Pain Education, No Script Provided Ep 4. Definitions and Clinical Descriptors

We examine the IASP definition of pain, why shared language matters, and how sloppy semantics derail research and care. We contrast barriers to recovery with causes, clarify differences between nociceptors and nociception, and use sensitization and nociplastic as hypotheses that guide better reasoning.

• using the IASP definition to ground assessment
• distinguishing nociceptors, neurons, and nociception
• reframing biopsychosocial as barriers to recovery
• identifying sensitization without overpathologizing
• applying nociceptive, nociplastic, neuropathic as hypotheses
• avoiding conflations like “pain signals” in clinic and AI
• aligning treatment dosing to irritability and mechanism

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Chapters

• 0:00 Setting The Stage And Goals
• 3:18 The IASP Definition Of Pain
• 6:50 Why Shared Semantics Matter
• 10:30 Biopsychosocial: Barriers Not Causes
• 17:45 Nociception As A Foundational Assumption
• 24:03 Conflations In AI And Literature
• 32:13 Mechanistic Terms: Receptors To Process
• 38:48 The Nociceptive Apparatus Explained
• 45:13 Sensitization: Peripheral And Central
• 51:33 Nociplastic As Hypothesis Of Mechanism

Transcript

Eric: 0:12

H ello and welcome to the Massage Science Podcast. My name is Eric Purves. I'm a course creator, educator, researcher, RMT, and advocate for evidence-based care. Today is episode four of my seven-episode series with Monica Noy. In this episode, we further discuss the definition of pain and explore the meaning and relevance of the clinical pain descriptors per the IASP. Monica's course, Pain Education No Script Provided, is now available for purchase on our website, thece.com. Thank you for being here, and we hope you enjoy this episode. Hello, everybody, and welcome to episode four of our Pain Education No Script Provided. Conversations with the wonderful Monica Noy. Today we're going to talk about the definition of pain, some of the sensory or clinical pain descriptors, and we'll see what other wonderful things come up in this conversation. So thanks, Monica, for being here again.

Monica: 1:15

Thank you very much for having me.

Eric: 1:17

Let's start off with the definition of pain. This is something that I think a lot of people know. And if they don't know, you should know, I feel.

Monica: 1:29

They should know. I don't think enough people know, actually.

Eric: 1:33

That goes back to that gap in knowledge thing that we've talked about before. Not enough people know. And so for those that whether you know or you don't know, what is the definition of pain? And then the second question is that is why is this important and how is does this help us treat or think or clinically reason those that hurt?

Monica: 1:54

Yeah. So let me start with one caveat, two caveats maybe. One is just reiterating that there is a massive knowledge gap in healthcare practitioners' knowledge of mechanisms and management of pain. And it's massive, it's a pit of knowledge gap. So if people don't know the definition of pain, that's not unsurprising. And also if they know several definitions or several understandings of pain, that's not necessarily unsurprising. But I like to start with that only because that's the hardest thing for people to accept is that they actually don't know enough. And the second thing is that most of this information is not proprietary. I've collated it, I've put it together, I've presented it in a particular way. But this is not, I didn't invent this information. This is not information that I made up in any way. With that, when we go to the definition of pain, we're talking about the definition of pain that comes from the International Association for the Study of Pain. And we're talking about that definition for the reason that it is at this particular time a consensus, a scientific consensus definition that's used or should be used for research and clinic. And I'll go through the definition and then I'll just get on my high horse about something. So the current definition is an unpleasant sensory and emotional experience associated with or resembling that associated with actual or potential tissue damage. And that was updated very minorly in 2020. That's the 2020 update. If there's an argument, we can't, nobody can win it, and nobody can really even talk about it. Semantics matter.

Eric: 4:20

That makes 100% sense because if you ask a group of 30 people what the definition of pain is, or what is pain, just to what is pain? That's the question I often ask in my courses, and you will get probably close to 30 different responses.

Monica: 4:37

That I'm trying to see if I have an AI. I've taken AI down some logical sinkholes basically regarding the definition of pain.

Eric: 4:48

Oh wow.

Monica: 4:49

Yeah, I've got some of them. I'm gonna have to look at them. You keep asking a question while I find this AI thing.

Eric: 4:55

Yeah, mine was more of a statement. It was just saying that the understanding from so coming from a profession, say massage, osteopathy, anyone in the MSK world, we should have a very strong understanding, or at least that we should understand the definition or know the definition of pain. Because if you're helping somebody that is comes to see you because they are experiencing pain, if we don't understand what that means from a I think you said a scientific consensus, then how are we supposed to provide the best treatment for it? How are we supposed to understand?

