Chest myositis: causes, symptoms and effective treatment methods

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Autoimmune myositis is a group of autoimmune rheumatic diseases that cause inflammation and weakness of the muscles (polymyositis) or skin and muscles (dermatomyositis). To date, it has already been proven that coronavirus infections can cause viral myositis - about 30% of patients infected with various coronavirus infections demonstrate increased levels of muscle enzymes - indicators of the disease.

Muscle pain (myalgia) is one of the most common primary symptoms of the new coronavirus disease. In a WHO report based on an analysis of the symptoms of more than 50,000 COVID-19 patients in China, muscle pain was listed as one of the first symptoms of the disease in 15% of cases. In patients with severe disease during bed rest, muscle weakness is observed within a week, which is associated with type 2 muscle fiber atrophy. It also develops as a result of the use of muscle relaxants that block neuromuscular transmission - they are used for mechanical ventilation in patients with extensive lung damage.

To date, no direct evidence of direct muscle damage from COVID-19 has been obtained - no viral particles were found in the muscles of those who died from the new coronavirus infection. But necrosis of muscle tissue was recorded. Therefore, a hypothesis was put forward about immune-mediated damage to muscle fibers, that is, the indirect influence of the virus (autoreaction of the body). Statistics show that the majority of recovered patients with musculoskeletal system disorders recover, but for a certain portion of recovered patients the consequences can be significant. And all of them are explained by the body's autoimmune reaction.

Symptoms

• symmetrical muscle weakness;
• joint pain;
• difficulty swallowing;
• heat;
• fatigue;
• weight loss.

Autoimmune myositis is characterized by inflammatory and degenerative changes in the muscles (polymyositis) or muscles and skin (dermatomyositis). Manifestations include symmetrical muscle weakness, occasionally sensitivity, muscle replacement with fibrous tissue, and in some cases atrophy of the pelvic and shoulder girdle muscles develops. Muscle weakness may develop slowly or suddenly, gradually worsening over weeks or months. Pain and inflammation in the joints are noted by about a third of patients. Sometimes damage to the lungs and heart occurs, leading to irregular heart rhythms (arrhythmias), shortness of breath and cough. Over time, joint contractures may develop. Autoimmune myositis may also overlap with other autoimmune disorders, such as systemic lupus erythematosus, systemic sclerosis, and mixed connective tissue diseases.

Common symptoms of myositis that should make you see a doctor

One of the typical signs of any inflammation is pain. This is a kind of cry from the body for help. With myositis, pain is localized in the muscles. It can have a different character. The main symptoms of diagnostic significance are:

• pain syndrome;
• the presence of dense hyper-irritable zones (trigger pain points) in muscle tissue;
• increased muscle weakness and decreased muscle mass
• redness and swelling of the skin over the affected area;
• local (sometimes general) increase in temperature, fever;
• movement disorders.

Any of these symptoms (and especially a combination of several) is a serious reason for immediate contact with a specialist!

Diagnostics

It is based on the analysis of the clinical picture and laboratory assessment of muscle dysfunction by determining the concentration of the enzymes aldolase and creatine phosphokinase, as well as MRI data, electromyography and muscle tissue biopsy. The determination of antinuclear antibodies is indicated.

To make a diagnosis of autoimmune myositis, as many of the following 5 criteria must be present:

• weakness of proximal (located close to the center of the body) muscles;
• characteristic rash;
• increased activity of muscle enzymes (creatine kinase, aminotransferase, aldolase);
• muscle disorders detected by electromyography or MRI;
• changes detected by muscle biopsy (defining test)

An accurate diagnosis is made based on biopsy data - for polymyositis and dermatomyositis, chronic inflammation with foci of degeneration and partial regeneration of muscle tissue is typical. The biopsy must be obtained from muscle consistent with one or more of the following:

• weakness on clinical examination;
• presence of signs of muscle swelling on MRI;
• presence of changes in electromyography in the paired muscle.

Laboratory testing confirms or reduces the suspicion of myositis, allows us to assess its severity, as well as identify cross-sectional changes and complications.

Diagnosis of myositis at the Med&Care clinic

As mentioned above, different forms of the disease have their own clinical picture. If myositis is suspected, a neurologist at our clinic will interview and examine the patient and prescribe the necessary tests and studies.

