Pain in muscles and joints: causes, treatment in a clinic in St. Petersburg

If you feel pain or discomfort in your muscles and joints, you should immediately seek medical help from an experienced doctor at the spine clinic. In the human body, all systems work in interconnection, so often one problem leads to another. Pathologies of bone tissue entail changes in muscle function and vice versa. Many patients at the Osteopathic Spine Clinic complain of muscle and joint pain. And the symptoms are more typical for older people, but they also occur in young people. This condition has a medical name - myoarthralgia.

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Causes of pain in muscles and joints

Unpleasant symptoms lead to:

degenerative processes (osteochondrosis, protrusion, disc herniation) and joint inflammation (arthrosis, spondyloarthrosis, spondylolisthesis);
scoliosis, poor posture, prolonged stay in one position;
entry of viruses and bacteria into the joint (for example, rubella pathogens);
autoimmune diseases;
violation of blood circulation and metabolic processes;
taking certain medications;
weakening of the muscle corset;
stress, shock.

That is, it is not a disease, but a combination of symptoms and causes.

How does it manifest?

Some patients complain of lumbago, acute, aching or constant pain, many note aching bones. In some cases, inflammatory processes are accompanied by high fever and symptoms of intoxication. Weakness and stiffness often occur. Symptoms of muscle and joint pathologies, as a rule, often recur, and the degree of their severity depends on the provoking factor:

If the pain is caused by damage to muscle fibers, then it is felt in a certain place and intensifies with pressure. It manifests itself more strongly when changing body position and loads.
Myoarthralgia, provoked by inflammation, leads to night pain that subsides after morning warm-up.
Degenerative processes are characterized by pain during physical activity, which subsides with rest.

In addition to pain, swelling, swelling of the joints, and numbness of the limbs may occur. Sometimes patients note that discomfort increases with hypothermia and stress.

What is the threat?

Pain in muscles and joints is a dangerous symptom that has many causes; it always requires urgent help from a specialist. Moreover, there is a risk of developing degenerative processes and serious complications of diseases. It is important to start treatment on time to avoid severe consequences and disability. An accurate and timely diagnosis is needed.

Diagnostics

At the initial appointment, the doctor will examine you, assess your condition, complaints, and study your medical history. Based on the data obtained, an examination will be prescribed, which may include diagnostic methods such as:

Ultrasound and ECG;
MRI, CT;
Radiography;
Laboratory research.

Features of neuropathic pain in joint damage

T.G. SAKOVETS

Kazan State Medical University, 420012, Kazan, st. Butlerova, 49

Tatyana Gennadievna Sakovets – assistant at the Department of Neurology and Rehabilitation, tel., e-mail: [email protected]

Joint lesions of various natures are widespread in the population; they are the most common cause of disability, but there is still no clear understanding of the nature of joint pain. Joint diseases can be an independent nosological form, as well as a manifestation of the pathology of other systems or a reaction to another pathological process. Carefully designed studies using experimental models of arthritis and appropriate methodological approaches will clarify all the mechanisms and aspects of the formation of neuropathic pain in arthritis and develop adequate pain therapy.

Key words: neuropathic pain, joint diseases, joint pain.

TG SAKOVETS

Kazan State Medical University, 49 Butlerov St., Kazan, Russian Federation, 420012

Features of neuropathic pain in the affected joints

Sakovets T. G. - Assistant Lecturer of the Department of Neurology and Rehabilitation, tel. (843) 237-34-66, e-mail

Joint lesions of various nature are widespread in the population. Though they are the most common cause of disability, there is still no clear understanding of the nature of joint pain. Diseases of the joints can be of independent nosological form or a manifestation of other systems pathology, or a response to a pathological process. Carefully designed studies using experimental models of arthritis and related methodological approaches will clarify all aspects of the formation and mechanisms of neuropathic pain in arthritis, and help to develop an adequate anti-pain therapy.

Key words: neuropathic pain, joint diseases, joint pain.

