Pain Education, No Script Provided Ep 5. Rethinking Inflammation

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Chapters

• 0:00 Welcome And Series Context
• 3:20 How “Inflammation” Became A Catchall
• 6:20 Acute vs Chronic: Misapplied Models
• 9:35 Ethics Of Provoking Inflammation
• 13:08 PRP, Prolotherapy, And Gray Areas
• 18:43 Redefining Inflammation As Innate Immunity
• 22:53 Low-Grade Inflammation And Metabolic Stress
• 28:03 Clinical Puzzles: Migrating, Fluctuating Pain
• 32:13 Nociception, Thresholds, And Sensitization
• 36:33 When Therapy Can’t Help: Autoimmune Flares
• 41:13 Honesty, Consent, And Scope
• 44:38 Neuroinflammation And Central Sensitization
• 50:03 Amplification, Allodynia, And Mechanisms
• 54:53 Where Neurogenic Fits In

Transcript

Eric: 0:13

Hello and welcome to the Massage Science Podcast. My name is Eric Purvis. I'm a course creator, educator, researcher, RMT, and advocate for evidence-based care. Today is episode five of my seven-episode series with Monica Noi. In this episode, we focus our discussion on inflammation, and Monica proposes that we adopt a new understanding of inflammation that encompasses more than the classic signs of redness, swelling, and heat. Thank you for being here, and I hope you enjoy this episode. We'll try and stay on topic, but we know that's probably not going to happen. Tangents are probably going to happen. They are encouraged and expected. So today we're going to talk, we're going to try to talk a little bit, or a lot of depending on how it goes, on the topic of inflammation. Monica, wonderful. Thank you again for being here.

Monica: 1:19

Thank you very much for having me again. Yes, we started off. Eric and I started off before this, basically trying to solve all of the problems of musculoskeletal health education. So we're running a little behind time.

Eric: 1:35

I've often thought that the unrecorded conversations that I have with you or with other guests, those should probably be in like a bloopers episode or a bloopers reading or something. Because there's so much, or even a highlight, maybe it's not bloopers, but even a highlight one. Because I think some of the conversations that don't get recorded are actually really profound.

Monica: 1:56

Yeah. Yeah. And we're talking about things where just, yeah, this is big stuff. Yeah. We can also talk about inflammation, which is also big stuff.

Eric: 2:04

Yes.

Monica: 2:06

In in terms of pain. I think one of the reasons for getting into this was that I was looking through some of the papers that I had been provided to look through just with regard to things like neuroinflammation, because you'd asked that question about talking about neuroinflammation. And I realized I wasn't actually that knowledgeable about it. I'm still not. I often have to look back on the inflammation inflammation, on the inflammation again and again just to keep up to date with it. But that word inflammation got to the point of just being used to the point of meaninglessness for everything. And without a really good understanding of what we actually meant by inflammation. And so everyone who had like a disease or whatever, it's inflammatory. And then there's all these clean diets and all this sort of stuff, anti-inflammatory diets as though the whole body is some sort of inflamed mess, all of these kinds of things. So again, it was one of those things that got to you got to blame for a lot of different things without really having a good understanding of what that meant.

Eric: 3:24

It's trended. It became this trendy explanation for everything. Yeah. If you hurt, if you were sick, it was inflammation, inflammation, without really identifying what that meant.

Monica: 3:39

And it and technically maybe not wrong in terms of that inflammation's involved. In terms of what that means for what we can do or what it means for the person and for our learning about inflammation. So one of the things that I think when I read this one paper that I've broken down with the deck was like the definition of pain. Like we had an understanding of inflammation based on tissue damage and injury for the most part. So when you come out of school, that's your understanding of inflammation. And then when there are things like chronic diseases or chronic pain, where inflammation is used as part of the disease process or part of the healing process or part of the irritation process, whatever it might be, the thought process is that the inflammation is what we learned of it in a tissue damage situation where there's swelling, there's heat, there's bringing of blood to that area, there's certain healing molecules, immune responses that come with it, but it's very specific, perhaps in its function. And that's how we understand it. And then that got translated, I think, to that whole body inflammation. A person has fibromyalgia or a person has some other either illness label or autoimmune inflammatory autoimmune condition. And there's this kind of whole as bolus translation of what inflammation means in that context. And it isn't the same, right? It isn't the same kind of a thing. I think that's why this particular paper appealed to me because it had a it had the nice history part of it, which allowed me to see, oh, here's how the knowledge of inflammation changed over time. Here's how we came to learn about it over time. And that gives us a better understanding for what it means for us, kind of thing.

Eric: 5:49

The historical definition or understanding of inflammation was applied to every region of the body. So if you said inflammation due to another health condition, another disease, the understanding was that it involved the immune responses with the heat and the increased circulation. But that's what you're saying is that's not the case. There is some similarities between the responses, but it's not that red hot swelling.