The most informative instrumental diagnostic method for myositis is ultrasound of soft tissues and ultrasound angiography. Our medical center uses modern expert class ultrasound equipment TOSHIBA APLIO CV. It allows you to detect inflammation of muscle tissue (foci of hyperechogenicity), fibrous layers (hypoechoic areas), abscesses and other pathological processes.

To confirm the diagnosis, electromyography is sometimes used to help evaluate the electrical activity of muscles.

The following are a good help to the doctor:

• General blood analysis. It allows you to confirm or exclude infectious myositis (accompanied by an increase in ESR, the number of leukocytes and neutrophils) and a parasitic form of pathology that provokes the growth of eosinophils.
• Blood test for creatine phosphokinase. Exceeding the permissible norms of this enzyme indicates damage to muscle cells.
• Rheumatic tests that help identify local or systemic autoimmune diseases. Of particular diagnostic value is the analysis for myositis-specific autoantibodies (MSA).
• Biopsy. Taking a biopsy allows you to see structural changes in muscle tissue, the vessels that feed it and nearby connective tissue.

Treatment

• corticosteroids;
• immunosuppressants (methotrexate, azathioprine, mycophenolate mofetil, rituximab, tacrolimus)
• intravenous immunoglobulin;
• gentle motor mode (until inflammation subsides).

In acute illness, glucocorticoids (prednisone) are the treatment of choice for initiating therapy. For severe illness with dysphagia or respiratory muscle weakness, pulse corticosteroid therapy (methylprednisolone) is indicated. A decrease or normalization of enzyme levels is observed after 6–12 weeks, after which the dose of prednisone is gradually reduced. At the same time, to minimize the effects of corticosteroids, a second (non-steroidal) drug (methotrexate, tacrolimus or azathioprine) is prescribed.

Causes of thoracic myositis

The skeletal muscles of the human chest are constantly in action, even when other muscle groups are resting - after all, we breathe continuously. Under unfavorable conditions, the muscles of the thoracic region are susceptible to inflammation - thoracic myositis. Let's call these conditions:

• previous diseases (viral, infectious), metabolic problems;
• pathologies of the thoracic spine;
• cold, damp, drafts;
• long-term preservation of anatomically incorrect posture;
• overwork of the pectoral muscles;
• injuries;
• local infection.

The risk group includes people engaged in sedentary work, as well as heavy physical labor.

Osteoarticular pain in the thoracic spine and chest

N.V. PIZOVA

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Doctor of Medical Sciences, Professor, State Budgetary Educational Institution of Higher Professional Education "Yaroslavl State Medical Academy" of the Ministry of Health of Russia The article discusses in detail the causes and mechanisms of the occurrence of vertebrogenic pain syndromes.
A differentiated approach to therapy is presented, taking into account the pathogenesis and stage of the underlying disease. The advantages of using combination drugs (diclofenac and B vitamins) in the treatment of patients with back pain are described. Back pain is one of the most common sufferings of modern people. It is associated with significant economic losses caused by temporary and even permanent loss of ability to work in young and middle-aged people. Back pain accounts for up to 6% of all direct costs for the treatment of various diseases, 15% of all days of disability and 18% of causes of disability [1]. Acute and chronic back pain can be manifestations of any disease. And a doctor of any specialty faces two main tasks - to identify the cause of pain and to find a medicine that adequately helps with it.

All back pain syndromes can be classified into the following categories:

1. by reason – vertebrogenic and non-vertebrogenic; 2. by mechanism – reflex, compression, against the background of instability of the spinal motion segment (SMS), vascular, inflammatory; 3. by localization - local, reflected and irradiating; 4. by duration – acute and chronic.

During life, back pain occurs in 70–90% of the population, and in 20–25% it is registered annually. In the vast majority of patients, as a result of the therapy, pain is relieved within 4 weeks. However, 73% of patients develop at least one exacerbation during the first year [2, 3, 4]. Thus, according to a Russian study, the most common location of pain (576 patients - 60.6%) was the back. According to medical documentation, back pain was regarded as dorsopathy in 417 (72.4%) patients and as a consequence of intervertebral disc herniation in 104 (18.1%). 34 (5.9%) patients had osteoporotic fractures of the vertebral bodies, and 21 had other causes of back pain [5].

