ways. The perception of pain depends not only on the location and nature of the injury, but also on the conditions or circumstances under which it occurred, on the psychological state of the person, his individual life experience, culture, and national traditions. Individual perception of pain is influenced by gender, age, social factors, ethnic characteristics, and religion. 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 such interaction will be the individual nature of the pain sensation and the form of the patient’s response to pain. According to this model, behavior, emotions, and even simple physiological reactions change depending on a person's attitude to current events. The sensation of pain can persist and be maintained, including due to expected unpleasant consequences of damage, which are often exaggerated by man, and in some cases even overly dramatized. The patient’s personal position and beliefs, his individual strategies for overcoming difficulties, as well as his attitude towards treatment influence both the intensity of pain and the effectiveness of the therapy. In other words, the severity of the damage and the intensity of pain often do not correlate with each other.

Pain sensation is a consequence of activation of the nociceptive system. This can occur at the level of either nociceptive receptors in tissues or nociceptive afferents when peripheral nerves are damaged, or when central nociceptive structures are damaged or dysfunctional.

Chapter 1. Physiology and pathophysiology of pain

1.1. Nociceptive system

The perception of damaging stimuli is carried out by nociceptors - sensitive receptors that are responsible for the transmission and encoding of damaging stimuli. Nociceptors are free nerve endings of peripheral A-delta and C-fibers, the bodies of which are located mainly in the spinal ganglia and the trigeminal ganglion. Nociceptors are widely present in the skin, subcutaneous tissue, periosteum, joints, muscles and internal organs.

Nociceptors can be activated by a strong mechanical stimulus (puncture) or thermal stimulation (heating or cooling), as well as by the action of a number of chemicals (such as inflammatory mediators) that cause pain in minimal concentrations. Because of their varying sensitivity to mechanical, thermal, and chemical stimuli, nociceptors represent a heterogeneous group. Some nociceptors respond exclusively to chemical stimuli, others to mechanical and/or temperature ones. Some nociceptors (“silent” nociceptors) under normal conditions do not respond to any of these stimuli and become excitable after tissue damage or inflammation. Chemical substances(algogens) capable of activating nociceptors are divided into three groups: tissue algogens, released into the extracellular environment when tissue is damaged from mast cells (histamine), platelets (serotonin, ATP), neutrophils (leukotrienes), macrophages (interleukin 1, tumor necrosis factor α), endothelium (interleukin 1, tumor necrosis factor α, endothelins, prostaglandins, nitric oxide); blood plasma algogens(bradykinin, kallidin); algogens released from peripheral endings C-nociceptors (substance P, neurokinin A, cocalcigenin).

IN In most cases, the stimulating effect of algogens on the peripheral endings of nociceptors is realized through their interaction with the corresponding membrane receptors. Thanks to the achievements molecular biology Currently, receptors for bradykinin, serotonin, prostaglandins, ATP, capsaicin, nociceptin, histamine, hydrogen ion, etc. have been identified on the nociceptor membrane.

The spread of excitation from the nociceptors of the trunk and limbs is carried out with the help of weakly myelinated A-delta fibers and unmyelinated fibers - C-afferents - which are part of the mixed somatic nerves.

IN dorsal roots of spinal nerves and sensory root of the trigeminal nerve A-delta and C-afferents are sent respectively to the spinal cord and medulla oblongata, where signal transmission to 2nd order nociceptive neurons occurs. An important role in the activation of these neurons belongs to excitatory amino acids (glutamate, aspartate), as well as substance P, neurokinin A and cocalcigenin. Excitatory amino acids (glutamate, aspartate) are contained in more than half of the neurons of the spinal ganglia and

