Thursday, September 12, 2013

How do we control pain?

Nowadays it is not known so much about it, but enough to know that we are able to control the pain. For example, we know that placebo effect can make us feel better by thinking we are given a drug, or when we get hurt but we don't feel the pain within the next hours, and we have also noticed that not everybody faces the pain in the same way. The main reason is that the perception of pain depends on the circumstances  and emotions involved in this situation. In terms of evolution, feeling pain could be disadvantageous in stress or emergency situations since our body must care about surviving. However, pain is something essential in the opposite situations in order to prevent further damages.  

This is due to the descending control of pain which goes from the brain to the spinal cord and let our brain select those pain stimuli we want to feel.  A lot of different areas in our brain has been identified to inhibit the transmission of pain sensation at the level of the spinal cord. 
One of these areas is the rostral ventrolateral medula, which is located in the nucleus raphe magnus where a serotonergic pathway (release serotonin) is derived and projected to the spinal cord, thus inhibiting pain transmission. This pathway is the final part of a system that begins in another levels, in fact, the nucleus raphe magnus receives information from periaqueductal gray matter, which receives information from the cortex and the limbic system. The cortex has an important role in the thinking process, while the limbic system is responsible of the emotions and our behavior, as well as of the sense of smell and other functions. Therefore, it could be thought we can control these structures in order to elaborate the necessary information to restrict the pain sensation. 

Describing in detail, rostral ventrolateral medula is made up from neurons, including on-cells and off-cells. On-cells act by activating the transmission of pain impulses, while off-cells act by inhibiting that trasmission when they are activated. These cells are the target of opioids such as morphine, which inhibits the action of on-cells and activates off-cells which produces an interruption of pain, thus causing an analgesia

It is quite similar in a stress situation or the effects of placebo in our body, which are capable of activating endogenous opioid system by producing substances that are similar to morphine which binds to the same receptors and activate the descending pain control system. As a result, a strong analgesia will be caused by the stress or the supply of that drug. 
There are some evidences to show the endogenous opioid substances our brain produces are essential for analgesia. For example, naloxone, an opioid antagonist, blocks the analgesic placebo effect, while other drugs antagonize cholecystokinin (an anti-opioid) and increase analgesic placebo effects.

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Translation made by Alba Daza Molina