Chronic back pain is observed in 20–25% of cases, and this category of patients accounts for up to 80% of the economic costs associated with pain in this localization [6]. Chronic pain is the result of a complex interaction between biological, psychological, social and cultural factors that make its diagnosis and treatment difficult [7, 8]. Chronic back pain can be classified as nociceptive, neuropathic, inflammatory, dysfunctional, or can be mixed when there are characteristics of several types of pain [9]. Although their causes and clinical manifestations are different, the mechanisms by which these types of pain occur may overlap, and a patient may develop chronic back pain with components of more than one type of pain.

The source of back pain can be pain impulses associated both with the spine itself - vertebral factors (ligaments, muscles, periosteum of processes, fibrous ring, joints, roots), and with other structures - extravertebral factors (muscles, visceral organs, joints). Traditionally, thoracalgia, like other pain syndromes, depending on the cause, is divided into vertebrogenic (pathogenetically caused by changes in the spine) and non-vertebrogenic pain syndromes. Vertebrogenic thoracic syndromes include damage to the thoracic roots due to intervertebral disc herniation, spinal canal stenosis, spondylolisthesis and instability, and arthropathic syndrome due to degenerative lesions of the facet and costotransverse joints. Vertebrogenic causes of pain in the thoracic spine also include relatively rare malignant neoplasms of the spine (primary tumors and metastases), inflammatory (spondyloarthropathy, including ankylosing spondylitis) and infectious lesions (osteomyelitis, epidural abscess, tuberculosis), as well as compression fractures of the vertebral bodies due to osteoporosis. The cause of non-vertebrogenic pain syndromes can be pathology of internal organs and muscle pain syndromes, which can be formed under the influence of both vertebrogenic and non-vertebrogenic changes. Therefore, the division into vertebrogenic and non-vertebrogenic pain syndromes can be considered quite relative. In addition, psychogenic pain syndromes (panic attacks and hyperventilation disorders) are a possible cause of nonvertebrogenic chest pain.

Clinical syndromes in spondylogenic thoracalgia include [10]:

1. local vertebral syndrome, often accompanied by local pain, tension and soreness of adjacent muscles, pain and deformity, limited mobility or instability of one or more adjacent segments of the spine; 2. vertebral syndrome at a distance; 3. reflex (irritative) syndromes: referred pain, muscular-tonic, neurodystrophic syndromes, autonomic (vasomotor, etc.) disorders, etc.; 4. compression (compression-ischemic) radicular syndromes; 5. spinal cord compression syndrome (ischemia).

Vertebrogenic pain syndromes are conventionally divided into reflex (occurring in 85–90% of cases) and compression (observed in 10–15% of cases). Reflex pain syndromes arise due to irritation of the receptor apparatus in muscles, tendons and fascia, ligaments, spinal joints, intervertebral discs, etc. due to the formation of nociception sites with a local nonspecific inflammatory reaction. Under conditions of activation of the synthesis and release of pro-inflammatory and algogenic substances (substance P, kinins, prostaglandins, leukotrienes, cytokines, nitric oxide, tumor necrosis factor, etc.), the excitability (sensitization) of nociceptors increases. As a result, a powerful flow of nociceptive afferentation is formed, which enters through the dorsal roots into the neurons of the dorsal horns of the spinal cord, from where it reaches the central parts of the nervous system (reticular formation, thalamus, limbic system and cerebral cortex) along the ascending nociceptive pathways, causing an NMDA-dependent increase in these structures intracellular calcium concentrations and activation of phospholipase A2. The latter stimulates the formation of free arachidonic acid and the synthesis of prostaglandins in neurons, which, in turn, increases their excitability [11, 12]. At the same time, in the posterior horns of the spinal cord, the flow of pain impulses through interneurons activates the neurons of the lateral horn with activation of adrenergic (sympathetic) innervation and motor neurons of the anterior horns of the spinal cord. Activation of the latter leads to spasm of the muscles innervated by this segment of the spinal cord (sensorimotor reflex). Muscle spasm is an additional source of pain due to the activation of muscle nociceptors due to its shortening, the development of neurodystrophic changes and impaired microcirculation in muscle tissue. As a result, a vicious circle closes: “pain, neurogenic inflammation - increased protective muscle tension, pathological changes in the muscles - increased pain,” which contributes to the development of persistent reflex muscle-tonic syndrome [11, 12, 13]. Normally, there is a strictly balanced relationship between the intensity of the stimulus and the response to it. The antinociceptive system exercises descending inhibitory cerebral control over the conduction of pain impulses and inhibits the transmission of pain stimuli from primary afferent fibers to interneurons. The interaction of these structures results in a final pain assessment with an appropriate behavioral response. However, long-term preservation of nociceptive impulses leads to the formation of stable pathological connections, the appearance of pronounced dystrophic changes in surrounding tissues, which, in turn, become a source of pain signals, thereby increasing peripheral pain afferentation, which contributes to the depletion of the antinociceptive system [11, 12, 13] . The chronic course can be facilitated by inadequate treatment of acute pain, excessive limitation of physical activity, a “painful” personality type, low mood, in some cases the patient’s interest in long-term disability, aggravation of existing symptoms or a “rental” attitude towards the disease. With a long course of the disease, pathological changes occur in the roots with the development of axonal and/or demyelinating processes.

