Pain syndrome after. Chronic pain syndrome. Therapy for abdominal pain

Description:

From a medical point of view, pain is:
- a type of feeling, a kind of unpleasant sensation;
- a reaction to this sensation, which is characterized by a certain emotional coloring, reflex changes in the functions of internal organs, unconditioned motor reflexes, as well as volitional efforts aimed at getting rid of the pain factor.
- an unpleasant sensory and emotional experience associated with real or perceived tissue damage, and at the same time a reaction of the body that mobilizes various functional systems to protect it from the effects of a pathogenic factor.

Prolonged pain is accompanied by changes in physiological parameters (blood pressure, pulse, pupil dilation, changes in hormone concentrations).

Symptoms:

Acute pain.
Acute pain is defined as pain of short duration of onset with an easily identifiable cause. Acute pain is a warning to the body about the current danger of organic damage or disease. Often persistent and acute pain is also accompanied by aching pain. Acute pain is usually concentrated in a specific area before it somehow spreads wider. This type of pain is usually highly treatable.

Chronic pain.
Chronic pain was originally defined as pain that lasts about 6 months or more. It is now defined as pain that persistently persists beyond the appropriate length of time during which it would normally end. It is often more difficult to heal than acute pain. Particular attention is required when addressing any pain that has become chronic. In exceptional cases, neurosurgeons may perform complex surgery to remove parts of a patient's brain to treat chronic pain. Such an intervention can relieve the patient of the subjective sensation of pain, but since signals from the pain site will still be transmitted through neurons, the body will continue to react to them.

Skin pain.
Skin pain occurs when the skin or subcutaneous tissue is damaged. Cutaneous nociceptors terminate just below the skin and, due to their high concentration of nerve endings, provide a highly precise, localized sensation of pain of short duration.
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Somatic pain

Somatic pain occurs in ligaments, tendons, joints, bones, blood vessels, and even the nerves themselves. It is determined by somatic nociceptors. Due to the lack of pain receptors in these areas, they produce a dull, poorly localized pain that is longer lasting than that of skin pain. This includes, for example, sprained joints and broken bones.

Inner pain.
Internal pain arises from the internal organs of the body. Internal nociceptors are located in organs and internal cavities. An even greater lack of pain receptors in these areas of the body leads to more dull and prolonged pain, compared to somatic pain. Internal pain is particularly difficult to localize, and some internal organic injuries represent “attributed” pain, where the sensation of pain is attributed to an area of the body that is in no way related to the site of the injury itself. Cardiac ischemia (insufficient blood supply to the heart muscle) is perhaps the best known example of attributable pain; the sensation may be located as a separate feeling of pain just above the chest, in the left shoulder, arm or even in the palm. The pain attributed may be explained by the discovery that pain receptors in internal organs also excite spinal neurons that are excited by skin lesions. Once the brain begins to associate the firing of these spinal neurons with stimulation of somatic tissues in the skin or muscle, pain signals coming from the internal organs begin to be interpreted by the brain as originating from the skin.
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Phantom limb pain is a sensation of pain that occurs in a lost limb or in a limb that is not felt through normal sensations. This phenomenon is almost always associated with cases of amputations and.

Neuropathic pain.
Neuropathic pain (“neuralgia”) can appear as a result of damage or disease to the nerve tissues themselves (for example,). This can impair the ability of sensory nerves to transmit correct information to the thalamus (a part of the diencephalon), causing the brain to misinterpret painful stimuli even when there is no obvious physiological cause for the pain.

Psychogenic pain.
Psychogenic pain is diagnosed in the absence of an organic disease or in the case when the latter cannot explain the nature and severity of the pain syndrome. Psychogenic pain is always chronic and occurs against the background of mental disorders: hypochondria, phobias. In a significant proportion of patients, psychosocial factors play an important role (dissatisfaction with work, desire to obtain moral or material benefit). Particularly strong links exist between chronic pain and depression.

Causes:

Depending on the mechanism and type of damage, it happens:
- occurs when one of the parts of the nervous system (central and peripheral) is damaged;
- noceptive pain (from the Latin noci - damage), associated with damage to skin tissue, muscles or internal organs;
- mixed pain (has signs of the above types).

