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Chapter 22. Pain

Pain is one of the most frequent manifestations of diseases and pathological conditions. In addition to the mechanisms of perception, transmission and analysis of pain sensations, the patient’s personal characteristics are extremely important in the perception of pain. The peculiarities of the psychological state largely determine the formation of pain and reaction to pain.

Depending on the duration of the existence of the pain syndrome, pain may be divided into following categories:

  • acute;
  • chronic.

Acute pain is caused by irritation of pain receptors due to a damage to organs and tissues. Such pain plays adaptive, signaling role. An important feature of acute pain is its duration, which corresponds to the duration of the healing processes of the damaged tissue. In diseases of the nervous system, acute pain occurs, when peripheral nerves (traumatic, ischemic neuropathy), spinal roots (radiculopathy, dorsalgia caused by a herniated intervertebral disc) are affected.

The perception of acute pain is determined by the action of a wide range of chemicals called algogens, the formation and release of which occurs due to acute tissue damage. There is a group of tissue algogens, which include histamine, leukotriene-1, endothelins, prostaglandins, as well as algogens circulating in the blood — bradykinin, callidin and substance P, neurokinin A, calcitonin gene-related peptide (CGRP) derived from nerve endings. The products of arachidonic acid metabolism are of great importance: prostaglandins synthesized under the action of cyclooxygenase-2 (an inducible isoform of the enzyme). Pain-reducing effects of nonsteroidal anti-inflammatory drugs that block the activity of the enzyme are associated with a decrease in their formation.

The duration of chronic pain exceeds the period necessary for normal healing. Chronic pain refers to pain when the duration of pain exceeds 3 months. Unlike acute pain, which indicates trouble in the body and performs a protective function, chronic pain itself has a maladaptive effect on the body, accompanying structural and functional disorders in internal organs, the cardiovascular system, causing emotional and mental changes. Due to these features of chronic pain, it is considered pathological.

Pathophysiological basis of chronic pain is thought to be a complex restructuring of the system of perception, conducting and analyzing pain sensations. Increased response to a painful stimulus (hyperalgesia), increased sensitivity of the central mechanisms of pain perception, inhibition of the antinociceptive (analgesic) system play a significant role. A complex set of changes in PNS and CNS leads to the formation of a pathological algic system, a substrate of chronic pain syndrome. The structure of this system includes both PNS and CNS (the posterior horn of the spinal cord, thalamus, reticular formation, and other structures). An important role is played by the structures of the cerebral cortex, which largely determine the attitude to the pain syndrome, its emotional coloring.

Neurotransmitters, substances that enhance and modulate the action of neurotransmitters (substance P, neurokinins, somatostatin, etc.) play a significant role in chronic pain. The involvement of activating neurotransmitter systems, in particular those controlled by glutamic acid (NMDA receptors), contributes to the activation of the mechanisms of plasticity of the nervous system with the enhancing of existing synapses and the formation of new interneuronal connections (synaptogenesis).

The Melzack and Wall theory of gate control helps to understand the mechanisms of pain formation. Pain impulses enter the posterior horn of the spinal cord through thin fibers. The passage of pain signals can be blocked by an impulse entering the posterior horn through thick myelinated fibers from skin receptors (thermal, mechanical) or due to signals descending from the nuclei of the brainstem. Activation of these systems accompanies the production of chemicals in the neurons of the gelatinous substance of the posterior horn that block the passage of pain impulses. At the same time, nociceptive impulses do not reach the overlying structures, since the “gate” for the passage of the pain signal is closed.

Mechanisms that block pain impulses (antinociceptive system) are located at different levels of the CNS and include the raphe nucleus, some nuclei of the reticular formation, specific and non-specific thalamic nuclei, structures of the motor and sensorimotor cerebral cortex. The mediators of the antinociceptive system are enkephalins, serotonin, GABA.

Clinical manifestations of chronic pain can be causalgia, allodynia, hyperpathy, hyperalgesia. Chronic pain is observed in subacute and chronic polyneuropathies (for example, diabetic), some forms of brain damage.

In addition, the following types of pain may be distinguished:

  • nociceptive;
  • neuropathic.

Nociceptive pain (usually acute) is caused by irritation of pain receptors (nociceptors); it occurs with acute tissue damage, regresses with the development of reparative processes, and is resolved with the use of analgesic drugs. Since nociceptive pain occurs due to damage to organs and tissues, it can be considered as somatogenic.

Neuropathic pain is caused by damage to the central or peripheral structures of the nervous system. Its occurrence is not associated with irritation of nociceptors; to a small extent, it is relieved by the use of non-steroidal anti-inflammatory drugs. Mononeuropathies and polyneuropathies, radiculopathy, damage to the nerve plexuses (plexopathy) and nodes (ganglionitis) can lead to the neuropathic pain. Central neuropathic pain is a rare syndrome, which can be caused by damage to the sensory systems at various levels (spinal cord, brainstem, thalamus, cerebral cortex). Finally, there is a psychogenic pain, which occurs without a structural damage to the nervous system; in the pathogenesis of psychogenic pain, a significant role is played by the patient’s personal characteristics. Psychogenic pain often occurs in patients with somatoform disorders.

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