Anatomy of the nociceptive system

Perception of damaging effects is carried out by nociceptors. Nociceptors, first discovered in 1969 by E.Perl and A.Iggo, are unencapsulated endings of A8 and C-afferents. Depending on the modality (the nature of the stimulating stimulus) nociceptors are divided into mechanonociceptors, thermoconceptors and polymodal nociceptors.

The first neuron of the nociceptive path from the trunk and extremities is located in the spinal ganglia, from the head and face - in the trigeminal ganglion. Most of the nociceptive afferents also enter the spinal cord through the posterior roots and terminate on the neurons of the anterior horn. Swedish neurohistologist B.Rexed in 1952 proposed the separation of the gray matter of the spinal cord, which now bears his name - the Reksed plates.

The nociceptive information processed by the spinal neurons rushes to the brain through the spinotalamic (including the neo-and palaeospinotalamic tract), the spinal mesenterphalic, spinaloretic pathways and 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, block excessive nociceptive flow. Nociceptive information from the head and face is transmitted through the trigeminal nerve system.

[1], [2], [3], [4], [5]

Classification of pain

There are three main types of pain syndromes:

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

Nociceptive refers to the syndromes that occur when nociceptors are activated in trauma, inflammation, ischemia, and stretching of tissues. The nociceptive pain is divided into somatic and visceral. Clinically, post-traumatic and postoperative pain syndromes, pain associated with inflammation of joints, muscles, cancer pain, pain in cholelithiasis, and many others are distinguished.

Neuropathic pain is pain that occurs as a direct consequence of a damage or illness affecting the somatosensory system. The most striking examples of neuropathic pain are neuralgia, phantom syndrome, pain in peripheral neuropathy, deafferentation pain and thalamic pain syndrome.

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

In clinical practice, it is often necessary to meet with mixed forms of pain syndromes (combined pain syndrome), which is appropriate to reflect in the diagnosis for building therapeutic tactics.

It is very important to divide the pain by temporal parameters into acute and chronic. Acute pain occurs as a result of nociceptive exposure, which may be due to trauma, disease, and muscle and internal muscle dysfunction. This type of pain is usually accompanied by neuro-endocrine stress, the severity of which is proportional to the intensity of the exposure. Acute pain is "designed" to detect, localize and limit tissue damage, so it is also called nociceptive pain. The most common types of acute pain: post-traumatic, postoperative. Pain in childbirth, as well as pain associated with acute diseases of internal organs. In most cases, acute pain is resolved alone or as a result of treatment for several days or weeks. In cases where, due to impaired regeneration or improper treatment, pain persists, it becomes chronic. Chronic pain is characterized by what remains after the resolution of the acute phase of the disease or after a time sufficient for cure. In most cases, this period varies from 1 to 6 months. The cause of chronic pain may be peripheral nociceptive effects, as well as dysfunction of the peripheral or central nervous system. Neuroendocrine response to stress is weakened or absent, marked sleep disorders and affective disorders are noted.

Important from the theoretical and clinical standpoint is the classification proposed by GN Kryzhanovsky (1997,2005), who divided pain into physiological and pathological. Normally, pain is a mechanism of etiologic protection. Its appearance induces adaptive functions aimed at eliminating nociceptive effects or direct pain. Pathological pain loses its protective functions, it has a disadaptive and pathological importance for the body. Overpowering, severe, pathological pain causes mental shock disorders, disintegration of the central nervous system, frequent suicidal actions, structural and functional changes and damages in the internal organs and cardiovascular system, dystrophic changes in tissues, violation of autonomic functions and endocrine system, secondary immune deficiency. Myological pain can occur with various forms of somatic pathology and pathology of the nervous system, acquiring the status of an independent nosology.

Manifestations of pathological pain (Kryzhanovskii GN, 1997)

• Causalgia
• Hyperpathy
• Hyperalgesia
• Allodinia
• Expansion and appearance of new receptive zones
• Reflected pain
• Spontaneous bouts of pain without provocation
• Increase in the intensity of pain during a spontaneous or provoked attack
• Permanent, persistent pain, not dependent on stimulation

Having discovered the listed clinical signs, the doctor can confidently diagnose the patient's pathological pain with possible fatal consequences. Especially I would like to dwell on the explanation of terms connected with the concept of "pain",
since in practice, doctors do not always use them correctly.

• Allodynia - Perception of non-nociceptive stimulation as a pain
• Analgesia - Lack of perception of pain
• Anesthesia - Lack of perception of all kinds of sensitivity
• Anestesia dolorosa - A feeling of pain in the area of the body that is in anesthesia
• Dysaesthesia - Unpleasant or pathological sensations with or without stimulation
• Hypoalgesia - Weakened response to nociceptive stimulus
• Hyperalgesia - Excessive reaction to nociceptive stimulus
• Hyperesthesia - Excessive reaction to weak non-nociceptive stimulus
• Hyperpathy - A combination of hyperesthesia, allodynia and hyperalgesia, usually associated with increased reactivity and persisting after the cessation of irritation.
• Hypoesthesia - Decreased skin sensitivity (ie tactile, temperature and pressure sensations)
• Neuralgia - Pain in the zone of innervation of one or more nerves
• Paresthesia - Pathological sensations perceived in the absence of explicit stimulation
• Causalgia - Intense, burning, often - unbearable pain

[6], [7], [8],