The causes of pain are conventionally divided into two groups:
external causes (burn, injury, etc.);
internal causes (intoxication, inflammation, circulatory disorders (ischemia) in tissues and organs or, for example, compression characteristic of heart pain).

Treatment:

For treatment the following is prescribed:

Non-medicinal:
physiotherapy,
procedures using cold (compresses) or heat,
different types of massage;
electrical stimulation (the action is based on the activation of specific centers of the spinal cord that inhibit the conduction of pain impulses);
acupuncture treatment (acupuncture).

Today the list of painkillers is very large and varied.
However, one must understand that most of the drugs suppress pain impulses in the brain, but do not eliminate the cause of the pain itself (for example, in case of heart disease). Moreover, all medications have some side effects. It is important to consult a professional physician before starting to take medications to treat pain.

> Pain syndrome

This information cannot be used for self-medication!
Consultation with a specialist is required!

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, the functioning of internal organs changes, and activity increases aimed at getting rid of the effects of the damaging factor. 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 from a 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, paroxysmal or constant, severe or moderate, you should call an ambulance. First of all, this concerns pronounced discomfort in the abdomen and in the heart area (behind the sternum). People with a variety of traumatic injuries, chemical and thermal burns need emergency care. 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.

Pain syndrome, which is most often described as “suddenly occurring, sharp, stabbing pain” in one or another part of the body, directly related to neurology - this is in medical language the so-called neuralgia - the result of damage to the peripheral nerves. When a nerve or a group of them is damaged, this causes all of the above symptoms, characterized by one succinct word: “acute pain.”

Description of the disease

The peculiarity of neuralgia, in contrast to, say, neuritis, is that the former are distinguished by signs of irritation, and for the latter - loss of nervous functions. In medicine, neuralgia of the following groups of nerves is distinguished: femoral, spinal or, in other words, intercostal, cervical and, finally, cranial. In the last group, lesions of the trigeminal and glossopharyngeal nerves are distinguished.

Symptoms of pain syndrome

The symptoms of neuralgia are determined primarily by which nerve or area of nerves is affected and which group it belongs to.

Trigeminal or facial neuralgia affects the part of the cranial nerves that control movement and sensation in the mouth and face. Here the most susceptible are the ophthalmic nerves and those located in the upper part of the jaw. The lower ones specialize more in chewing movements. The main nerves in the facial area are the trigeminal nerve and the so-called Gasserian ganglion, which communicates with the thalamus and spinal cord.

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Accordingly, the symptoms of neuralgia of this group of nerves are as follows: “shooting” pain, short-term and periodic, however, very acute; this pain causes increased lacrimation, drooling, and redness in the trigeminal nerve area. With mechanical irritation, jaw movements, and so on, the pain intensifies. If the mandibular nerves are involved, tics and twitching are possible.

With neuralgia of the pterygopalatine ganglion, pain is observed in the area around the eyes, at the base of the nose, in the area of the upper lip, and teeth. It can flow and radiate downward, that is, into the neck, or upward, into the temple. Externally, there is abundant production of tears, redness of the eyes, swollen eyelids, swelling, and excessive salivation. Glossopharyngeal neuralgia is characterized by pain in various areas of the tongue, as well as the pharynx. Possible dry mouth, taste sensations are abnormally transformed.

With intercostal neuralgia, pain occurs when moving, bending the body, turning. Often it is even painful for the patient to take a deep breath. In case of damage to the external nerve of the thigh, aching pain in this area, a burning or tingling sensation, and a false sensation that something is crawling on the skin are observed. Sometimes there is numbness.

Causes

There are many factors that can cause neuralgia. However, among the most common are: severe frostbite, hypothermia; ongoing or past inflammation; mechanical impacts, such as: injuries, blows, bruises; tumor formations; intoxication. A psychological condition such as stress or excessively acute negative experiences can also cause symptoms. In addition, demyelinating processes can also contribute to the appearance of neuralgia.

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Treatment of pain syndrome

First of all, it should be noted that the diagnosis and detection of neuralgia can only be carried out and carried out by a neurologist. The professional begins by studying the complaints and external examination of the patient, after which he examines the possible causes of the disease, which are also considered separately to eliminate the possibility of detecting side diseases and clarify the diagnosis.