Diseases of the musculoskeletal system are the most common cause of disability in the modern world, and the prevalence of these diseases is growing at an alarming rate. Joint pain is widespread in various populations, but there is still a lack of clear understanding of the nature of joint pain. The whole variety of joint pathologies can be reduced to two forms - arthritis (inflammatory lesions of the joints, regardless of the immediate cause - infections, autoimmune processes) and arthrosis (dystrophic-degenerative lesions). About 80% of all patients with joint diseases are patients with osteoarthritis.

During inflammation, the receptors become hypersensitive to mechanical stimuli under the influence of neuropeptides, eicosanoids, and excitation of proteinase-activated receptors is noted. Immunocytes also influence the formation of pain in arthritis. The most obvious cause of joint dysfunction is chronic or episodic pain, which leads to psychological distress and decreased quality of life. Modern methods of antalgic therapy have limited effectiveness and a number of undesirable side effects, which thereby excludes the possibility of their long-term use.

The perception of damaging stimuli is carried out by nociceptors - sensory receptors that are responsible for the transmission and encoding of damaging stimuli [1]. Due to their varying sensitivity to mechanical, thermal and chemical stimuli, nociceptors represent a heterogeneous group [2]. Stimulation of pain receptors is carried out by mechanical, temperature and chemical stimuli.

The knee joints are innervated by sensory and sympathetic nerve fibers. Postganglionic sympathetic fibers are located near the blood vessels of the joints, where they regulate the blood supply to the joint, influencing the level of vasoconstriction. Nociceptive nerve fibers have a small fiber diameter, typically less than 5 µm, and are either unmyelinated (C-fibers) or myelinated with free nerve endings without a myelin sheath (Aδ-fibers) (type III and type IV nerve fibers, respectively). These slow-conducting fibers typically have a high activation threshold and respond only to potentially harmful mechanical stimuli.

Substance P and cocalcigenin (calcitonin gene-related peptide (CGRP), released by some C-fibers, are involved in the regulation of local blood flow and vascular permeability. A number of unmyelinated C-fibers in the dorsal root ganglia are activated by stimulation receptors with a specific irritant adenosine triphosphate, which is released when cell membranes are exposed to various damaging factors and contributes to the occurrence of peripheral sensitization. A common property for all nociceptors is a higher threshold for their activation compared to mechano- and thermoreceptors that respond to tactile, thermal or cold stimulation.

In rats and cats, 80% of all afferent nerve fibers in the knee joint are nociceptive [3], indicating the importance of the ability to sense excessive and potentially harmful joint movements. Pain receptors are located throughout the joint, including the capsule, ligaments, menisci, periosteum and subchondral bone [4]. Most distal sections of type III and IV afferent fibers lack myelin sheath and perineurium; these parts of the nociceptive receptors are thought to be responsible for the perception of pain. Electron microscopy reveals type III and IV nerve fibers with an hourglass-shaped terminal and multiple onion-shaped zones, which is typical for perception zones. It is in the “ball-like” structures at the terminals of free nerve endings that the pain perception of joints is formed. The question of how nociceptive information is converted into an electrical signal propagating along sensory nerves to the central nervous system (CNS) still remains unclear. The absence of a myelin sheath on sensory “free” nerve endings means that the axolemma of these fibers is likely to undergo significant stretch during joint movements. The recent identification of mechanodependent ion channels of types III and IV afferent nerve fibers of the knee joint identifies the mechanism responsible for mechanotransduction in the joints [5]. The current theory is based on the concept that joint movement generates shear stress on the axolemma of “free” nerve endings, which leads to the opening of mechanically dependent ion channels. The result is depolarization of nerve endings and the generation of action potentials, which are subsequently transmitted to the central nervous system, where they are decoded. If potentially dangerous joint movements are observed, the frequency of impulse generation in the afferent nerve increases sharply and the central nervous system interprets this nociceptive activity as pain. The formation of a multicomponent pain sensation is ensured by a complexly organized nociceptive system, which includes a network of peripheral nociceptive neurons and nociceptive neurons located in many structures of the central nervous system.

During inflammation, the main changes occur in the plasticity of the peripheral and central nervous systems, when the pain sensitivity threshold decreases, which leads to allodynia and hyperalgesia. Pain in arthritis is formed by stimulation of the so-called silent nociceptive receptors. These afferent nerve fibers are in an inactive state in unaffected joints, however, after damage to the joint tissues and/or induction of inflammation, these pain receptors are activated and begin to transmit nociceptive information to the central nervous system. This additional stimulation of peripheral “silent” nociceptive receptors is one of the factors contributing to the formation of pain in arthritis.

