Pain Education, No Script Provided. Ep 7, Making an MSK Pain Assessment

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Transcript

Welcome Back And Series Finale

Eric 0:12

Hello and welcome to the Massage Science Podcast. My name is Eric Purves

Why Pain Assessment Gets Missed

Eric 0:16

. I'm a course creator, educator, researcher, RMT, and advocate for evidence-based care. My apologies for the large gap between these last two episodes. Life happens and other priorities pulled me away. And then I was away overseas for a much-needed vacation. But I'm happy to be back and hopefully can share a few more episodes in the next few weeks. Today is the final episode of my seven-episode series with Monica Noi. In this episode, we have a discussion about making a musculosqueletal pain assessment. This episode should help to put some of the pieces together about how to integrate the information from this series into something that is clinically useful. As always, thank you for being here, and I hope you enjoy this episode. Here we are, episode seven with the most amazing Monica Noi. I've really enjoyed making these. Monica says she's enjoyed having these conversations too, and we hope that all you listeners out there are in enjoying these and getting something valuable from them. I've dropped a few hints to some people that have I've spoken to recently about this, and they're so excited. And this one here today is our gonna be our final module discussion. And this is gonna be on making a musculoskeletal pain assessment. All about putting this information together into something we can use in the clinic.

Speaker 1:45

Yes. And this again is not caveat, is not mine. I I, with permission, stole this from John Quinna who put this together. And then I've certainly added to it since to clarify my own understanding of things and just to present it to various different audiences and create a little bit of a tool that we might be able to use. I'm sure there are probably more creative people out there who could make it better. Hopefully, in the future, that will happen.

Eric 2:18

It's such a great idea because we learn how to assess joints and muscles and conditions where pain is, I would say, almost always the primary concern or complaint.

Speaker 2:33

Yeah, it's a very, very high percentage. Yeah.

Eric 2:35

Yeah, but we don't ever actually learn how to make a pain assessment.

Speaker 2:39

Yeah. And it turns out there, I don't want to say different types of pain, but there are certainly different presentations. And there are some presentations where people present with something that doesn't necessarily make sense to us as clinicians, but it tells you that there are mechanisms going on that will change how it is that we clinically reason for our treatment. We're used to the really mechanical kind of stuff, where it's joint related or muscle related. And we can we can more easily reason things out, although we might get into the trigger point on this one. So especially for massage therapist. That's always been a fun one for me. So yeah, so it just enables us to be able to say, based on what this person is coming to me with, I can understand some of the hypothetical mechanisms that may be occurring and what that might mean, or how I address this person with treatment.

unknown 3:43

Yeah.

Speaker 3:45

So that's where we're going. So that's what that deck is. Yeah, that's what that deck is.

Assessment Versus Diagnosis Boundaries

Eric 3:49

Well, let's again just you go ahead, just uh tell us a little bit more about maybe some of the preamble stuff that's that sits before making a diagnosis or before making an assessment. Sorry. I think that's the key thing is it's assessment versus diagnosis, not the same thing.

Speaker 4:04

Yes, yeah, we're not making a diagnosis in a on a medic in a medical sense because it's not something that we are really allowed to do. So it's really assessment and impression for our own benefit, not necessarily for us to quote unquote explain pain, explain that person's pain to them. Although some of the neurological information can be useful to people depending on who they are and what they like. But again, usually I try and contextualize things. If I haven't already done it, I'll certainly contextualize this making a pain assessment within the within the operational paradigm that we exist within, which is biomedicine. And a lot of allied health professions or what might be called alternative as well, health professions. Some people will call it alternative or complementary, depending on where they're coming from. But a lot of the time we don't realize that we actually are educated within a biomedical construct and a biomedical paradigm. So we use these biomedical constructs all the time. We use anatomy, physiology, neurology, pathology, all of those kinds of informations. They don't come from our professions. They come from a biomedical perspective and we draw on them for our purposes. So we're not in any way, this is our foundation. And I think that it becomes challenging because people often criticize biomedicine and often criticize the paradigm in which we not only exist but are educated and want to distance themselves from that.

Eric 6:06

But would you say, sorry, Monica just interrupt for sure?

Speaker 6:09

Yeah, no, no.

Eric 6:10

Uh would you say though that so people say biomedicine is bad? This other way, this complimentary, not biomedically is better. But would you say that the philosophy though that the complementary ones are doing is still very biomedically based?