In special cases, as well as for a more thorough study of the patient’s condition, additional equipment may be used for examination. Most often, these procedures are used when exposure to trauma is identified as the underlying cause of neuralgia. In this case, referrals are issued for a procedure such as electroneurography. If it is suspected that neuralgia is caused by a herniation or protrusion of an intervertebral disc, the patient is referred for magnetic resonance imaging of the spine or individual groups of nerves. The same procedure is prescribed if a tumor is suspected in the soft tissues.

Further, if there is an accurate diagnosis, the neurologist offers various methods of treating pain. These could be medications against seizures, additional intake of B vitamins, drugs that promote relaxation; at the patient’s request, physiotherapy and acupuncture can be prescribed. Depending on the type of nerves affected, more specific treatment is proposed, for example, massage or exposure to infrared rays for trigeminal neuralgia; drugs novocaine and lidocaine for intercostal neuralgia and others. It is also possible to perform operations under general anesthesia, again, only if indicated by a doctor.

Every person has felt pain at least once in their life. This is an extremely unpleasant condition that everyone wants to get rid of as quickly as possible. Pain in different areas of the body accompanies many diseases and is a signal that there are problems in the body. Sometimes pain does not occur immediately, but in the later stages of the disease. Then it is much more difficult to fight the disease than at the very beginning of the disease.

Pain is a protective reaction of the body that helps to take measures against the disease. After all, when the disease is asymptomatic, as a rule, there is no treatment. Having felt painful symptoms, a person urgently seeks medical help.

The concept of pain syndrome

Nerve endings, which permeate all tissues of the body, play a major role in pain sensations. Pain is localized where pathological processes occur. Unpleasant sensations often spread to the organs, tissues and systems associated with the affected area. Everything in the human body is interconnected.

How can a person with pain feel?

Pain in a specific place or several places;
pain without specific localization;
increased sweating (“dropping into sweat”);
increased urination;
swelling in the sore spot;
redness of the sore spot;
heat in the face or whole body;
dizziness;
severe muscle weakness;
nausea, vomiting;
bloating;
difficulty moving, lameness;
difficulty chewing food, swallowing;
fear of light and sound;
loss of consciousness;
periodic changes in the location of pain;
changes in sensations when changing body position.

Other sensations are possible depending on the type of disease, its stage, and the individual characteristics of the body.

Neurology deals with the classification and study of pain syndromes.

Types of pain syndrome

Pain syndromes are acute and chronic.

Acute pain syndrome manifests itself once in a specific area of the body. Example: stomach pain due to indigestion, appendicitis; The knee joint aches after suffering from a sore throat.

Chronic pain can bother the patient many times, interspersed with periods of remission, during which nothing hurts. They can be dull, aching, spread to different areas of the body, but the main sign of chronic pain is that it worsens periodically, occurring in one area. Example: stomach pain due to chronic cholecystitis; one or both knees ache due to the weather.

Origin of pain syndrome

In medicine, pain syndromes are also classified according to their origin and associated location.

Neuropathic – occurs due to injuries and infections with damage to the central nervous system. This group includes types of headaches of a neurological nature.

Radicular (vertebrogenic) – combines all types of pain in the back and spine. Most often they are caused by dorsopathy, especially osteochondrosis of various parts of the spine.

Anococcygeal - pain in the coccyx and back of the perineum. The causes may be chronic constipation, diseases of the pelvic organs, oncology, etc. pathologies localized in a given area of the body.

Abdominal – attacks of pain are associated with pathological conditions of the gastrointestinal tract: poisoning, tumor, diseases of the gastrointestinal tract, symptoms of infections, etc.

Patellofemoral - pain is localized in the knee joint. Knee pain can be caused by injuries, complications of infections or viruses, or joint diseases.

Myofascial – pain occurs due to muscle tension and spasms. Palpation reveals tense, painful muscles with areas of even greater compaction. Usually, so-called trigger points are felt; when pressed, the pain intensifies and affects other areas of the body.

Myofascial syndrome is very common in the human population. Its reasons may be:

Staying in an unnatural position;
hypothermia;
depression;
stress;
physical overload;
diseases of the musculoskeletal system (bones, joints, ligaments, etc.);
developmental pathologies.

