Testing nerve versus musculoskeletal pain before treatment

But we did the opener techniques to reduce pressure in the individual foramen transiently to see if we could ease their sciatica. And this group did so much better than the other group. By eight days, these people were, their worst parameter was 65% better. And this is back pain, leg pain and disability emitted by two independent instruments. You're listening to the Restoring Human Movement podcast, where movement experts discuss the latest evidence-based practices to help you and your clients move with mastery. And now, your host, Dr. Sebastian Gonzales. Hey everyone, it's Dr. Sebastian Gonzales, your host for the brand new rebranded podcast.

This is called the Now, the Restoring Human Movement podcast. This is session number 91. We're not starting back at zero, but we're going to rebrand it to better identify with what you're going to get from these types of podcasts. So, that was a roughly about 15 second bumper of the interview I'm going to have today with Michael Shacklock. He is a great, I don't want to say diagnostician, like he, we went to, I went to his seminar, Clinical Neurodynamics, just a few months ago. And it was amazing, amazing to be able to use tools to screen out types of nerve conditions. If you rule them in versus out, we might have a musculoskeletal problem, we might have a neurological problem.

And it's not always pins and needles based, which is actually very, it was surprising to me to see. And I've been using these at the office, and I have some clinicians come in, they're like, what the heck is this, right? So, it's a relatively new thing, at least in our profession, and it's amazing to see. So, Michael's going to go through a lot of that today with you guys. If you are young clinicians, you're going to want to listen to this because it's going to absolutely blow your mind, and you're going to want to buy his book. If you're a, this is going to be a little bit technical today. So, if you're a patient, you might have to tune out a little bit, and I'll try to write something a little bit more simple to understand.

But we might go through some storytelling, which is probably going to interest you guys. Just kind of a rough idea, just so you understand what we're going to be looking into today is, actually, right before you recorded this podcast, I have a patient, I had a patient in with a shoulder condition that, with pain lifting overhead, and she said it feels like a pinch at the top right there, especially when she's back into the shoulder-packed position. And we find that, actually, she goes up into that position, and all I have to do is move her hand from fingers to the ceiling to fingers forward, kind of like you're waving, and we can turn her pain on and off like a switch.

So, that's a very not-standardized version of a neurodynamic test, but if you consider what we're doing there, there's really no direct connection other than fascia and vessels and nerves, which come from the shoulder to the hand directly. So, nothing about wrist movement should really affect that shoulder. So, in that case, we're looking at a neurodynamic problem, when in the past, I would have treated it as a shoulder impingement. Do you understand what I'm saying here? Okay. So, this is going, if you understand that concept, and you're interested, this is going to be a very interesting podcast for you guys.

Now, this is session number 91. If you're looking for all the show notes, please go on to my website, p2sportscare.com. We have a pretty comprehensive search function at this point in time, and look up Michael Shacklock podcast, and you're going to find all the transcription and everything there. Now, I thought also what we would do to kind of sub out all those old podcasts had little bits and pieces of kind of my life, and just so you guys can learn about who is actually speaking with you and sharing this information, and I thought I would just go into some, like, kind of almost like personal story corner.

So, it'll be a little bit more contained. I won't spend too much time talking about it. Either that or I'll go very into depth, but then we'll go right into the podcast. That'll be roughly the format going forward here. Now, just a real quick personal story about me, in case you guys don't know me that well. It's probably one interesting thing that people find interesting about me is that I owned a coffee roasting business, and at least for a period of time, I would tell people, like, hey, like, they're like, hey, what do you do for work? Well, I'm like, well, I own a coffee roasting business, and I practice sports medicine.

And they're like, you own coffee? A coffee business? I love coffee. So, it's funny that they would really gravitate onto that. It's kind of a unique job, and I had that business for about two years, and then we recently closed. But we actually roasted coffee over a barbecue with a stainless steel drum that I created. And then we eventually, I made a bigger one that would actually do about 10 pounds at a time. And then after that, we kind of focused more on nitrogen cold coffee, which is becoming much more popular now. Actually, when we started, there was literally no place you could find it. And even where I live right now, that's probably a good 20 minutes drive before you find one that's really good.

So, I know a lot about coffee, more than I probably ever should. But because of that, when I meet people for coffee, we really got to get specific on the spot because I do not enjoy burnt coffee because there's a lot of that around. All right, so thanks for spending the time to listen to this podcast, guys. I'm very appreciative that you spent about an hour or so with me. I know you could be doing a ton of other things, so make sure you do something productive when you're doing this. Go do the dishes, walk the dog, drive a bit, exercise, whatever you got to do. But I hope this is a good learning experience for you.