When Biomedicine Gets Misused

Speaker 6:27

Yeah, 100%. Everything we do is biomedically based because we're using biomedical sciences in order to construct whatever we'll get into this in a second, but whatever kind of thought processes we have about that. The problem being that I'm just gonna get to this paper which I present. This is actually a good paper. It's an osteopathic paper, but it's not related to only osteo. It's called the fallacy of osteopathic anatomical possibilism. Actually, it's not called that, but that's what it's about. So it's called it's all connected, so it all matters, and the fallacy of osteopathic anatomical possibilism. So we take this biomedicine, we take all of the sciences, and then we manipulate them through a different perspective, through a massage therapy or an osteopathic or a chiropractic or a physiotherapy perspective, that A is sometimes deficit of some of the sciences that are out there, but also has this problem where we impose relationships on structures or on systems or on relationships between what we do and how a person reacts or how their systems react or whatever it might be. And because we're thinking, well, I did this and this happened, so let me fill in the gaps as to mechanistically how this happened. And that is often based on a perspective that is about well, it's possible, I guess, because it's all connected, and and then we can basically say anything that we want to, we can construct these elaborate mechanistic possibilities. So that can often happen within our professions, and that's one of the reasons I try and contextualize this, where it's like we come from biomedicine. So it's like there's all this idea that we may have to pay attention to other kinds of traditions, but for some reason we try and distance ourselves from biomedicine, and that is one of the founding traditions of our professions.

Eric 8:50

So this is this is such a great paper, and I read it last year when it first came out. So admittedly, right now it's been over a year since I read it. But the it hit on so many key points that are a problem in our manual therapy MSK world.

Speaker 2 9:15

Yeah.

Eric 9:16

Because the one quote that here it says it's the imagined, exaggerated or implausible relationships claimed to exist between anatomical structures. And this is such a thing that we see in, I can only speak from a massage therapy perspective, but I'm sure I'm not alone because osteopaths are doing it too, and I'm sure chiros and physios are. Oh, I understand. Is we make these clinical impressions or a diagnosis based on this very convoluted the toe bones connected to the ankle bone, connected to the knee bone, connected to the hip bone reasoning process that is impossible. Because you could say anything's connected to anything, exactly, which does end up happening, exactly. And it gets if we're going back to uh making an assessment or into trying to better understand pain or some of the causal stuff we've hit on in most of these episodes, there's no end.

Consequence Versus Cause In MSK Pain

Speaker 10:18

No, there may be no end, yeah, absolutely, and that makes it very that's good for the profession that you're in because you're able to have explanations for things that go on and sound perhaps confident about those or reasoned about those kinds of things. It's oh, this didn't work, that's because this issue is here, or this, and I have to deal with this first, or I have to deal with that first, or some other kind of thing that's going on. And it misses where connections might actually be reasonable. And in a pain situation, and I'm just I'm gonna use me as an example because I've talked about my ankle, which I I did a number on, and it's healing. I think I did a I haven't had a scan because therapists are the worst patient, so I haven't actually got to have anything looked at. I can wait there, it's healing, but where there was very much, where it was very much contained to the ankle at a certain point, I'm pretty sure probably to on a ligament, definite tissue damage, swelling, all of that kind of thing, very specific acute related pain, which makes sense. As the healing process has gone on and this happens, is that the whole limb starts to become what Asav has called a no-susceptive, like a a no susceptive origin, basically. And that relates to how the nerves might change in sensitivity related to the injury, which is described in the paper that he that was dropped recently, which was the adhere to the aphorism paper that he just dropped, which relates to a functional capacity that might be inherently advantageous on an evolutionary level. But basically, what I have is a sore tender ankle, but my whole leg hurts, right? In some to some degree or another. There's sensitivity there, my whole foot is sensitive, and that kind of relates to what we understand happens when there's tissue damage in relation to the injury. So that's connected, that's connected in a very reasonable, explainable, physiological way. So then we'll if we make up these other possibilities for connection, we miss the ones that do exist and how they may impact what it is that we do on a treatment basis.

Eric 13:51

That's such a key thing that I'm glad you brought that up. And something that I try to in my courses I try to address as well is that the everything that we see clinically, everything that somebody experiences as a patient, things like you said, where there's been tissue damage, but the whole leg becomes a nosoceptive like I know, I don't know.

Speaker 14:17

I'm trying to think of the word.

Eric 14:18

A nociceptive canister.

Speaker 14:19

Yeah, it's like a cause, basically.

Eric 14:21

Yeah, yeah. We can explain or understand what's happening with a person based on physiology or neurophysiology, yeah, or those nociceptive processes sensitivity. If we know to be able to do that, yeah, if we know, but we can always it's a more right or a less wrong approach. I think it's a more right approach than trying to connect these fascial lines or these joint loading things, which is a relevance for those things. I don't know, I don't know anymore.

Speaker 14:55

But we're going to see. So if I look at myself in a mirror, I will see a weight-bearing shift. I will see that my foot is externally rotated. I'll see, and I'll be able to match that with the tension that I'm feeling in my glute. A therapist might see that my iliacs don't necessarily align, that my thorax perhaps is somewhat rotated because I'm compensating for whatever weight-bearing shift because of this issue with my ankle. So we will see these things as therapists when someone has this kind of an injury. But what we do is not think about those as reasonable ways in which someone might actually deal with an injury or pain and the growing uh sensitivity or a no-susceptive area. But we will see them as causal for the pain that person's having. Oh, you're not weight-bearing properly because your hips are out of alignment or because your thorax is rotated, or because whatever it might be. And so we flip it to be causal rather than actually consequential and reasonably so.