Chapter 1. Physiology and pathophysiology of pain

are released from their central presynaptic terminals in the dorsal horns of the spinal cord under the influence of nociceptive impulses. It is believed that the implementation of physiological nociceptive reactions (for example, a protective withdrawal reflex) during the release of glutamate is mediated through AMPA receptors, while NMDA receptors ensure the development of long-term hyperactivity of nociceptive neurons, which may underlie the formation of hyperalgesia. Cocalcigenin (or calcitonin gene-related peptide) provides excitation of nociceptive neurons of the dorsal horn under thermal, mechanical and chemical damaging influences. The synthesis of this peptide by nociceptive neurons increases sharply during inflammation of peripheral tissues. Substance P is found in more than 90% of neurons containing glutamate. With tissue damage, an increase in the concentration of substance P in the dorsal horn of the spinal cord correlates with an increase in the excitability and reactivity of nociceptive neurons in the dorsal horn.

Nociceptive neurons of the dorsal horns of the spinal cord form ascending tracts ( spinothalamic, spinoreticular and spinomesencephalic), carrying out nociceptive signals to various subcortical parts of the brain and thalamic nuclei.

From the thalamic nuclei, pain signals enter the cerebral cortex, which is the highest integrative link of the nociceptive system. Great importance in the analysis of nociceptive information is given somatosensory cortex, insular cortex, anterior cingulate cortex, anterior frontal cortex, and posterior parietal cortex. The somatosensory areas of the cerebral cortex evaluate pain signals, forming sensations associated with the localization, intensity and nature of the pain sensation. The associative areas of the cerebral cortex (the insular cortex, the anterior part of the cingulate cortex, the prefrontal cortex and the posterior part of the parietal cortex) ensure the formation of the mental components of pain and the appropriate behavior associated with it. In turn, the cortical sections have close bilateral connections with the thalamic nuclei, structures of the limbic system (amygdala, hippocampus, fornix, septum, entorhinal cortex), reticular formation of the brain stem, and hypothalamus. This organization of the nociceptive system under conditions of damage ensures the inclusion of not only sensory and motivational-affective components of pain, but also memory mechanisms and autonomic reactions.

Thus, the nociceptive system, which ensures the formation of pain, is multi-level and hierarchically organized.

1.2. Antinociceptive system

The activity of the complexly organized nociceptive system of humans and animals is controlled by the endogenous system of inhibition of nociceptive signals, or antinociceptive system. Activating nociceptive

Chapter 1. Physiology and pathophysiology of pain

tive signals, the structure of the antinociceptive system using a loop feedback inhibit the transmission of pain impulses, inhibiting nociceptive neurons in the dorsal horns of the spinal cord, reticular formation, and thalamic nuclei.

Electrical stimulation of the structures of the antinociceptive system, especially the raphe nuclei, the central gray matter of the brain stem, and the tegmental nuclei of the midbrain, causes pain relief in humans and animals.

There are close anatomical bilateral connections between the structures of the antinociceptive system, uniting individual formations into a single network and ensuring the selective activation of neurochemical mechanisms of pain inhibition. The opioidergic, serotonergic, noradrenergic and cannabinoid systems of the brain are of greatest importance in the neurochemical mechanisms of pain relief.

1.3. Pathophysiology of nociceptive pain

All pain syndromes, depending on the etiopathogenesis, can be 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 arise due to activation of nociceptors during injury, inflammation, ischemia, and tissue edema. Clinically, they include: post-traumatic and postoperative pain syndromes, pain due to inflammation of the joints, myofascial pain syndromes (MFPS), vascular pain, pain in cancer patients, angina pain, pain due to cholelithiasis, etc.

As a rule, when superficial tissues are damaged, patients experience severe pain. If muscles or bones are involved in the pathological process, a feeling of dull, aching pain occurs. This pain increases with movement and decreases with rest. Somatic pain is usually well localized and clearly felt in the affected area. The pain that occurs when visceral organs are damaged is usually poorly localized, as it is transmitted mainly through C-fibers, and is perceived as deep, compressive, and cramping. It may be accompanied by nausea, vomiting, changes in heart rate and depth of breathing, and profuse sweating. With pathology of the visceral organs, along with deep pain, zones of reflected pain (Ged-Zakharyin zones) appear.