So, without any further ado, let's get into Michael Shacklock's interview, the author of Clinical Neurodynamics and also the owner of the seminar series called The Neurodynamic Solution. Here we go. Hey, everyone. Joining me now is Michael Shacklock. Hey, Michael, what's going on? Hi, how are you doing? Doing great. I'm glad we were able to link this up because after your seminar, I was just blown away by the amount of neurodynamic findings I find now on people that I would have thought were only musculoskeletal before. Okay, that's interesting. Neurodynamics has been around for 20 or 30 years now, but what I feel we're doing is getting more skillful.

And, you know, in the day, these days where your knowledge is power and skills are nothing, it's really important to keep those skills going. And we're doing studies at the moment that are in the cadavers that are looking like we can really be much more specific than even I ever imagined. You know, structural differentiation. We're now showing we can move a nerve with great emphasis compared with other tissue. So, for me, skills are really important and I'm glad you're finding them useful. Yeah, totally. And I know I looked on your site last night and I saw that you had the brachial plexus plus total shoulder movement plus finger movement.

That was interesting to see just the hint of movement was still a larger differentiation than total movement, although it went more. Yeah, look, I think you could summarize that by saying less can be more. Yeah. Or less can be more informative. For example, if you do a large movement of a limb, you'll get more nerve movement, but you also produce a lot of movement in other tissues. So, the difference between the two systems is not apparent. But if you slow everything down, make a small movement, keep the musculoskeletal stable, and move the nerve from a different location to the wrist extension for the brachial plexus.

In the right situation, you can often produce a bigger difference in movement between the two systems. And that then, diagnostically, can become more informative. So, again, less can be more. Totally. I can feel you're going to have a lot of great little quotes like that throughout this. I listened to a couple of your podcasts recently. There was the Jetpack and also two movement guys had you on recently. Yes, that's right. Yes, yes. Well, so then I thought this one would be, the listenership seems to be more so clinicians. And I've definitely had a lot of interns in my office over the last few months.

And they see these tests and they don't even know that these tests even exist or how to differentiate between neurological versus MSK or musculoskeletal. Can you kind of lead us into that a little bit and just a couple of cases that you might maybe thought used to be musculoskeletal or that might wow the listener in the beginning here so they carry on to the end of the podcast? Yes, to me, there's a couple of situations. Just imagine that we're doing a clinical reasoning exercise and a patient comes to you with certain symptomatology or presentation. If you asked a large number of clinicians who experienced a neurodynamics, what two most important criteria in a subjective would make you get suspicious about a nerve aspect to the problem and therefore justify doing a neurodynamic test as part of the physical examination?

To me, that would be radiating pain and pins and needles. And so when someone has those two features, that's one of the most common alarm bells or clues that we might consider a neural aspect to the problem. And I'm thinking more in the cases of a musculoskeletal problem that has a neurodynamic aspect. I'm not thinking of idiopathic peripheral neuropathies, generic peripheral neuropathies, diabetic neuropathy. I'm not so much thinking of those, although we can integrate some of our treatments with some of those people. And so in that context, I would say a limb pain that comes from the spine, so cervicobrachalgia, would be an example.

And to me, precise technique in that situation can be used to rule out a neurodynamic aspect. For example, if you do the neurodynamic test, if you get to the end, reproduce the person's cervicobrachalgia, and you change the wrist position, and it does not change the limb pain or the neck pain, we would argue that that eliminates a neurodynamic problem for that particular patient. So even though we're using a neurodynamic test to find it as a neurodynamic aspect, we're actually also using it as an exclusion test. So if it fails on the basis that it reproduces a patient's pain and it changes with a remote movement like extension for a nerve root problem, then we would say that that suggests a neurodynamic aspect of the problem.

That's one case. The other second case would be someone who has a neural aspect to, say, wrist pain. Now, there are different forms of wrist pain, of course. One would be carpal tunnel syndrome. Another one would be a fall on the outstretched hand with wrist pain, but no pins and needles or radiating pain. Now, we would not normally think of, oh, median nerve neurodynamic aspect to that. We'd probably think of, you know, musculoskeletal problem, but we can also do a neurodynamic test for that problem. And instead of using wrist movement to differentiate it at the end of the test, we would use lateral flexion of the C-spine to change the movement of the nerve at the wrist to see if that changes the wrist pain.