Eric 16:04

I like that word, consequential.

Speaker 16:08

Yeah.

Eric 16:09

The things that we see, those traditional kind of musculoskeletal structural changes that you see, are because they're consequential to the fact that you injured your ankle and you have this socioceptive environment in your leg.

Speaker 16:25

Yeah, yeah. And then you're dealing with it in various different ways. Now, does that mean you weren't hurt somewhere else? No, it might have even mean that as a therapist, when you see these things that you've been trained to see, where there's maybe some postural changes, there's weight-bearing changes, there's something that you see that is uneven, it doesn't mean that you treating what you feel as tension or muscle tension in a certain area related to that isn't helpful because it could very well be helpful to for the person to not feel that tension, even though it might build back up again because they're still dealing with it. But it may be helpful for them to not feel it if it's causing discomfort or various other reasons. It may, who knows, help them weight bear better on this injured ankle as part of a recovery. It's hard to know. We can't like necessarily make these one-on-one correlations, but the important point is to not make them causal because that's where the anatomical possiblism comes in. Where we see these things and we're like, I can explain why you're having this pain. So hold on, I started with this pain. Maybe you can explain how that changed something about what I'm feeling.

unknown 17:49

Yeah.

Eric 17:50

And this just goes back to that knowledge gap, which we've been saying every episode and started with was that huge knowledge gap is that because there might not be that pain education or the pain knowledge to help explain things, we come up with other stories, other rationale to try to explain what we see and feel and what the person experiences. Because people are trying to fill in that gap. And unfortunately, the gap has traditionally been filled in with 100-year-old belief-based ideals.

Why More Neuroscience Is Not Enough

Speaker 18:26

Yeah, and and observational things as well, where we can like this happened, therefore, this must be the reason it happened. And yeah, and then they become law, and then they become something that we start to extrapolate to everybody. And that becomes quite problematic as well. And I used to think it was because we just were missing some sciences. So maybe if we had more neuroscience or neurophysiology, then we would be able to connect the dots. But it goes way beyond that with regard to pain education, because there's it's such a conflated field already. And we're starting to see much more information coming from neuroscience related to susception and pain, but that has to infiltrate through the goal that we might have, instead of actually being able to say, oh, we are like pain experts or we're pain therapists or whatever it might be, is that is that while we're getting our ducks in a row with all of this information, that we can at least limit the misinformation.

Speaker 2 19:35

Yes.

Speaker 19:36

That might be the biggest thing that we can do is to not make these massive assumptions.

Eric 19:44

The idea that neurophysiology, neuroscience, education would make a difference is something that I thought for a while too. And I remember having conversations with people early days into looking at some information and talking about, let's say you want to talk about trigger points. We talked about now, we're gonna talk about later if you want. It's up to you. I'll leave you in charge of the trigger point thing. But I remember somebody being like, oh, I I learned we learned all this neurophyphysiology or all the neuroscience I needed in school, and then and they'd been practicing for 40 years, and they thought that was enough, and that explained all the things they need to know about pain or trigger points and stuff. And I think that is a closed-minded way of thinking because it's incomplete. We need to know you need to know the neuroscience. I think it helps to know like synapses and receptors and receptor types and different fibers and the how things work in the spinal cord with through the dorsal ganglion and interneurons and blah blah blah. You get all that. I think that's important, but the context of it needs to be how is this relevant to pain?

Speaker 20:54

Yeah. And not only that, but if we're gonna go for trigger points, this is the trigger points are indicative of a problem that exists related to anatomical possibility, where there's a piece of information that's come out, it uses forms of anatomy in science, basic science. It provides a perspective that gets taken up and becomes accepted knowledge. And this happens not just with trigger points, this happens with a lot of other kinds of things. The the paper that that just dropped, the adue to an aphorism, why no susception is necessary for pain, describes the same sort of thing, but with relation to the idea that no susception is neither necessary nor sufficient for pain, which was the aphorism that they are analyzing. But that has become that sort of came out. There was certainly some science behind what was presented, like a lot of neuroscience actually behind what was presented, but it was provided through a particular perspective, and this became accepted image that people are now like, yeah, no, we can have pain without some sort of neurological uh component, which on a science level isn't supportive. But the trigger point that was an example of that, where it became just accepted. So part of it is not just that we don't necessarily didn't necessarily have the pain knowledge that we needed, but part of it was also there was a refusal to address the critiques that became evident in the description of the trigger. It was a hyp it was basically a testable hypothesis that when tested didn't really stand up. Like parts of it did. There were parts that could be checked and shifted to an a different question. And then we could look at that question and study that. But it is it's just accepted as a given. And that becomes a real problem. So the thing Yeah, go ahead.