In addition to complaints of constant pain, patients with nociceptive pain develop zones of increased pain sensitivity (zones of hyperalgesia). There are primary and secondary hyperalgesia. Primary hyperalgesia develops in the area of ​​damaged tissue, secondary hyperalgesia is localized outside the damaged area, spreading to healthy tissue. The development of primary hyperalgesia is based on phenomenon of peripheral sensitization

Chapter 1. Physiology and pathophysiology of pain

(increased sensitivity of nociceptors to the action of damaging stimuli). Secondary hyperalgesia occurs as a result central sensitization(increased excitability primarily of nociceptive neurons of the dorsal horns of the spinal cord).

Sensitization of nociceptors occurs due to the action of algogens coming from the blood plasma and released from damaged tissue, as well as from the peripheral terminals of C-nociceptors. Neuropeptides of C-nociceptors have a pro-inflammatory effect and, released upon activation of C-nociceptors, lead to the development of “neurogenic inflammation”, causing vasodilation and an increase in their permeability. In addition, they promote the release of prostaglandins, cytokines and biogenic amines from mast cells and leukocytes, which in turn, acting on the free nerve endings of nociceptors, increase their excitability.

The presented mechanisms of increased excitability 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.

The leading mechanism of sensitization of central nociceptive neurons is the long-term depolarizing effect of glutamate and neurokinins on the membranes of nociceptive neurons of the dorsal horn. Last years were also marked by the discovery of the important role of immune and glial cells and the cytokines, chemokines and growth factors they secrete in this process. In addition to sensitization of nociceptive neurons in the dorsal horn, tissue damage initiates an increase in the excitability of nociceptive neurons in overlying centers, including the nuclei of the thalamus and the somatosensory cortex of the cerebral hemispheres.

Thus, peripheral damage triggers a cascade of pathophysiological processes affecting the entire nociceptive system - from tissue receptors to cortical neurons, causing persistent changes in excitability in them, which are manifested by an increase in pain sensitivity.

The severity and duration of peripheral and central sensitization during nociceptive pain directly depend on the nature and duration of tissue damage. In cases of tissue healing, the phenomenon of peripheral and central sensitization will also disappear, and vice versa, the longer the damage and inflammation persist, the longer the pain sensation will be. For example, in patients with degenerative joint disease, the progression of the disease will be accompanied by an increase in the duration of pain.

1.4. Pathophysiology of neuropathic pain

Neuropathic pain, as defined by experts from the International Association for the Study of Pain, is a consequence of primary damage or dysfunction nervous system. However, at the 2nd International Congress on Ne-

Chapter 1. Physiology and pathophysiology of pain

ropathic pain (2007) proposed changes to this definition. According to this proposal, neuropathic pain refers to pain resulting from direct damage or disease to the somatosensory system. Neuropathic pain can occur when both the peripheral nervous system and the central structures of the somatosensory analyzer are damaged. The causes of damage to the peripheral nervous system can be metabolic disorders, trauma, intoxication, infectious process, mechanical compression, vitamin deficiencies. The causes of neuropathic pain due to damage to the structures of the central nervous system - the central nervous system (in the domestic literature, such pain syndromes are also called “central pain”) are considered to be injuries to the spinal cord and brain, ischemic and hemorrhagic strokes leading to a deficiency of somatosensory sensitivity, and demyelinating diseases ( multiple sclerosis), syringomyelia, etc. Neuropathic pain most often occurs in the form of painful diabetic polyneuropathy and postherpetic neuralgia. Not only neurologists encounter painful polyneuropathies; this pathology is often observed in rheumatic diseases - periarteritis nodosa, rheumatoid arthritis, systemic lupus erythematosus. At least a third of cancer patients suffer from neuropathic pain due to the impact of the tumor on nerve structures, nerve damage from chemotherapy, radiation therapy, or major surgery.