And again, it's used in diagnosis of a neurodynamic aspect to the wrist pain, but it's not necessarily carpal tunnel syndrome. Right. So, you did say something there that actually, I remember going through school, that definitely when there's radiating or pins and needles, that would be something where we would think of nerve root pain or some type of neurological pain. And obviously, we jump around to things like carpal tunnel and so on. But I've experienced, at least since the seminar, that there's a lady that came in today, actually, before we were talking, that she had neurodynamic positive findings into the shoulder with overhead pressing.

But it wasn't really pins and needles. It was just pain. So, do you find that is the symptomatology really indicative a lot of a neuro problem or are there other qualifiers? Yes, I think there's a really important point here, and that is that a neural aspect to the problem doesn't necessarily mean a neuropathy. And so, you can get – what I'm trying to put forward out there is that neurodynamics is way beyond neuromobilization plus some neurosciences. It's relating nervous system mechanical function and physiology, of course, with how we move because, really, how we move influences the nerves profoundly.

For example, if we depress the shoulder, the cost of the space reduces and applies pressure to the brachial plexus. So, if someone has a shoulder dyskinesia with referred pain down the arm, then we might deal with the dyskinesia as part of managing a brachial plexus irritation. But that doesn't mean a plexopathy. That doesn't mean, say, numbness and paralysis. It can be mechanical irritation and a sensitivity of the connective tissues of the nerve, the neural tissue, in relation to pain production with activity. And that's a neurodynamic – that has a neurodynamic aspect, but it's not necessarily a plexopathy or a neuropathy.

So, by spreading this definition out, we're actually integrating it more effectively with how we move. Well, it's interesting that the – I know that in our profession, we kind of get – we're supposed to cluster into these diagnoses that are just, you know, plexopathy or cuff tear or whatever. It almost seems like there's gradients of these things when we're taking into account the person that has shoulder dyskinesis, you know? Oh, yes, absolutely. And I'm quite, what do I say, firm. I'm quite firm about my conceptualisation of where neurodynamics is placed in the whole biopsychosocial aspect of clinical problems.

And we have medical diagnosis of disease and pathology. That's a medical doctor's job. And some of those produce a dysfunction which may or may not be symptomatic. We know that pathology is not always symptomatic. Dysfunction is not always symptomatic either. But then symptomatology often relates to dysfunction. And to me, skills are so important in determining if a functional problem relates to the current patient's symptomatology. And that's where physical testing and treatment's really important. So, I mean, function's critical. I agree. I totally agree. I had heard the podcast that you did with the two movement guys the other day, or I heard it this morning.

And actually, one thing that stuck out with me a lot with there is that you mentioned this lady that came in before. She was a worker and that had the pins and needles into her arm, but she had shoulder depression. And you had mentioned how you treated it unconventionally for musculoskeletal, but conventionally for neurological, and then you reversed them. Can you go into that a little bit? Because I think that's interesting. You're really hitting on some interesting points here. I think that's very astute of you, that there are some critical elements of how we deal with nerve problems in relation to how we move.

For example, if we have a shoulder dyskinesia, the sort of the bad patterns are elevation, anti-rotational protraction, and that's partly related to hyperactivity of levodoscapially and maybe upper trapezius and pectiles minor. And that usually relates to reduced activity in serratus anterior and lower trapezius, okay? Now, we would say that's a bad pattern, but if you look at what happens at the costoclavicular space, that reduces pressure on the plexus. So for an inflamed or irritated plexus, it could be really good. So what's good for the musculoskeletal is not always good for the nervous system, and what's good for the nervous system is not always good for the musculoskeletal.

And that's called Model B. There are two models, and that's called Model B. When the two don't work together, well, they can be in conflict, and then we need clinical strategies to resolve that competing set of influences. Is it often Model B? I'm guessing it's usually Model A. That's why it's called Model A. Well, yeah, that's a good – it's very influenced by the anatomy and biomechanics. So, for example, if you follow the brachial plexus from the city spine, it starts off with spinal nerves, of course, and then it merges into a plexus. But the scalenes, anterior middle scalene, when they contract, they press on the plexus.