Important! Pain syndrome is always caused by pathology. It may be a temporary disorder that is treatable and goes away permanently. But a more serious disease is possible, which can become chronic and persist for a long time, sometimes for life.

Psychologically, primary cases of acute pain are the most difficult to experience. A person encounters unpleasant sensations for the first time, does not know what is happening to him and what measures need to be taken. If the pain is severe, if the usual rhythm of life collapses, the patient may begin to panic and depression. You need to urgently consult a doctor and undergo an examination. In case of exacerbation of chronic diseases, the patient most likely previously consulted doctors. The reason why the pain has returned may not be clear to him.

Important! Chronic patients need to undergo regular follow-up examinations to exclude possible complications and minimize exacerbations.

Treatment methods

Treatment of pain syndrome is carried out comprehensively and has two main goals:

Relieving pain symptoms, restoring the patient’s activity, improving his physical and psychological condition.
If it is impossible to completely eliminate pain, reduce it to a minimum and restore the body as much as possible.

Symptomatic relief of acute pain prevents chronic pain syndrome and includes elements of psychosomatics.

Important! We must understand that pain accompanies a disease that needs to be cured. Relieving pain with analgesics is often only a temporary measure. This is not eliminating the causes of pain.

Therapy depends on the type, nature and stage of the disease that became the root cause of the syndrome.

Non-steroidal anti-inflammatory drugs are often prescribed to relieve pain and inflammation in the affected tissues. To relieve chronic pain syndrome as a result of muscle spasm, muscle relaxant drugs are used, which contribute to the rapid restoration of normal muscle tone.

It is effective to treat chronic pain syndrome by injecting corticosteroids into the site of inflammation and degenerative changes. Medicines are injected into joints and active (trigger) points. For chronic pain syndrome, psychotropic drugs (antidepressants, anticonvulsants) can be used.

If there are no contraindications, physiotherapy, manual therapy, and various types of massage are performed. Warming procedures, mud therapy, and folk remedies help with many pains.

To cure myofascial pain syndrome, the patient is given injections of painkillers and vitamins. Posture is corrected and muscles are strengthened using special corsetry. Therapy is complemented by physiotherapy, massage, treatment with leeches, and acupuncture.

To treat abdominal pain syndrome, the main thing is to establish its exact cause. The patient may be prescribed antispasmodics, antidepressants, and muscle relaxants.

Anococcygeus pain syndrome, depending on the cause, is treated differently. The basis of treatment is sedative and anti-inflammatory drugs. Physiotherapy plays a great role in healing a patient with this syndrome. Electrophoresis, UHF, balneotherapy, massage are used.

Treatment of vertebrogenic syndrome begins with providing the patient with complete rest. Therapy is carried out with non-steroidal drugs that relieve inflammation. Massage and rehabilitation course are required.

Patellofemoral syndrome in the early stages is well treated with ointments and compresses. At the same time, rest and the absence of unnecessary stress during the first months are important. In some cases, surgical intervention is resorted to.

It is easy to “trigger” neuropathic syndrome, bringing it to a stage where treatment will be difficult. A number of medications are prescribed: anesthetics, antidepressants, anticonvulsants. Acupuncture and electrical neurostimulation help.

People perceive pain syndromes individually. The mood and even the physiological functions of the body depend on this perception. Stress, psychological trauma, and panic can provoke a psychosomatic nature of pain in the absence of visible causes or exceeding these causes.

Therefore, to treat patients with pain syndromes, psychotherapy is also practiced, aimed at reducing fear of an attack of pain. This is done by rehabilitation doctors and psychotherapists, whose goal is to restore to patients the strength, desire, and sometimes the meaning to effectively fight the disease.