Monica: 5:31

Right, exactly. And that's that's the hard part, is that and one of the reasons we're doing this is partly because, in on an educational sense, there are a couple of streams of understanding within the pain world. One of them being very popular, but not particularly science-based, and one of them being not very popular, much more complex, but more grounded in science. And the people don't even understand that they're not using or they're contradicting the consensus definition definition of pain when they start saying things like pain is a biopsychosocial phenomenon, or pain is the result of biopsychosocial or biological, psychological, and social factors. Because now you've taken a definition, uh, you basically actually taken a definition out of it, or that understanding out of it. And now it's now you're talking about something else completely. And we're trying to have these conversations related to a definition that we can all perhaps understand, but that definition's been bypassed. In a lot of ways that people talk about it, or in a lot of the ways that it's used in research, you know, in definitely in a lot of ways it's used in clinic.

Eric: 6:53

Tell me a bit more about your thoughts about the I mean we've I know we've mentioned this in previous episodes about the biopsychosocial. So pain is a biopsychosocial phenomenon. Because I know that is a that's a common idea, narrative out there, and I know I have been I've perpetuated that in the past. I don't think as a buy, yeah. I don't think I do, I'll admit, I don't think I do it as much anymore. I don't think I do it anymore. I try not to. But tell me uh about the problem with that, just so listeners can have a better understanding of what you mean.

Monica: 7:24

We talked about that a little bit last time when we talked about the the whole biopsychosocial for pain phenomenon being heuristic in terms of it becomes this very shortened learning thing where people say pain is a biosychosocial phenomenon, and then suddenly anything that comes from the biological, the psychological, the social realm is fair gain, and it becomes very causal then for pain, which when we take it to a logical conclusion, when it's used in that heuristic way, is basically uh it's your fault if you have pain. Right? It's something about your biology, something about your psychology, or something about your social status that contributes to the cause of your pain. And so if we take it to that kind of, and I know people are gonna think that's extreme, but that's where it goes on a clinical level. That's where people take it on this clinical level. Because now they're looking into something someone has said within an intake about stress in their life or something else, and then that becomes the treatment target for their pain. Or some other thing become and we've already done this, we've already done this on a biological level in a million different ways. It's posture, it's a rotated vertebrae, it's they sprained their ankles seven years ago. That's why they have like shoulder pain now, it's whatever it might be. There's we have all of the biomechanical reasons, we've already looked at all of that. We already have all of those pain is because of this type thing, and now we're just hooking on psychological or social, we're maintaining the same narrative with structure, we're just changing the category. I like that, and all of that's just a category error.

Eric: 9:29

Yeah, I like how you just how you described that that it's the same narrative structure, but we're using a different category or a different causal to explain it.

Speaker 2: 9:36

Yeah.

Eric: 9:37

Now, would it be more right or less wrong? I think we've talked about this before. Depends on how you want to classify it. To say that those psychosocial factors could contribute to an overall experience of how the person is living with their pain. Could it amplify, could it turn the volume up or turn the volume down on their pain? Or are those things completely irrelevant? What's your what's the no?

Monica: 10:02

Those things have been around for a long time. We have yellow flags. Yellow flags are barriers, psychosocial barriers to recovery. So that makes it that's not a cause of your pain. That's a barrier to recovering from what is going on, which makes much more sense. You already have pain. Now we can look at what are the social determinants or the specifically the yellow flags, which might be psychosocial barriers to recovering. And maybe then that is you can't afford treatment, or you're in a category of persons who is usually discriminated against with regard to pain, or there can be a whole bunch of different factors that might come into play. Stress could absolutely be one of them. If someone has a high stress job, that becomes what we can see in some of the note-taking blue flags. So there's a work-related barrier to recovery. But to think of them as this biopsychosocial for pain, it's we've taken away the barrier now. We've changed it into something else. Barriers have been there for a long time, right? These understanding of psychosocial barriers has been there for a long time. So, no, they are not irrelevant in any way, shape, or form. The problem that I think we have with not understanding where our consensus semantics and meanings come from and how they are used at the moment and how they might change is really detrimental to the person who's has pain. Because now we're just gonna pick a target out of the air, and it's the target that we are most familiar with, and that the person deigns to actually share with us because they maybe trust us with something that they're telling us, but they're not gonna tell us everything, they're not telling us their life story, they're coming in with a particular perspective, and we're now cherry-picking that perspective to say that's a psychosocial contributor, whatever, however, we or influence, however we like to say it for pain, though what we're doing is targeting as a treatment, so we're treating it as a cause.

unknown: 12:25

Yeah.