The pathophysiological basis of neuropathic pain syndromes is a violation of the mechanisms of generation and conduction of the nociceptive signal in nerve fibers and the processes of control of the excitability of nociceptive neurons in the structures of the spinal cord and brain. Damage to nerves leads to structural and functional transformations in the nerve fiber: the number of sodium channels on the nerve fiber membrane increases, new atypical receptors and zones for generating abnormal ectopic impulses appear, mechanosensitivity occurs, and conditions are created for cross-excitation of dorsal ganglion neurons. As a result, an inadequate response of the nerve fiber to irritation is formed, which contributes to a significant change in the pattern of the transmitted signal. Increased impulses from the periphery disorganize the work of central structures: sensitization of nociceptive neurons occurs, the death of inhibitory interneurons occurs, neuroplastic processes are initiated, leading to new interneuron contacts of tactile and nociceptive afferents, and the efficiency of synaptic transmission increases. Under these conditions, a special pain symptom complex is formed, which is clinically manifested by a combination of negative symptoms in the form of partial or complete loss of sensitivity (including pain) and positive symptoms with the simultaneous appearance in the affected area of ​​unpleasant, often pronounced, pain in the form of allodynia, hyperalgesia, dysesthesia, hyperpathia.

Inflammatory and degenerative diseases of the joints and spine, myositis, bursitis, tendovaginitis and periarthritis of various localizations, which, according to international classification diseases of the 10th revision comprise class XIII - diseases of the musculoskeletal system and connective tissue, which are in fourth place in terms of prevalence after diseases of the circulatory system, breathing and digestion. In the practice of a therapist, patients with diseases of the musculoskeletal system are encountered quite often. According to WHO, over 4% of the population globe suffer from various diseases of the joints and spine. In more than 30% of cases, temporary disability and in 10% of patients' disability are associated with rheumatic diseases.

Currently, musculoskeletal pathology has become the focus of attention of the entire world scientific community. It is known that the main symptom uniting rheumatic diseases is pain in the joints and spine of varying degrees of severity. Let's look at the basic mechanisms of pain formation in rheumatological pathology, and also consider character traits rheumatic pain, regardless of nosological affiliation, and then the nature of the pain syndrome in some rheumatic diseases.

The main mechanisms of pain in rheumatology and their manifestations are as follows::
Nociceptive (activation of pain receptors)
referred pain
arthralgia
myalgia
myofascial syndrome (MFS) (trigger points)
Neuropathic pain
algoneurodystrophy
carpal tunnel syndrome
Psychogenic pain
discrepancy between complaints and objective signs of pain
non-localized nature of pain, its migration
treatment failure
numerous "crises"

Typically, damage to peripheral joints and the spine in rheumatic diseases is accompanied by moderately severe but persistent pain, the intensity of which changes in a certain way during the day. Traditionally in rheumatology, it is customary to distinguish two main types of arthralgia: inflammatory and mechanical.

Inflammatory joint pain observed in chronic arthritis. They are worse at night and in the morning, often accompanied by morning stiffness. After warming up, pain and stiffness decrease. Symptoms of this kind are characteristic of an inflammatory process that occurs as a result of the immune system’s reaction to a foreign antigen, when the immune response does not eliminate the damaging factor, and it persists in the body, maintaining the chronic course of the pathological process. Neutrophils, lymphocytes, and macrophages accumulate in the affected joint, which produce proinflammatory cytokines, prostaglandins, leukotrienes, free oxygen radicals and other compounds that mediate the development of inflammation.

Mechanical pain characteristic of degenerative joint damage in patients with osteoarthritis. They are more pronounced at the end of the day and in the first half of the night, decreasing in the morning. After physical activity, the pain intensifies, but subsides with rest. A type of mechanical pain is starting pain, which occurs immediately at the beginning of the movement and subsides as it continues. Osteoarthritis pain may be partly due to trabecular microfractures and venous congestion in bone tissue. However, the key role in its occurrence appears to be played by the development of a chronic inflammatory process.