The term “osteochondrosis” was proposed in 1933 by the German orthopedist Hildebrandt to designate involutional changes in the musculoskeletal system [14]. Osteochondrosis (Greek osteoon - bone, chondros - cartilage, osis - suffix denoting a pathological condition) is understood as a congenital or acquired degenerative-dystrophic cascade process, which is based on disc degeneration with subsequent secondary involvement of adjacent vertebral bodies, intervertebral joints and ligaments . In turn, the intervertebral disc is a component of the intervertebral symphysis - a complex connection of the vertebrae in the spinal column. In the symphyses of the spine, unlike synovial joints, between the surfaces of the vertebrae covered with hyaline cartilage, there is not synovial fluid, but a specific formation of a cartilaginous nature - an intervertebral disc consisting of a nucleus pulposus and an annulus fibrosus. The first is close in morphological structure to hyaline cartilage due to the high content of proteoglycans, hyaluronic acid, type II collagen and water. While the annulus fibrosus refers to fibrous cartilage with a high collagen content (up to 68%), mainly due to type I collagen in the outer plates of the ring, and rich in sulfated glycosaminoglycans integrated into large proteoglycan molecules, with their characteristic ability to retain water [11, 15]. However, despite the existing differences in the morphological structure of synovial joints and intervertebral symphyses, there is an opinion about the similarity of arthrosis changes occurring in them, expressed in an imbalance of anabolic and catabolic processes in the cartilage matrix [16]. An imbalance of the most important homeostatic processes leads to a decrease in the synthesis of complete collagens and proteoglycans by chondrocytes. Non-sulfated glycosaminoglycan, hyaluronic acid, is no exception, ensuring the formation of matrix proteoglycan aggregates and the hydration of the nucleus pulposus, which plays the role of a protective cushion (due to hydration and changes in its volume). Changes in the quality and quantity of hyaluronic acid in osteochondrosis lead to a decrease in the content of bound water in the nucleus pulposus and destruction of the collagen network, especially in the pericellular zones of chondrocytes [17, 18, 19]. The latter is primarily associated with an increase in the synthesis of metalloproteinases (collagenase, stromelysin), ultimately leading to the complete disappearance of the pericellular collagen network and the loss of shock-absorbing properties of the intervertebral disc as a whole.

Osteochondrosis and spondyloarthrosis are provoked by identical pathogenetic factors, in response to which in the involved structures of the SDS (including two adjacent vertebrae and the intervertebral disc, the own articular, musculo-ligamentous apparatus, the vascular system, as well as the section of the spinal cord corresponding to this level, roots and spinal autonomic ganglia with their connections within this segment) there is a release of biochemically and immunologically active mediators that interact with sensitive receptors, which, in turn, triggers complex and not yet fully understood neurophysiological mechanisms of the formation of pain sensations [11]. It has been established that the source of pain can be an anatomical structure innervated by unmyelinated fibers or containing substance P (or peptides similar to it) [20, 21]. The intervertebral disc has long been considered a formation indifferent to the generation of pain impulses, since no nerve endings were found in it. More detailed anatomical and histochemical studies showed the presence of thin nerve endings in the outer third of the fibrous ring - 1-2 segments above or below its exit [11, 18, 19].

Another source of pain is considered to be the facet (facet) joints, the synovial capsule of which is richly innervated by articular nerves, which are branches of the posterior branches of the spinal nerves, and small accessory nerves from the muscular branches. Due to their vertical orientation, the facet joints offer very little resistance to compression, especially during flexion. Most likely, this slight resistance is due to stretching of the capsular ligaments. Under conditions of extension, the facet joints account for 15 to 25% of compression forces, which can increase with disc degeneration and narrowing of the intervertebral space [11, 21]. With sudden unprepared movements associated with rotation of the body, lifting heavy objects, when working with arms raised above the head, facet syndrome often occurs. The pathogenesis of this syndrome is associated with the convergence of the articular surfaces of the facet (facet) joints and their blocking when the load on the joint and its ligamentous apparatus increases. Pain associated with facet syndrome in the thoracic spine can range from mild discomfort to severe intensity and be severely disabling. It usually increases with extension and decreases with flexion of the spine and can be reflected on the anterior surface of the chest. Below and above the level of joint blocking, a reflex spasm of the erector spinae muscle is often detected [22, 23, 24, 25, 26].