Eric: 12:26

Thank you for clarifying that because that's how I understand it too. So that's confirming to hear what you're saying. But what we do see, particularly with some of the online arguments people have, is that, well, you're telling me the biopsychosocial is completely irrelevant. These other things are like it's this all or nothing kind of thing. And I I appreciate that you said that yes, these things are barriers, but they're not these causal rationale. And I that's for me, I feel that's a really important point for people to understand.

Monica: 12:58

And because we don't have enough knowledge, because we don't have enough knowledge on mechanisms, well, what has allowed us to jump into those spaces where we think we can target it, uh, target something about someone's thoughts and feelings or a state of being as causal for pain, even though we're we're trying not to think it's causal for pain, but that's what's happening. Because we don't have that knowledge, we're not understanding the foundational mechanisms that are occurring. So this particular course comes from the foundational assumption, which can be fairly robustly supported by science, by basic science, that no susception is necessary for pain, it may not be sufficient.

Eric: 13:54

I love that. So simple yet complex.

Monica: 13:57

So in any report of pain, and I'm not talking about emotional pain because then we start to get into a whole other subject that is a different realm. Pain gets used in a lot of different ways. But we're talking about manual therapists, we're talking about people who people come in and report bodily pain. And if someone reports bodily pain to you, the underlying foundational assumption of any therapist should be that no susception has occurred, sufficient for that person to be aware of the sensation. Whatever else is going on, that's part of the intake. But that's your foundational assumption. Whether you can see anything that you know we often associate with tissue damage or not, then it doesn't matter.

Eric: 14:54

I love that to the point there's no deception is present if someone comes in reporting bodily pain. I find that when I hammer that point home and I introduce that point, I really emphasize it over the course of courses that I teach. Easier in in-person courses because you have more exposure to somebody again and again. And it really helps, I feel, the clinician to think, okay, if this person's reporting bodily pain, they hurt, and they hurt in this area, shoulder, yeah, face, whatever it might be. My goal as a therapist should not be to put more, I can just put this air quotes, no seception into that area. Not to make it more noxious, not to make it hurt more, which goes back to the conversation we had last week about is it ever okay to purposely try to hurt someone?

Monica: 15:45

Yeah, how ethical responsibilities with relationships, which goes back to the knowledge gap.

Eric: 15:50

Yeah, exactly. And so I feel that then it's the you're it changes how you think as a therapist to say, what can we do to make this area have less or for to have less no sympathy. I don't know, that's probably not the right term, but like that to have less to hurt less, to have less of this kind of noxious stimuli, whatever that might be. Embracing that as a clinician and also trying to teach that as an educator, it really shifts how people think or should and how they're interacting and how they're behaving when they're treating that area with a hands-on nor movement-based intervention.

Monica: 16:25

And the other aspect to that was when I go through this course, especially this one we're talking about is deck three. So it's based on a lot of the definitions. So when we're going through this and then eventually get to making a pain assessment based on understanding a lot of these constructs and definitions, this is not something that we're doing so we can quote unquote educate a person who has pain. Because, especially if someone has chronic pain, like they're the one who should be educating you. But this is for our understanding of the mechanisms that might be occurring. And I say might because what we have are what John Laquinna calls hypothesis of mechanism rather than an understanding that, oh, you have no supplastic pain or you have neuropathic pain. It's like these are hypothesis of mechanism based on the report that the person provides to us and the symptoms that go along with that. That gives us an understanding of their of the mechanisms that may be occurring for nosoception that are related to the pain that they're reporting, which is really our understanding and allows us to clinically reason. It's not a tool with which we can now educate, and I hate that term when it comes to using it with patients because that that takes away the idea of conversation rather than just sharing knowledge. But it's not necessarily something we need to be telling that person in front of us, just that we understand that these things may be occurring and it gives us an understanding of why a treatment may or may not be a good idea, and B, what kinds of treatment may or may not be good ideas and or doable andor something we would be able to help with.

Eric: 18:22

Thank you for that. I think that's important for a very clear understanding about why this is important. So I appreciate that, Monica. Thank you. You were looking for some AI.

Monica: 19:16

Oh, yeah, I'm through. I don't have it here as actually. Um I was I did I went the took chat down there, and I've got to get back into my chat, but then that's gonna take me a little bit of time, and I'm not good with the multitasking. But it's I went to chat. Hold on, let me see if I can just go to their LLM.

Eric: 19:38

And Monica has found her AI information.

