Types of pain and major groups of antinociceptives. Nociceptive sensitivity and its physiological role

The concept of pain is an unpleasant sensory and emotional experience associated with real or perceived tissue damage, and at the same time the reaction of the body, mobilizing various functional systems to protect it from the effects of a pathogenic factor.

Classification Neurophysiological (depending on the mechanism of pain) 1. Nociceptive § Somatic § Visceral 2. Non-nociceptive § Neuropathic § Psychogenic 3. Mixed

Nociceptive pain is pain caused by damage to the musculoskeletal system or internal organs and is directly related to the activation of peripheral pain receptors (nociceptors)

Theories of pain perception A theory authored by M. Frey II. The theory, authored by Goldscheider I.

I. The theory, authored by M. Frey According to her, there are pain receptors in the skin, from which specific afferent pathways to the brain. 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.

II. Theory by Goldscheider Postulates that any sensory stimulus reaching a certain intensity can cause pain. In other words, there are no specific pain structures, and pain is the result of the summation of thermal, mechanical, and other sensory impulses. Initially called the intensity theory, this theory later became better known as the "pattern" or "summation" theory.

Types of nociceptors. Mechanosensitive and Thermosensitive nociceptors Activated only by intense, tissue-damaging pressure or thermal stimulation. And their effects are mediated by both A-delta and S fibers. Polymodal nociceptors Respond to mechanical and thermal stimuli. A-delta fibers respond to both light touch, pressure, and pain stimuli. Their activity corresponds to the intensity of the stimulus. These fibers also "conduct" information about the nature and location of the painful stimulus.

Types of nerve fibers. Type I (C-fibers) very thin weakly myelinated 0.4-1.1 microns in diameter Type II (A-delta fibers) thin myelinated (1.0-5.0 microns in diameter)

Types of nerve fibers. Communication with different types pain: Type I (C-fibers) Secondary pain is associated with its afferent stimulation (long-latency) Type II (A-delta fibers) Primary pain is associated with its afferent stimulation (short-latency)

Substances that cause functional and structural restructuring of nociceptors Plasma and blood cell algogens › › › Bradykinin, kallidin (plasma) Histamine (mast cells) Serotonin, ATP (platelets) Leukotrienes (neutrophils) Interleukin-1, tumor necrosis factor, prostaglandins, nitric oxide ( endothelium, macrophages) C-afferent terminal algogens › Substance P, neurokinin A, calcitonin

Antinocyptic neurotransmitters Øopidergic system of beta-endorphine M-, D meta and lei-enkefalin D-d'Dinorphine K-endomorphine M- ØSerotonergic system SEROTONIN 5 HT 1, 5 HT 2, 5 HT 3, 5 HT 4 ØReraderergic system Norerenaline A 2 AAR, a 2 BAR, A 2 car. AR ØGABA-ERGIC SYSTEM GAMBA-Cl(-), GABA-Gi-proteins Ø CANNABINOIDS ANANDAMIDE, 2-ARACHIDONYLGLYCERIN CB 1, CB 2

SOMATOGENIC PAIN SYNDROMES Arise as a result of activation of nociceptors in case of: - injury, ischemia, inflammation, stretching of tissues

Nociceptive (somatogenic) pain I. Somatic Superficial (early, late) II. Visceral Deep Origin Area Skin Connective tissue. Muscles. Bones. Joints. Internal organs Forms of pain Prick, pinch, etc. Muscle cramps, joint pain, etc. Cardialgia, abdominal pain, etc.

I. Somatic pain Superficial pain Early pain is a "bright" in nature, easily localized sensation, which quickly fades with the cessation of the stimulus. It is often followed by a late one with a latency of 0.5 -1.0 sec. Late pain is dull, aching in nature, it is more difficult to localize it, it fades more slowly.

I. Somatic pain Deep pain As a rule, dull, difficult to localize, tends to irradiate into the surrounding tissues.

II. Visceral pain Occurs with rapid and severe stretching of the hollow organs of the abdominal cavity (renal pelvis). Spasms and contractions of internal organs are also painful, especially due to improper circulation (myocardial ischemia).