Monica: 6:22

Yeah. It's almost like we've put it an acute inflammation into a chronic state. So it's like we take what we understand by acute inflammation, and then we've transferred that to perhaps a chronic state. When someone's in a chronic state, that's the same sort of inflammatory process that is going on. Because we understand it, because that's how we learned about it. That's our understanding of it. And we see sometimes it becomes harder to see, which I'm using myself as a as I guess an indicator here, because this is not going to be the same for everybody, but for myself, that was a heuristic. It was an easy way of thinking about inflammation and understanding inflammation. And then you didn't understand the nuances in relation to other conditions that might also be characterized by inflammation. Now you're just like, oh, this is bad kind of thing. It's it's this person's subject to this particular process that occurs. And that's related to a healing process. In terms of what we see with chronic conditions or inflammatory autoimmune conditions, inflammation has nothing to do with healing.

Eric: 7:40

I was gonna say that, but that point is so important because there's a lot of therapies out there that try to sell their mechanism of effect by creating an acute and inflammatory response to heal or to fix or to repair.

Monica: 8:00

Yeah.

Eric: 8:01

What do you think about the thing?

Monica: 8:02

Which mechanistic mechanistically might make sense depending on what the condition is. Because that is the process we understand is that when you have that acute state, the function of one of the functions related to inflammation is a healing aspect. And so I can understand that or see that from a mechanistic perspective. But I think that aspect of things, especially when we start to relate it to a chronic condition, becomes really challenging because we see it as a part of a healing state. We see it as a part of a healing process. And in the chronic state, it's not. We see it as bad, but we don't really necessarily know why. And the other part of part of that is when we look into the paper, is the neuroinflammation as well. So we can have very discrete nerve-related inflammation. So we're not going to see swelling, we're not going to see heat, we're not going to see those cardinal signs. We're not going to necessarily see an influx of molecules related to healing, although we will be seeing immune responses and immune interactions, not even just responses, it's really interactions with niceception. So yeah, so it becomes a very kind of a different process.

Eric: 9:34

One thing I just wanted to rewind back for a second, just because I'm just curious about so things. So I'm thinking about, and we'll talk about the neuroinflammation and stuff because that's to me as fascinating information and how that role with the no seep no susceptible apparatuses. I we'll get to that, but I one just clarification here is you said from a mechanistic perspective, creating an inflammatory response in an injury can help. What are your thoughts about those like things like say prolo or PRP friction or PRP or whether the goal is to try to increase inflammation to speed healing or to repair tissues? I know the evidence for those things is all not good, but from a mechanistic perspective, you said that inflammation, yes, but in though it can can be useful. But in those applications for, say, these chronic musculoskeletal concerns, does it make sense to provide an inflammatory treatment to try to help that?

Monica: 11:19

On a chronic basis, probably not, but it would depend on the issue for the PRP, the use of the PRP. Some of the papers I've read are not necessarily terrible. It's like anything else in terms of some form of outcome that we see, that you'll see that there are some positive responses, and that you'll see that there are neutral and/or negative responses. And there's nothing that, like, if we were to have a vaccine or an antibiotic study where you would just be like, that's it now becomes unethical not to provide the treatment. We don't see those sort of studies, but there are certainly some at least mechanistic type justifications that may be used depending on the condition. So I'm not necessarily going to rule that out, but I think that in in every case, things have to be taken into consideration as to why something like this would be used, under what circumstances, and what the kind of goal of that is. And usually things like that are very specific. They're not doing whole body therapy. This is something that's really specific to a joint. There's usually some diagnosis along with that joint as well.

Eric: 12:37

Yeah, I was just curious because I was just thinking about putting this pieces from some of our previous conversations. Because I know a lot of those types of treatments for let's say like tendons, ligaments, joints that involve scraping techniques, things like that, it can be quite irritating.

Monica: 12:52

Yeah.

Eric: 12:53

The goal is to increase inflammation. I was just thinking about how that relates to previous discussions we had where the ethical question was, is it ever okay to try to hurt somebody? That's why I think it creates this gray area. So that's why I was asking what your thoughts were, because it puts me in this state of, I don't know. Which is a good place to be.