One of the causes of chest pain may be Tietze's syndrome, first described by Tietze in 1921. This syndrome is a relatively rare condition characterized by the presence of nonspecific benign reversible painful edema in the area of ​​the II (in 60% of cases) or III costal cartilage. In 80% of cases there is a unilateral lesion limited to one costal cartilage. The pain is usually well localized, but can radiate along the entire anterior surface of the chest wall, as well as into the shoulder girdle and neck. There are no redness, increased temperature and other changes in the skin over the affected area. The pain usually resolves spontaneously after 2–3 weeks, but often persists for several months, and residual swelling can persist for up to several years. The disease usually develops at a young or childhood age. Its causes are unknown [22, 23, 24, 25, 26].

One of the most common causes of chest pain is costosternal syndrome. This syndrome is much more common than Tietze's syndrome. With costosternal syndrome, palpation in 90% of cases reveals multiple areas of pain: in the left parasternal region, below the left mammary gland, in the projection of the pectoral muscles and sternum. There is no local edema in costosternal syndrome. The cartilages of the II and V ribs are most often affected. When the upper costal cartilages are damaged, pain irradiates to the heart area. The pain usually worsens with chest movement. The disease is more common in women after 40 years of age [22, 23, 24, 25, 26].

Another common cause of chest pain is slipping rib syndrome. The syndrome is characterized by intense pain in the projection of the lower edge of the costal arch and increased mobility of the anterior end of the costal cartilage, usually the X and less often the VIII and IX ribs. This condition is believed to be of traumatic origin and is associated with recurrent subluxation of the costal cartilage during trunk rotation. Unlike the overlying ribs, the cartilaginous parts of which form the sternocostal joints, the cartilaginous parts of the VIII–X ribs form articulations with the cartilaginous parts of the overlying ribs using the external intercostal membrane. This zone is anatomically the weakest area of ​​the chest, prone to injury. Following damage to the cartilage joint, the free cartilaginous part of the rib deviates upward, moving in the vertical or anteroposterior direction when breathing relative to the overlying cartilage, which is accompanied by pain and a characteristic clicking sensation. The pain, as a rule, is sharp or shooting in nature, localized in the upper quadrant of the abdominal wall and provoked by hyperextension of the chest when raising the arms up. In the acute stage of the disease, the patient often takes a forced position with the torso tilted forward and to the painful side to reduce tension in the abdominal wall muscles attached to the costal angles. In some cases, the displaced costal cartilage can injure the perichondrium of the overlying rib and the intercostal nerve. Pathognomonic for this condition is the test described by Holms, which consists of pulling the edge of the rib anteriorly with a bent finger. In this case, a typical pain pattern is reproduced, accompanied by a characteristic click. Carrying out such manipulation on the healthy side is not accompanied by the described phenomenon. The diagnosis can also be confirmed by infiltrating the space between the separated cartilage and the rib with 5 ml of 0.5% lidocaine solution, leading to complete regression of pain 10 minutes after the procedure [22, 23, 24, 25, 26].

Diffuse idiopathic skeletal hyperostosis (Forestier disease) is a disease that is relatively common in middle-aged and elderly people, mainly in men. The main symptoms are usually mild to moderate pain and a feeling of stiffness in the thoracic and lumbar spine. Upon examination, increased thoracic kyphosis, limited range of motion in the thoracic spine and chest excursion are determined. Local pain is often detected on palpation of the thoracic and lumbar spine. To confirm the diagnosis of diffuse idiopathic skeletal hyperostosis, it is necessary to conduct radiography of the spine, which reveals hyperostosis, most pronounced in the thoracic region and manifested by linear ossification along the anterior surface of four adjacent vertebrae or more with preservation of radiological clearing between bone deposits and vertebral bodies, as well as relative preservation of the height of the intervertebral gap. Also characteristic is the formation of osteophytes between the bodies of neighboring vertebrae, interlocking with each other in the form of “bridges” [22, 23, 24, 25, 26].