Monica: 19:43

Yeah, chat and also Gemini keep, and probably all of them will, if you're logged in, will keep your prior things that you've done. One of the things I tried to do was take AI down a bit of a narrative understanding of pain. So basically asking a bunch of suggestions. This one doesn't quite have the very beginning. I had asked some questions and it had asked me for characteristics. I was describing a mechanistic explanation for a particular phenomenon. They said, but they said, would you like a specific example from the field of biology, psychology, or another domain? And I said, I would. What is a neural mechanism in psychology related to pain? And then they said it was related to descending pain modulation system, which illustrates how the brain can regulate the perception of pain through a mechanistic exploration. And then they showed how it works. So they give you some. Neuroscience related to that. And so what I did was I said, before we go further, can you resolve this conflation you wrote? No susceptive pathways which carry pain signals from the body to the brain. That was the conflation. Do you know what the conflation was from talking about there?

Eric: 21:03

Above the no-susceptive pathways bringing pain signals.

Monica: 21:06

Yeah, it was the pain signals. Not everyone gets that. Unless they understand the definition of pain and how the definitions that they have had related to the biopsychosocial don't really carry.

Eric: 21:18

And there is just for people that saying there is no such thing as a pain signal.

Monica: 21:22

Exactly. So it's it's yeah, these are the some of the conflations that occur. And one of the reasons we need to go through these definitions so we understand what we're talking about. But the but chat is ever so gracious whenever you point out a problem and they're like, Great cat, you're absolutely right to question that phrasing. Let me clarify. No susceptible pathways does not equal pain itself. So they they go on and they say the statement is common but misleading simplification, right? Corrected version. No susceptible pathways carry signal about potentially harmful, noxious stimuli to the brain, not pain per se. And then they give me, and then they start talking about various other things. So then they'll give, they give a lot more explanation than is actually required. And as they do that, they start to mess up in terms of the conflation. Because chats only taking the information that's out there, and the information that is out there is incredibly conflated in terms of how the definition of pain is used and how all of the kind of terminology around it is used. So we start to get a lot of problems with how they do it. So, what did they do? I said, no susceptive pathways transmit information about tissue damaging or threatening stimuli to the brain where this input can be processed and interpreted as pain. Did I pick up on that one? I think I asked the question: how can a neural mechanism dampen pain perception through descending inhibition when perception requires the sensation of pain? Perception implies that no susceptive signals were sufficient to reach awareness of the person as a sensation of pain. And chat, ever so gracious. You're raising an excellent and foundational question in the physiology and neuroscience of pain. Here's how we can untangle it. And so we go on, and then it tries to untangle it, and in its untangling, it just conflates the whole time. Then I get to, I don't even read all of its things, but I get on the first conflation, and then I'm like, if a person experiences no sensation of pain because of descending modulation, how can they perceive it? Because they've gone on to say this happens in various ways. And then you're asking a subtle and crucial question that gets to the heart of what perceiving pain really means. And you just can just go on with chat. It was like they go, they keep going. And then my question is, what are pain signals? Because they've gone back to using terminology that conflates pain. And throughout it, like within the first start of their explanation, which is like three paragraphs long for the question, they just they use conflated language. So I go back to what are pain signals? Excellent question, because the phrase pain signals is widely used and often misleading. And then they go on and give me a whole tirade of explanation. And then I'm like, you're right, the brain interprets that information as pain, but only in certain contexts. If pain is a human experience, how can the brain interpret neural signals as pain? Why would the brain interpret these signals as pain only in some circumstances? Then chat recognizes you're asking a deep and absolutely critical question. The one that cuts across neuroscience, philosophy, uh, psychology, and philosophy of mind. Let's take it step by step. And as they go step by step, they use language that conflates all the time. They just go back and bat. And then I ask the question, what is the brain-body system? And that comes from their prior explanation. And it just goes on. So now we start to see that they're using binaries and they're using just the understanding that is out there. So when I say to my students, because we can use chat GTP and some of the stuff that we do because it helps to conflate information. But I'm like, if you're using chat, if you're using any large language learning, large language model to help you with pain information, you are in trouble. Yeah, you are going to get it wrong because large language models will not get it right. The information that exists is not correct, it's conflated. So what you will get is conflation. But anyway, it goes on. Like it's super long. Yeah. Every time. I'm like, are you saying that the brain can interpret neural signals as pain? It's just, it just goes on and on. And then I've got I finally got to the end of it where I said, I think I said to it, do you now understand defined sensation and perception? They talked about a unified brain-body system, which retains dualism. And of course, I'm absolutely right in that. What do you mean by the brain interprets? All of these kinds of things. And I think I finally got to an understanding. I kept saying wrong. Try again, go back to the definition of pain as it's like explaining things. And I think I got to the end where I said, Do you understand why you cannot use this information anymore? And it said yes. And then it went, and then I asked it the definition of pain, it went straight back again.