Three Mechanisms For Pain Impressions

Eric 23:12

Sorry, just to clarify here. The thing with the trigger points, and this is from what I understand, is that the it's a clinical phenomena. We all have experienced feeling the traditional air quotes trigger point. People have had have a push on it. And as a therapist, maybe you feel something there, maybe you don't, but the patient feels something and you get that traditional referral. So there is a clinical reality to it. Clinical phenomenon. Okay.

unknown 23:42

Yeah.

Eric 23:43

And so that's I understand that too, and that's the way I think about it. But from a what's happening in the body from a physiological anatomical phenomena, it's not what that traditional Trevel belief was.

Speaker 24:00

No. And it also trigger points as being really problematic in a lot of ways because they led to this myofascial pain syndrome and some circular reasoning related to pain. But you're talking about when someone comes in with this sore mut sore spot in the muscle that has some of those characteristics, you're talking about someone who's reporting pain to you. And this is where the pain assessment comes in. And it's done by looking at various kinds, like contextualizing it, but also having a much better understanding of the clinical descriptors that are related to the mechanisms or the hypothesis of mechanism. And these are nosoceptive, osoplastic, and neuropathic. And so they have different kinds of descriptions related to them, so that we can start to understand what might be related to normal functioning of the nosoceptive apparatus and abnormal functioning. And then functioning related specifically to the nerves itself, but to a lesion or disease of the nervous system. So getting to know those things, which is part of what the course does, is contextualize some of those, but getting to know those clinical descriptors, it allows us to start to distinguish. And there's a this is not new. Like John didn't come up with this on his own. There's a table from Woolz from 2009 that has similar, similar setup. And there are other papers along the way that have categorized these things as well. Nosoplastic a little bit newer. Obviously, that's not in the Wolf table because that's a new one. But and there's they've also added like to nosoceptive inflammatory, just to consider what else might be going on in terms of when someone might have inflammation with relation to tissue damage. So all of these things become quite helpful for us. And then we can see where these things might be associated on different musculoskeletal levels. So what we might be dealing with most of the time on a musculoskeletal level, if it's non-problematic, we would might, we might more categorize as no susceptible hypothesis of mechanism, meaning we've got a normal functioning no susceptible apparatus in the area, and there might be inflammation, because if there's tissue damage or something along those lines. That there is one present. We should be able to actually have some indication that there may be one present based on the nerve symptoms that are present. And then nosoplastic, which was the newer one and has actually become a little bit of a problem because it keeps getting conflated with a whole bunch of different things. But it's just another way of describing a mechanism which is altered. It's an altered no susceptive mechanism. So it's not the same as no susceptible, it's there functioning in a capacity where you have particular symptoms that will indicate to you that that processing of information has been altered in some way. And that's usually allodinia and hyper hyperalgesia or other kinds of forms of sensitivity.

Eric 27:37

One thing just to clarify, just for listeners, also for myself, is so noseceptive is probably the thing we see most likely in the clinic, is kind of what you're saying. And would that be because I've seen some people conflate the two as nociceptive being more mechanical? Are those would that be a fair kind of comparison?

Speaker 28:01

Yeah, I think we could definitely correlate that in a way, because what we see is what we would describe as mechanical. So the descriptor for mechanical in various different places, but it's basically you'll see mechanical pain, which doesn't really make sense. But it's it may be no susception that's induced in from a from mechanical no susceptors based on movement, right? Movement relationship. So we start to see there are particular characteristics to that, that it's usually that pain is usually reproduced with load or stress on the joint or something like that. It's often associated with specific movements or specific positions, but it's not constant. So in a change of movement or position, it'll change unless there's a acute injury, then it's a different thing.

Eric 28:52

I have a question.

Speaker 28:53

It's generally yeah, generally localized, right?

Eric 28:57

Yeah, it's localized as I sit here doing this, it doesn't bug me. But if I bent over to pick up something from the floor, I can do it, but it's uncomfortable and I'm gonna change how I move to try to avoid it.

Speaker 29:08

Yeah.

Eric 29:08

Why that happened? I felt something twinge my back a little bit yesterday when I was at the gym.

unknown 29:12

Yeah.

Eric 29:14

Did I try to do too much? I don't know. Strain something. I did something, I upset tissue and mechanical. And so I would view that and I would explain that if it was a patient. I would say, yeah, this is I wouldn't say it's no susceptive, because we probably don't have no idea what that means, but I would think it's no deceptive nature. Something's irritating, it's normal.

Clearing Up Nociplastic Confusion

Speaker 29:35

You're not having any, you're not having any referral, nerve referral into the feet, you're not having it's not sensitive in some way, it's very much related to movement. So we start to see those characteristics. Yeah. And it gives us a little bit of an understanding of that they're not falling into this category or that category. So we can we can be more safe in the assumption that things are functioning as they should within this relationship. Now, there might be different reasons that's occurring, and that's another whole other level of assessment that we normally do anyway, whether or not we might be thinking, oh, they might have a disk issue for these reasons, or because there's an x-ray, or there's degeneration that can be seen. So it's like we can start to think of other contributing factors that might be there, or as you said, overuse, or something along those lines. So we'd have to tick off a level of those boxes any. And so we'd be looking at all those things. But yeah, so we would correlate those. We would categorize those in particular ways.