So a set of scalenes that are reasonably loose or not hyperactive is good for the scalenes, but that also is good for the plexus. That's Model A. So they work together. So to release – or help the plexus, you would release scalenes. That's interesting. Go ahead. Yeah, so go further out where you get into the costoclavicular space, and that's Model B. So physical treatments for costoclavicular space area may be – and shoulder dyskinesia might be quite different from higher up in between the scalenes. Well, it's interesting that the – I feel like there's a theoretical perfect spot of movement, you know, that let's just say we want shoulder depression, we want some stabilization in the GH joint or whatever that might be.

And it's kind of foreign to what I think we kind of learn from other movement perspectives, which – but – I mean, I think it's correct. But it's interesting because I'm sure a lot of listeners have not heard it that way yet. No, no. It's – look, this is a developing subject of neurodynamics, and for me, it's critical that we start understanding specifics because if we just – we all know that general can work with some people, but unfortunately, at the moment, there's a big sway of the pendulum in favour of general, which I think, you know, it's absolutely perfect for some people. And the specific can't work without the general, and if we – but if we get skilled at doing – rather than having a philosophical position of one or the other, if we're skilled at both, we and our patients have more choice.

And to me, that's what it's about, skills and choice. Nice. The – I know we – I guess we didn't go too much into actually what neurodynamics is yet from a definition perspective, but I guess – I guess I want to start to you before I, you know, open you up to that, is that you do have a book, which I did buy. It's amazing. It's good. The seminar is great. So anyone listening who – I know we're in an audio format right now, but the demonstrations that you did with the TheraBands, as well as the pictures in your book, I think, speak a lot to the understanding of the physics of it. But can you kind of tell everyone about neurodynamics just as a theoretical – or I don't want to say theoretical model.

They said there's a couple of cornerstones, yes. For me, the definition – the definition for me would be mechanics and physiology of the nervous system as they relate to each other. So, you know, if the mechanical function of the nervous system is perfect, your viscoelastic behaviours, normal slidings, normal tension behaviours are all normal, compressibility is all normal, that's not going to produce a problem in the physiology. But if there's pathomechanics, such as compression, stretch, excessive stretch, and so forth, in that we know that changes the physiology, particularly in relation to blood flow and sensitivity.

Conversely, if there's something abnormal in the physiology, such as inflammatory problem, a nerve can become scarred or develop mechanical issues. We know now that if a nerve doesn't slide normally, its tension behaviour along its course changes. And that we now know that lumbar and nerve roots, for instance, lose their capacity to slide in the frame by up to 90%, which is a massive change. These are usually from scar tissue and disc protrusion, of course. We've also shown, our groups have shown that people who have disc protrusion have reduced spinal cord movement with the straight leg raise.

And so there are now correlations being made between physical problems and synoptology, in relation to nervous system movement anyway. That's one side. The other thing is, for me, there's been a really, especially in physical therapy anyway, there's been a big emphasis placed on flossing or sliding of nerves or neuromobilisation or tensioning. There are different terms used and different methods used. But to me, that's only part of the story. Because if the nerve's compressed, for instance, which is the most common cause from a musculoskeletal perspective, we're applying force to a nerve that's already forced on.

So at best, we're probably producing an adaptive response. I'm not sure that we're producing a corrective or a leviative response. So my PhD is at the moment on how to do this differently. And we're applying some really different principles. And so far, our first clinical trials have really, really good results. So we're kind of flipping it. But my definition to the next step would be clinical neurodynamics, would be clinical application of mechanics and physiology of the nervous system, as they relate to each other, and are integrated with musculoskeletal function. And so I mean, that's the key.

That's the next step. Well, so you mentioned that clinical trial you're doing. I know that you're excited about it. Because I know you talked about it in the seminar. It's funny. When you do clinical trials about all this stuff, you get real scared. Well, you get scared. Because if it goes bad, you've still got to publish it. And you've got to start, you know, you don't understand what happened. But fortunately, ours worked out really well. Can you describe that? Because I think it's definitely an interesting one. Yeah, sure. I can't talk too much about it. Because I'm just putting the last dots and T's on it now.

And it's going to be submitted very, very soon. But I'll just briefly describe it. We had people come into an emergency hospital, the emergency department at a local hospital with acute... People would come in naturally for all sorts of causes. But the ones we invited to join the study were those with low back pain and sciatica, acute severe sciatica. And we put them into two groups, got them into hospital, did MRI and electrophysiology on them to make sure that they had a radiculopathy and that they... We established a cause which is single-level disc protrusion, not multi-level or spinal stenosis or previous surgeries and stuff like that.