Eric: 27:00

Models need to be updated for sure. Yeah. Yeah.

Monica: 27:04

But it's not even it's not even an update. You can't update the large language model on pain because we don't have the updated information on pain. That is part of the problem.

Eric: 27:14

And this is a thing we could have a whole episode, I'm sure, just on on the use or misuse of AI, but we see that all the time, people using it and using it to confirm what they want to hear. Because that's what it does. Unless you tell it otherwise, it will tell you what you what it actually want what you want to hear. And you have to how the how you answer ask the questions is and how you respond to it makes you better.

Monica: 27:39

And for some of it, it's not bad. Like I've you I've looked at AI definitions for critical thinking, and it's reasonable, but I knew the definitions beforehand, so I could go and check. And I know this information for pain, so I can check it. But if you don't know it, you think what you're getting, but what you're getting is a conflated mess. Yeah. That probably fits with some of your worldview view, because your world view, if you've gone into any kind of biopsychosocial or what we understand as biomechanical causes for pain, and all of these things that we've mixed together that we're trying to then find explanations for, you're going to find that in your large language, in your AI.

Speaker 2: 28:19

Yeah.

Monica: 28:20

Because it comes from the same sources that you got from it to begin with, with a little bit of research maybe mixed in there on a neuroscience level. But even in neuroscience research, the conflation, there's at least one conflation in most papers, and it can be a meaning conflation. So if it becomes something about meaning, then it becomes a problem for the message of the paper. Sometimes it's just the language, the way the language is used. And it's and it's a paradox because we don't have we don't have a way of measuring what the right information is at this point, because we don't actually necessarily know 100% what the right information is. We can maybe what we can logic is the wrong information. We don't necessarily have can say this is 100% the right information, but we can logic that this is the wrong information. And that's what getting into these definitions means. It means using that to help you logic what the wrong information is.

Eric: 29:26

So we talked about the definition of pain. Let's talk about some of the mechanistic definitions. Why don't you start with those? Take your pick of which one you want to start with.

Monica: 29:33

Yeah, so we look at the main ones no, no susceptive neuron. So no susceptor and no suceptive neuron are different. Noxious stimuli, no secession, which is the action, and then sensitation, sensitization in various ways, because the conflation around sensitization is pretty significant as well. And those are the kinds of things that we're going to be looking at, again, coming from an IASP perspective, so that we can see what it means when we put those particular definitions in place. And also that what we're understanding is. So when we go back to this, it's the foundational part of this no script provided, because it comes from this view that no susception is necessary for pain. So then understanding what a no sceptor is, what a no suceptive neuron is, what a noception is, is actually really important because you can then understand why and in what circumstances the nosoceptor is activated. The other understanding of that is, and the other definitions that we get into are the clinical descriptors, which is nosoceptive, gnosis plastic, and neuropathic, which have pain after them, but they are not actually pains. They are clinical descriptor descriptors or hy hypothetical descriptors of mechanism.

Eric: 31:01

That is an important distinction is that those are often taught or described as a type of pain. Because that's receptive pain, neuropathic pain, gnosyplastic pain.

Speaker 2: 31:13

Yeah.

Eric: 31:14

That's would be a very long podcast to go into the differences amongst all those, so I know just we'll touch on those. The one thing though I thought would be an important thing to just touch on without going into too many details would be just a quick description or uh difference between nosciceptors, nosyceptive neuron, and nosyception. What's the and why are those three things different or how are they different and why is it important to understand the difference?

Monica: 31:43

Yeah, so one's a sensory receptor, which is more at the kind of end of things, it is the receptor part of it that transduces and encodes noxious stimuli.

Eric: 31:55

That's the noseceptor.

Monica: 31:57

Yeah, that's no, that's noceptor, yeah.

Eric: 31:59

Yeah.

Monica: 32:00

Then the neuron is the central or peripheral neuron that's capable of encoding noxious stimuli. And then you have nosoception, which is the process, the neural process of encoding and processing that stimuli. And so one's a receptor, one's a neuron, one's the process in relation to that. So then we just have an understand, have an understanding that there's component parts of the nosoceptor neuron. We understand what those component parts do and where they are, and then the process of that. So we also have the peripheral and central understanding as well.

Eric: 32:45

Brilliant.