Monica: 13:15

I think we I think to some degree we can categorize that particular thought process around the ethical part of things to be non-invasive versus non-invasive versus invasive, where we might have a different set of standards or processes for consent that we're going through in what is happening with that person and in relation to the treatments that are being provided. Because surgery is something in which there is absolute harm caused to a person because someone is cutting their skin andor their joint andor drilling out the bone to stick a piece of metal in. But the sort of end goal is better function, less pain, whatever the case may be. So there's this is so not doing anything in that case would be quite possibly doing more harm. So it doesn't really, that that ethical question perhaps doesn't apply in the same sense as it would in a manual therapy situation where you're putting physical pressure on a person with the belief that putting physical pressure on a person to the point where it causes them pain, so it activates no susception, would be the thing that is going to solve their problem or change their pain or whatever the case may be. It's a somewhat difficult, different ethical question, but certainly I need to think a little bit more about that as well. That's not something that I would say is going to be settled in my mind at this point.

Eric: 14:56

It just kind of came to my mind as you were talking about inflammation. I wanted to just throw that out there. No, that's good.

Monica: 15:01

Especially when we have treatments like that that are a bit like, are they good? Maybe in this situation, but could they cause more harm? Possibly in this situation. So we have this again, we have this spectrum with which the treatments are not, we can't, we couldn't guarantee there's certainly probably subsets of people for whom it would be more helpful than for other people.

unknown: 15:24

Yeah.

Eric: 15:25

To be determined.

Monica: 15:27

Yes. Yeah, yeah. Things to be looked into.

Eric: 15:30

Yeah.

Monica: 15:32

Yeah.

Eric: 15:33

Okay. So we were talking before I took us on the side tangent there. So we promised at the beginning there probably would be some tangents. Thanks for following along for all the listeners. You said that in this section of the course, you talk about a redefinition of inflammation.

Monica: 15:52

Yeah, so this person, this paper was asking the question, is it time to redefine inflammation? And I think that's because our definition of inflammation, like one of the things that they said, and I'd have to get a look at what their problem was, is that it's basically based on it was based on function, I believe. Their proposed definition based on the history that they showed and the sort of mechanistic understandings that we have related to inflammation in various different states, was that they were proposing that inflammation is the innate immune response. We know it is part of the immune response to harmful stimuli such as pathogens, injury, and metabolic stress. So it includes tissue injury, obviously, we understand that occurs. But also when they talk about metabolic stress, they're talking about cellular insults. So cellular insults can be things where we look at chronic day-to-day issues like a lot of smoking, not sleeping well, bad diet, not exercising enough, high levels of stress, all of those combined things are metabolic stress. There's metabolic insult on a kind of ongoing day-to-day, plus also pathogens, illnesses that diagnosed illnesses or germs that might be causing illness. And that inflammation is the innate immune response. Where inflammation is the innate immune response to harmful stimuli such as pathogens, injury, and metabolic stress, and innate being that first line defense. So there's innate and adaptive, this is the first line defense. I'm saying that inflammation is an inherent part of the immune response, as well as but it takes different forms depending on the response of that particular issue, of the particular issue. The author, and I should I'll I can give you the link to that paper as well, but the author made a comparison chart, which sort of outlined some of the differences in the inflammatory kind of responses, which was really helpful. I thought it was a great, really great, helpful chart. So the chart had infection, tissue injury, low-grade inflammation, because they talk about low-grade inflammation, and then autoinflammatory diseases, which would include autoline type inflammatory diseases. So something that's using the something related to the immune system and in relation to the inflammation. There was cause mediators, signs, the C-reactive protein response, the purpose for it. We're the ones who define the kind of purpose and whatever the mechanism for triggering it was. So most of these, most of these purposes were two of the purposes, so infection and tissue injury, which we can understand infection as an invasion and tissue injury, obviously something's happened. But we're talking about defense and also healing and repair. Low grade inflammation was talked about as a restoration of homeostasis. And that was in this low-grade inflammation where the C reactive protein testing would be very low. But low grade inflammation isn't necessarily quote unquote normal. It's usually something that's seen in chronic conditions, chronic, perhaps chronic metabolic issues and things that have an illness label to them that have a where inflammation is blamed, which makes sense, right? There's a metabolic malfunction. This is that kind of cellular insult, right? That metabolic cellular insult. And they all are, they all contain, so the mediators of it are all the molecules and cells of immune responses, of the innate immune responses. So we get all of those different kinds of cellular components that are there, which are described in the paper as well. So it's all the same, it's all the same kind of responses that occur as that first line response. But where other issues might have classic signs of inflammation, where some Something like an RA flare will have heat and will have swelling. So the joints will flare up, et cetera. So you'll start to see those kinds of same metabolic responses that you might have with also tissue injury, where you're also going to see swelling, you might see heat, there's tenderness, there's various other things that go on. In low grade inflammation, where you have this metabolic malfunction, the there you don't see the classic signs of inflammation. And so this gives an explanation, basically, for why if someone has a label of fibromyalgia where low-grade inflammation is considered one of the characteristics where C-reactive protein tests aren't going to show up, where people will be saying oh it's inflammation, because there might be other kinds of signs that there might be inflammation that like stiffness and various other things might occur. But we don't, it gives us a little bit of a different understanding then because we're not looking for those cardinal signs. We're not going to see the cardinal signs of inflammation.