An additional process that contributes to arthritic pain is peripheral sensitization, in which the activation of nociceptive receptors is altered and afferent nerves become hypersensitive to both normal and excessive potentially harmful joint movements.

Experimental studies have shown that the induction of acute synovitis with intra-articular injection of kaolin and carrageenan reduces the pain sensitivity threshold of types III and IV afferents of the knee joint. The frequency of generation of action potentials from these mechanosensory nerves increases dramatically during both hyperflexion and hyperextension of the knee joint.

It is believed that this increase in neuronal conductance and hyperexcitability is interpreted by the central nervous system as joint pain. This process is the neurophysiological basis for the occurrence of allodynia and hyperalgesia in acute inflammation of the joints. A decrease in the mechanical threshold of excitation and increased impulses along afferent nerve fibers were identified in an experimental model of acute osteoartitis [6], as well as in adjuvant-induced chronic arthritis.

The persistence of neuronal hyperactivity in the absence of various mechanical stimulation in an experimental model of arthritis has also been described, which is consistent with the theory of awakening “silent” nociceptive receptors. Spontaneous firing of sensory nerve fibers is associated with joint pain in patients with arthritis. Peripheral sensitization of joint afferent nerves is a source of pain in arthritis.

Thus, a deeper study of the mechanisms and mediators responsible for the generation and maintenance of sensitization of joint nerves is necessary for the development of new drugs that help alleviate pain in arthritis.

Factors that change joint mechanosensitivity and implement nociception can be divided into two types: mechanical factors and inflammatory mediators.

After an injury or infection, a natural inflammatory response is often observed in the joints, which mainly affects the synovium (synovitis). Inflammatory mediators released within the joint by neurons, immunocytes, synoviocytes and vascular endothelium promote further recovery. These same inflammatory mediators also affect the sensory nerve fibers of the joint, leading to their excitation or sensitization. In experimental medicine, the local effect of various inflammatory mediators on the tissues of a healthy joint causes an increase in the impulses of articular afferents, and symptoms similar to the clinical manifestations of arthritis arise. The identification of inflammatory agents that cause neuropathic pain is currently underway, and the results of these studies will be of great importance in identifying promising therapeutic targets for joint damage.

Neuropeptides are a family of chemical transmitters that are released from nerve terminals of the autonomic nervous system and slow-conducting joint afferents. Neuropeptides released locally from the axons of sensory neurons are involved in neurogenic inflammation. Among numerous high-molecular-weight compounds, substance P, neurokinin A, calcitonin gene-related peptide, and vasoactive intestinal peptide (VIP) are the most important in the activation of nociceptive neurons; their levels increase in arthritis.

The neuropeptide FQ nociceptin/orphanin (N/OFQ) is also known as a modulator of mechanosensitivity in joint pain. N/OFQ (opioid-like neuropeptide), found in the CNS and peripheral nervous system (PNS), controls central pain mechanisms. The impact of N/OFQ on the activity of sensory neurons of the knee joints is characterized by a certain dualism, which is determined by the amount of N/OFQ, the degree of mobility of the knee joints and the presence of inflammation processes in the joint tissues [7]. In experimental models, when performing full rotation of the knee joints in the case of acute inflammation, the usual concentration of N/OFQ leads to sensitization of joint afferents, however, during excessive rotation of the knee joints, a high level of N/OFQ determines the desensitizing effect on mechanosensitive nerve fibers.

Eicosanoids (prostaglandins, leukotrienes, lipoxins, thromboxanes and endocannabinoids) are metabolites of arachidonic acid. The role of prostaglandins in the inflammatory process and nociception in joint damage has been most studied. Prostaglandins are formed during a series of physicochemical reactions involving various enzymes, while arachidonic acid is oxidized under the influence of cyclooxygenase. Prostaglandin endoperoxides are formed as intermediate products of prostaglandin biosynthesis. Tissue-specific synthases and isomerases convert these chemically unstable intermediates into prostaglandins, thromboxanes and prostacyclins.