In 1906, J. J. Dejerine and G. Raussy first gave a detailed clinical description of pain after a stroke. Dejerine-Roussy syndrome (central or thalamic pain syndrome) was intense unbearable pain in patients with thalamic infarction, which included: acute burning pain of the hemitype, decreased all types of sensitivity, hyperpathy, hemiparesis, mild hemiataxia, muscle dystonia. Along with motor and sensory disorders, such a patient also experiences severe cognitive impairment and depression. It is believed that the severity of pain experienced correlates with the severity of cognitive impairment and depression. Post-stroke pain can lead to suicide attempts. The development of post-stroke pain is observed in 12-55% of patients. Typically, pain develops within 3-6 months after a stroke, but it is not uncommon for pain to appear during the first month. Post-stroke pain syndrome from the point of view of pathogenesis is heterogeneous, and in its structure one can distinguish central pain, post-stroke pain, pain associated with spasticity, shoulder pain, tension headaches, and complex regional pain syndrome.

For a long time, the development of central post-stroke pain was associated only with damage to the thalamus. However, the introduction of neuroimaging methods into modern clinical practice has made it possible to establish that central post-stroke pain develops both with damage to the thalamus and outside the thalamic structures. Central post-stroke pain can occur when the somatosensory analyzer is damaged at any level - the cerebral cortex, thalamic nuclei, structures of the medulla oblongata and spinal cord. According to epidemiological studies, central post-stroke pain develops in 1-12% of patients. A number of authors believe that ischemic stroke more often leads to the development of central pain than hemorrhagic stroke. Central post-stroke pain belongs to the group of neuropathic pain syndromes and, according to experts from the International Association for the Study of Pain (IASP), is a direct consequence of damage or disease to the central parts of the somatosensory system.

The most frequently cited hypothesis about the nature of central neuropathic pain is Head and Holmes's concept of a disruption of the inhibitory influence of the lemniscal somatosensory system on the ascending paleospinothalamic system. Later hypotheses about the mechanisms of formation of central pain are essentially a detailing of the concept of Head and Holmes about the interaction of “specific” lateral and “nonspecific” medial brain structures. For example, L.A. Orbeli (1935) attached importance in the mechanisms of development of central pain to the imbalance between the lemniscal and extralemniscal systems of the brain. K. Winther (1972) devotes significant attention to the disruption of afferent interaction between the impulse flows of epicritic and protopathic pain. Electrophysiological studies conducted in patients with central pain syndromes suggested that hyperactivation of neurons in the medial thalamus when the lateral thalamic nuclei are damaged occurs through the reticular thalamic nucleus. According to the thermosensory input limitation hypothesis, central pain occurs due to a decrease in cold inhibitory influence on the processing of pain information. The author's assumption is based on the fact that in central pain syndromes, a decrease in temperature sensitivity occurs earlier than pain, and in some cases it is the only sensory deficit. In most cases, patients with central pain syndrome experience burning or freezing pain in the area of decreased temperature sensitivity, and the degree of pain is proportional to temperature hypoesthesia.

Damage to the central structures of the somatosensory system leads to disruption of the mechanisms that control the excitability of nociceptive neurons in the central nervous system and changes the nature of interaction in the systems that regulate pain sensitivity. Due to disruption of inhibitory and excitatory processes, central sensitization of nociceptive neurons develops with long-term self-sustaining activity. An increase in the excitability and reactivity of nociceptive neurons during central pain syndrome is observed in the dorsal horn of the spinal cord, thalamic nuclei and somatosensory cortex of the cerebrum.

Central post-stroke pain can have a limited area and be localized in any part of the body or spread throughout the hemitype. In patients with brainstem lesions, pain may be limited to one half of the face or localized to the opposite side of the trunk or extremities. The distribution of pain according to the hemitype is characteristic of a thalamic lesion.

The presentation of central post-stroke pain fully or partially corresponds to the localization of sensory disorders and correlates with the area of cerebrovascular damage. Approximately 80% of central postinsulin pain occurs in the parietal cortex. Central post-stroke pain is characterized by a combination of negative and positive sensory phenomena in the area of pain localization. Disorders of temperature (cold) and pain sensitivity are observed in more than 90% of patients, while disturbances of other types of sensitivity (tactile, vibration) are less common. At the same time, allodynia, hyperalgesia, and hyperpathy are diagnosed in the painful area. One patient may experience several types of pain. Constant spontaneous pain is more often described as burning, tingling, cold and pressing, and periodic pain is tearing and shooting in nature. The intensity of pain can vary throughout the day, under the influence of provoking factors. The main factors leading to increased pain may be cold, emotional stress, physical activity, fatigue, and weather changes. Anxiety and depressive symptoms aggravate the course of the pain syndrome. The pain may decrease with rest, distraction, and disappears during sleep. Many patients find relief from warmth.

