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How Pain Works, Part III – Nociception

Larger version below!

Larger version below!

The science of pain is actually very interesting, and involves everything from chemistry to cultural studies and everything in between. It can get complicated, but we’ll keep things simple and understandable while remaining as accurate as possible. Here we will start with some of the basic science of how potential pain is detected and transmitted through the body.

If you missed the last few “How Pain Works” articles, visit the pain education section


Pain Mechanisms

As you can imagine, there are countless injuries, conditions, and diseases that can lead to pain. For example, pain in your big toe may be due to slamming your foot in a door, dropping something on it, cutting your toenail too far, being bitten by a snake, and so on. While the possibilities are endless, they all share similar “mechanisms” by which the painful event is detected, transmitted, and experienced.

There are many mechanisms of pain that help explain the variety of experiences people can have, such as “nociception” (which we will start with here), “neuropathic pain”, “central sensitization” and more. 1 These mechanisms can overlap and interact, and most pain involves a combination. At the end of this series, you should have a basic idea about many of them!

Nociception – The Pain Transmission System

When you roll your ankle, or pull a muscle in your lower back, pain is usually immediate. In these cases, pain is acute – meaning new or sudden. Acute pain often originates from nociception – the nervous systems way of detecting, transmitting and processing potential damage. This potential damage is detected by nociceptors – a kind of nerve ending (sensory receptor) found all over your body. 2

Once nociceptors are activated, they send signals through peripheral nerves to the spinal cord, which then travel to the brain. 3 The signals are processed at each stage of transmission, with the brain arguably playing the largest role in how pain is consciously experienced. 4

Nociception

Notice this is labeled the anatomy of “nociception” – not “pain”!

People often refer to nociceptors as “pain receptors” – but that’s not quite right. Nociceptors actually detect the same sensations as other receptors (pressure, temperature, etc). However, nociceptors have a higher threshold of activation, meaning that they require a stronger than usual stimulus before sending a signal to your brain. 2 In a way, they are the “danger” nerves, telling you that something intense is happening – and therefore, you should pay some attention! Nociceptors are kind of like alarms.

There are three main categories of nociceptors that are useful to know:

  • Mechanical – Mechanical pressure is perhaps the most common cause of pain. If you roll your ankle, your ligaments are being stretched too far, which can set off mechanical nociceptors.
  • Temperature – Extreme temperatures are another common cause of pain – if you touch something very hot, you’ll set off temperature nociceptors, which may signal pain even before you get burned!
  • Chemical – Chemicals can activate nociceptors too. For example, when you have an injury or infection, the affected area becomes inflamed. Inflammation is an important first step in your body’s healing process – it brings blood and important chemicals to the damaged area to aid in the the repair process. Some of these inflammatory chemicals also affect pain in a couple of ways. Chemical might activate nociceptors to produce pain (sometimes constantly), and some chemicals can lower the threshold of activation in other nociceptors, making you more sensitive to pain in general! 2 This is why an injured body part seems to hurt with even the slightest movements.

Generally, “nociceptive” pain makes sense – you can usually pinpoint a cause (“it hurts here, because this happened”), and it behaves in a predictable way. Most of the pain people feel every day can be explained by the nociceptive mechanisms described. There are many examples: like when you hit your knee on a corner, drink hot coffee before letting it cool, and (sorry, this next one is gross, but it’s a good example of pain sensitivity increased by inflammation) touch a sore pimple.

Many pain medications (NSAIDs and Opioids) work by blocking the chemicals that lower pain thresholds. This is why they seem to work, especially for primarily nociceptive pain. But remember, this is only one of the many reasons why things can hurt, so these pain medications only help so much.

Nociception vs. Pain

Nociception doesn’t always result in pain, nor is is nociception the only way you can experience pain. There are many cases in which something can activate a nociceptor without pain being experienced (like during sports, for example). The the opposite is true too – there are cases in which you can experience pain without nociception. There are many reasons for these exceptions, and we will start talking about them next time.

The important thing to understand now is that nociception and pain are not the same thing. That’s why it’s wrong to call nociceptors “pain receptors”, and nociception “pain signals”. 5 Nociception is simply a sensory signal indicating potential harm. Pain is a conscious experience, and whether nociception ends up being perceived as pain depends on many more factors.

Like what? To be continued…


References *

ResearchBlogging.org1. Smart KM, Blake C, Staines A, Doody C. Self-reported pain severity, quality of life, disability, anxiety and depression in patients classified with ‘nociceptive’, ‘peripheral neuropathic’ and ‘central sensitisation’ pain. The discriminant validity of mechanisms-based classifications of low back (±leg) pain. Man Ther. 2012 Apr;17(2):119-25. doi: 10.1016/j.math.2011.10.002. Epub 2011 Nov 9. PubMed PMID: 22074733.

2. Basbaum AI, Bautista DM, Scherrer G, & Julius D (2009). Cellular and molecular mechanisms of pain. Cell, 139 (2), 267-84 PMID: 19837031

3. Giordano, J. (2005). The neurobiology of nociceptive and anti-nociceptive systems. Pain Physician, 8(3), 277-90.

4. Apkarian AV, Baliki MN, Geha PY. Towards a theory of chronic pain. Prog Neurobiol. 2009 Feb;87(2):81-97. doi: 10.1016/j.pneurobio.2008.09.018. Epub 2008 Oct 5. Review. PubMed PMID: 18952143; PubMed Central PMCID: PMC2650821.

5. Moseley, G. L. (2012). Teaching people about pain: why do we keep beating around the bush?. Pain Management2(1), 1-3.

* Remember, nothing is set in stone. As pain researcher Lorimer Moseley says: “the biology of pain is never really straightforward, even when it appears to be”. Research is ongoing, science keeps updating, and this article will probably be updated regularly.

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    2 Responses to How Pain Works, Part III – Nociception

    1. Rachel Meeks says:

      Just beginning to dabble in this approach on pain – I suffer from chronic pain, and I’ve been looking for anything that will help because I can’t stay on Vicodin forever! Looking forward to reading more. :)

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