It should be noted, however, that even with arthritis, the intensity of pain does not always correlate with the severity of other signs of inflammation. Severe pain syndrome is sometimes observed with an almost complete absence of joint swelling and normal laboratory test results. It can be assumed that in such cases the intensity of pain may increase due to factors such as impaired microcirculation, muscle spasm, and a decrease in the threshold of pain sensitivity.

So, distinctive feature Rheumatic pain is closely related to inflammation, which in one form or another accompanies all rheumatic diseases. The inflammatory process in rheumatic diseases does not have any specific symptoms, it occurs as a reaction of the body to the action of various damaging agents and in most cases becomes chronic due to constant pathogenic stimulation. Features of its development and localization determine the uniqueness of the clinical picture within each specific nosological form.

Polymyalgia rheumatica. The disease develops acutely. As a rule, suddenly and without apparent reason intense pain appears in the muscles of a jerking, cutting, pulling nature. The localization and nature of pain are stereotypical: the neck, shoulder girdle, pelvic girdle. In 100% of cases, the lesions are symmetrical, although at the very beginning the lesion may be one-sided. At the same time, pain is observed in at least two of these three areas. Pain can also occur in other areas of the musculoskeletal system (hips, legs, buttocks, back, even forearms), but not as naturally. Constant pain of a cutting, pulling, tearing nature sharply intensifies with movement. With rest, the pain usually subsides, although in 25–30% of cases its intensity remains. Night pain is often disturbing, which intensifies under the influence of body weight and pressure. The intensity of pain is related to the activity of the disease. Because of the pain, movements are limited: it is difficult for patients to stand up, sit down, raise their arms, place them behind their backs, it is impossible to enter a vehicle without help, etc. Morning stiffness and a feeling of stiffness after any period of immobility are typical.

Fibromyalgia. Clinically, fibromyalgia is defined as diffuse, symmetrical musculoskeletal pain of a chronic nature. The pain in fibromyalgia is monotonous, worsening after emotional stress and physical fatigue, as well as in a state of immobility, after cooling and postural strain. Pain is relieved after exposure to heat, massage, and rest. Despite the fact that the intensity of pain can change during the day, pain accompanies a person constantly, i.e. Subjectively, patients do not notice “light gaps.” The distribution of pain sensations is equally characteristic. Despite the fact that the patients themselves complain of local pain, upon active questioning, as a rule, everyone notes the presence of “pain everywhere.” Pain is the main cause of disability (about a third of patients do not work due to chronic pain). However, a pronounced dissociation between the low intensity of algic phenomena proper and the pronounced degree of maladaptation of patients is very characteristic of fibromyalgia. From a practical point of view, very important for the clinical verification of fibromyalgia is the study of its specific sensitive points, which are designated “tender points” (TP). One of the most characteristic features of these pain points is the reproducibility upon palpation of the pain that occurs spontaneously in patients. The number of points may vary. There are descriptions of the presence of up to 70 sensitive points in one patient. The importance of their study is also determined by the high degree of correlation between the amount of TR and the severity of the main clinical symptoms of fibromyalgia. “Fibromyalgic points” are located at the attachment points of muscles and tendons in a strictly symmetrical manner. The diagnostic criterion for fibromyalgia is pain on palpation of at least 11 out of 18 (9 pairs) of specific sensitive points: occipital region - the place of attachment of the m.suboccipitalis; neck region - anterior sections of the spaces between the transverse processes of C5-7; trapezius muscle - middle of the upper edge; supraspinatus muscle at its insertion; the zone of articulation of the 11th rib with the sternum along its upper edge; a point located 2 cm distal to the external epicondyle of the shoulder; in the gluteal region - the upper outer quadrant of the buttock along the anterior edge of the muscle; greater trochanter of the femur; in the area of ​​the knee joint - the medial fat pad.

