Pain: Is it really all in your head?

Pain is something experienced by many on a regular basis. Although it hurts, pain is actually a good thing. It tells a person that something is wrong and in need of attention. For example, if your hand touches a hot stove, you will immediately pull it away because you feel pain. If you didn’t feel pain from the hot stove, your hand would be damaged. Thus, pain can protect us from harmful stimuli and can be a positive thing. Pain can also have a dark side. In some cases, the pain experienced doesn’t have an obvious cause. This can leave the individual who is experiencing the pain wondering if they have a mental issue rather than a physical one. Individuals who experience chronic, widespread pain may not necessarily have something wrong with their heads, although that may be an issue. What is wrong is the functioning of pain signals. When pain signal dysfunction occurs, the activation of pain signaling becomes amplified, resulting in an increased sensation of pain.

There are four major components of how the body processes pain. The first thing that happens is called transduction. Transduction occurs when tissue is damaged which activates nerve endings. Next, transmission takes place. Transmission is where the message of “pain” is relayed through the body’s nervous system to the brain. Once the pain signal arrives in the various areas of the brain, the brain processes this information. What results from this is called pain perception. After the brain has an idea of what the severity and type of pain is, it will signal the body to help with pain modulation. Pain modulation is the nervous system’s attempt to reduce the transmission of pain signals [1].

Pain Modulation

Opioid medication is commonly prescribed to help with pain modulation by blocking pain signals. In addition to blocking pain signals, opioids can have an influence on neurotransmitters that play a role in decreasing pain perception and modulation. Opioid medication can inhibit the reuptake of serotonin and norepinephrine [2]. Serotonin can play a significant role in decreasing pain perception. One study found 5-HTP (the biochemical precursor to serotonin) administration to decrease fibromyalgia symptoms [3]. It could be postulated that the 5-HTP was converted into serotonin, thus decreasing the perception of pain. Norepinephrine can also play a significant role in pain modulation. Norepinephrine can actually stimulate the release of beta-endorphins (endorphins are the body’s naturally occurring opioids), which work to block pain signals [4]. Dopamine is another neurotransmitter influenced by opioid medication. One study showed an increase in dopamine levels in the nucleus accumbens of mice after Tramadol injection [5]. Dopamine can produce analgesic effects when its D2 receptor is stimulated [6].

Although treating pain with opioid medication can be effective, it often comes with unwanted side effects such as constipation and addiction. It may be beneficial to consider alternative therapies that can help manage pain before starting a prescription medication regimen. Additionally, consider assessing neurotransmitter levels to see where major imbalances may lie. Talk to your doctor today about Sanesco’s neurotransmitter assessment and TNT formulas. As we see, pain isn’t so simple, which could imply that its identification and treatment shouldn’t be either.

References

1. Osterweis, M., Kleinman, A., & Mechanic, D. (1987). Pain and disability: Clinical, behavioral, and public policy perspectives.
2. Grond, S.,& Sablotzki, A. (2004). Clinical Pharmacology of Tramadol [Abstract]. Clinical Pharmacokinetics, 43(13), 879-923. doi:10.2165/00003088-200443130-00004
3. Caruso, L., Sarzi, P., Cazzola, M., & Azzolini, V. (1990). Double-blind study of 5-hydroxytryptophan versus placebo in the treatment of primary fibromyalgia syndrome. J Int Med Res, 18(3), 201-209.
4. Binder W, Mousa SA, Sitte N, et al. (2004). Sympathetic activation triggers endogenous opioid release and analgesia within peripheral inflamed tissue. Eur J Neurosci. Jul;20(1):92-100.
5. Nakamura, A., Narita, M., Miyoshi, K., Shindo, K., Okutsu, D., Suzuki, M., . . . Suzuki, T. (2008). Changes in the rewarding effects induced by tramadol and its active metabolite M1 after sciatic nerve injury in mice [Abstract]. Psychopharmacology, 200(3), 307-316. doi:10.1007/s00213-008-1180-1
6. Jääskeläinen SK, Lindholm P, Valmunen T, et al. (2014). Variation in the dopamine D2 receptor gene plays a key role in human pain and its modulation by transcranial magnetic stimulation. Pain. Oct;155(10):2180-7.

Clinical Contributor

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