Eric: 21:48

But they know it's present, it's just gonna, it's not gonna lose the how you would expect inflammation.

Monica: 21:55

And yeah, some of those it's this wrist to restoration of homeostasis. So there's always this metabolic insult, and every time we have insults like that, we have this homeostatic process that goes on trying to get us back to whatever it's not trying to get us back, it's a constant process. But we're talking about with a metabolic malfunction where there's consistent metabolic stresses, there's consistent cellular insults over a variety of different ways.

Eric: 22:25

I find this stuff really fascinating because a couple years ago I started looking more into condition-specific and joint-specific research. And some of the stuff that I kept coming up was they used the term metabolic insults or metabolic stress stressors, and seemed that a lot of the unexplained or unknown conditions, things like frozen shoulder and non-specific low back pain, whatever that means. These ones they seem to think had these metabolic stressors that I guess we you take a step back and you look at this inflammatory homeostatic process, I guess how where it's how it's manifesting in somebody could present as these pain presentations that we don't really have a specific simple diagnostic criteria because it doesn't fit the normal acute injury inflammation.

Monica: 23:21

Yeah. Is that and this makes sense too?

Eric: 23:25

Paige with understanding that?

Monica: 23:26

Yeah, because it makes sense when we get to the making a pain assessment, because one of the aspects of making a pain assessment is also looking at whether or not there are these signs of this kind of continued, these continued stresses if someone has this particular issue along with it, which would there's low energy, there's fatigue, there's sleep issues, there's digestive issues, there's a whole bunch of different things that fit into this category that would then give us an idea. There's also this inflammatory response that's consistent, that's low enough to not hit the triggers for testing, but is significant enough to not necessarily be normal to be to be a sign of metabolic malfunction. And that gives us a better understanding of what the case may be because when we look at things like an auto-inflammatory disease, where someone has an inflammatory flare-up within that disease, you have one of the cardinal aspects of that will be pain. People will have the painful joints where it flares up. They'll have a where you have might have this inflammatory response, you're going to continue to have the pain. And that makes sense as something that would activate a chemical nose, chemical nose exception sufficiently, right? To result in pain. And then this, what we might find with something where you have low-grade inflammation, there might be I don't know enough about what it means to have a low CRP response of whether or not the likelihood is that there's peaks and valleys within that response. It would unlikely be a steady state, which would make again sense for why someone might have pain in areas that one day where they may not feel it the next day, where things move, where they shift, where it isn't always the same sort of thing, where someone might have trouble walking because they have knee pain one day and then the next day they don't have pain in that area and they have it somewhere else, or various other states of things that might be going on. It makes it very challenging because what we're trained to do is look at any body part that the person says, I have pain here, and then we'll find a dysfunction for that to say, oh, that's the reason that you're having pain. And we might do that by saying you have a postural issue or some other thing that we can blame them for, where it's like they're not been sitting for too long, or maybe it's your shoes, or I don't know, it could be a bunch of different things where we're actually talking about not just an immune response that relates to low-level inflammation, but also that has a bidirectional communication with no susception.

Eric: 26:34

To understand this stuff, and I don't think you need to understand it fully, but it helps, I guess. But just the kind of calls notes version of this, and from what I understand, and you're helping by listening and having these conversations, so thank you again. This helps to explain a lot of the weird I'm gonna put that in air quotes, weird pain presentations that we would see clinically where yes, somebody has pain one day, not the next. Or it's they or they were like, Oh, my pain's moving around my body. Like that can be very uh scary for patients. I can make them feel like things are really bad or really confused, they're afraid to do things because last time I did that thing, my knee hurt, and then so I don't want to do that thing anymore, but then now I do this thing, my back hurts. We all know those clinicians, you understand what we're talking about.

Monica: 27:23

Very yeah, yeah.

Eric: 27:25

But I guess that this knowledge helps to make sense of why that might be occurring in some people.

Monica: 27:32

Yeah, yeah. It just gives us an understanding, it's another mechanistic understanding of why a no secession sufficient for a sensation of pain would be activated in different ways. So if someone's living with this metabolic stress, these metabolic stresses, they have an illness label, they might have other comorbidities along with it, but they have basically a low-grade inflammation that is a sign of that metabolic malfunction. There's this consistency that's going on. They're still living their lives like everyone else does. They can still have some other issue that happens, land too hard on a pavement or whatever else might be. So there's then there's other forms of activation of noseception related to the joints or related to muscles or whatever it might be. But there might just be, in that case, it takes less to reach a threshold for sufficient noseception. So there's no necessary, there's no dysfunction there necessarily.