Eric 30:35

I think that's the thing that we're looking for that you're talking about with these things, is that there's your correlations or associations, but not they're not causal. So you'd see this, and that would be correlated with.

Speaker 30:48

Yeah, like there's a definitely relationship between what we might categorize as no susceptible and what we might see on a clinical picture as being really associated with these particular elements.

Eric 31:01

One thing I wanted to ask you about nosyplastic pain, just for clarification. Yeah. My understanding of nosyplastic pain is it's just in the periphery. It's only stuff that happens outside the spinal cord.

Speaker 31:15

So is that correct? This may be where there's some, maybe where there's some challenge there. So it's pain that arises, that the definition is pain that arises from altered nosoception, despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors, or evidence for disease or lesion of the somatosensory system causing pain. So the idea of the idea, I'm just going to go back up to this, the idea of no susceptible is due to the activation of nosoceptors, and we generally tend to relate that to a peripheral aspect. And I was looking at the definitions. I was looking at the definitions and I use this as an explanation. But there's nothing in the definitions that specifically ties nosusception or nosoceptors to uh the periphery.

Eric 32:19

So even though it says for nocy plastic causing the activation of peripheral nociceptors, there could be central mechanisms.

Speaker 32:27

That's a that's saying there's no evidence there. So we're seeing this particular activation, but what we're not seeing is evidence of peripheral nociceptor activation.

Speaker 2 32:41

Okay.

Speaker 32:42

So it's not saying that it's only perusal no sysceptive activation, is my understanding. And give me one second, because I'm gonna up to the ISP terminology. Because I kept going back and forwards to this, and I can never quite understand. I can never not understand, but I keep I can't be keeping things in my head. Actually, I've got all the definitions on my deck, but this is easier. Because no susception is the neural process of encoding noxious stimuli and then gnosisceptor. Okay, this is where, yeah, no, this is where it does go to the periphery. That was my that's my error. I might have to review what I wrote. So gnosceptor is the high threshold sensory receptor of the peripheral somatosensory nervous system that's capable of transducing and encoding noxious stimuli. So the gnosoceptor, when we talk about nosoceptive hypothesis of mechanism, that's where we associate that with the periphery, right? With peripheral nosoceptors.

Eric 33:48

Yes.

Speaker 33:49

An activation of those gnosisceptors that are in the periphery. However, the clinical descriptor for nosoplastic is that it's arising from altered nosoception, and nosoception is not periphery, right? It's related. So nosusception is the neural process of encoding noxious stimuli. And encoding can occur in both the peripheral and the central nosoceptive neurons. So that's not related specifically to periphery. It's just that when you see this altered no susception or evidence of altered no susception, we don't see evidence of peripheral activation. We're trying, it's basically a rule. It's basically a way of saying we don't see evidence of a disease or lesion of the nervous system. We don't see evidence of what we would otherwise classify as a no susceptive mechanism. So what we're left with is evidence that tells us that there's an alteration in that no susceptive process.

Eric 35:01

And we're not sure where that's coming from.

Speaker 35:04

And we're not sure where that's coming from.

Eric 35:05

Yeah.

Speaker 35:06

But it's not specific to peripheral.

Eric 35:09

It's just saying we don't have to see activation of the peripheral.

Speaker 35:11

We don't see activation of peripheral. I think that is not that there isn't, just that we don't have evidence of it.

Eric 35:18

I think that's a confusing definition because I've had this conversation with a few other people over the years, and I've listened to other people talk about it, and there's a lot, it's confusing. There needs to be something. I don't know what it is. I don't have a suggestion right now, but I do know from just I'm trying to understand what the heck nostoplastic is unclear. And I think it's because the definition is itself unclear.

Speaker 35:43

Yeah, and there's been a few papers written on it, and some of those unfortunately conflate it. Others are trying to give a better explanation of it. And this was my understanding of for reading some of those papers, and also because I came across the same thing where I was confused. And other people had come across, I was in one pain forum where they basically said it's it's specifically peripheral and all that sort of stuff, and then at the same time conflated it with central sensitization. Anyway, it was when I was like, okay, everything is a bit weird. But from what I can understand and just being able to articulate it this way, is that the no susception is altered. It is not no susceptible in the way that we would understand that as related to activation of peripheral nociceptors in what we associate with that mechanical understanding or perhaps inflammatory understanding. And it so the system is altered, and we don't have evidence of activation of peripheral nociception. Not that isn't. We don't have evidence of no neuropathic mechanism. So does that make sense?

Eric 37:02

I get it. Yeah, I understand. Yeah, it's I just wanted some clarity on that because I have seen the same thing that you were saying, is that I've seen the common description or common discussion around it is it's just peripheral nosy scepters.

Speaker 37:17

Yeah, that's the common, the that's the common discussion.

