“Pain endings”, “pain transmission” and “pain pathways” – these terms are in wide use by health professionals, including scientists who should know better. It really drives us crazy in the education and clinical world and it must be unhelpful for patients as there is no such thing as pain endings, pain transmission and pain pathways.
These terms suggests that pain has a source in body tissues which often leads to repeated and excessive diagnostic and therapeutic hunts for culpable structures in tissue. It denies the role of the brain in pain construction and I believe enhances chronic pain and makes it more difficult to manage.
Nociception, nociceptive pathways and transmission of nociception are the correct terms. Nociception is not pain, it is not a necessary requirement for pain, sometimes the brain will evaluate it, weigh up what else is going on and construct pain.
If you believe in pain endings and pain pathways from tissues you may also believe in love endings, love pathways and love transmission from the genitals.
Feel free to name anywhere the error has been made. I probably made the error a while back. This may be one of the best things we can do for the world’s chronic pain epidemic.
Here is a start:
Wikipedia has the error “A free nerve ending (FNE) is an unspecialized, afferent nerve ending, meaning it brings information from the body’s periphery toward the brain. They function as cutaneous receptors are essentially used by vertebrates to detect pain”
WebMD has the error in the otherwise great section on fibromyalgia. “there are roughly 20 different kinds of nerve endings in your skin that tell you if something is hot, cold, or painful”
The error is most dangerous when it is in children’s science websites. Comments like “pain travels up…” are common
Just Google the terms, read the literature – the errors are everywhere.
Let us know your finds.
Of course you are right, however some physicians try and explain an ethereal unseen factor. When you feel pain radiate or it is felt in three parts I,e buttock, thigh and calf. It is distinct from pain which is associated with one site. If we just used a medical term patients would not get a grasp to localise pain. There has to be room for both Clinical and Everyday. Imagine chatting to a friend and attempting to explain – that’s difficult, we try and simplify into common English.
The fact is you are right with regard to the clinical terminology. Here is the obvious. Joe Soap uses common English when making a web search, he is not schooled in medical terminology. He will use pain in leg, radiates up, sharp pain, burning pain in an attempt to find out what is wrong with him. So stating the obvious common English plays a fundamental role in pointing to the correct information. I would never be so absolute for the exclusion of the people you wish to reach.
Although pain is felt in the brain after a signal is received, a signal is sent to the site of an injury, it warns us something is wrong but at that site a cocktail of chemicals are manufactured (common English), these chemicals help protect the injured site. Now sent to involves a pathway brain, spinal cord, peripheral nerves. At the end of the day the physician translates our Russian into Clinical English – what harm is there? Naming and shaming may be more damaging than one realises. We are not all Puritans in a global Village nor should we be.
“What harm is there” – I think this is the whole point of the post; there is GREAT harm in conflating nociception with pain.
Perhaps more than anything else, this error has perpetuated the idea that pain is of the body/from the body/produced in the body and therefore led to the erroneous conclusion that pain = harm/damage in the body.
While entire industries and professions have built themselves on this false foundation, people in pain have continued to suffer as they seek the “treatment” that will “fix” their bodies and therefore eradicate their pain.
I’m not 100% sure of what you mean with “Although pain is felt in the brain after a signal is received, a signal is sent to the site of an injury, it warns us something is wrong but at that site a cocktail of chemicals are manufactured (common English), these chemicals help protect the injured site.”
But I would beg to differ on a number of points –
Pain is not “felt in the bran” it is a construct of the brain. Semantics? Absolutely not.
Pain does not necessarily mean that “something is wrong” – again, this is at the core of the issue with chronic pain and the reason that people in pain will continue to seek treatment that proposes to fix the tissue that they believe are involved – usually believing this because their therapist told them so.
This problem has been around far too long, and if a bit of naming and shaming is what it takes to make people take notice and to change, I’m all for it.
Quick check; I typed “pain fibres” into Google Scholar – 2,180 results in .03 seconds.
Since 2012 – 108 results, just a couple;
Back pain in space and post-flight spine injury: Mechanisms and countermeasure development
JV Sayson, J Lotz, S Parazynski, AR Hargens – Acta Astronautica, 2013 – Elsevier
… discogenic pain . Endplate nerves are prototypical pain fibres that demonstrate nociceptor markers such as the neurotransmitter substance P and high affinity nerve growth factor receptor trk-A .