Eric: 28:38

And that was my question too. Was how does this impact nociception? Was it due to the nociceptive system or to the nociceptors?

Monica: 28:52

Yeah, so this is basically so we one of the reasons for looking at this related to inflammation is partly in relation to not just the so if we're talking about, and this is it's not like this this redefined inflammation is the new definition, but this gives us an understanding of we have differences with relation to perhaps not just what we might consider the purpose of inflammation at the time, but also that it's part of an immune response. And we know that there are bidirectional communication responses with the noseceptive apparatus and immune responses. There are receptors on the nociceptive neurons for immune molecules. So nosoceptors can both provide communication toward the immune responses, but also will accept communication from immune cells or molecules. So we do have this communication between the two systems, which is in this situation with this paper, one system, right? We're not talking about something that's separated. We're talking about inflammation as part of the innate immune response.

Eric: 30:18

Okay, gotcha. Yeah. It sensitizes or lowers low, like I think you said before, lower lowers the threshold for so possibly in a low-grade inflammation setting for sure.

Monica: 30:31

And that's not even that's not neuroinflammation, which we still haven't talked about.

unknown: 30:35

Yeah.

Monica: 30:35

But yeah, we can do that in a second. One of the other things I wanted to say was one of the things this chart had, which I found also really helpful, and also is backed up by some of the information with relation to nose deception as well, is that the purpose for different kinds of inflammation, so relating to infection, tissue injury was healing repair, and then related to low-grade inflammation was restoration of homeostasis and auto inflammatory diseases. There's no reason, right? There's no apparent purpose. We're not talking about healing. We're talking about a genetically based dysfunction. We're not talking about something where we're going to have this defense, we're going to have this healing. We're not even going to have restoration of homeostasis. There's no purpose in an auto-inflammatory condition or an autoimmune condition with an inflammatory as a primary aspect. There's no reason for the inflammation. So that helps us also start to make sense of when we're making an assessment and we're trying to clinically reason how we can be of use in this situation. It's in those situations we can't, we really can't. If someone's going through an autoimmune flare-up, medication's the thing that's gonna make the difference. We're not gonna make the difference for that person in that particular situation.

unknown: 32:08

Thank you.

Eric: 32:09

Does that make sense? Hopefully the people listening understand. I think I understand. I understand enough to know that I need to know more.

Monica: 32:17

I think it's because when the people come to us with pain, yeah. That's what they come to us with. And someone with an autoinflammatory condition may have flare-ups in their joints, pain in their joints, but we're talking about a dysregulation that's that has a particular trigger that then leads to pain that has that doesn't heal, it's not about healing, it's not about defense, it's not about homeostasis, it's it's it's completely dysfunctional in terms of that other situation. So we have to be careful as musculoskeletal therapists to to say that we can be helpful in any sense of the word in a situation like that. Because on an ethical level, again, if we know that's occurring, and that person perhaps isn't medicated or perhaps doesn't maybe we suspect an auto-inflammatory that hasn't been ruled out, for us to continue without that rule out would be ethically traumatic.

Eric: 33:22

What are your thoughts about and I agree with that, and I think that's a good point you made. What are your thoughts, though, about so say there's been that diagnosis? They know they've got some systemic inflammatory problem or fibromyalgia or whatever the whatever diagnosis they have. Our role, we know we can't fix it, we know we can't change it. The role I would assume for most of us then would just be symptom management.

Monica: 33:51

In a in a in a flare state for an auto inflammatory disease. But I don't know if it would get it.

Eric: 33:55

Well, yeah, I would say in a flare state, I would assume that if someone knows, they probably wouldn't be coming in for therapy if they were, but I don't know.

Monica: 34:01

Some sometimes people do because they're in pain, and it might be the case that part of the problem is that someone could be in a flare, go to a musculoskeletal therapist, and be feeling better the next day. But now there's this sort of fallacious thinking of one thing caused another.

unknown: 34:20

Yeah.

Monica: 34:21

And and now there's this understanding that, oh, we can help people, but in any given situation, there's a sort of a natural time course to that in terms of significance of what we could do. Might a person feel slightly better after a treatment, maybe, but if they're in an auto-inflammatory disease flare, it's just chaperous to think that we would be able to actually do anything for them at that time for that condition, for that reason. Yes. Yeah, no.

Eric: 34:49

I was just thinking from a clinical perspective. Sometimes people come in with stuff and they just want you to do something. And you and in which case, if I think if I'm gonna think out loud here, so I could totally be wrong.

Monica: 35:03

Yeah.

Eric: 35:03

And I'm okay with that. The if someone comes in, they're having an acute flair, and they just they want you to do something. Ethically, as long as we don't make any big promises and we just try to do something somewhere that makes them feel not worse, I guess that's the best we can do. And is there do you see a problem or I think we need to be honest. I think that's honesty, yeah.

