Nociception VS. Pain

Over the last 2 years I have spent countless hours reading about, taking courses on, and learning all about the science behind pain. It has been a revelation to learn so much in stark contradiction to what I was taught in both undergraduate as well as graduate school regarding pain, biomechanics, posture, and mechanisms of manual therapy. Each of these are topics sufficient for lengthy discussion on their own. However, in this post I plan to address a very basic concept that is integral to a more accurate understanding of how pain works. I find on a regular basis when talking with both colleagues and patients that the difference between nociception and pain is poorly understood.

By basic definition nociception is the encoding and processing of potentially harmful stimuli in the nervous system.⁴ In more detail it can be described by stating that “specialized peripheral sensory neurons known as nociceptors alert us to potentially damaging stimuli at the tissues by detecting extremes in temperature and pressure and injury-related chemicals, and transducing these stimuli into long-ranging electrical signals that are relayed to higher brain centers.”¹ 

There are many different types of nociceptors in the body, but generally speaking there are three main categories of nociceptors that are useful to know. These are mechanical, chemical, and thermal.

• Mechanical – Mechanical pressure is perhaps the most common cause of pain that you would think of or experience on a daily basis. If you bang your shin on the corner of the bed, you have soft tissue damage, which can set off mechanical nociceptors.
• Thermal – temperatures that exceed a normalized threshold are another common cause of pain – if you touch something very hot, or very cold you’ll set off temperature nociceptors, which may result in the experience of pain even before you get burned!
• Chemical – Various chemicals can activate nociceptors as well. For example, when you have an injury or infection, the affected area becomes inflamed. Inflammation is very important as it brings blood flow to the damaged area to aid in the repair process. Some of these inflammatory chemicals such as prostaglandins, cytokines, and substance P for example can also affect pain in a couple of ways. These chemicals can activate nociceptors to produce signals to the brain, or they could lower the activation threshold of neighboring mechanical and temperature nociceptors which will make you more sensitive all stimuli in general.³ This is why an injured body part seems to hurt with even the slightest movements or pain can seem to spread to nearby areas that weren’t damaged.

If people are familiar with the idea of nociception at all, you will regularly hear them refer to nociceptors as “pain receptors”. However, as you can see by the definitions above, that’s not correct. Nociceptors actually detect the same sensations as other receptors in the body. However, nociceptors have a higher threshold of activation, which means that they necessitate a more robust than usual stimulus before sending signals to your brain. ³ Again, it is more appropriate to refer to nociceptors as danger receptors instead of pain receptors.

Conversely, pain has been defined as a “complex constellation of unpleasant sensory, emotional and cognitive experiences provoked by real or perceived tissue damage and manifested by certain autonomic, psychological, and behavioral reactions.”² Pain is an experience, not just a sensation. It involves current emotional status, belief systems, past experiences, fear, stress, nociception, among many other issues.

As you can see, nociception is one factor that contributes to the multi-factorial higher level processing in the brain subsequently leading to the possible output of pain from the brain based on actual or perceived danger to the body. An everyday example of this is when you’re out working in the garden, focused on planting your cucumbers, squash, and beans when suddenly you look down to notice the blood streaming down your arm. Five minutes ago you snagged the back of your forearm on the rose bushes just enough to break the skin and cause bleeding. Clearly there was enough mechanical nociception that occurred to signal the brain. However, you were in your happy place of gardening and heavily focused on the task at hand, so your brain “ignored” the incoming nociception and deemed that danger message benign. Subsequently causing it to refrain from generating an output of pain to alert you. 

The opposite can be seen in the patient with phantom limb pain. They have had an above the knee amputation, yet they consistently feel pain or even itching in their foot. How can one feel pain in a foot that isn’t present with receptors to send “pain messages” up to the brain? That amputee feels pain due to the brain perceiving danger due to a host of factors. It then synthesizes those factors including, but not limited to the emotional and psychological trauma of losing the limb, past experiences, current stress level, etc. 

 So remember…

“nociception is neither sufficient nor necessary to create pain”.

-Lorimer Mosely

1.       Dubin AE, Patapoutian A. Nociceptors: the sensors of the pain pathway. J Clin Invest. 2010;120(11):3760-72. 
2.       Terman GW, Bonica JJ. Spinal mechanisms and their modulation. In: Loeser JD, Butler SH, Chapman CR, Turk DC, eds.Bonica’s Management of Pain . 3rd ed. Philadelphia, Pennsylvania, USA: Lippincott Williams and Wilkins; 2003:73. 
3.       Basbaum AI, Bautista DM, Scherrer G, & Julius D (2009). Cellular and molecular mechanisms of pain. Cell, 139 (2), 267-84 
4.       Loeser JD, Treede RD. The Kyoto protocol of IASP Basic Pain Terminology. Pain. 2008;137(3):473-7.

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