In the projection of pain zones, high activity of cyclooxygenase is detected, which is presented in the form of two isoforms (COX-1 and COX-2). COX-1 is present in almost all tissues of the body; in platelets it ensures the conversion of arachidonic acid into thromboxane. COX-2 is obligately present in the brain and renal cortex. In other tissues, COX-2 expression is induced by certain stimuli, for example, it increases during inflammation. COX-2 is not typically expressed in joints, but is found in significant amounts in the synovium, macrophages, and endothelial cells of patients with rheumatoid arthritis.

The endocannabinoid anandamide is enzymatically synthesized from free arachidonic acid and ethanolamine, formed during the hydrolysis of N-arachidonylphosphatidylethanolamine with the participation of phospholipase D. Anandamide is a non-selective ligand that binds to CB1 and CB2 cannabinoid receptors coupled to G-proteins. CB1 receptors are localized primarily in the CNS and PNS, while CB2 receptors are associated with immunocytes. CB1 receptors modulate the release of excitatory and inhibitory transmitters, determining the modulation and perception of pain.

In the joints, high doses of anandamide cause excitation of multimodal sensory nerves, indicating the pro-pain effect of endocannabinoids. The pronociceptive effect may be due to the non-selective action of anandamide, which acts on both types of CB receptors to excite them. Some authors have suggested that low doses of anandamide may possibly cause an antinociceptive effect. Experiments are currently underway to clarify the role of the selective effects of CB1 and CB2 agonists on joint mechanosensitivity when stimulating these two receptor subtypes.

Based on the activation method, all ion channels discovered to date can be divided into different groups [8]. Some channels are activated when a certain potential is reached on the cell membrane (voltage-activated K-, Na-, Ca-channels) or when the configuration of the cell membrane changes with the formation of action potentials. A number of ion channels open when chemicals activate receptor binding sites on the channel molecule.

Various ion channel ligands are involved in the development of neuropathic pain. Many different types of ion channels are present at pain receptor terminals, and their activation is directly or indirectly required for the processing of nociceptive signals. The opening of voltage-dependent sodium channels determines the depolarization of afferent nerve endings and the propagation of action potentials along nociceptive nerve fibers. Sodium channels are generally blocked by tetrodotoxin, but a significant number of sodium channels present on small neurons are resistant to tetrodotoxin and their primary function is to modulate nociceptive neurotransmission.

Chronic inflammation with accompanying pain syndrome is accompanied by an increase in the number of sodium channels and, accordingly, the frequency of impulse generation along the nerve fibers of various tissues.

Calcium channels are also involved in the conduction of nociceptive impulses [9]. Other chemical compounds that contribute to joint sensitization are bradykinin, histamine, adenosine and nitric oxide. The study of new potential agents that realize pain and the neurobiology of nociception continues to identify drugs that relieve algic joint manifestations.

Recent advances in the field of molecular technology and the development of effective pharmacological research methods make it possible to study the features of the formation of pain in arthritis. However, the mechanism of persistence of chronic pain is not well understood; it is unclear why in some cases episodic pain in arthritis is clearly nociceptive in nature, while other patients have chronic joint pain with neuropathic characteristics. At present, the reason underlying the lack of direct correlation between the degree of inflammation and damage to the joint and the level of pain has not been studied.

Carefully planned studies using experimental models of arthritis and appropriate methodological approaches will clarify all the mechanisms and aspects of the formation of neuropathic pain in arthritis for adequate selection of antalgic therapy.

LITERATURE

1. Kukushkin M.L., Tabeeva G.R., Podchufarova E.V. Pain syndrome: pathogenesis, clinical picture, treatment: clinical recommendations. - 2011. - 79 p.

2. Kukushkin M.L. Neurophysiology of pain and analgesia // Pain, joints, spine. - 2011. - No. 2.

3. Hildebrand C., Oqvist G., Brax L. et al. Anatomy of the rat knee joint and composition of a major articular nerve // Anat. Rec. - 1991. - Vol. 229. - P. 545-555.

