Pathological pain of peripheral origin

Pathological pain of peripheral origin

 This form of pathological pain occurs in chronic stimulation of pain receptors (nociceptors), damaged nociceptive fibers, spinal ganglia and dorsal root. These structures are often a source of intense and constant nociceptive stimulation.

Nociceptors are activated in chronic inflammation (such as arthritis), the action of the decay products of tissues (eg, in tumors), and others. Chronically damageable (for example, when squeezed scars, overgrown bone and so forth. ) and regenerating the sensory nerves, degenerative changed (under the action of various hazards, endocrinopathy) and demyelinated fibers are very sensitive to various humoral effects, even those for which they do not react under normal conditions (for example, to the action of epinephrine, K +, etc. ). Sites such fibers are ectopic source of constant and significant nociceptive stimulation. A special role is played by such a source neuroma - the formation of randomly overgrown nerve fibers, which occurs when they are disordered and difficulty increase. These endings are sensitive to a variety of mechanical, thermal, chemical and endogenous factors (eg, catecholamines). Therefore, the pain attacks with neuroma, as well as nerve damage can be triggered by different factors (for example, emotional stress, adrenaline action).

 Nociceptive stimulation from the periphery of attack may cause pain if she overcomes the so-called " gating control" in the rear horns (Melzak, wall) consisting of a brake unit substantia gelatinosa neurons. These neurons control the flow entering the posterior horns and the ascending nociceptive stimulation. This effect can occur when intense afferent stimulation or by brake failure " gate-control. "

Pathological pain of central origin

This form of pathological pain associated with hyperactivation of nociceptive neurons in the spinal and supraspinal levels. Such neurons form aggregates which are pathologically enhanced excitation generators. In the formation of the generator in the posterior horns of the spinal cord there is a center of origin of spinal pain syndrome in education in the nuclei of the trigeminal nerve - trigeminal neuralgia, in the nuclei of the thalamus - thalamic pain syndrome.

In the early stages of the disease process twinge due to the activation of the generator is triggered by nociceptive stimuli with certain directly related to the receptive field generator; the late stages of an attack provoked by stimuli of various intensities from different fields of the receptor, and can also occur spontaneously. Feature bout of pain (paroxysmal, continuous, short, long, and so forth. ) depends on the characteristics of the generator function and pathological systems. Character same pain (dull, sharp, localized, diffuse, and others. ) is determined by what education systems have become parts of nociceptive pathological algic system.

The generator in the central office can occur nociceptive system, such as in dorsal horns after prolonged nociceptive stimuli from the periphery. In these circumstances, the pain of peripheral origin initially becomes the central component and becomes pain of spinal origin. This situation occurs when causalgia, neuromas and damages afferent nerves, neuralgia, etc.

The generator in the central nociceptive apparatus may also occur when deafferentation, due to increased sensitivity deafferentized nociceptive neurons and the violation of the brake control. Deafferentatsionnye pain syndromes can occur after limb amputation, nerve transection and posterior roots, after a break or transection of the spinal cord. Thus the patient may feel pain sensitivity or lacking in nonexistent body (e. g., non-existent in the limbs of the body parts following transection of the spinal cord). This type of pathological pain is called phantom (from the word «fantom» - a ghost). It is due to the central generator activity, the activity of which is not dependent on nociceptive stimulation from the periphery.

The generator in the central parts of the nociceptive system may occur in infectious lesions of these departments (herpetic and syphilitic lesions), trauma, toxic effects. In the experiment, thesegenerators and associated pain syndromes are reproduced by introducing appropriate department system nociceptive substances causing violation brake (tetanus toxin, penicillin) or activate nociceptive neurons (potassium ions and so forth. ).

The central office of the nociceptive system may form secondary generators. Thus, after the generator rear horns of the spinal cord after a certain time in the thalamus secondary generator may occur. Often, the localization of the primary generator in the spinal cord in order to prevent the receipt of his impulses in the brain, producing a partial (break of the ascending tracts), and in severe cases even a complete transection of the spinal cord of conductive paths.