They're excluded. And then we divide them into two groups randomly. One group had steroid therapy and opioid analgesics and walking and flexing forward regularly. The other group had exactly the same thing. But we did the opener techniques to reduce pressure in the individual foramen transiently to see if we could ease their sciatica. And this group did so much better than the other group. By eight days, these people were... The worst parameter was 65% better. And there's back pain, leg pain and disability measured by two independent instruments. How long were they in the opener positions with that?

Oh, that's a good question. I was surprised. You know, it's funny when you do something repeatedly, you don't actually add it up. I've been doing it for more than 20 years. And I didn't realize how much people were in the open position in the first eight days. Normally, it's about a one-minute position. And they were told to do it five times. Do that set five times a day. And it increased after six days and so forth. But after eight days, these people were in the open position for 4.6 hours. Oh, really? It's a lot of time. And after 14 days, it was 16 hours. Were they... Because I know that one of the opener positions for lumbar is legs off table.

Were they in that aggressive position or were they more of like... Yeah, they were. It's funny we say aggressive. It's actually aggressive. But remember that the nerve root's under pressure and the frame and positioning technique reduces pressure. So it actually... It's like putting your foot up on a cushion for a sprained ankle. It looked like you just got comfortable right there. Yeah, I'm getting very comfortable here. Yeah, so it's actually... As long as it doesn't provoke pain, in fact, it eases their limb symptoms, which is the objective, it actually does. It's really quite a safe technique.

But we limit it to one minute because we don't want to stretch the disc in that position for too long. Right. So actually, that was going to lead into my next question because the... As I was thinking about, we talked... Because we talked the other day about this clinical trial and we talked about in the seminar too. I kept being reminded of the... I think in the last podcast I heard you talk about it with, you said you're applying first aid to the nerve and then... Because there are symptoms of the leg pain that are excruciating. They're really nerve-based. They're not disc-based, right? A lot of people...

I think you've got to subgroup them, actually. I think there's groups out there that have limb-referred pain. Somatic-referred pain can be from the set joint and many of the ligaments in the spine can do it. Disc obviously can do it. And so that's not quite the same as referred pain from the nerve root due to pressure. And so what we would do clinically would be evaluate their movement patterns, provoking and easing ones, and decide whether it's a pressure mechanism or a tension type mechanism. And so these people who would actually be worse, the leg symptoms would be provoked with extension and ipsilateral lateral flexion and eased with flexion.

It's like a subgroup. It's a subgroup. Were you actually... Were you doing it or did you have people do it with... Were you the one actually applying? No, she was a physio who was working with a neurologist. And it was a collaboration. And they said, look, we're going to do a clinical trial. And I said, whoa, please, please. If you're going to use my stuff, please come. Please talk to me. And they just did it really well. And I've been involved in the methods and stuff like that. And we're writing it up now. And luckily, it went really well. Luckily, we're very fortunate to collaborate with a neurologist in the hospital.

And they admitted these people. It was a very controlled environment. Yeah, it was a kind of a... It was serendipitous to some extent. But at the same time, it was all planned in advance. The opportunity was serendipitous. So, I definitely going through that first seminar, you talked about the vessel or the vein of the nerve. And I found that demonstration really helpful to kind of... And actually, pressing on my own hand, I got a couple of veins in the hand. I'm like, dang, that doesn't take any pressure to really occlude that thing. Very little pressure. Look, we've looked at nerves under ultrasound, neurovascular bundles.

And if you do a cross-section of a neurovascular bundle, and you were talking about your ulnar nerve before, just come up your arm a bit. There's a neurovascular bundle there. And you can see the artery, the vein, and the nerve. And, of course, the artery is pulsing quite aggressively, more vigorously. You can see it quite clearly. And the vein pulses much more softly. Instead of going, boosh, boosh, it goes, whoosh, whoosh, whoosh, whoosh, whoosh, whoosh, whoosh. You sound just like the pulse on there. Well, I've heard it before. And it's very soft. And if you actually compress the head, you can see it all happening.

Compress the head onto the neurovascular bundle and see what collapses first. It's always the vein. And that mechanism exists inside nerve because the nerve is a neurovascular bundle. It's got axons, arteries, veins. So it's the same mechanism. So when you occlude it, because I know that nerves have different sensations when they're affected. So when they're, I know we talked about being pressurized. At what point would, or actually, I guess, I don't know if it even matters from, you know, clinical perspective. If we know a nerve is affected and an opener technique works with it. I guess I'm asking, like, you know, burning pain versus increased tone of a muscle versus atrophy versus, you know what I mean?