Cancer-related neuropathic pain: pharmalogical options
J Clancy – British Journal of Nursing, 2012 – internurse.com
… pump (hence blocking sodium and/or potassium and/or calcium channels) of pain fibres and/or inhibiting the production and secretion of substance P (ie the excitatory pain neurotransmitter secreted at pain fibre synapses)
Clearly, this problem is everywhere, from the hospital ward to the International Space Station….
This confusion is quite widespread. The Human Brain Book by Rita Carter is a wonderful resource for patient education. The majority of images and explanations are fantastic. However, Carter’s explanation of pain is very frustrating to read. It is clear that she is “trying” to make the right point, but her imprecise language undermines her efforts to explain that pain does not equal tissue damage.
She writes “The feeling of pain is not actually caused by an injury in itself. In order to experience pain, it must be made conscious. This requires activity in brain areas involved in emotion, attention, and assessing significance. Such activity can create the pain experience in the absence of a cause”
It’s an interesting start, but she follows it with:
– “Pain-transmitting nerve fibers permeate almost every part of the body.”
– “pain transmitted by a C fiber”
– “opiates then dampen the pain signals carried in those nerve endings”
– “Pain signals are transmitted to several areas of the cortex”
– “pain signals traveling up from the site of the injury”
– “An intensely imagined experience generates almost identical brain activity to the equivalent “real” experience, so an imagined state of physical ease may be achieved even as pain fibers in the body are being stimulated.”
Unfortunately, I cannot share this otherwise amazing resource with my patients. Carter inadvertently promotes the exact misunderstanding she is trying to resolve.
I was surprised to here Fernando Cerraro, the current head of the IASP, mention pain pathways in a podcast interview with Ginger Campbell (Brain Science Podcast) just a few weeks ago.
Sorry. Fernando Cervero.
Yep, I remember thinking the same thing, That phrase, “pain pathway” whenever I hear it is a real clanger.
Dr Cervaro did seem to be using the phrase in a slightly different way:
“If you think about vision, when we have first the sensors in the retina, and we have pathways through the brain, and we have a piece of the cortex, and the visual cortex, and all that, the way we study the process of visual perception is following that visual path. Now, whether pain has something like that, or not, is also controversial; because if it is not a sensation, then we shouldn’t have it. Why do we need to have a pain pathway, or pain-specific elements within our brain, if it is not a sense like vision or hearing.”
“Dr. Cervero: Of course. What this approach implies is that if you have an
abnormal, or excessive—or whatever you want to call it—stimulation of a normal sensory pathway, then it would be a painful event. So, you didn’t need to have a specific pain pathway, it would be the result of an abnormal activation of an existing sensory pathway from another method. Whereas, if you think of pain as having some sensory components… And I think that the truth is somewhere in between. Pain does have an important sensory component, but it also has added emotional and cognitive elements. So, there are, in fact, some elements of a pain pathway in the brain.”
However, for mine, suggesting that there is a pain pathway in any way, suggests that pain is an “entity”, a “thing” that exists (and can therefore be transmitted along a pathway) as opposed to a conscious experience that emerges as a result of certain activity within the brain.
In the same way, talk of a “visual pathway” is misleading. There are certain pathways that *information* travels along from the receptors in the retina, to various parts of the brain, but is this information “vision”? Like pain, incoming information along these pathways is neither sufficient nor necessary for a “visual” experience to be constructed- we can dream/imagine with our eyes shut, and equally we may not “see” when our eyes are open – ‘blindsight’ would seem to offer an amazing example of this, along with more ‘mundane’ optical illusions.
Nice one Byron! Talk about starting at the top!
This one is subtle, but I think it is still there:
Hum Brain Mapp. 2011 Oct;32(10):1592-601. doi: 10.1002/hbm.21131. Epub 2010 Sep 15.
Within-limb somatotopic representation of acute muscle pain in the human contralateral dorsal posterior insula.
Henderson LA, Rubin TK, Macefield VG.
Department of Anatomy and Histology, University of Sydney, Sydney, New South Wales 2006, Australia. email@example.com
It is well established that the insular cortex processes noxious information. We have previously shown that noxious inputs from the arm and leg are coarsely organized somatotopically within the dorsal posterior insula. The same has been shown for inputs from C tactile afferents, which mediate affective touch, and it has been suggested that the insula may be responsible for the localization of some somatosensory stimuli. Knowing the degree of spatial detail may have significant implications for the potential role of the dorsal posterior insula in the processing of noxious stimuli. Using high-resolution functional magnetic resonance imaging (fMRI), we compared insula activation patterns in 13 subjects during muscle pain induced by injection of hypertonic saline (5%) into three muscles within the same limb: shoulder (deltoid), forearm (flexor carpi radialis), and hand (first dorsal interosseous). Mapping the maximally activated voxels within the contralateral dorsal posterior insula in each individual subject during each pain stimulus revealed a clear somatotopy of activation within the contralateral dorsal posterior insula. Shoulder pain was represented anterior to forearm pain and medial to hand pain. This fine somatotopic organization may be crucial for pain localization or other aspects of the pain experience that differ depending on stimulation site.