Monica: 35:29

Yeah, but the honesty would be like I won't the likelihood is there'd be no change to the flare-up symptoms. And in fact, there's a possibility it could make things worse.

Eric: 35:41

Yeah.

Monica: 35:42

Yeah, you'd have to be honest in that situation. And I think part of the problem is if we don't understand that this is occurring and that we actually have no part to play in this, that people believe they have a part to play. And then they will pass that belief on to a person who's having that flare-up and and not are no longer a and not being honest with themselves because they lack the knowledge to be honest with themselves. So I think that's part of it. I think part of it is understanding, okay, if we understand a little bit more about what we mean by inflammation in any particular given situation, and then are able to understand where that inflammation relates to the no-susceptive apparatus, then we can start to understand when we make this pain assessment, we can clear clear reason then how useful or not useful we may be in that situation. And in which case we might say, look, if you're having a flair, stay home, do the things, get that over with, and then we'll see you after that for something else. Because otherwise, there's a possibility there's wasting money on something that is in no way, shape, or form plausible to make a difference for them.

Eric: 37:03

Yeah, yeah. No, that makes sense. Thank you. Let's talk about neuroinflammation to finish off this conversation.

Monica: 37:12

Scroll on down. Yeah, so there's so neuroinflammation is a little bit newer again to me. So I've been looking into it, but it's I think before I was looking into I think and that's another reason I was looking into inflammation, so I can understand like what's the difference between inflammation on this standard level and neuroinflammation, whatever that means, because it is it is certainly believed that there's it's implicated in chronic pain and chronic pain states. And it relates to at least from the papers I'm talking about. I'm just gonna go to the bottom paper because it relates to central sensitization as well of no susception. So whenever I say central sensitization, I'm gonna say of no susception, so that we understand that is the difference. We're not talking about peripheral sensitization, then we're talking about brain and spinal cord. And then also immune response. The immune responses related to it. You have spinal cord cells that might become. So this is from I'm just looking at this is from a paper that was posted related to fibromyalgia. And then so these cells become sensitized through the immune responses, which includes things like cytokines, which we know are pro-inflammatory cells, so various other pro-inflammatory cells, and then those nerves are more likely to create an impulse. That's where your threshold gets lower, and then you'll get these this generation of no susception in the central area, and then that results, it's sufficient enough to result in pain. And then you get you can get distortion, or that's where people say there's amplification of signals because there's changes in thresholds, there's changes in sensitivities in these cells. And that can come from nosoceptors, or it can come from other types of neurons as well. You can still get messaging or whatever from other types of neurons, and then there's distortion where there's uh central change in noseception.

Eric: 39:28

And you're saying that's occurs centrally, so spinal cord brain.

Monica: 39:33

But related to central sensitization, but you can have messaging, so neural messaging from touch nerves as well. That, and that's from the periphery, but that goes to the spinal cord, right? Goes to the spinal cord, and that's where the sensitivity is. There's changes in the spinal cord nociceptors and neurons, and that's where you'll get the signal changing, and that's where you might get the amplification, or you get the neuronal firing that's sufficient for pain or other kinds of issues, such as allidemia. Where you'll see it peripherally, you'll see it peripherally because you'll have this connection from touch receptor to the spinal cord, and so you'll see the symptoms peripherally.

Eric: 40:27

Yeah, because the signal that shouldn't be painful, let's use that word flippantly painful, is perceived or is experienced as being painful because even though it's a light touch or is amplified in the spinal cord and then

Monica: 40:44

There's changes of in the in the message. Yeah.

Eric: 40:50

Because yeah, when I teach my pain I do my my I know as much pain science stuff as I used to because I'm get bored of it. I don't know. I've done it so many times. You want to do other things, but I do touch on a little bit, and that's one thing I do mention. And but I try and make it as simple as possible. I say there can be these changes that occur in the spinal cord, acts as an amplifier. So signals come in, they get amplified and sometimes distorted, and the person may feel it peripherally, like you said.