Difficulties in diagnosing central post-stroke pain are due to the varied clinical picture, the presence of different types of pain in one patient and the lack of clear diagnostic criteria. Decreased cognitive function, depressive symptoms, and speech impairment in a patient after a stroke can cause difficulties in identifying signs of post-stroke pain. Diagnosis should be based on a medical history, the results of a clinical neurological examination, and the use of neuroimaging methods (computed tomography or magnetic resonance imaging). When collecting anamnesis, it is necessary to find out the sensory characteristics of pain, its location, prevalence, intensity and duration. Sensory characteristics of neuropathic pain are “burning”, “shooting”, “stabbing”, “like an electric shock”, “burning”, “chilling”, “piercing”. Screening questionnaires for neuropathic pain (DN4, PainDetect) can provide some assistance in diagnosis.

Many stroke patients also experience "crampy" pain. A prospective observational study demonstrated a strong association between the development of spasticity and pain. 72% of patients with spasticity develop pain, while only 1.5% of patients without spasticity experience pain.

It is currently believed that post-stroke spasticity is a reflection of a combined lesion of the pyramidal and extrapyramidal structures of the brain, leading to a decrease in inhibitory effects mainly on α-motoneurons of the spinal cord. The development of spasticity impairs motor function, promotes the development of contracture and may be accompanied by painful muscle spasms. Spastic dystonia and pain lead to a decrease in the functional capabilities of patients and their rehabilitation. The risk of developing spasticity is higher in patients with severe paresis, low Barthel scores, post-stroke central pain and sensory deficits. The leading role in the treatment of post-stroke spasticity is played by therapeutic exercises, which should begin from the first days of stroke development and be aimed at training lost movements, independent standing and walking, as well as preventing the progression of spasticity and the development of contractures. In clinical practice, muscle relaxants (tolperisone, tizanidine, baclofen) are most often used to treat post-stroke spasticity, the use of which can improve motor functions, facilitate care for an immobile patient, relieve painful muscle spasms, enhance the effect of physical therapy and prevent the development of contractures.

Currently, direct evidence has been obtained that the muscle relaxant effect of tolperisone is associated not only with inhibition of the activity of voltage-dependent Na+ channels, but also with a decrease in the release of excitatory neurotransmitters. In particular, using a model of an isolated nerve, it was found that the addition of tolperisone to the incubated medium at a dose of 100 µmol/l reduces the permeability of sodium ions by 50%. A comparative study of the effect of tolperisone and lidocaine on seven types of voltage-gated sodium channels showed that tolperisone, like lidocaine, has a blocking effect on the activity of sodium channels, but the degree of blocking in tolperisone is less pronounced. Significant differences between the two drugs in the restoration of sodium channel activity were demonstrated for three types of sodium channels - Nav1.3, Nav1.5 and Nav1.7, which are not related to the conduction of pain impulses, while the duration of inactivation for channels like Nav1.8 related to nociceptive impulses, lidocaine and tolperisone were similar.

Studies conducted on dorsal root ganglion cells found that tolperisone inhibited voltage-dependent sodium conductance at concentrations at which it inhibited spinal reflexes. Moreover, tolperisone had a significant effect on voltage-gated calcium channels. These data allowed the authors to assert that tolperisone exerts its muscle relaxant effect primarily by inhibiting the presynaptic release of neurotransmitters from the central terminals of afferent fibers through a combined effect on voltage-gated sodium and calcium channels.

Thus, tolperisone, by blocking sodium and calcium channels in nociceptive afferents, is able to suppress the secretion of excitatory amino acids from the central terminals of primary afferent fibers, weaken the frequency of action potentials of motor neurons and thereby inhibit mono- and polysynaptic reflex reactions in response to painful stimuli. This action of tolperisone provides effective control of spasticity and muscle pain.

In addition to its effect on muscle tone, tolperisone has the ability to enhance peripheral blood circulation. This effect is associated with the blockade of alpha-adrenergic receptors localized in the vascular wall. Increased blood circulation in the muscle may be an additional factor preventing the sensitization of muscle nociceptors during muscle spasticity under conditions of pain impulses.

