Inflammation

Inflammation

As we know from current literature, pain is muti-dimensional. Injury and pain is not the cause and effect relationship it was once thought to be. Why do two people of identical demographic stub their toe on a door and one feels more pain than the other? There is no way to know for sure. You could go so far as to say one person had more emotional trauma during childhood. Or one person had a meal with more processed carbohydrates that day. Now let’s say one person expresses the negative emotions we are all too familiar with when catching the corner of the coffee table with our little toe. Why does that person feel better faster?

Mechanisms of pain and pain sensitization all operate in the brain. The peripheral nerves responsible for signaling pain are type III and type IV nerve fibers. They synapse via glial cell in lamina II, IV, V, and VI of the spinal cord. The pain signal is sent to the brain via spinothalamic tract to the thalamus where the limbic system processes and stores information.

The type IV fibers that sense pain and start the cascade of synaptic activity up to the brain are also known to give off sensations of their own. Activated type IV fibers release Calcitonin gene related peptide (CGRP) and substance P, both promoting an inflammation response. The inflammatory response excites immune mediating cells like macrophages, mast cells, and endothelial cells to carry out the appropriate mechanisms for protecting the body. However, when there is over activation of the type IV fibers these inflammatory mediators are called on far too often. This results in excess inflammation throughout the body.