Dermatomyositis-polymyositis. Dermatomyositis is characterized by predominant damage to skeletal muscles and skin. In cases where there are no skin changes, they speak of polymyositis. Inflammatory lesions of striated muscles are the main and earliest symptom of dermatomyositis-polymyositis. It is based on necrotizing polymyositis. All skeletal muscles can be damaged simultaneously or sequentially. However, at the onset of the disease, the most typical symmetrical damage to the skeletal muscles is predominantly in the proximal parts of the limbs, neck and back, while the distal muscles of the limbs are damaged less frequently and insignificantly. In severe cases, all striated muscles are involved in the pathological process, including facial, oculomotor, chewing, lingual pharyngeal, laryngeal and esophageal muscles, as well as respiratory muscles, myocardium, sphincters of the rectum and bladder. In the early stages, muscle syndrome manifests itself as fatigue. Subsequently, increasing weakness of predominantly symmetrical muscle groups of the shoulder girdle, neck and proximal region is noted lower limbs– myopathic syndrome. In the acute phase of the disease and during exacerbations, patients note pain in the affected muscles, especially during active movements. Palpation reveals swelling, dough-like consistency and soreness of the affected muscles. The skin over them is swollen. In contrast to neurogenic damage, tendon reflexes and sensitivity are preserved, and muscle weakness does not decrease after taking proserin and its analogues. During periods of remission, swelling and soreness of skeletal muscles disappear, muscle strength is gradually restored. However, as the disease progresses, muscle atrophy increases with each new exacerbation due to the replacement of dead muscle fibers with fibrous tissue. In this case, muscle weakness becomes permanent, the muscles become thinner and acquire a woody density.

Eosinophilic myalgia syndrome, diffuse fasciitis with eosinophilia. Manifestations of muscle damage in eosinophilic myalgia syndrome are sudden myalgia. A year after the onset of the disease, myalgia persists in more than 50% of patients. Severe painful muscle spasms are observed in 43-90% of patients with chronic eosinophilic myalgia syndrome. Myopathy develops at the onset of the disease or later; in most cases, its cause is permyositis, less often - myonecrosis or microangiopathy. Biopsy reveals necrosis and edema of interstitial tissue and muscle fibers, eosinophilic infiltrates.

Systemic lupus erythematosus. In almost all cases of systemic lupus erythematosus, joint pain occurs. Pain in one or more joints may last from a few minutes to several days. When the disease is highly active, the pain can be persistent, with the development of inflammation and swelling of the joint. The phalanges and wrists of the hands are especially often affected, knee joints. Joint damage is usually symmetrical. Morning stiffness of the joints is characteristic: after waking up in the morning, pain in the joints is especially pronounced, and movements in them are difficult; it takes some time to “diverge” and develop the joints.

Rheumatoid arthritis. Articular syndrome in rheumatoid arthritis has a number of features: persistent pain, intensifying with movement and weakening at night and at rest; fairly quickly arising limitation of movements in the joints; gradually developing deformities, contractures, subluxations and ankylosis. Joint damage is combined with progressive muscle atrophy. Rheumatoid nodules form in the skin (the histology of the nodule reveals a specific rheumatoid granuloma).