Monica: 32:46

So that we know where they are and that they go from, they send messages from one to another, and that's part of the process. And the process itself is what you may have heard termed, so rather than looking at it just on a single gnosoceptor level, because when we look at the different gnosisceptors, the sensory receptors and the neurons that are out there, we're looking at when receptors encounter noxious stimuli that are specific to types of gnosoceptors. So they may be mechanical or chemical or what's the other one? Thermal. Mechanical chemical thermal. You can have changes from mechanical nosoception to something that now picks up chemical as well as mechanical. So depending on the stimuli, you can then have also alterations in this the capacity of the sense of the receptor as itself. And that makes it much more complex for understanding what's happening on a nosoceptive level. So when then we're talking about nosoception, we're talking about an apparatus. We're talking about the understanding is that there's a specialized sensory apparatus that is related to pain, as there is for sight, as there is for hearing and taste and touch. We have specialized sensory neurons that are related to the sensation of pain. And this is not something that is out of the glue. This comes from the gate control theory.

Eric: 34:27

From the 60s.

Monica: 34:29

Yeah. So this was a something that was established back then as a an understanding of this apparatus.

Eric: 34:38

The nociceptive apparatus. This is where I I feel that some of the confusion and when comparing that to other sensory components, like sight or hearing, or taste, any other sensory system has a very distinct apparatus associated with it.

Monica: 34:59

Has specialized sensory knowledge.

Eric: 35:01

Yeah, specialized sensory. And whereas it's not that's not commonly how it's understood or taught when it comes to pain, is there being this specialized sensory apparatus specific to pain. But there is, and that's the no-seceptive apparatus.

unknown: 35:17

Yeah.

Monica: 35:18

And that goes back to that foundational understanding of the sort of primary mechanistic understanding is uh no seception being this necessary component to pain.

Eric: 35:32

I guess the one thing that would make the no-suceptive apparatus or not the one thing, but the thing, the fundamental thing is that it's everywhere.

Monica: 35:40

Yeah, so we have receptors. Yeah, we have receptors and neurons.

Eric: 35:45

Oh, but I'm saying so compared to say sight or sound or taste, that those specialized sensory neurons are located in a defined area.

Monica: 35:54

Right.

Eric: 35:55

Where it's no scept the nociceptive or uh no sceptive apparatus.

Monica: 35:59

Yeah, peripheral peripheral noseceptors, yeah.

Eric: 36:01

Are everywhere.

Monica: 36:02

Yeah.

Eric: 36:03

Yeah. You name it.

Monica: 36:04

They're in the primarily like largely skin around joints, but we also have them in other areas as well.

unknown: 36:11

Yeah.

Eric: 36:11

Yeah, they're in and around muscle tissue and around bone and around viscera, they're around all the things.

Speaker 2: 36:18

Yeah.

Eric: 36:18

So when we have an injury or a stimuli that's noxious, you feel that. And because those Oceptors are being stimulated, yeah. Yeah, okay. Yeah, that's how I understood the too. Yeah.

Monica: 36:32

So I try and figure out, and this might be wrong, and I know that I know that there is more information coming up soon about the actual definition of pain and also no susception. And that will be something along a more of a professional kind of commentary on and a logic commentary on why some of these definitions may need to change to have them make them make more sense to us in a uh research level and also an understanding of no susceptors and this no susceptible apparatus. So that is coming up, but just in terms of the the definition of pain right now, where it says resembling so an emotional experience associated with or resembling that associated with actual potential tissue damage, my understanding then of potential tissue damage is something that activates noserception sufficient to reach awareness. So someone will have a sensation of pain, but then may or may not be reached the level of tissue damage. Was my kind of understanding. It's it's or a way of figuring that out for myself. But I think that there are it makes sense with what I'm like trying to figure out with all of the different definitions and how to then approach that on a mechanistic level.

Eric: 37:56

And we talked about that before, I believe, about the last episode or the one before about you know sufficient when if someone is we we can't tell if it's actual or potential tissue damage. It's just there's noxious stimuli is sufficient enough for the person to have that in the case.

Monica: 38:15

Yeah, but the act of no susception that's necessary. That's necessary for a report of pain. You mentioned something but sufficient to get reach their awareness.

Eric: 38:30

Yes, to reach their awareness, that's key to reach the awareness. Because if you're not aware, then you can't experience pain.

Monica: 38:37

Yeah, it doesn't necessarily have to be reported, they it can be non-verbal as well. So there may be no suggestion occurring where people can't report, but it may be observed that you would assume that this would be painful to the person because of what you're observing.

Eric: 38:51

And I believe that's one of the six sub points of the definition, which we don't need to get into, but I think one of those is it doesn't have to be verbally reported. Yes. For the experience of pain to be real.

Monica: 39:05

Exactly.

