Nociceptive pain

Nociceptive pain syndromes arise as a result of activation of nociceptors in damaged tissues. Characterized by the emergence of zones of constant soreness and increased pain sensitivity (lower thresholds) at the site of injury (hyperalgesia). Over time, the zone of increased pain sensitivity can expand and cover healthy tissue areas. Isolate primary and secondary hyperalgesia. Primary hyperalgesia develops in the area of tissue damage, secondary hyperalgesia - outside the injury zone, spreading to healthy tissues. The primary hyperalgesia zone is characterized by a reduction in the pain threshold (PB) and the pain tolerance threshold (PPB) for mechanical and temperature stimuli. The zones of secondary hyperalgesia have a normal pain threshold reduced by PPB only to mechanical stimuli.

The reason for the primary hyperalgesia is the sensitization of nociceptors - unencapsulated endings of A8 and C-afferents.

The scatisation 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, endothelin, prostaglandins, etc.) formed in our blood (bradykinin) secreted from C- afferents (substance P, neurokinin A).

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

The zone of secondary hyperalgesia can be significantly removed from the site of injury, or even be on the opposite side of the body.

As a rule, the 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 input into cells through NMDA-regulated channels activates early response genes, which in turn through effector genes alter both neuronal metabolism and receptor potential on their membrane, resulting in long-term neurons becoming hyperexcitable. Activation of early response genes and neuroplastic changes occur within I5 minutes after tissue damage.

Subsequently, neuronal sensitization can occur in structures located above the dorsal horn, including the thalamus nuclei 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 the perception of pain and the functioning of the antinociceptive system. An important role in this is played by opioidergic and serotonergic systems, and corticofugal control is one of the components in the mechanisms of analgesic action of a number of drugs.

Experimental studies have shown that the removal of the somatosensory cortex, responsible for the perception of pain, delays the development of the 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 coloration of pain, not only retards development, but also reduces the onset of pain syndrome in a significant number of animals. Different zones of the somatosensory cortex are ambiguous regarding the development of the pathological algic system (PAS). Removal of the primary cortex (S1) retards the development of PAS, the removal of the secondary cortex (S2), in contrast, 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 are described: true localized visceral pain; localized parietal pain; irradiating 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-Ged zone) is caused by the convergence of visceral and somatic impulses on neurons of a wide dynamic range of the spinal cord.

[1], [2], [3]