Pathogenesis of nociceptive pain Injurious factor Primary hyperalgesia in the area of ​​damaged tissue (phenomenon of nociceptor sensitization)

Structures and substrates that cause nociceptive pain. The sequence of stages in the onset of pain The first danger Formation of alkogenic substances Nociceptor Afferent Spinal cord, fiber (A-delta, C) Supraspinal CNS. Stages of information processing Formation and release of harmful substances Transduction and transformation Conduction Central processing

Realization of pain. Sensory-discriminative component Reception, conduction and processing of nociceptive signals Affective (emotional) component Vegetative component Motor component Pain assessment (cognitive component) Expression of pain (psychomotor component)

Physiological purpose of nociceptive pain. Nociceptive pain is a warning signal about the occurrence of disorders (damage) in the body, which opens the way to the recognition and treatment of many diseases.

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 long-term 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, 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 body. 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 ...

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 is most often acute pain, with all its inherent characteristics ( see Acute and Chronic Pain). 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 understandable 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 long-term 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. 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 at all 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. (Table 1). 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.

Neuropathic pain is much more diverse than nociceptive pain in terms of its clinical characteristics. This is determined by the level, extent, nature, duration of the lesion, and many other somatic and psychological factors. With various forms of damage to the nervous system, on different levels and stages of development of the pathological process, the participation of different mechanisms of the genesis of pain may also be different. However, regardless of the level of damage to the nervous system, both peripheral and central pain control mechanisms are always activated.

General characteristics of neuropathic pain are persistent nature, long duration, ineffectiveness of analgesics for its relief, combination with vegetative symptoms. Neuropathic pain is more commonly described as burning, stabbing, aching, or shooting.

Various sensory phenomena are characteristic of neuropathic pain: paresthesias - spontaneous or sensory-induced unusual sensations; dysesthesia - unpleasant spontaneous or induced sensations; neuralgia - pain spreading along one or more nerves; hyperesthesia - hypersensitivity to a normal non-painful stimulus; allodynia - the perception of non-painful irritation as pain; Hyperalgesia is an increased pain response to a painful stimulus. The last three concepts used to refer to hypersensitivity are combined with the term hyperpathy. One of the types of neuropathic pain is causalgia (sensation of intense burning pain), which occurs most often with complex regional pain syndrome.

Table 1. Levels of damage and causes of neuropathic pain

The mechanisms of neuropathic pain in lesions of the peripheral and central parts of the somatosensory system are different. Suggested mechanisms for neuropathic pain in peripheral lesions include: post-denervation hypersensitivity; generation of spontaneous pain impulses from ectopic foci formed during the regeneration of damaged fibers; ephoptic propagation of nerve impulses between demyelinated nerve fibers; increased sensitivity of neuromas of damaged sensory nerves to norepinephrine and certain chemical agents; decrease in antinociceptive control in the posterior horn with damage to thick myelinated fibers. These peripheral changes in the afferent pain stream lead to shifts in the balance of the overlying spinal and cerebral apparatus involved in pain control. At the same time, cognitive and emotional-affective integrative mechanisms of pain perception are obligately switched on.

One of the options for neuropathic pain is central pain. These include pain that occurs when the central nervous system is damaged. With this type of pain, there is a complete, partial or subclinical impairment of sensorimotor sensitivity, most often associated with damage to the spinothalamic pathway at the spinal and / or cerebral levels. However, it should be emphasized here that a feature of neuropathic pain, both central and peripheral, is the lack of a direct correlation between the degree of neurological sensory deficit and the severity of the pain syndrome.

With damage to the sensory afferent systems of the spinal cord, pain can be localized, unilateral or diffuse bilateral, capturing the area below the level of the lesion. The pains are constant and are burning, stabbing, tearing, sometimes crampial in nature. Against this background, various paroxysmal focal and diffuse pains may occur. An unusual pattern of pain has been described in patients with partial lesions of the spinal cord and its anterolateral parts: when pain and temperature stimuli are applied in the zone of loss of sensitivity, the patient feels them in the corresponding zones contralaterally on the healthy side. This phenomenon is called allocheiria ("other hand"). Lermitte's symptom known in practice (paresthesia with elements of dysesthesia during movement in the neck) reflects the increased sensitivity of the spinal cord to mechanical influences in conditions of demyelination of the posterior columns. There are currently no data on similar manifestations in demyelination of the spinothalamic pathways.