Eric: 39:05

Yeah, yeah. I just wanted to say, because you said something a few minutes ago about sensitization. And I don't want to quote you what you said because I can't remember, but can you just tell us a little about sensitization and maybe how that term is misused or misunderstood in common discussion?

Monica: 39:25

Yeah, so the term sensitization is increased responsiveness of sensory neurons. And so it it's seen via particular symptoms that occur. And when when it gets used in particular ways as uh synonymous for particular conditions along with something like nosoplastic. It gets used as synonymous with nosoplastic as well, which is a mechanism that says that there is altered nosoception. That nosoceptive neuron is uh altered in its function. And sensitization specifically is an increase with relation to the neuron itself, an increase in responsiveness.

Eric: 40:14

Because it's central the term that you're you hear central sensitization.

Monica: 40:20

Yeah, and peripheral sensitization.

Eric: 40:22

Peripheral sensitization. And from what I understand, central sensitization obviously is something that we don't know. It's not a diagnosis, it's a clinical descriptor based on allodinia and hyperalgesia or secondary hyperalgesia, is that correct?

Monica: 40:42

Yeah, so it's it's an increased rate. Responsiveness responsiveness of no susceptible neurons in the central nervous system. And peripheral is the same, but in the peripheral nervous system.

Eric: 40:53

Yes.

Monica: 40:54

And then if we understand that we have these peripheral neurons and these central neurons, and they uh have different things that they do, one of them has receptors that trick transduce and encode, and another is more encoding, and messages change from from in format from peripheral to central. So then we start to get changes in the messages. But what we're talking about is really there's this increase in responsiveness of any of the messages.

Speaker 2: 41:22

Yeah.

Monica: 41:22

And then we see that if we're going to infer some sort of sensitization, then we're looking for things like allodinia and hyperalgesia and other forms of sensitivity.

unknown: 41:34

Right.

Eric: 41:34

Yeah, so sensitization, whether it's peripheral or central, could still have would clinically that would present as alludinia and hyperalgesia. Is that correct?

Monica: 41:44

Yeah, but other things do too. You can have a mechanism that increases uh peripheral sensitivity, which means that the peripheral noserceptor will have been altered in some form, but it doesn't necessarily relate to a chronic illness in terms of something like breaking a bone or an ankle sprain or something along those lines. You might have sensitivity above and below the tissue damage as it's healing. So it's gonna hurt more, you will display hyperalgesia. You may in that area, you may have allodinia theory, right? Where it hurts to touch, but it's not a dysfunction necessarily on a chronic in a chronic sense. It's uh it's more of a altered function for a particular injury or during that healing. It makes sense for that injury, it's gonna go away. The function will change. But it tells you there's a mechanism there, right? There's a mechanism that's occurring, and and you can tell because this is the display that you have, right? Or the symptoms that you're reporting.

Speaker 2: 43:03

Yeah.

Monica: 43:04

But we wouldn't say if someone has a recent sprained ankle, but they can you but you press above that area and they say it really hurts, so it's really light pressure, but they're saying that really hurts more than you think it should. You wouldn't then infer central sensitization from that.

Eric: 43:25

It's a normal process. That's the thing that is I want people to listen, the listeners to understand, and people take the course, is that these sensitizations these aren't always pathological.

Monica: 43:36

Well, exactly. Distinguishing that is one thing, and to make sure that people aren't necessarily saying, oh, this is going to go on to chronicity or whatever it might be because you have these particular symptoms and these particular mechanisms. And so the mechanisms get this is where the conflation comes in because the mechanisms start to get blended into one another.

unknown: 43:58

Yeah.

Monica: 43:59

And then we start to think, oh, because this is happening. But if someone has chronic pain and they have they have allidemia and hyperalgesia and other kinds of sensitivities that are that don't really make sense, they may be there on any given day or not. Things change. They might have difficulty wearing certain types of clothing, or then other days it's fine, or it can be a bunch of different things like that. Then you might start to infer that there is a centrally sensitized apparatus. Because now they have allodina and hyperalgesia, and not all of it makes sense for any kind of other mechanism of injury that you might consider.

Eric: 44:45

Thank you for making that distinction. Last question for today, last topic for today. So in five minutes or less, can we do it? Gnosyplastic. This is I know a new mechanistic pain descriptor. Just share some thoughts about that, please.