Diagnosis of vertebrogenic pain syndromes includes establishing the nature of pain and their relationship with static and dynamic loads, identifying trigger points, and symptoms of tension in nerve trunks. Computer and magnetic resonance imaging and radiography are important for determining the nature of the process and assessing the extent of existing changes. To determine the functional state of the roots, determine the location and stage of their damage, electroneuromyography is used [2, 6, 12, 13]. Already during the first examination of the patient, one should exclude danger symptoms (“red flags”) that are generally recognized for dorsalgia, namely, pay attention to the presence of fever, local pain and local increase in temperature in the paravertebral region, which are characteristic of an infectious lesion of the spine. A tumor (primary or metastatic) may be supported by an unreasonable decrease in body weight, a history of malignant neoplasm of any location, persistence of pain at rest and at night, as well as the patient’s age over 50 years. Spinal compression fractures are more common with trauma, corticosteroid use, and in people over 50 years of age. With a tumor lesion of the spinal cord, pain can be constant or recurrent, appear at rest and decrease with movement, often leads to sleep disturbance, forcing you to move or sleep in a forced position, for example, sitting. Against the background of constant pain, lumbago, provoked by coughing or sneezing, is often noted. Motor and sensory disturbances corresponding to the level of damage are identified. With syringomyelia and multiple sclerosis, pain may also be observed, the localization of which depends on the area of ​​damage to the spinal cord.

Other causes of damage to the thoracic roots may be herpes zoster with the development of postherpetic neuralgia, diabetes mellitus, and fractures of the thoracic vertebrae. The pain in these cases, as a rule, is long-lasting, intense, localized in the area of ​​the corresponding segment, has a tightening or burning character, is often accompanied by short shooting pains, and can be lancinating. The pain intensifies at night and with movements in the thoracic spine. Hyperesthesia, hyperalgesia and hyperpathy are often detected in the affected segments. To clarify the diagnosis, radiography, CT, and MRI of the thoracic spine are necessary. In case of rib injuries, the interosseous nerves can be affected, which is accompanied by acute superficial, burning pain in the area of ​​their innervation. The pain intensifies when inhaling or when moving the chest, reminiscent of the pain of pleurisy. As a rule, a small area of ​​segmental hyperalgesia or hyperesthesia is detected, which occurs even when one nerve is affected.

After identifying the cause, mechanism, nature and duration of the pain syndrome, the issue of selecting adequate therapy is decided. Treatment should always be individualized. It depends on the nature of the underlying disease and is divided into undifferentiated and differentiated therapy. The main objectives of undifferentiated therapy are to reduce pain or the patient's reactions to pain and eliminate autonomic reactions. The main direction of differentiated therapy for back pain syndromes is the influence on their pathogenetic mechanisms; treatment also depends on the phase of the underlying disease. The basic principles of conservative treatment include: 1) drug treatment using analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), dehydration, vascular and phlebotonic agents, angioprotectors, antihypoxants, antioxidants, muscle relaxants, B vitamins, biostimulants, chondroprotectors, desensitizing agents, immunocorrectors, neuroprotectors , metabolites, anticholinesterase, absorbable and vegetotropic drugs; 2) reflex treatment using acupuncture, laser therapy, physiotherapy, massage (segmental), thermal procedures, physical therapy (physical therapy), manual therapy, local irritants; 3) orthopedic treatment involving immobilization, traction therapy, massage, exercise therapy, manual therapy; 4) local anesthetic treatment with the appointment of irrigation with chlorethyl, blockades, dimexide applications, analgesic and anti-inflammatory ointments, gels, and patches.

The first and fundamentally important task facing the doctor is pain relief as quickly and effectively as possible. NSAIDs are the most widely used drugs for symptomatic pain management [27]. They are quite effective, easy to use, inexpensive and generally well tolerated. It should be noted that the effectiveness of NSAIDs as analgesics is determined not only by the peripheral effect associated with a decrease in the synthesis of prostaglandins, as well as other mediators of pain and inflammation in damaged or inflamed tissues.