Despite the large representation of antinociceptive systems in the brain stem, its damage is rarely accompanied by pain. At the same time, damage to the pons and lateral sections of the medulla oblongata is accompanied by algic manifestations more often than other structures. Central pains of bulbar origin are described in syringobulbia, tuberculoma, tumors of the brain stem, and in multiple sclerosis.

Dejerine and Russi described intense unbearable pain within the so-called thalamic syndrome (superficial and deep hemianesthesia, sensitive ataxia, moderate hemiplegia, mild choreoathetosis) after infarcts in the area of ​​the thalamic thalamus. The most common cause of central thalamic pain is a vascular lesion of the thalamus (ventroposteriomedial and ventroposteriolateral nuclei). In a special study that analyzed 180 cases of thalamic syndrome in right-handers, it was shown that it occurs twice as often when the right hemisphere is affected (116 cases) than the left (64 cases) . It is curious that the identified predominant right-sided localization is more typical for men. Domestic and foreign studies have shown that thalamic pain often occurs when not only the thalamic thalamus is affected, but also other parts of the afferent somatosensory pathways. The most common cause of these pains are also vascular disorders. Such pain is referred to as "central post-stroke pain", which occurs in approximately 6-8% of cases of stroke. . Thus, the classical thalamic syndrome is one of the options for central post-stroke pain.

The mechanisms of central pain are complex and not fully understood. Recent studies have demonstrated great potential for functional plasticity of the central nervous system in lesions at various levels. The obtained data can be grouped as follows. Damage to the somatosensory system leads to disinhibition and the appearance of spontaneous activity of deafferented central neurons at the spinal and cerebral levels. Changes in the peripheral link of the system (sensory nerve, posterior root) inevitably lead to changes in the activity of thalamic and cortical neurons. The activity of deafferented central neurons changes not only quantitatively, but also qualitatively: under conditions of deafferentation, the activity of some central neurons that were not previously related to the perception of pain begins to be perceived as pain. In addition, under conditions of “blockade” of the ascending pain flow (damage to the somatosensory pathway), afferent projections of neuronal groups at all levels (posterior horns, trunk, thalamus, cortex) are disturbed. At the same time, new ascending projection paths and corresponding receptive fields are formed rather quickly. It is believed that since this process occurs very quickly, it is most likely that spare or “disguised” (inactive in a healthy person) pathways are not formed, but are opened. It may seem that in conditions of pain, these shifts are negative. However, it is postulated that the meaning of such a “desire” for the obligatory preservation of the flow of nociceptive afferentation lies in its necessity for the normal operation of antinociceptive systems. In particular, the insufficient effectiveness of the descending antinociceptive system of the periaqueductal substance, the major raphe nucleus, and the DNIK is associated with damage to the pain afferent systems. The term deafferent pain is accepted to refer to the central pain that occurs when the afferent somatosensory pathways are affected.

Certain pathophysiological features of neuropathic and nociceptive pain have been identified. Special studies have shown that the activity of opioid anti-pain systems was much higher in nociceptive than in neuropathic pain. This is due to the fact that in nociceptive pain, the central mechanisms (spinal and cerebral) are not involved in the pathological process, while in neuropathic pain there is direct damage to them. An analysis of works devoted to the study of the effects of destructive (neurotomy, rhizotomy, chordotomy, mesencephalotomy, thalamotomy, leucotomy) and stimulatory methods (TENS, acupuncture, stimulation of the posterior roots, OSV, thalamus) in the treatment of pain syndromes allows us to draw the following conclusion. If procedures for the destruction of nerve pathways, regardless of its level, are most effective in relieving nociceptive pain, then stimulation methods, on the contrary, are more effective in neuropathic pain. However, the leading in the implementation of stimulation procedures are not opiate, but other, not yet specified, mediator systems.

There are differences in approaches drug treatment nociceptive and neuropathic pain. To relieve nociceptive pain, depending on its intensity, non-narcotic and narcotic analgesics, non-steroidal anti-inflammatory drugs and local anesthetics.