Eric 37:20

And and then so there's something happening in those peripheral nosoceptors only is the way it's I've heard. And I've seen other people talk about, and could you said I think you said they could fight it with central sensitization. I've seen that too, where nosoplastic pain is a peripheral weirdness. Yeah, peripheral demonstration, peripheral weirdness from central changes. And that one didn't seem right to me either. But yeah, it's yeah.

Speaker 37:49

So there could be there could be activation of peripheral nosoceptors, and there could be activation of central no suceptors. And they and yes, and so it's not limited, it's basically looking at no susception on an apparatus level. It's just distinguishing it from the other clinical descriptors that we have, which is no susceptible and neuropathic. And no susceptible being, yeah, what we talked about, and then neuropathic being a lesion or disease of the nervous system.

Eric 38:21

So if it's not one of those things, and the person has pain.

Clinical Examples Of Nociplastic Pain

Rethinking Trigger Points As Pain

Speaker 38:24

And the person has pain with specific evidence of sensitivity, which is that allidinium hyperalgesia, and there can be other levels of sensitivity as well. But but yeah, those are and so that would be the sort of characteristic of that as being a mechanism. So within a central sensitization, as it's currently defined, nosoplastic would be a possible mechanism within that particular issue, right? It's not the issue, it is one of the mechanisms that would exist probably within a centrally sensitized state. There would be an alteration of gnosis. Yeah, it's interesting actually. It is, it's a lot, and it helps to really talk about it and clarify it. And I will, you know, the next time someone asks me that, I'll have to sit and think about it for a while before I can clarify it like that. And hopefully, when when Anissa John or ASAP listened to this and I've got this wrong, the table uh clarify that for me. But I think from my understanding, which is it's the closest I can get to there. But when we look at when we look at something in that making a pain assessment, so some of the examples that are given would be if there was an impairment of the apparatus that led to altered nosoception, which is the gnosoplastic. Examples of that might be an impairment that would have this particular mechanism, would be chronic low back pain without any other kind of explanatory findings. So it's like someone has this sort of sensitivity there's maybe some tenderness in the area, some low back pain, but there's nothing that would otherwise explain the symptoms and the sensitivity. Complex regional pain syndrome falls under that. It is a mechanism that would be evident within that particular condition because it presents having alodinia and hyperalgesia and other forms of sensitivity. And the person who may have an illness label, right? Fibromyalgia, IBS, myof pain syndrome, various other things like that, where you would have evidence that there is a nosoplastic mechanism in relation to that particular issue. Again, not the whole issue. It's a mechanism within that issue. So one of the other things with nosoplastic impairment that I have in this is that you have a recurrent set sore spot on the body. That would be a local impairment, a local nosoplastic impairment. So a local alteration of nosoception.

Eric 41:37

So if you're an on so you're saying if you have an ongoing sore spot, they're like, oh, that's my spot.

Speaker 41:43

Yeah. When you press on it, there's a referral.

Eric 41:46

Yeah.

Speaker 41:46

You have those considerations.

Eric 41:48

Yeah. That would be uh characteristic of a gnosyplastic, a localized gnosyplastic.

Speaker 41:55

Yeah. So if we do a pain assessment, and I don't want to spoil it for everyone, but it is a fun one to look at and people forget. So we have this phenomena. We have a sore spot on the body, could be reported as spontaneous, it could be in response to pressure, palpation, when people have carry a purse or something, and just, oh my God, it really hurts. It could be anywhere in the body where there's muscle. No known mechanism of injury necessarily, right? These things might certainly be correlated with states of tension and various other things. There could be a referral pattern when you press on it. And you could have a referral down the arm, you could have a referral up, which, if we look at those referral patterns, they're usually following nerve pathway, right? It makes anatomical nerve pathway sense. Possible torque band that may or may not be palpable, right? People often feel that there's like a there's some sort of tightness within the muscle, like some sort of band of tightness. And there could be a possible twitch response with regard to palpation. So something that happens in the that muscle, that twitch response. So in terms of a pain assessment, what we're looking at are character. Okay, so we got phenomena. And then if we go to characteristics of this trigger point, when we're trying to make a pain assessment, we're then going to look at how we can characterize what this means and what sort of mechanisms might be at play. So if we've got this sore spot on the body where we have this, anywhere there's muscle, etc., it can be both spontaneous pain, so without stimulus, or stimulus-induced reports of pain as well. So we have two. So it's not one thing or the other, it can be possibly both. There's likely that people have pain at rest. The aggravating factors can be various, as well as the relieving factors. And the aggravating factors and the relieving factors may be the same at any given time. So it's like in one day it might be relieving to apply heat, the next day it may actually be aggravating. It can include movement. Movement might be aggravating, or it might be relieving. Sustained positions or inactivity might be aggravating, might be relieving. Rest, pressure, all of those kinds of things. Pressure can be relieving, could be aggravating. So those things don't necessarily pattern. They're not consistent. And then there is it can be localized, a localized spot with a referral pattern as well. So you press on it, you get this referral. It's irrelevant. The time of day is irrelevant. This can occur at any time, or these elements can occur at any time of day. It's it might you might wake up with it, you might not. It could happen during the day, it might not. There's some characteristic descriptions that are actually more neuropathic. So there's stiffness, hot, burning, dull, aching, times and descriptions of pain. You can have others as well, along with sharp, and you can also have omigran associated. And then the intensity is variable, it might linger after the stimulus is removed. And it can vary depending on the stimulus. So it might be that for some people, the a small amount of pressure will cause a response or a report where that's a large amount of pain. So once you start to look into that, you start to get the understanding that there may be various mechanisms and there may be evidence of halodinia or hyperalgesia in relation to that source bar. So there's some form of alteration or sensity sensitivity in that mechanism.