The most widely used NSAIDs are from the group of non-selective cyclooxygenase (COX) inhibitors. Basic recommendations for the use of NSAIDs (in monotherapy or in combination with other analgesic drugs): 1) their use is advisable for acute or chronic diseases and pathological conditions manifested by pain associated with both inflammatory and degenerative damage to the musculoskeletal system, acute trauma and surgical interventions; 2) the duration of NSAID use depends on the duration and intensity of pain in a particular situation; 3) to relieve acute pain, it is advisable to prescribe parenteral forms of NSAIDs or those that give the most pronounced analgesic effect with a minimal risk of side effects; 4) for a long course of treatment, NSAIDs with a medium or long half-life are recommended, taken orally or in the form of rectal suppositories. These drugs are characterized by good analgesic and anti-inflammatory effects and provide relatively quick relief from pain.

In modern medicine, diclofenac, which is one of the most frequently prescribed painkillers, is recognized as the recognized standard for the treatment of diseases with severe pain. Like other NSAIDs, dilofenac inhibits the activity of the COX enzyme, which is involved in the formation of prostaglandins from arachidonic acid. Diclofenac also inhibits the activity of the enzyme lipoxygenase. According to Russian studies, with the simultaneous administration of diclofenac and B vitamins, a higher Cmax value was observed compared with the use of diclofenac alone [28]. To increase the therapeutic effect of diclofenac, while minimizing its dose as much as possible, using B vitamins, a highly effective combination drug Neurodiclovit was created, one capsule of which contains 50.0 mg of diclofenac, 50.0 mg of vitamin B1, 50.0 mg of vitamin B6 and 250.0 mcg vitamin B12. B vitamins have a wide range of pharmacodynamic properties and participate as coenzyme forms in most metabolic processes. It is known that thiamine (vitamin B1) has a significant effect on the regeneration processes of damaged nerve fibers, provides energy for axoplasmic transport, regulates protein and carbohydrate metabolism in the cell, affects the conduction of nerve impulses, and promotes the development of an analgesic effect. Pyridoxine (vitamin B6) is a cofactor for many enzymes acting in nervous tissue cells, participates in the synthesis of neurotransmitters of the antinociceptive system (serotonin, norepinephrine), supports the synthesis of transport proteins and sphingosine, a structural element of the nerve fiber membrane. ensures the delivery of fatty acids to cell membranes and the myelin sheath. Cyanocobalamin (vitamin B12) ensures the delivery of fatty acids to cell membranes and the myelin sheath. The use of vitamin B12 promotes not only remyelination (due to the activation of the transmethylation reaction, which ensures the synthesis of phosphatidylcholine in nerve cell membranes), but also a decrease in the intensity of pain, which is associated with the intrinsic antinociceptive effect of high doses of cyanocobalamin [29]. Experimental studies have shown that vitamin B1 alone or in combination with vitamins B6 and B12 is able to inhibit the passage of pain impulses at the level of the dorsal horns of the spinal cord and thalamus [30]. B vitamins function as coenzymes in metabolism, in particular in nervous tissue, which enhances the analgesic effect of diclofenac. When using B vitamins in the treatment of pain, one should remember that their analgesic properties decrease accordingly: B12˃B6˃B1 and that the multivitamin complex (B1+B6+B12) has a more pronounced analgesic effect than monotherapy with vitamin B1, B6 or AT 12. In the treatment of acute back pain, a combination of B vitamins with NSAIDs is more effective than NSAID monotherapy [31]. The drug is used for inflammatory and degenerative diseases of the joints and spine (chronic polyarthritis, rheumatic and rheumatoid arthritis, ankylosing spondylitis, osteoarthritis, spondyloarthrosis). Neurodiclovit has a low incidence of unwanted complications and good individual tolerability, which allows it to be recommended for widespread use in the treatment of patients with osteoarticular pain in the thoracic spine and chest.

The main therapeutic measures of individual forms are presented in Table 1.

Table 1. Basic treatment measures

Literature:
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Clinical manifestations

Thoracic myositis is characterized by a number of symptoms:

• local painful sensations, aggravated by active and passive movements, touch;
• radiating pain to the neck;
• inability to take a deep breath;
• swelling of tissues and redness of the skin in the area of ​​inflammation.

In elderly patients, the pathology must be differentiated from ischemic heart disease.

When the superficial muscles are predominantly affected, the patient's upper limb functions are impaired. When you try to raise your arm, severe pain occurs. Discomfort when inhaling and exhaling is not so pronounced.

Active movements in the limbs are difficult

If the deep muscles of the chest are involved in the pathological process, the patient begins to experience serious breathing problems.

Important! If the above symptoms appear, consult your doctor as soon as possible. The price of delay is your health.