Osteoporosis. The main complaint patients make is back pain. The pain may be episodic and associated either with awkward movement or with lifting heavy objects. Patients often complain of “fatigue and aching back pain” after being forced to stay in one position or walk. They are concerned about the “feeling of heaviness” between the shoulder blades and the need to rest repeatedly during the day, preferably in a lying position. Complaints of joint pain, gait disturbances, and lameness are less common. Taking non-steroidal anti-inflammatory drugs does not relieve pain. Its severity may vary in the same patient at different periods of time. The causes of back pain with osteoporosis can be: compression fracture of the spine or partial fracture with periosteal hemorrhage, mechanical compression of ligaments and muscles, kyphosis thoracic spine, decreased height and shortening of paraspinal muscles. With a fresh fracture of the vertebral body, acute pain occurs, radiating like radicular pain into the chest, abdominal cavity or thigh and severely limiting movement. The pain intensifies with minimal movement, lasts 1-2 weeks, then gradually subsides over 2-3 months. A decrease in the height of the vertebral bodies and an increase in anteroposterior curvature at the fracture site leads to an increase in lumbar lordosis. Therefore, over the next 3-6 months, back pain gradually decreases. Compression fractures of the vertebrae and creeping deformity inevitably lead to decreased height and severe thoracic kyphosis, which causes pain from pressure on the ribs, iliac crests, and intervertebral articular surfaces. Such patients live for years with dull chronic pain in the back, ribs, and pelvic bones. They have a characteristic gait - they walk slowly and carefully, climb stairs with visible difficulty, and enter city transport. The pain increases when walking, any physical activity. There may be girdling pseudoradicular pain in the chest, abdominal cavity, ribs. Many patients exhibit some degree of sensitivity to concussion and complain of pain “in all the bones.” Progressive changes in posture also lead to shortening of the paraspinal muscles, which actively contract, causing pain from muscle strain. This is one of the main causes of chronic back pain. Such pain is often localized not in the spine itself, but paravertebrally. The pain intensifies with prolonged standing and decreases with walking. Most patients with osteoporosis complain of a significant decrease in performance and increased fatigue. Prolonged back pain contributes to increased irritability, agitation and even the development of depression; patients also often lose weight. Decreased height and a protruding abdomen also contribute to the patient’s emotional discomfort.

Chronic pain syndrome is a fairly common pathology that can cause mental illness. Chronication of pain is a consequence of disruption of the nervous system. Many authors consider chronic pain syndrome as an independent disease. Neuralgia, tingling, body aches - key features most diseases that cause suffering to millions of people. Experts say that every fifth person on the planet is faced with the problem of chronic pain.

Doctors often use a method of elimination to determine the functional nature of painful sensations in the patient’s body. Chronic soft tissue pain syndrome is also a diagnosis of exclusion. At the same time, unpleasant manifestations of a different nature may be practically absent. And in this case, the patient is diagnosed with “chronic pain syndrome.” As a rule, painful sensations are localized in the back, heart, joints, abdomen and head.

Biological role of pain

Such discomfort by their biological origin they are a danger signal and evidence of a disruption in the functioning of organs or their systems in the body. In medical practice, chronic pain syndrome is often considered as a sign of some pathology that occurs due to injury, tissue damage, inflammation or ischemia. At the same time, negative sensations are formed as a result of the coordinated work of a whole complex of defensive reactions aimed at eliminating dysfunctions. Based on the information presented above, we can conclude that a person’s full life is impossible without normal perception of pain.

Abdominal pain

Chronic abdominal pain syndrome is a common illness registered among both children and adults. There are many factors that provoke the development of pain in the abdominal area:

Therapy for abdominal pain

The main role in the treatment of abdominalgia (chronic) belongs to methods of mental influence. In the treatment of pathology, hypnotic sessions are quite effective, behavioral psychotherapy. To influence the central mechanisms of pain, antidepressants (Fluoxetine, Paroxetine, Amitriptyline) and anti-anxiety (Closepam, Diazepam), desensitizing (Tavegil, Suprastin) and anti-hypochondriacal (Frenolone, "Sonapax") means. Non-narcotic analgesics - Diclofenac, Nimesil - are used as painkillers. Good results are obtained when using methods of manual therapy, underwater traction, physical therapy and acupuncture.

Pain in the heart area

Chronic heart pain syndrome is a frequently reported disease, the etiology of which is associated with many reasons:

  • psychogenic diseases;
  • myocardial infarction;
  • spine pathologies;
  • dysfunction of the peripheral nervous system;
  • myocardial dystrophy;
  • pulmonary embolism;
  • myocarditis;
  • arterial hypertrophy;
  • heart defects;
  • hypertrophic cardiopathy;
  • pericarditis;
  • pleurisy;
  • angina pectoris;
  • pneumonia;
  • mitral valve prolapse;
  • diaphragmatic abscess.

How to treat?