Eric 46:18

And all the stuff you described sounds very similar to trigger point ideals.

Speaker 46:26

Yeah, but also you can match some of that with someone who has fibromyalgia.

Speaker 2 46:32

Yeah.

Speaker 46:33

Or someone who someone has myofascial pain syndrome, which is what the trigger point is supposed to be, like causal of. Now you've got a bunch of mechanisms that are possibly in relation, a bunch of neurological mechanisms related to pain that are existing.

Eric 46:51

And that it helped that they exist and understanding them helps to explain the patient experience as well as the clinical experience of what we see and feel and what the person sees and feels.

Speaker 47:04

And it also helps to explain why treatments apparently are incredibly varied in terms of what they do, but also not necessarily very helpful.

unknown 47:17

Yeah.

How Treatment Can Backfire

Speaker 47:17

Do we get rid of trigger points? Like certainly in some cases, or what we could classify as trigger points. Certainly in some cases, people can be treated and they'll they may never experience that again. But what we see in terms of why the trigger point was associated with myofascial pain syndrome is that these are recurrent, that these don't go away. So here we are pressing like crazy on areas in the body that may actually have mechanisms that are altered. And so now you're creating and you're a no-susceptive trigger. You're you're a noxious stimuli, basically. You're you become a mechanical noxious stimuli by digging around with a needle or pressing around with your thumb or whatever other digging that you might do to set off this, what's the word called? Referral, to set off this referral, or to like we go then to the whole pain treats pain like idea of things. And what you may actually be doing is creating more problems for something that's already a problem.

Eric 48:36

And then people feel better eventually, and the therapist can then take credit for it, even though they may have prolonged.

Speaker 48:46

Totally. Then they'll come back the next week and have a source area again.

unknown 48:52

Yeah.

Speaker 48:52

Because there's been this temporary change in something about the sort of no-susceptive environment or some sort of down regulation, or I think it's called DNIC. I can never remember what other yeah.

Eric 49:05

DNIC is, I think, the term that they used in animal studies and conditioned pain, CPM, conditioned pain modulation is what's used in human studies.

Speaker 49:14

Yeah, which is super problem.

Eric 49:16

Is that correct? Am I remembering those correct? Yeah.

Speaker 49:18

I I have read that in a paper recently. Yeah.

Eric 49:20

Yeah, I think I read that. You probably read the same paper.

Speaker 49:23

And it's yeah, it's but some of those mechanisms might be there where there's this, where there's something that happens when you press, and then there's some form of inhibit inhibition that occurs, and then someone feels better afterwards. We have a condition that keeps uh recurring.

unknown 49:45

Yeah.

Eric 49:48

It's all fan fantastically interesting stuff, and it it really challenges us to think differently about what it is we're doing and why it is we're doing it, and to give us a reality check on how good are we at treating pain? We tend to remember our successes and probably forget our failures, and we are probably we all have the best of intentions helping people that hurt, and no one, and I think that sometimes when you talk about the stuff when you challenge us, some people can be offended and say, Hey, are you telling me what I'm doing is useless or I'm no good? And that's never even slightly what we're trying to get at.

Building A Safer Learning Bridge

Speaker 50:31

Nor the big caveat here is that this is not necessarily our fault in terms of not having the pain knowledge. We understand this is a massive knowledge gap. And I think that that actually, I understand it's a massive knowledge gap, you understand it, but I think that that is not well understood, is that we have this massive knowledge gap and we don't have the education we need to be able to necessarily fill that gap in a way that would make us reasonable in knowledge and mechanisms and management. So when we're out here challenging the constructs, it's not because we're trying to tell people that they're wrong, it's because we want people to know that they're missing information and that we're starting to get much more of the information that they're missing. Now of course it does challenge the information that's been used to fill in the gaps and the people might be using on a daily basis.