Monica: 45:03

This is where we're talking about a descriptor. It's technically an error in language use to say no supplastic pain. Because no soplastic is a clinical descriptor, and that's what John was saying is a hypothesis of somatic mechanism or a hypothesis of mechanism. So terminology-wise, it should be no susceptive hypothesis of mechanism, no supplastic hypothesis of mechanism or no susceptible hypothesis of mechanism. So what's that what that's telling us is that based on what this person is presenting, they only have pain with movement. They have it specifically within a journey. It's related to a mechanism of injury. They would probably, their mechanism is the most susceptive. The hypothesis is it's a no-susceptive mechanism, perhaps no susceptible inflammatory if there's a subacute stage with that as well. But it's pain that arises from activation of no sceptors. When you see something that might lead you to think that nosoception is altered, such as the hyperalgesia or allodinia, then you're going to say nosoplastic hypothesis of mechanism, which is pain arising from nosoceptors that are altered in some way. There has been an alteration of how that gnosoceptor is functioning.

Eric: 46:30

That's the best definition I've heard or best description I've heard of anybody differentiating that or describing that so that people can pause.

Monica: 46:38

The current definition there's a couple of things in current definitions that aren't quite delineated properly in some of the definitions, just on a language level. But the current definition is pain that arises from altered nosoception, despite no clear evidence of actual or threatened tissue damage causing activation of peripheral gnosisceptors or evidence or disease. So it says here despite no clear evidence of actual or threatened tissue damage, that is causing activation of peripheral noseceptors or evidence of disease or lesion of the somatosensory system causing pain. Think that could be more easily written. It's pain that arises from altered nosoception. So the noseception is altered in some way, you're getting evidence of that from the hyperalgesia or the allodenia. There may not be clear evidence of any kind of tissue damage, which would give you an explanation for why that is altered. And there may not be any evidence of neuropathic symptoms which would tell you that there's a disease or a lesion of the nervous system. But you will still have something that tells you that most ofception is altered. It's not synonymous with central sensitization, it's not synonymous with a disease label, an illness label like fibromyalgia. It is just a mechanism possibility. It allows you to go on from that place.

Eric: 48:23

Is there a hypothesis of what causes gnosy plastic? Why would the gnosy scepters be altered? Why would they be firing at a lower threshold?

Monica: 48:38

Maybe. Or it's uh when we say hypothesis of mechanism, it's a testable hypothesis. Okay. Which again, I'm not a neuroscientist. I'm trying very hard to keep up with a lot of the kind of neuroscience research that's coming out with related to nosoception and nosoceptors, but that's not my expertise. What I am able to tell you is that on a clinical level, I see this is my hypothetical understanding of the mechanism that is occurring, which allows me to then understand a little bit more with regard to their symptom picture. It's not for me to educate my patient, it's for me to understand when we get back to that foundational level of no susception is necessary, a necessary component of her pain, that we have no susception occurring and that it may be altered in some way.

Eric: 49:34

I love that. I think in the course, when you do the course and we you present this in more detail, and there's the interaction with students who will be zooming in with us. Hopefully that'll start that'll start to make a little more sense.

Monica: 49:47

Yeah. Yeah. Yeah.

Eric: 49:51

I think we'll probably about an hour, so we'll just leave it at that because I think if we start on.

Monica: 49:57

We could go. Because we could go on forever.

Eric: 50:00

Next episode with one, we will probably cover a few things that maybe we didn't get to today and talk about the next deck of material, the next group of material.

Monica: 50:11

Yeah, yeah. Because once we get to that making a pain assessment can might be, I can't remember if that's the next one or not, or inflammation might be. I think I do a thing on inflammation, which is really interesting. But but yeah, when we get to making a pain mechanism, these things making a pain assessment, these things come in really handy to understand that. And then that helps us with a little bit more to go into the critical reasoning of why or why not that we may think of a treatment.

Eric: 50:40

Yeah, it's a good way to end it. Because the question always comes, what do I do with this? Why? How why is this important? Why is this relevant? Those are listening made this far.

Monica: 50:50

Yeah, why this is important is that we don't jump to conclusions about something else that might be going on that neglects to bring this foundational component in.

Eric: 51:05

Yes. Yes. I love it. That's it.

Monica: 51:08

I'm done then.

Eric: 51:09

Yes. Thanks, Monica, until next time.

Monica: 51:12

You're welcome.

Eric: 51:13

Thanks. Thank you for listening. To listen to more of these episodes, please subscribe on your favorite podcast network. If you enjoyed this episode, please share to your favorite social media platforms. To connect with me, I can be reached to my website, the CEBE.com, or send me a DM through Instagram at Eric underscore pervis underscore C E B E, or you can find me on Facebook at Eric Pervis RMT. If you would like to support my podcast, please consider making a small donation. This can be done by clicking on the support button or heading over to buymeacoffee.comslash hello O B.