Anticholesterol diet therapy is indicated for the treatment of heart disease. Authorized products include:

  • nuts;
  • seafood;
  • veal;
  • berries, fruit drinks;
  • lentils, beans, peas;
  • vegetable soups;
  • cereal porridge;
  • seeds;
  • fermented milk products (kefir, yogurt, low-fat cottage cheese);
  • fruits, vegetables, dried fruits;
  • unrefined vegetable oils (peanut, rapeseed, corn, sunflower, flaxseed, maize, olive);
  • bran bread;
  • natural marmalade;
  • rosehip decoction;
  • skimmed milk;
  • sea ​​fish (hake, pollock, sprat, herring, cod, navaga, tuna, salmon, sardines, haddock, halibut);
  • chicken fillet;
  • natural juices.

To restore the functioning of the heart and nervous system, doctors prescribe a course of physical therapy. The presented method of treatment is indicated for the following pathologies:

  • stable angina pectoris;
  • post-infarction cardiosclerosis.

Physiotherapeutic treatment methods include the following procedures:

  • magnetic therapy;
  • electrophoresis;
  • electrosleep;
  • aquatherapy;
  • balneotherapy (treatment with mineral baths);
  • low-energy laser radiation.

The choice of therapeutic treatment regimen depends on the etiology of the disease and diagnosis. If conservative treatment methods are powerless, then surgical intervention is performed.

Causes of pain in the pelvic area

Chronic pelvic pain syndrome - current problem many women and men. The development of prostatitis is the main cause of occurrence in representatives of the stronger sex. In women, this pathology most often manifests itself for a reason related to the morphofunctional characteristics of their pelvis. Patients often consult a doctor with complaints of prolonged, periodically intensifying pelvic pain, which is localized in the lower abdomen. Chronic pain in the pelvic area is a rather “vague” and diverse concept, since most diseases of the pelvic organs (for example, urological, proctological, gynecological) can be accompanied by similar manifestations. There are many reasons that provoke the development of chronic pain in women.

Gynecological reasons:

  • uterine fibroids;
  • polyps of the uterine mucosa or;
  • foreign body in the pelvis;
  • tuberculosis of female genitalia;
  • intrauterine contraception;
  • prolapse of the internal genitalia;
  • Allen-Masters syndrome;
  • ovarian cyst;
  • postoperative lymphoid cysts;
  • abnormalities of genital development;
  • carcinogenic formations in the body and cervix;
  • painful periods syndrome;
  • ovarian cancer;
  • atresia of the cervical canal;
  • postoperative adhesive disease.


Urological and gastroenterological reasons:
  • bladder cancer;
  • urethritis;
  • urolithiasis disease;
  • anomaly of kidney development;
  • urethral diverticulum;
  • cystitis;
  • ureterocele;
  • inflammation of the paraurethral glands;
  • colon cancer;
  • hernias;
  • constipation;
  • Crohn's disease;
  • colitis.

Neurological, musculo-ligamentous and bone causes:

  • neuralgia;
  • abscess of the iliopsoas muscle;
  • coccydynia;
  • femoral or ventral hernia;
  • iliac bone sarcoma;
  • hip dysfunction;
  • myofascial syndrome.

Chronic pelvic pain syndrome: treatment in men

Treatment depends on the etiology of the disease. In the presence of chronic neuropathic pain syndromes, the following groups of medications are prescribed:

  • anticonvulsants;
  • α-blockers;
  • analgesics;
  • muscle relaxants;
  • nonspecific anti-inflammatory and desensitizing drugs;
  • plant adaptogens;
  • membrane stabilizers;
  • tranquilizers;
  • sedatives;
  • phosphorus preparations;
  • novocaine blockades;
  • neuroleptics;
  • immunosuppressants;
  • anticholinesterase drugs;
  • corticosteroids.

Chronic pain syndrome: treatment in women

In the absence of clearly defined gynecological pathology, reflexology is prescribed. If signs of depression are detected, antidepressants can be used. If neoplasms are detected in the pelvic area, surgical intervention is indicated. As a rule, laparoscopy is performed in the absence of a positive result from conservative methods of therapy.