In the treatment of neuropathic pain, analgesics are usually ineffective and are not used. Drugs of other pharmacological groups are used.

For the treatment of chronic neuropathic pain, antidepressants and anticonvulsants are the drugs of choice. The use of antidepressants (tricyclic antidepressants, serotonin reuptake inhibitors) is due to the insufficiency of the serotonin systems of the brain in many chronic pains, usually combined with depressive disorders.

In therapy various kinds neuropathic pain widely used some antiepileptic drugs - anticonvulsants (carbamazepine, difenin, gabapentin, sodium valproate, lamotrigine, felbamate) . The exact mechanism of their analgesic action remains unclear, but it is postulated that the effect of these drugs is associated with: 1) stabilization of neuronal membranes by reducing the activity of voltage-dependent sodium channels; 2) with activation of the GABA system; 3) with inhibition of NMDA receptors (felbamate, lamictal). The development of drugs that selectively block NMDA receptors related to pain transmission is one of the priorities. . Currently, NMDA receptor antagonists (ketamine) are not widely used in the treatment of pain syndromes due to numerous adverse effects. side effects associated with the participation of these receptors in the implementation of mental, motor and other functions . Certain hopes are associated with the use of drugs from the group of amantadines (used in parkinsonism) for chronic neuropathic pain, which, according to preliminary studies, have a good analgesic effect due to the blockade of NMDA receptors. .

Anxiolytic drugs and neuroleptics are also used in the treatment of neuropathic pain. Tranquilizers are recommended mainly for severe anxiety disorders, and neuroleptics for hypochondriacal disorders associated with pain. Often these drugs are used in combination with other drugs.

Central muscle relaxants (baclofen, sirdalud) for neuropathic pain are used as drugs that enhance the GABA system of the spinal cord and, along with muscle relaxation, have an analgesic effect. Good results have been obtained in the treatment of postherpetic neuralgia, CRPS, and diabetic polyneuropathy with these agents.

Mexiletine, an analog of lidocaine that affects the operation of sodium-potassium channels in the peripheral nerve, has been proposed in a number of new clinical studies for the treatment of chronic neuropathic pain. It has been shown that at a dose of 600-625 mg per day, mexiletine has a clear analgesic effect in patients with pain syndrome in diabetic and alcoholic polyneuropathy, as well as in post-stroke central pain. .

special clinical research it was shown that in neuropathic pain the level of adenosine in the blood and cerebrospinal fluid was significantly reduced compared to the norm, while in nociceptive pain its level was not changed. The analgesic effect of adenosine was most pronounced in patients with neuropathic pain. . These data indicate insufficient activity of the purine system in neuropathic pain and the adequacy of the use of adenosine in these patients.

One of the directions in the development effective treatment neuropathic pain is the study of calcium channel blockers. In preliminary studies of HIV-infected patients suffering from neuropathic pain, a good analgesic effect was obtained with the use of the new calcium channel blocker SNX-111, while emphasizing that the use of opiates in these patients was ineffective.

Recent experimental work has shown the role immune system in the initiation and maintenance of neuropathic pain . It has been established that when peripheral nerves are damaged, cytokines (interleukin-1, interleukin-6, tumor necrosis factor alpha) are produced in the spinal cord, which contribute to the persistence of pain. Blocking these cytokines reduces pain. The development of this area of ​​research is associated with new prospects in the development medicines for the treatment of neuropathic chronic pain.

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 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.

nociceptive painis a medical term used to describe pain from physical injury. Examples would be pain from a sports injury, from a dental procedure, or from arthritis. Nociceptive pain is the most common type of pain people experience. It develops when specific pain receptors (nociceptors) are affected by inflammation, chemicals, or physical injury.

What is the difference between nociceptive and neuropathic pain?

Nociceptive pain is usually acute and develops in response to a specific situation. It passes when the affected part of the body is restored. For example, nociceptive pain from a broken ankle goes away when the ankle heals.