Symptoms

The main problem in the diagnosis and treatment of chest myositis is that patients often confuse this disease with intercostal neuralgia. Many of the symptoms of both diseases are very similar.

• The patient feels aching pain that intensifies with movement and palpation.
• Upon palpation, compactions can be detected - foci of the inflammatory process.
• If purulent myositis occurs, the patient’s body temperature rises and chills are possible. The pain will intensify. The muscle becomes denser, it may swell, and the skin will take on a reddish tint.

Myositis of the chest occurs relatively suddenly. This usually occurs as a result of severe muscle strain or after an injury. The pain syndrome associated with this disease increases over time. These sensations lead to muscle contraction. If nothing is done to alleviate the condition, the body will begin to independently protect itself from pain. This will occur through muscle tension and, as a result, restriction of joint mobility. Ultimately, all this can lead to atrophy.

In addition to common symptoms, some patients may experience headaches and increased skin sensitivity. The condition is affected by weather conditions and time of day. Sometimes the unpleasant sensations go away on their own, but then relapses occur.

You can distinguish myositis from neuralgia by one main criterion: if it is myositis, pain during palpation will be felt in the entire area, and if it is neuralgia, then painful points will be clearly defined.

Why is it necessary to treat thoracic myositis?

There are several reasons, let’s focus on the main ones.

• Firstly, neglected thoracic myositis risks becoming chronic and negatively affecting the quality of life.
• Secondly, if inflammation of the pectoral muscles is not treated, it can spread to neighboring muscle groups - the neck, larynx.
• Thirdly, the patient’s body, trying to avoid pain, reflexively takes an unnatural posture, which affects the health of the thoracic spine.

We see that in the absence of adequate treatment for thoracic myositis, problems grow like a snowball. At the same time, early contact with a doctor is an important factor in complete recovery.

Treatment

Most often, when treating thoracic myositis, doctors give preference to methods that allow the patient to be cured as quickly as possible with minimal use of medications.

Such old but relevant remedies as manual therapy and hirudotherapy (leeches) quickly relieve pain and successfully eliminate inflammation in the chest muscles. At the same time, self-healing mechanisms are launched in the patient’s body.

Massage increases blood circulation in the pectoral muscles, eliminates stagnation of waste and toxins, relieves swelling, breaks up compactions, and returns muscle tone and activity.

does not treat thoracic myositis. If you notice symptoms of the disease, immediately contact your doctor.

Cosmetic procedures are contraindicated during pregnancy and lactation.

How to treat myositis?

Treatment of any inflammatory processes requires an integrated approach, since in addition to relieving acute and painful symptoms, it is important to influence the cause of their occurrence. It is advisable to begin treatment of both acute and recurrent forms with drug correction, and after regression of symptoms, continue therapy with physiotherapeutic methods and physical therapy.

Medications

You can get rid of pain and stop inflammation during myositis with the help of drugs from the NSAID group. Combination drugs are considered the most effective, for example, combinations of paracetamol and ibuprofen (“ Ibuklin ”, “ Next ”) or a combination of diclofenac with paracetamol (“ Panoxen ”). The group of drugs with a rapid analgesic and anti-inflammatory effect also includes meloxicam ( Movalis , Amelotex ) and Aertal , a drug based on aceclofenac, a derivative of acetic acid and related compounds.

Painkiller Next

Drug treatment of myositis can also be supplemented with the following medications:

Questions for the doctor

Specialist in the treatment of myositis

Which doctor treats myositis? From time to time I am bothered by vague chest pains, I would like to undergo a full examination.

Hello! If acute myositis develops, it is most logical to contact your local physician. The doctor will issue a certificate of temporary incapacity for work for the entire period of active inflammation, draw up a diagnostic plan (perhaps it will include consultations with specialized specialists) and treatment.

After the acute stage of the disease subsides, its causes should be understood. Here you may need to be examined by an infectious disease specialist, immunologist, endocrinologist, parasitologist, rheumatologist, neurologist, traumatologist, vertebrologist and other doctors.

What are the pectoral muscles for?

Muscles not only help a person make active movements, but also maintain the vertical position of the body, and also take part in breathing. Anatomically, the chest is represented by several important muscles.

Table: Chest muscles:

The muscles involved in the act of breathing work constantly. Even if some of the fibers fail, the person experiences serious discomfort, because the painful sensations prevent him from taking a normal breath.