Neuroscience and pain 3: Interaction of the neuroimmune system and somatic tissues

Neuroscience and pain 3:

Interaction of the neuroimmune system and somatic tissues


In myotendinous or other viscoelastic tissues, the immune system has the function of phagocytizing damaged cells, as a consequence of overload, overstretching, compression or hopoxia.

Damaged cells release substances that reduce the intensity of the stimulus to generate the action potential – state of nociceptive hypersensitivity by activation of adjacent terminals, generate a nociceptive hypersensitivity by activation of afferent terminals,
in chronic pain the damage is repetitive, there is no healing time and there is persistent inflammation, the mast cells will release histamine, bradykinin, proinflammatory cytokines, will generate this activation of the afferent terminals already mentioned, increasing vascular permeability, this gives infliltration of immune cells, and these, in turn more production of inflammatory cytokines. Macrophages and local damaged cells generate the release of more cytokines, in the acute phase is perfect, but if this is not corrected, over time, there will be increased peripheral sensitisation, remember that these mast cells are related to the immune system and therefore with the sympathetic system.

Muscular alterations do not depend on the primary damage to the muscle (massage therapists, this is important for us) and there is loss of fine postural system regulation.

In the chronic the damage is repetitive, there is no healing time and the inflammation is persistent, this chronic inflammation will have prolonged macrophages and there will be secondary tissue damage due to the prolonged and numerous presence of the famous macrophages, with prolonged phagocytic activity and the presence of cytotoxic radicals that generates more pain…
This not only affects the tissue of the lesion but also the tissue surrounding the lesion, and gives rise to fibrosis of this tissue, which could be related to endometriosis but the mechanism of action would be different,
And with increased pain, there is hyperalgesia, muscle weakness, cytokines in the bloodstream, systemic inflammatory effects, diffuse tissue damage and hypersensitivity to pain. This leads to a loop of tissue pain and system hyperactivation which, according to some authors, a problem like sacroiliitis, ends up with fibromyalgia.

Muscle disturbances are not dependent on primary muscle damage:
With pain and pain loop and cytokines that produce more pain and more cytokines, there is also fat infiltration in the muscle, as well as fibrosis and structural changes (hypotrophy, tonic fibres – they start to become fasic fibres, for this it is not necessary that there is tissue damage, it happens when it is a chronic problem).

Initial alterations mediated by neural activity (e.g. reflex inhibition) long term changes possibly mediated by excess central and peripheral release of substance P (related to inflammation and immune system).
1 response system is neural and second is humoral, because the humoral pathway is already adapted.

The neuroimmune system related to motor control, astrocytes and glia cells can produce inflammation in the central nervous system. A nociceptive pain becomes a central inflammation, if there is hyperprotection of the sympathetic system it will be related to the autonomic nervous system.

Sensitization of peripheral neurons results in lowering of the excitability threshold for nociceptive firing which results in a greater need for load to avoid nociceptive discharge which increases basal muscle tone. This means that if it hurts to make a movement, the musculature and the system need more control of the movement to avoid generating pain, but to control more, more tension is needed to activate the protective sympathetic system, and for that increase the basal system, thus activating the autoimmune system,

The increase of fibrosis and the infiltration of muscular fat, this leads to the decrease of the capacity of muscular control and to move the spine (effector organ of the neural system), this generates limitation and distortion of the movement, it will develop around a different biomechanical axis, and this alters the quality of the afferent information originated by these tissues, and therefore there will be an efferent response according to the information received and it will affect with alterations of the autonomic nervous system.

Brain – peripheral tissues interaction

Local somatic structures generate information that generate long-term alterations in the central nervous system.

Is it chronic pain that produces a decrease of grey matter in the brain or is it a previous decrease of grey matter that promotes chronic pain?

Peripheral modulates central structure, peripheral input produces changes in the central nervous system.
Human studies experience pain related structure treated with surgery or infiltration after 6 months, in patients who improved symptoms the prefrontal cortex returned to the size and width of the previous prefrontal cortex and altered functional activity and returned to the condition of the controls.

This says that the changes are reversible if we treat the pain and sensitivity hyperactivity/local hyperresponsiveness, sympathetic protective system


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