The body contains specialized nerve cells called nociceptors that detect harmful stimuli that damage the body, such as extreme heat or cold, pressure, injury, or chemicals. These warning signals are transmitted through the nervous system to the brain, resulting in nociceptive pain. This happens very quickly in real time, which is why people remove their hand if they touch a hot oven. Nociceptors can be found in internal organs, although their signals are not easily identified and may not always be felt. The information provided by nociceptive pain can help the body protect and heal itself.

What is neuropathic pain?

neuropathic painis a medical term used to describe the pain that develops when nervous system damaged or not working properly due to illness or injury. It differs from nociceptive pain in that it does not develop in response to any particular circumstance or external stimuli. People can suffer from neuropathic pain even if the limb is missing. This condition is called phantom pain, which can develop in people after an amputation. Neuropathic pain is referred to as nerve pain and is usually chronic. Many different conditions and diseases cause neuropathic pain, including:

• diabetes;
• stroke;
• cancer;
• cytomegalovirus;
• amputation.

Diagnostics

In order to receive proper treatment, it is very important to determine whether a person is suffering from neuropathic or nociceptive pain.

Chronic low back pain is a very common complaint, but in 90% of cases, doctors cannot identify a physical cause. Often, some of the symptoms that people experience when , is neuropathic pain.

A diagnostic test has been developed to help clinicians identify the presence of both neuropathic and nociceptive pain. This test is now widely used to assess neuropathic pain in many different conditions and diseases, including rheumatoid arthritis.

When filling out the questionnaire, the patient will be asked to answer 9 questions. Seven questions will ask you to rate different sensations of pain on a scale of 0 to 5. You also need to answer how long the pain lasts: from -1 to +1. The higher the score, the higher the level of neuropathic pain a person experiences.

People with diabetes are advised to monitor for symptoms of neuropathic pain, especially in the legs. neuropathic pain in lower limbs very common in people with diabetes and is a major cause of amputation. Neuropathic pain in people with diabetes often begins with numbness, weakness, or a burning sensation. This pain may worsen at night, making it difficult to sleep.

Location of nociceptive and neuropathic pain

The most common systems in which nociceptive pain develops are the musculoskeletal, which includes joints, muscles, skin, tendons, and bone. Internal organs such as the intestines, lungs, and heart can be affected by nociceptive pain, as can smooth muscles.

Approximately half of all people with diabetes experience diabetic peripheral neuropathy (DPN), which is nerve pain that affects the legs and arms. Fingers usually start to hurt first. People with diabetes may also develop neuropathy in other parts of the body, including the front of the thighs, the area around the eyes, and the wrists. Many people with cancer experience neuropathic back, leg, chest, and shoulder pain due to tumors that affect the spinal cord. They may also experience neuropathic pain due to drugs or surgery. The lower back is one area where people can experience both neuropathic and nociceptive pain.

Symptoms and treatment

It is important to keep in mind that a person can experience neuropathic and nociceptive pain at the same time. Paying attention to key differences can improve the quality of life of people suffering from pain and help them get the right treatment.

Because nociceptive pain can develop anywhere, it can have many different characteristics. Pain may occur at the time of injury, but there may be pain in the morning or during exercise.

Treatment for nociceptive pain depends on the cause. Unlike neuropathic pain, nociceptive pain often responds well to opiates such as codeine.

Symptoms of neuropathic pain

People with neuropathic pain report symptoms such as:

• sharp, shooting, burning or stabbing pains;
• tingling;
• numbness;
• extreme sensitivity;
• insensitivity to heat or cold;
• muscle weakness;
• pain worse at night.

As with nociceptive pain, one of the first and most important steps in the treatment of neuropathic pain is the treatment of the underlying disease.

Individuals with diabetic peripheral neuropathy should take medications to help control their diabetes. A doctor may prescribe medication to reduce the pain and injury associated with this condition.

People with oncological diseases people with neuropathic pain may benefit from anticonvulsants, local anesthetics, and antidepressants. Treatment will depend on the specific cause of the pain.

It is estimated that 42.2-78.8% of people who undergo limb amputation will suffer from phantom pain. Research shows that one of the best treatments for neuropathic pain in phantom pain is prevention. If a person receives pain medication prior to amputation, they are less likely to develop phantom pain.

Literature

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