Do you, are different clinical expressions, do they reflect different mechanisms? Is that what you mean? Yeah, like the, is it always that the vessel, or always that there's light pressure on it, which affects the nerve in maybe different manifestations? Oh, look, I think initially, yeah, initially, yes, but given time, it probably converges or starts to, sorry, starts to spread out rather into different mechanisms, which might all finalize to be quite similar. For example, if you put severe pressure on a nerve straight away, you know, it'll get paralyzed. You might develop pins and needles for a short time, it'll go paralyzed.

But if you push on a nerve very softly, and there's no response at all symptomatically, and keep it there for a long time, eventually, it'll become paralyzed as well, because you get a neuropathy. But in the interim, you might get pain, you might get aches, you might get throbs, you might get movement-related symptoms, you know, pins and needles, there's all sorts of things you could get. So probably the ones that have movement-related pain to me are probably less severe and more modifiable, and that's my favorite kind of neurodermic problem to treat. The ones that don't have much pain and they're paralyzed, that's really hard.

That's usually a biomedical problem, you know. I don't think we do that well with them. I think we do better with the people who have movement-related nerve pain or posture-related nerve pain. Do you find these people would then have positive electrodiagnostic testing all the time? No, that's in the balance, in my opinion. It's just some people who do, some people who don't. And the electrophysiology mostly looks at large fibers, and there's now been some good studies that show people with neural entrapment syndromes don't always have abnormality in conduction, but they can have evidence of small fiber neuropathy, because a conduction test has emphasized large fibers.

So there's probably going to be more research showing that there are different components to a neuropathy, and different people have different aspects to their neural problem or neural dysfunction. You know what I really enjoy about talking with you, and I enjoy this seminar too, is that you're very calm in the way you cite out the research. You're almost like middle of the road, like, hey, this is what it is. Just take it. Well, thanks. Yeah, research to me is critical. Evidence research, I tend – I'm not very good at it, but I'm trying not to use the word evidence. I'm trying to use the word research instead, because some of the early studies, particularly neurodynamics, were hailed as evidence, and our understanding has been flipped on its head, and so they really weren't evidence at all.

They were the current status, or they were the most recent research. But, for example, early studies did not find loss of nerve movement in people with neural syndromes, but since then it's been found on numerous occasions. And so we can misinterpret or jump too quickly as new knowledge comes, instead of being a bit more circumspect and saying, well, you know, blah, blah, blah, blah, this is how it is. This is the current status, but, you know, these are the further options. And one of my concerns these days is that the clinic is way more complex than a research study. And we have one small study, and we generalize from it, and often it's wrong.

Not the study, but how we use that study, or several studies. So to me, you know, I'm any time willing to quite research, but only on the basis that it's current research. It's not necessarily all the answers. It's a bit more knowledge. Well, I definitely appreciate in your book you put all those references straight away right in there. Oh, thank you. To me, research is critical. Really important. You mentioned, I remember this at the seminar as well, and you just said it a little bit ago, is that so people that have had disc injuries have decreased cord slide. How do you get that back, and how much can it come back?

Yeah, that's a good question. Well, we found that, and I should rightly acknowledge my colleague, who's leading this line of research, collaborating in detail. Marinko Radez, a Croatian physio, a physiatrist, who's finished his PhD now on this, and he developed a method of measuring non-invasively spinal cord movement with straight leg raise. So we're able to use now spinal cord movement as a looking glass into lumbar nerve root behavior. So we know you need the straight leg raise to move the nerve root to move the cord. And so if the cord doesn't move, it probably means the nerve roots are not moving either.

And we also know from other studies that have directly measured nerve root movement at surgery and people with disc protrusion, that the nerve root movement is impaired in a lot of these people. And we found it a 66% reduction in spinal cord movement in people with disc protrusion. Now, what do you do? Is it scarring of it, or is it? We didn't get to the point of finding exactly the minutiae of exactly why the nerve root wasn't moving. We only looked at spinal cord in people with disc protrusion. So maybe if we went back and did a retro study on what was going on there, we would find more. But we didn't specifically go into the little details of why that nerve root's not moving.

