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Nociceptive pain

 
, medical expert
Last reviewed: 08.07.2025
 
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Nociceptive pain syndromes occur as a result of activation of nociceptors in damaged tissues. Typically, zones of constant soreness and increased pain sensitivity (decreased thresholds) appear at the site of damage (hyperalgesia). Over time, the zone of increased pain sensitivity can expand and cover healthy tissue areas. Primary and secondary hyperalgesia are distinguished. Primary hyperalgesia develops in the area of tissue damage, secondary hyperalgesia - outside the zone of damage, spreading to healthy tissues. The zone of primary hyperalgesia is characterized by a decrease in the pain threshold (PT) and the pain tolerance threshold (PTT) for mechanical and temperature stimuli. Secondary hyperalgesia zones have a normal pain threshold and a decreased PTT only for mechanical stimuli.

The cause of primary hyperalgesia is sensitization of nociceptors - unencapsulated endings of A8 and C-afferents.

Sesitization of nociceptors occurs as a result of the action of pathogens released from damaged cells (histamine, serotonin, ATP, leukotrienes, interleukin 1, tumor necrosis factor a, endothelins, prostaglandins, etc.), formed in our blood (bradykinin), released from the terminals of C-afferents (substance P, neurokinin A).

The appearance of zones of secondary hyperalgesia after tissue damage is due to sensitization of central nociceptive neurons, mainly the posterior horns of the spinal cord.

The zone of secondary hyperalgesia may be significantly distant from the site of injury, or even located on the opposite side of the body.

As a rule, sensitization of nociceptive neurons caused by tissue damage persists for several hours and even days. This is largely due to the mechanisms of neuronal plasticity. Massive calcium entry into cells through NMDA-regulated channels activates early response genes, which in turn, through effector genes, change both the metabolism of neurons and the receptor potential on their membrane, as a result of which neurons become hyperexcitable for a long time. Activation of early response genes and neuroplastic changes occur within 15 minutes after tissue damage.

Subsequently, sensitization of neurons can also occur in structures located above the dorsal horn, including the nuclei of the thalamus and the sensorimotor cortex of the cerebral hemispheres, forming the morphological substrate of the pathological algic system.

Clinical and experimental data indicate that the cerebral cortex plays a significant role in pain perception and the functioning of the antinociceptive system. The opioidergic and serotonergic systems play a significant role in this, and corticofugal control is one of the components in the mechanisms of analgesic action of a number of drugs.

Experimental studies have shown that removal of the somatosensory cortex, responsible for pain perception, delays the development of pain syndrome caused by damage to the sciatic nerve, but does not prevent its development at a later date. Removal of the frontal cortex, responsible for the emotional coloring of pain, not only delays development, but also stops the occurrence of pain syndrome in a significant number of animals. Different areas of the somatosensory cortex have an ambiguous relationship with the development of the pathological algic system (PAS). Removal of the primary cortex (S1) delays the development of PAS, removal of the secondary cortex (S2), on the contrary, promotes the development of PAS.

Visceral pain occurs as a result of diseases and dysfunctions of internal organs and their membranes. Four subtypes of visceral pain have been described: true localized visceral pain; localized parietal pain; radiating visceral pain; radiating parietal pain. Visceral pain is often accompanied by autonomic dysfunction (nausea, vomiting, hyperhidrosis, instability of blood pressure and cardiac activity). The phenomenon of irradiation of visceral pain (Zakharyin-Geda zones) is caused by the convergence of visceral and somatic impulses on neurons of a wide dynamic range of the spinal cord.

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