Monica: 41:17

Yeah. But it's not that we can't have peripheral changes as well, but it's very, it's very local inflammation. So it's it's local to the nerve, to the ganglia, and there are certain kinds of changes or features that might go with it that might one of the things that we talk about with pain is related to tissue damage and this idea that we can't see the tissue damage, but it must be something else. It must be psychology or social situations, and then people start to find different reasons for why someone has pain when there's no observable damage. But neuroinflammation and other forms of inflammation over time can create tissue damage. Right. So there is definitely damage associated with it. There can be changes in the vasculature around it. There can be different ways in which barriers in terms of central, I think there's permeability that occurs in different places. There's infiltration of cells that shouldn't be there. There's different inflammatory medias that are also produced and activation of different cells centrally. You'll have the glial cells as well being activated. We start to see that actually there can be differences in damage occurring, but we don't see it. And there's another chart. This particular paper gives a chart which compares inflammation, neurogenic inflammation, and neuroinflammation. And the neurogenic inflammation is one thing I always keep forgetting about. That results in rapid plasma extravasation. I guess that's like a is it like vaso is opening? Because it's that an edema before the infiltration of immune cells. So it plays a role in inflammatory diseases such as asthma, psoriasis, and contributes to pain conditions such as migraines, CPRS, and after things like bone fractures. This one's comparing these. We haven't really talked about neurogenic inflammation. I don't quite fully haven't got that quite fully down yet. But when comparing inflammation and neuroinflammation in terms of location features and role in when someone has pain, the inflammation we usually see peripheral tissues, skin and muscle. There are, it is there in our internal organs, but usually we don't see that in the brain in the way that we're thinking about this kind of inflammation. Usually it's related to disrupting the blood vessels, there's the edema, there's immune infiltration. These are the cardinal signs of inflammation. And then we also know that there's um that healing response, that defense response, depending on what the issue is. So we have that. And then usually we'll have pain more with the acute phase and less. So there'll be less pain response or pain feeling as things start to heal and move from acute to less acute. But there's there can also be a transition then from acute to chronic. There will be a change in how that that pain is felt in a particular way. Even in a chronic pain situation, generally it's not described on the whole as an acute pain situation. The descriptions will be different. But not that there can't be flare-ups that just are described in similar ways. Neuroinflammation, PNS and CNS. So we have the nerves, the dorsal root, the trigeminal ganglia, and then the spinal cord and brain for the CNS. So that can disrupt the blood-brain barrier. There's an infiltration of immune cells, there's an activation of peripheral and central grial cells, production of inflammatory cytokines, transition from acute, and then the role in pain. Again, there's a transition from acute to chronic, and then maintenance with regard to people who have chronic pain. But neuroinflammation is nerves, like we're talking PNS, CNS, more specific and direct to the nerves, and very specific in relation to the directional communication with the immune system.

Eric: 46:11

That's a lie.

Monica: 46:13

Yeah. That's a lot. Yeah.

Eric: 46:15

It is.

Monica: 46:15

And part of it is just trying to figure out it is just trying to figure out okay, where do we put this information in our clinical reasoning when someone comes in with these particular symptoms? And in terms of, especially in terms of here we are, we work in musculoskeletal care for people, and we see a lot of people who have pain. Anyone from chronic pain who has they may have also associated musculoskeletal issues, and to people who have sprained an ankle and now maybe their ankles healing, but they've got back pain because they've been limping for a bit. There could be a bunch of different reasons that we see people. And for a long time, pain had been treated in very much the same way. And then when BPS came in, chronic pain got treated even worse because now it will no susception was removed. Right. Before that, it was there, we just had lots of different uh possible reasons that we could we could find lots of physical dysfunctions that we might be able to blame for that. But then we were finding physical and mental and social dysfunctions that could be blamed for that. And this idea that part of that relates very much to that innate immune response and inflammatory response and inflammation related very much to the nerves itself, and where we put that with clinical reasoning. Because we can't treat that.

Eric: 47:51

Which is important because, like you said, we said earlier about the honesty and the understanding and communicating that we might make this worse.

Monica: 48:02

Yeah, we might make this worse, or we might provide people with information that makes them think they have a problem they don't have.

Eric: 48:11

Yes.

Monica: 48:11

Which can be a physical problem, or maybe it's a mental problem, or maybe it's some other problem, because we then remove a mechanistic quality, or we just don't know about it. This is part of the education, is there aren't mechanisms of inflammation, immune response that lead to sensations of pain that on a manual therapy level we can't treat. But we do need to understand. We may be able to offer some helpful information, not this. Patients don't need to know this, but some helpful and honest information to say, you know what, you might feel better after a treatment, but it wouldn't be surprised, it's not surprising if this pain were to last this long, because this is our understanding of the process. Are you on medication? If someone's not medicated, if there's an autoimmune condition suspected, that that would be an advocacy role that we have in terms of saying here's the things we can think that we may be able to rule out, andor get your doctor to provide you with medication for that may be way more helpful than something else that you might be doing.

