Causes of pain
The pain response in the body is triggered under the influence of two key factors that threaten tissue viability.
The first factor is disruption of the integrity of protective integuments. Any damage to membranes poses a threat to homeostasis (the constancy of the internal environment). In this case, pain performs a crucial control function. It acts as a strong negative biological drive, which creates motivation in a person to get rid of the source of pain as quickly as possible.
The second factor is changes in oxygen metabolism levels. Pain occurs when oxidative processes are disrupted or normal blood access to tissues ceases (ischemia or hypoxia develops). The body responds to this systemically: the autonomic nervous system is activated, predominantly its sympathetic division. This has a pronounced compensatory character, as sympathetic stimulation aims to improve oxygen supply to the affected organ and restore tissue nutrition (trophism).
General principles of nociception
In physiology, there is the "specificity" theory, according to which pain is perceived by specialized receptors — nociceptors. Structurally, they form plexiform networks in the skin, muscles, and certain internal organs.
A crucial feature of pain sensitivity is the discrepancy between the excitation of a single receptor and the actual sensation of pain. A single impulse is not enough. According to the "intensity" theory, for a person to feel pain, multiple excitations of numerous receptors are necessary. The pain sensation is always the result of spatial and temporal summation of sensory stimuli from a strong impact.
Classification: Mechanonociceptors (Type I)
According to L.N. Smolin's classification, the first type of pain receptors is mechanonociceptors. Their membrane depolarizes exclusively as a result of mechanical displacement. They are localized in the integumentary membranes, deep tissues, visceral organs, and vessel walls. Their main function is monitoring tissue integrity.
Several groups of mechanonociceptors are distinguished:
- Cutaneous with Aδ-fiber afferents. They respond only to mechanical stimuli, ignoring heat and chemicals. They feature narrow receptive fields and rapid adaptation. They are responsible for epicritic (primary, sharp) pain.
- Epidermal with C-fiber afferents. Also activated mechanically only, do not respond to temperature fluctuations. They have narrow fields and easily adapt.
- Muscular with Aδ-fiber afferents. Located on the surface of muscles and at the junction points into tendons. They are excited by strong pressure from blunt objects. They adapt rapidly.
- Articular with Aδ-fiber afferents. Located in joint capsules. They are activated only under extreme conditions: during excessive bending or unnatural twisting of the joint.
Classification: Polymodal C-nociceptors (Type II)
The second type of receptors is excited by the action of a whole complex of strong stimuli: mechanical, thermal, and chemical. They respond to substances that disrupt normal oxidative processes in tissues (histamine, acetylcholine, acid solutions). Signals from them are transmitted predominantly via C-fiber pathways. The physiological role of this group is to monitor the respiratory function of tissues.
Polymodal receptors are divided into the following subgroups:
- Cutaneous (type 1): activated by a combination of mechanical stimulus and strong cooling (down to 15 °C).
- Cutaneous (type 2): respond to mechanical impact and strong heating. Unlike many other receptors, they adapt slowly.
- Subcutaneous: require simultaneous strong skin pressure and administration of chemical substances.
- Muscular: respond to all types of stimuli, including specific chemical markers of inflammation (bradykinin, histamine).
- Receptors of internal parenchymatous organs: localized mainly in the walls of small arterioles.
简述：主题相关问答
What types of pain are distinguished according to the clinical and pathophysiological classification?
According to clinical and pathophysiological classifications, several main types of pain are distinguished.
- Somatic pain — subdivided into superficial (skin irritation) and deep (receptors of muscles, joints, tendons).
- Visceral pain — associated with diseases of internal organs.
- Nociceptive pain — occurs in response to tissue damage and activation of pain receptors.
- Neuropathic pain — caused by damage to structures of the peripheral or central nervous system.
- Nociplastic pain — mentioned as a factor in complex regional pain syndrome.
In addition, by localization and character, epicritic, protopathic, phantom, and referred pain are distinguished, and by the time of formation — early and late.
Through which pathways is the pain impulse transmitted to the brain?
The transmission of the pain impulse to the brain is carried out predominantly via the spinothalamic tracts.
- Lateral spinothalamic tract (tractus spinothalamicus) — the main highway in the lateral funiculus of the spinal cord, whose fibers cross to the opposite side and carry impulses to the thalamus.
- Neospinothalamic pathway — conducts fast, localized pain to specific nuclei of the thalamus (VPL).
- Paleospinothalamic pathway — transmits slow, affective-motivational pain to non-specific (intralaminar, reticular) nuclei of the thalamus.
From the thalamic nuclei, the signal is transmitted to the cerebral cortex (specifically, the postcentral gyrus) via the thalamocortical tract for final analysis.
Which neurotransmitters are involved in the synaptic transmission of the pain signal in the spinal cord?
A number of neurotransmitters are involved in the synaptic transmission and modulation of the pain signal in the spinal cord. The main excitatory ("nociceptive") neurotransmitters of pain released at the level of the dorsal horns of the spinal cord include:
- Glutamate — the mediator of fast pain in the neospinothalamic pathway.
- Substance P (Substance P) — a tachykinin involved in the transmission of slow pain (paleospinothalamic pathway) and exerting a modulatory enhancing effect on the transmission of nociceptive impulses.
Additionally, modulators act at the first relay station: histamine, neurotensin, cholecystokinin, norepinephrine, serotonin, as well as inhibitory neurotransmitters — GABA and enkephalins, which suppress the pain signal.
What is the antinociceptive system and what endogenous substances are involved in it?
The antinociceptive system is a regulatory system that ensures the inhibition of nociceptive neuron activity at the levels of the dorsal horns of the spinal cord, the brainstem reticular formation, and the thalamus. Its function is to suppress pain impulses and provide pain relief.
The main endogenous substances of this system are opioid peptides:
- Endorphins — include $\alpha$-, $\beta$-, and $\gamma$-fractions.
- Enkephalins — have a wider localization in the central nervous system.
These neuropeptides bind to opiate receptors, inhibit the sensitivity of second-order neurons to pain mediators, and inhibit their release, causing a state of hypoalgesia or analgesia.
To avoid confusing fibers: Aδ-fibers (A-delta) mean Attack (mechanical displacement) and Acute (sharp, primary, epicritic pain). C-fibers mean Assorted (polymodal: they gather all stimuli — mechanics, temperature, chemistry).
课堂与考试常见问题
Does the excitation of a single nociceptor cause a sensation of pain?
No, there is a discrepancy between the excitation threshold of an individual receptor and the occurrence of a sensation. Pain only occurs as a result of the summation of multiple sensory stimuli.
What chemical substances are capable of exciting polymodal C-nociceptors?
Such stimuli include solutions of acids (sulfuric, acetic, hydrochloric), acetylcholine, histamine, and bradykinin, which disrupt oxidative processes in tissues.
Why is the sympathetic nervous system activated during tissue ischemia?
This is a compensatory reaction of the body to oxygen deprivation. The activation of the sympathetic division of the autonomic nervous system helps improve blood supply to the affected organ and restore tissue trophism.
该主题的其他拓展内容
- Morphological structure of plexiform networks of free nerve endings
- Receptor adaptation mechanisms: the difference between fast and slow adaptation of nociceptors
- Features of pain impulse conduction along Aδ- and C-fibers
- Intensity theory and the processes of spatiotemporal summation of pain
- The role of the autonomic nervous system in compensating for tissue hypoxia in pain syndrome
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