Inflammation
Inflammation essentially consists of a great dilatation of blood
vessels next to the opening of the pores, allowing a permeable pathway
for fluids, substances and cells from the bloodstream to the tissues;
these tissues increase their volume and temperature.
Pain nerve activation induces the release of certain neurotransmitters
that dilate vessels and open the pores, causing tissue inflammation
along the releasing sites. This is called "neurogenic inflammation".
Some of the implicated neurotransmitters are CGRP (calcitonin-gene-related-peptide),
NKA (neurokynine A) and Substance P (SP).
Some blood cells are also activated in specific circumstances,
especially when they detect the presence of microbes, releasing
substances that attract other systemic defense cells, which create
vessel and pore dilatation, opening a pathway for these cells to
reach tissues. This is known as "humoral inflammation";
some of the released substances are prostaglandins and leukotrienes.
It has been shown that neurogenous and humoral inflammation potentiate
each other and that both processes are implicated in back pain.
This explains the efficacy of treatment with anti-inflammatory agents,
since they hinder prostaglandin production and interfere in the
interaction between humoral and neurogenic inflammation.
In back pain, inflammation is essentially a consequence of a release
of neurotransmitters, together with pain nerve activation and, secondarily,
of the start of a humoral inflammation process. Nevertheless, after
the onset of inflammation, this in itself becomes an added aggravating
factor:
On the one hand, released substances at the onset of humoral inflammation
are able to activate pain nerves, thus increasing pain. At the same
time, pain releases the neurotransmitters involved in neurogenic
inflammation, which increases inflammation, creating a vicious circle.
On the other hand, at increased tissue volume the risk for nerve
compression also increases which in turn worsens the causal lesion.
For example, in a disc
herniation, inflammation may increase the herniated pulpous
material, or decrease the fissure opening of the fibrous fold from
where it protruded.
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