Anatomy of the nociceptive system

The perception of damaging effects is carried out by nociceptors. Nociceptors, first discovered in 1969 by E. Perl and A. Iggo, are non-encapsulated endings of A8 and C-afferents. Depending on the modality (nature of the exciting stimulus), nociceptors are divided into mechanonociceptors, thermonociceptors and polymodal nociceptors.

The first neuron of the nociceptive pathway from the trunk and limbs is located in the spinal ganglia, from the head and face - in the trigeminal ganglion. Most of the nociceptive afferents enter the spinal cord through the posterior roots and end on the neurons of the anterior horn. In 1952, the Swedish neurohistologist B. Rexed proposed a division of the gray matter of the spinal cord, which currently bears his name - Rexed's plates.

Nociceptive information processed by spinal neurons is sent to the brain via the spinothalamic (including the neo- and paleospinothalamic tract), spinomesencephalic, spinoreticular tracts and the posterior columns of the spinal cord. The task of nociceptive information is to ensure recognition of the damaging effect and its localization, activate the avoidance reaction, and block excessive nociceptive flow. Nociceptive information from the head and face is transmitted via the trigeminal nerve system.

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Classification of pain

There are three main types of pain syndromes:

1. somatogenic (nociceptive pain),
2. neurogenic (neuropathic pain),
3. psychogenic (psychogenic pain).

Nociceptive syndromes include those that occur when nociceptors are activated during trauma, inflammation, ischemia, and tissue stretching. Nociceptive pain is divided into somatic and visceral. Clinically, posttraumatic and postoperative pain syndromes, pain during inflammation of joints, muscles, cancer pain, pain during gallstone disease, and many others are distinguished.

Neuropathic pain is pain that occurs as a direct consequence of injury or disease affecting the somatosensory system. Common examples of neuropathic pain include neuralgia, phantom limb syndrome, peripheral neuropathy pain, deafferentation pain, and thalamic pain syndrome.

Psychogenic pain occurs regardless of somatic, visceral or neuronal damage and is largely determined by psychological and social factors. It is believed that the determining factor in the mechanism of psychogenic pain is the mental state of a person. Probably, neuropathic pain is hidden under the mask of psychogenic pain, the mechanism of which we do not yet know.

In clinical practice, we often encounter mixed forms of pain syndromes (combined pain syndrome), which should be reflected in the diagnosis for developing treatment tactics.

It is very important to divide pain by time parameters into acute and chronic. Acute pain occurs as a result of nociceptive impact, which can be caused by trauma, disease, and dysfunction of muscles and internal organs. This type of pain is usually accompanied by neuroendocrine stress, the severity of which is proportional to the intensity of the impact. Acute pain is "intended" to detect, localize and limit tissue damage, so it is also called nociceptive pain. The most common types of acute pain are post-traumatic, postoperative, pain during childbirth, and pain associated with acute diseases of internal organs. In most cases, acute pain resolves on its own or as a result of treatment within a few days or weeks. In cases where pain persists due to impaired regeneration or improper treatment, it becomes chronic. Chronic pain is characterized by the fact that it persists after the resolution of the acute phase of the disease or after a time sufficient for healing. In most cases, this period varies from 1 to 6 months. Chronic pain may be caused by peripheral nociceptive effects, as well as dysfunction of the peripheral or central nervous system. The neuroendocrine response to stress is weakened or absent, and severe sleep disorders and affective disorders are observed.

The classification proposed by G.N. Kryzhanovsky (1997, 2005), who divided pain into physiological and pathological, is important from theoretical and clinical positions. Normally, pain is a mechanism of etiological defense. Its appearance causes adaptive functions aimed at eliminating nociceptive effects or direct pain. Pathological pain loses its protective functions, it has a maladaptive and pathological significance for the body. Overcome, severe, pathological pain causes mental shock disorders, disintegration of the central nervous system, frequent suicidal actions, structural and functional changes and damage in internal organs and the cardiovascular system, dystrophic tissue changes, disruption of vegetative functions and the endocrine system, secondary immune deficiency. Myological pain can occur in various forms of somatic pathology and pathology of the nervous system, acquiring the status of an independent nosology.

Manifestations of pathological pain (Kryzhanovsky G.N., 1997)

• Causalgia
• Hyperpathy
• Hyperalgesia
• Allodynia
• Expansion and emergence of new receptive zones
• Referred pain
• Spontaneous attacks of pain without provocation
• Increasing intensity of pain during a spontaneous or provoked attack
• Constant, unrelenting pain that is not dependent on stimulation

Having detected the listed clinical signs, the doctor can confidently diagnose the presence of pathological pain in the patient with possible sometimes fatal consequences. I would especially like to dwell on the explanation of terms associated with the concept of "pain",
since in practice doctors do not always use them correctly.

• Allodynia - Perception of non-nociceptive stimulation as painful
• Analgesia - Absence of perception of pain
• Anesthesia - Absence of perception of all types of sensitivity
• Anestesia dolorosa - A sensation of pain in the area of the body that is under anesthesia
• Dysesthesia - Unpleasant or abnormal sensations with or without stimulation
• Hypoalgesia - Reduced response to nociceptive stimuli
• Hyperalgesia - Excessive response to a nociceptive stimulus
• Hyperesthesia - Exaggerated response to a weak non-nociceptive stimulus
• Hyperpathia - A combination of hyperesthesia, allodynia, and hyperalgesia, usually associated with increased reactivity and persisting after stimulation has ceased.
• Hypoesthesia - Decreased skin sensitivity (i.e. tactile, temperature and pressure sensation)
• Neuralgia - Pain in the innervation zone of one or more nerves
• Paresthesia - Abnormal sensations perceived in the absence of obvious stimulation
• Causalgia - Intense, burning, often unbearable pain

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