Eric 51:36

What I'm excited for with this course and and I think it it's gonna be it's gonna be great. And actually, I know it's I know it's gonna be great. The no the having seen the content and having these conversations with you is has been super inspiring and is really challenged me to make sure that I think I know what I know and be and also reflect on the stuff I don't know, and that's okay, because we can't all know all the things, and I that is I think that's a important piece of information that people are gonna probably get from the course is that it's okay not to know everything, and we're here to try to fill those gaps. But this course is gonna be six or seven modules, seven modules, plus there's gonna be two support live webinars as well. So to help to fill that gap even more, because you're guaranteed you're gonna go through this stuff, you're gonna have questions, yeah. And then it starts with those live meetings are for there's gonna be an asynchronous discussion community where people can post questions or comments that's all gonna be will be monitored by you. And I think it's gonna be it's gonna be a safe, welcoming place for people to admit they don't know and to try to learn and for us to say that's a good question, we don't know either, but we'll try and figure that out for you and we'll maybe reach out to other people that know more than us. But I think it's I don't want people to view this content or this course to be something that's elitist or something that's special. It's for the person who wants to know.

Speaker 53:08

Yeah. So I'll reiterate the yeah, I'll reiterate the caveat again is that this is this information is not proprietary. I did not create this information. I simply put it together in a way that allowed me to explain it to myself and get a clearer picture of it. And hopefully we'll do the same thing for the people who are engaging with this. And to take that further, to take that even further than I have gone with it. That will be the goal eventually, is that there will be much more information and education related to the foundations of pain science and the neuroscience knowledge that we're getting more and more and ultimately for the person in clean. But I'm not gonna say it's not, it's challenging information. You and I have already been through probably fairly significant amounts of cognitive dissonance. Huge and had to navigate that so we do understand when people are feeling challenged and/or defensive with this information because it's going to lead for some people, especially especially it's gonna lead to some cognitive dissonance, it's gonna lead to discomfort in their thought processes.

Eric 54:32

Yeah, and that's why we're here. We'll be here to try to help you through that. Because to a lot of people, you hear this stuff and it seems a little maybe eggheady kind of academia stuff, and I don't understand what about what's that what am I supposed to do with that information? I think that's a normal initial reaction. But once you start to be able to integrate this stuff into your clinical reasoning and into making sense of what you with your patients or clients, people that come to see you, whatever terminology, customers that you want to use, everyone uses different stuff. It really is helpful to help put some pieces together. And yeah, and I think that are I don't think we could say more effective, but yeah, but are more likely to not have negative effects, maybe.

Speaker 55:25

Yeah, yeah, and maybe less harmful.

Eric 55:27

Less harmful, yeah.

Speaker 55:29

For sure. Yeah, and if I had a point, I'm not sure what that was. Or not completely lost it.

Eric 55:38

Any final thoughts?

Speaker 55:40

What were you talking about? Just then? What were you saying just then? It'll remind me of what I was thinking. Yeah.

Eric 55:47

Oh, I was talking about the Oh no, I got it.

Closing Thoughts And Next Steps

Speaker 55:51

It's that's our challenge, right? Our challenge is to help bridge that gap between the knowledge that does seem out of reach and a way that we can bring it to people who aren't gonna get to this sort of stage of putting together a course so they can understand the information. It's it's I've not just put this together, but I've re-evaluated and I've updated it several times. And I continue to look at it on a daily basis. And people aren't gonna do that. But we have to find a way to be able to, that's our challenge, to be able to say, look, we're taking this information. How can we make that understandable for you to simplify it without making it simple and without removing the nuance, but making it reasonable for you to be able to take to a clinical setting and have a better understanding of what might be happening for your patient and where you may or may not be helpful.

Eric 56:58

I think that's a perfect way to end it.

Speaker 57:02

Exactly. I want to end it.

Eric 57:05

I'm sure we could probably come up with some other things to talk about in the future. But this is this has been great, Monica. I've really enjoyed these seven episodes, and I'm looking forward to going back and listening to them. I did the first couple and they'll be coming out soon.

Speaker 57:21

I didn't also want to listen to it.

Eric 57:23

Don't listen to you, share them to your people.

Speaker 57:26

It's so hard to deal with how you sound to yourself when you're not used to listening to yourself.

Subscribe Share And Support

Eric 57:32

It's a great thing about editing software is it makes everybody sound better. Oh, what sound? I wish I'd use that early on in my teaching and podcasting careers because it definitely people listening to probably hopefully they'll notice that the last couple months of episodes sound much better than the first.

Speaker 57:51

It's like a zoom filter for your voice.

Eric 57:54

Yeah. Exactly. So that's great. That's fantastic, yeah.

Speaker 58:00

And we'll be engaging more, and I'm looking forward to also to getting this going, and hopefully that we can have a really positive impact on our communities and on people who have playing.

Eric 58:13

That's the goal. I love it. Thank you. Thank you for listening. I hope you enjoyed these series of episodes with Monica Noi. If you want to learn more about this topic, Payne Education, no script provided, is a self-directed course which is now available for purchase on my website, the CEBE.com. Please subscribe so you can be the first to listen to all my new upcoming episodes. And if you enjoyed this episode, please share to your favorite social media platform. To connect with me, I can be reached through my website, 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'd like to financially support this podcast, please consider making a small donation. This can be done by clicking on the support button or heading over to buymeacoffee.comslash hello.