The drug selectively weakens pathological muscle spasm without affecting, in therapeutic doses, the normal sensory and motor functions of the central nervous system (muscle tone, voluntary movements, coordination of movements) and without causing sedation, muscle weakness and ataxia. Tolperisone hydrochloride, unlike other muscle relaxants, causes muscle relaxation without withdrawal symptoms, which was proven in a double-blind, placebo-controlled study conducted according to GCP criteria.

Treatment of patients with central post-stroke pain remains challenging. Attempts to treat such patients with analgesics (including narcotic analgesics) have been unsuccessful. A recently published systematic review of eight randomized controlled trials on the treatment of post-stroke pain also does not add optimism. According to the authors' findings, the effectiveness of pharmacological agents (anticonvulsants, antidepressants, opioid analgesics) and non-pharmacological treatments (transcranial magnetic stimulation, acupuncture) for post-stroke pain ranges from low to very low. Considering the heterogeneous nature of central post-stroke pain, experts are increasingly discussing rational polypharmacotherapy based on the principles of evidence-based medicine. Of greatest interest in this regard is a systematic review and meta-analysis of clinical trials of drugs for the treatment of neuropathic pain published by a group of leading international experts. The quantitative analysis included 229 randomized clinical trials for the treatment of neuropathic pain published from 1966 to 2014. The assessment was carried out using a system for assessing the quality and level of evidence of recommendations - GRADE (Grading of Recommendations Assessment, Development, and Evaluation) and the Oxford Research Quality Rating Scale. A meta-analysis of effectiveness was conducted for the following drugs:

tricyclic antidepressants (TADs);
serotonin and norepinephrine reuptake inhibitors (SNRIs);
pregabalin;
gabapentin;
gabapentin with sustained release of the active substance;
enacarbyl;
other anticonvulsants (carbama-zepine, oxcarbazepine, topiramate, lacosamide, zonisamide);
tramadol;
opioid analgesics;
cannabinoids;
5% lidocaine patch;
capsaicin in high concentration in the form of a patch and cream;
botulinum toxin type A;
NMDA receptor antagonists;
mexiletine.

Depending on the proven effectiveness and degree of safety, the drugs were assigned to one or another line of therapy (Table).

As can be seen from the table, the first-line drugs for the treatment of neuropathic pain included gabapentin, pregabalin, duloxetine, venlafaxine and TAD.

The authors of the recommendations note that the choice of a particular drug in each specific case is determined by a combination of various factors, including possible risks of adverse events, the presence of comorbid disorders (depression and sleep disorders), features of drug interactions, the possibility of overdose or drug abuse.

As first-line therapy in patients with central post-stroke pain, the use of TAD, pregabalin, and gabapentin is recommended. Selective SNRIs, lamotrigine, opioids, and their combinations may also be used when first-line drugs are insufficient.

An important aspect in the treatment of central post-stroke pain is the clear setting of realistic goals for pain therapy and the formation of adequate expectations for the patient and relatives. Considering the torpid nature of the course of central post-stroke pain, the goal of therapy will not be to eliminate pain, but to reduce the intensity of the pain syndrome, expand the patient’s functional capabilities, and improve the quality of life. Compliance with the dosing regimen and titration of drugs, based on the individual sensitivity of the patient, will help maintain the patient’s compliance with the therapy. Low rates of effectiveness of pharmacotherapy for neuropathic pain, according to a number of studies, are usually due to suboptimal dosing and premature discontinuation of prescribed medications. The use of drugs with different mechanisms of action during complex pharmacotherapy can help improve the effectiveness of treatment. The physician should also ensure continuous monitoring of therapeutic and side effects. When monitoring, it is necessary to evaluate not only the intensity of pain, but also the qualitative sensory characteristics of pain (burning nature, lumbago, dysesthesia, allodynia, numbness), quality of sleep, severity of anxiety and depression, functionality and social adaptation. If conservative drug and non-drug therapy is ineffective, it is necessary to refer the patient to algological centers to resolve the issue of invasive treatment methods.

Literature

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