Eric: 49:36

Before we started recording, we were talking about one of the problems that people have in the entry to practice education is they don't want to remove stuff, and you talk about these kind of things here, and they're like, oh, if we take those things, uh these other things away, we take away your teddy bear, and you're giving us this other thing. What are we left with? People feel people often feel scared for change. They don't want to change. And so what I'm getting what I get from this these conversations is that this stuff could easily and should be actually and must be included in entry-to-practice education because it's negligent. And I've got in trouble. Some people have reached out to me before saying that by using the word negligent, but I'm gonna say it's negligent. Uh I don't care to not have this stuff uh introduced and to be part of an entry-to-practice education. Because what are we seeing? We're seeing people with this every day, and so few of us, I mean I don't know how many, but I'm gonna say I'm gonna say most people when they first enter practice aren't exposed to this kind of education or this kind of information. And it should be part of the foundation because I think it's a disservice to the public and to the people that are seeing as if we don't even like you said, if we don't recognize this stuff.

Monica: 50:51

And at the very least, it's uh having an awareness and an honesty to be able to say, you know what, I don't know.

Eric: 51:00

Yeah.

Monica: 51:01

To say you have pain, I can't see tissue damage, or something that I would be able to say has a response, could be used to explain your symptoms and to be able to say I don't know to that person and to yourself, to say, I don't have the information I need to know, to be able to know. And that's the knowledge gap that is so hard to get people to understand that they have, that they exist within. We have a massive knowledge gap that means we don't understand the mechanisms of management, and that our understanding should be much more robust in that. And if we don't have that, then to to at least be able to say, I don't have enough to understand what mechanisms might be occurring here. Just but to know that there are, to know that our limited education isn't sufficient to be able to quote unquote explain that.

Eric: 52:13

Which is why this course exists to try to fill that knowledge gap. And yeah, we uh that's the nice thing about the continuing education world is that we can try to fill those gaps. It sure would be nice if the gaps were smaller.

Monica: 52:30

Yeah. And we also talked before we recorded about the what I was saying about having the honesty you say I don't have enough, is like ego checking. We learn to be experts. We we are taught that when we learn this, we will be the expert in this.

Eric: 52:50

Fundamentally, by education like that. We were taught that all the time that your schooling is the best in the world, that you're gonna be the best therapist that ever existed. And that was from day one. Yeah, that attitude was put into us. And I think you want to be confident, but you don't you gotta be realistic too. And I reflect on or have reflected on. I'm glad I went to school when I did. I'm glad I liked my instructors, my colleagues. I got a great experience, but I really do wish that things were done a little bit different, differently.

Monica: 53:26

Yeah, I and I had a great time, and we learned a lot. And some of the I remember the doing a lot of anatomy and cutting, but drawing bones and cutting them out of cardboard and putting them together. There was a whole lot of we had study groups, there was a lot of camaraderie, it was fun, we had a good time, and it's not that there are like a lot of the foundational courses are not problematic. It's the reasoning that becomes problematic. It's what we do with that foundational science that starts to challenge those kind of ethical and what did you say it was it was not unreasonable, unreasonable. What did you say that people got up in arms about?

Eric: 54:17

I use the word negligence, and I've also used the negative.

Monica: 54:19

Negligent. That was it.

Eric: 54:21

Okay, sorry, yeah.

Monica: 54:22

Yeah. And I think that's the part of the education that's the problem is that it's easier for us to be negligent because part of it is that the knowledge doesn't always exist. And part of it is that the knowledge means change, that where the knowledge does exist, it means that once it's put into practice, something has to give, something has to change. And that's a direct, I don't want to necessarily use the word assault, but it is a direct challenge to people's livelihood.

Eric: 54:59

Yeah.

Monica: 54:59

And the way that they maybe have made money and got people to come back and all of that sort of thing. Don't get me started on the ethics of private quote unquote healthcare.

Eric: 55:17

We will maybe next episode we can unpack that a little bit.

Monica: 55:21

So we'll leave it with this, uh like a challenge for the people of the next episode. One of the things I do with making a pain assessment after we go through the pain assessment stuff is we make a pain assessment on a trigger point. And not on a trigger point, because clearly they don't exist, but on the we use the phenomena and characteristics to make an assessment on what would otherwise be labeled as a trigger point.

Eric: 55:51

I love that. Kind of leaves hopefully listeners hanging and be like, oh, what the heck is she talking about? Yeah, what are we doing?

Monica: 55:57

How do we do that? What does it mean for you to see a trigger point not as a trigger point, but to make a pain assessment and to provide mechanistic hypothesis of mechanism, like to provide hypothesis of mechanism of what is occurring on a sore spot within a muscle.

Eric: 56:16

We'll leave it there. That's great, Monica. Thank you. Yes. Till next time. Thank you for listening. If you'd like to learn more about this topic, Pain Education, no script provided, is now available for purchase on my website, the CEBE.com. To listen to more of these episodes, please subscribe on your favorite podcast network. If you enjoyed this episode, please like and share to your favorite social media platforms. And please don't hesitate to connect with me. I can be reached through my website, thece.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 EricPurvis RMT. If you'd 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 helloob.