4. Mach DB, Rogers SD, Sabino MC et al. Origins of skeletal pain: sensory and sympathetic innervation of the femur mouse // Neurosci. - 2002. - Vol. 113. - P. 155-166.

5. Heppelmann B., McDougall JJ Inhibitory effect of amiloride and gadolinium on fine afferent nerves in the rat knee: evidence of mechanogated ion channels in joints // Exp. Brain. Res. - 2005. - Vol. 167. - P. 114-118.

6. Schuelert N., McDougall JJ Electrophysiological evidence that the vasoactive intestinal peptide receptor antagonist VIP (6-28) reduces nociception in an animal model of osteoarthritis // Osteoarthritis Cartilage. - 2006. - Vol. 14. - P. 1155-1162.

7. McDougall JJ Peripheral modulation of rat knee joint afferent mechanosensitivity by nociceptin/orphanin FQ / JJ McDougall, M. Pawlak, U. Hanesch et al. // Neurosci. Lett. - 2000. - Vol. 288. - P. 123-126.

8. https://kpfu.ru/docs/ion channel.

9. Yaksh TL Calcium channels as therapeutic targets in neuropathic pain / TL Yaksh // J. Pain. - 2006. - Vol. 7. - R. 13-S30.

REFERENCES

1. Kukushkin ML, Tabeeva GR, Podchufarova EV Bolevoy sindrom: patogenez, klinika, lechenie: klinicheskie rekomendatsii, 2011. 79 p.

2. Kukushkin ML Neurophysiology of pain and pain relief. Bol', sustavy, pozvonochnik, 2011, no. 2 (in Russian).

3. Hildebrand C., Oqvist G., Brax L. et al. Anatomy of the rat knee joint and composition of a major articular nerve. Anat. Rec., 1991, vol. 229, pp. 545-555.

4. Mach DB, Rogers SD, Sabino MC et al. Origins of skeletal pain: sensory and sympathetic innervation of the mouse femur. Neurosci., 2002, vol. 113, pp. 155-166.

5. Heppelmann B., McDougall JJ Inhibitory effect of amiloride and gadolinium on fine afferent nerves in the rat knee: evidence of mechanogated ion channels in joints. Exp. Brain. Res., 2005, vol. 167, pp. 114-118.

6. Schuelert N., McDougall JJ Electrophysiological evidence that the vasoactive intestinal peptide receptor antagonist VIP (6-28) reduces nociception in an animal model of osteoarthritis. Osteoarthritis Cartilage, 2006, vol. 14, pp. 1155-1162.

7. McDougall JJ, Pawlak M, Hanesch U et al. Peripheral modulation of rat knee joint afferent mechanosensitivity by nociceptin/orphanin FQ. Neurosci. Lett., 2000, vol. 288, pp. 123-126.

8. https://kpfu.ru/docs/ion channel

9. Yaksh TL Calcium channels as therapeutic targets in neuropathic pain. J. Pain, 2006, vol. 7, rr. 13-S30.

Treatment of muscle and joint pain

Your treatment will be carried out by professional doctors in their field. With the symptoms that patients come to us with, neurological, orthopedic and other problems are possible. That's why we offer you a comprehensive approach. Osteopathic spine center provides treatment using methods such as:

Physiotherapy
Osteopathy
Hirudotherapy
Manual and reflexology
Kinesiology
Massage and much more.

The methods used in our spine clinic are proven to be effective for both acute and chronic pain. The clinic’s specialists competently combine various techniques. If necessary, medical blockades and drug treatment are used. But we always aim to ensure that patients take a minimum of pills and can do without surgery.

Why do they trust us?

Each specialist at our medical center has several specialized educations. This means that the doctor will be able to quickly and accurately identify the causes of illness or disease. A doctor who is a professional in several fields of medicine will be able to make a 100% accurate diagnosis and build the correct treatment plan. Our patients do not have to run to different specialists and waste valuable time, since they undergo all examination and treatment from one doctor.

When the first symptoms of pathology appear, contact the Osteopathic Spine Center. What will you get?

In 1-2 visits you will get rid of pain.
The mobility of muscles and joints will return.
The development of the disease will stop.

Your immunity will begin to recover, you will feel a surge of strength and vitality.