Copyright © 2010 Wiley-Liss, Inc.
It starts off so well, but then slips with “muscle pain” and “pain stimulus”.
That last one especially represents the slip from “noxious stimulus” to “pain stimulus”.
Thanks everyone for the posts,
It’s everywhere isn’t it?. I am only just realising how endemic it is since I started the blog post.
Also in common usage is “pain generator”. The term is quite evocative and you can often read “hunt for pain generators in tissues”. The term “muscle pain” and “joint pain” are wrong too. There is no such thing although we all use it. “Muscle contribution to a pain experience” is linguistically difficult but it is more truthful. I guess as long as we know the difference we are doing something.
What do we do about it? I too was enjoying Rita Carter’s book til I got to the section on pain and had to close it. Some of the other examples mentioned are quite subtle. Do we just leave the error and consider it harmless it as one contributor on the blog has suggested.
I don’t think it is harmless. Cognitions such as “I am hurting therefore I am damaged” and “I won’t do that because I could damage the part” have been robust predictors of chronicity for years. Only yesterday on the phone a person in pain said to me “its somewhere is the back they just haven’t found it yet”. Surely we owe society a better pain literacy?
Plus I think it’s quite easy and inexpensive to change. While some of us might not know the difference between nociception and pain and require an urgent update, many of us are plain lazy. I make the error in everyday language too.
A suggestion is that language can change to something like…. nerves endings sniffing the environment and continually reporting danger that the brain only sometimes listen to. Stories of how people can have severe tissue damage and no pain or minimal damage (eg a pin in a violinists finger and heaps of pain) should help. Alter all the body doesn’t tell the brain when it is in pain. The body reports degrees of danger – pain is ultimately a brain construction.
More examples out there?
Textbooks that my undergrads are prescribed are rife with them and it is incredibly frustrating when I am trying to teach them the ‘truth’!! E.g. Snell – Clinical Neuroanatomy, Bear – Neuroscience, Vander – Human Physiology, Kandel – Principles of Neural Science and many many many more. Pain receptors, pain fibres, the spinothalamic pathway aka the ‘pain and temperature pathway’.. How can we get these authors to update their terminology!?
I was enjoying getting to grips with glia and a world outside neurons in The Other Brain by R. Douglas Fields who is described as an “internationally recognised authority on neuron-glia interaction, brain development, and the cellular mechanisms of memory”.
When I got to Chapter 9: Glia and Pain, I thought this would be where it all comes together for me in the more familiar territory reading about pain. However, this was what I encountered:
“Before considering chronic pain and the role of glia, we need to understand some fundamentals of pain circuitry. It may come as a surprise to learn that your pain neurons are not located in your brain. They are not inside your spinal cord either, where you will find the motor neurons that issue commands to your muscles. Pain neurons are squeezed like an afterthought between each vertebra of the bony spinal column that rises as a series of bumps down the center of your back. In the space between each bone in your backbone there is a sack of pain neurons. You have one sack of pain neurons on each side of the spinal column at each segment in your articulated spine.”
He continues throughout the chapter to describe pain neurons, pain signals and pain circuits and that “pain can be stopped by silencing the pain neurons in the skin…[injecting] novocain blocks the ion channels that spark nerve impulses. If there are no nerve impulses, no signals of pain will reach the spinal cord”.
It was indeed a surprise to me that there are a sack of pain neurons and that these are squeezed in between my vertebrae and thank goodness pain signals can be stopped by silencing pain neurons…
With that I never finished the next 7 chapters.
Share your disappointment with this one, more so because the rest of the book was, for me, quite brilliant.
I tried to mentally insert “nociception” rather “pain” as I was reading, but as your example shows, this gets difficult.
Prof Paul Rolan recently gave an open lecture at Adelaide Uni – http://blogs.adelaide.edu.au/researchtuesdays/2013/01/11/breaking-the-pain-chain/
Some interesting research regrading the immune system and pain, but after starting so well, there were more “pain messages”, “pain detection” slipping in.
Are there extra marks off for doing this in a lecture aimed to share research and new ideas with the general public??