But more related to previous research. Now, what do you do about it? The problem, if someone said to me, hey, Michael, do a study on neuromobilization in these people, I would say, just wait a moment. Do not jump forward too far in this because this could produce a classic black hole study. A black hole study is using the wrong methods, wrong technique or wrong independent variable, producing no outcome and in falsely concluding that that treatment does not have the capacity to produce an improvement. You've got to do it in really controlled circumstances, then release it into the wild. And if it works in controlled circumstances, find out why it doesn't work in the wild.

Rather than going to the wild and not working and then just giving up. And so our study in the patients with lumbar adecopathy, we did it in hospital. We did it in an extremely controlled environment. So we knew what these people were doing. They weren't commuting to work in a vehicle. They weren't picking up the dogs, you know, and taking the kids to school and cooking dinner and lifting things out in the backyard in the garden. So what we did was step right back and instead of doing things in an uncontrolled way, we controlled everything and showed that it has a capacity to produce an improvement.

Then we're going to do a bigger trial in a less controlled environment. And if it doesn't work, find out why and what are the patients doing and what other variables might be contributing or contaminating an improvement. So clinical trials to me are scary and they've got to be done really well. And unfortunately, there's a lot of ones that could be improved considerably, but unfortunately, we've taken too much from those studies in terms of negative outcomes. Yeah, yeah. Yeah, so you didn't want your opener one to become a black hole study when it first started? Oh, that was my biggest study, you know.

I would have then had to gone back and do another study and then it would have been two competing studies, why one worked, why one didn't. And it's such a mess. For me, it was just a bit of a step back, do something clear, simple, find out what happens and then spread it out into a less controlled environment. To me, it's a really important aspect. I saw that you, I was looking through your site a little bit and I saw that, I couldn't help but stop on a section of an article that you wrote where it was like, it wasn't a rant, but it was like about nerves being stuck. Yes, that's right. Look, I don't do a lot on the social media these days, but I was just browsing a while ago and saw someone saying we should not be telling our patients their nerves are stuck because there's no evidence for it.

And I thought, well, you haven't been reading the literature. And so I thought, well, let's do a bit of dissection of what evidence is for and against. Let's do it in three phases. And, you know, how do you gain evidence? How do you read literature? And, you know, how would you interpret what goes on in relation to stuck nerves? And they lose 90% of their movement in lumbar adiculopathy. That's called a stuck nerve. Yeah. I saw reading through that thing, there was a, like you have a high, I don't know if you do your own font and text on that side or not, but it just, it kept highlighting that section.

Yes, yeah, I did. Now, having said that, it's a really good point, though. Would you tell someone who's got significant psychosocial mechanisms in their back pain and disability that they have a stuck nerve? And I would be reluctant to. Right. So how you present that's really important, but there's a positive spin to it. So, yeah, look, there are people who have disc protrusions and most likely they don't hurt. And we know that not all disc protrusions hurt. And actually, if you look at these videos on what flexion does for the disc, flexion can reduce disc protrusion of the annulus area. And it opens the frame and takes pressure off your nerve.

So regardless of whether it's stuck or not or whatever you want to call it, this is how you can deal with it. You must move. You've got to flex. You've got to do this other stuff. But on the flip side is people are allowed to know the truth and we are allowed to tell it to them. And there's a bit of evidence now. There's a recent study in England that showed that people, it was a very explorative study, showed that people who did not have radiology for low back pain felt less inclined to engage in rehabilitation. Less inclined. Yes. Now, they said these are patients who are experiencing a lack of radiology, saying we're frustrated at not being cared for here.

We want to know what the heck's going on in our back so we can make an educated decision about our own health. Now, one of the key things that people are promoting these days is negotiative aspect or inclusive aspect in its health decisions. Meet the patient where they are and guide them to a better place. Well, people are saying, well, if I don't have radiology, I don't know what's going on my back. I'm not doing exercises. I want to wait until I find out what's going on. And so some of these people said they felt more inclined to engage in rehab when they had some radiology to explain either anything important or find out that there's nothing serious.

That's interesting because, actually, the person I learned musculoskeletal ultrasound from, they had a saying in their clinic where they said it never felt so good to know what was wrong. So they had people come in that had not found positive findings on anything else, and they were able to identify them under ultrasound. And, like, sometimes the people just cry just knowing that there is something there that's not in their head. And I guess at that point, you can kind of decide whether they want to do something about it or not. But I can definitely agree with that. I don't know. Do you ever find, though, that people that know there's something there, they hold on to it at all?

Or they kind of take, they're like, well, I have an 8mm protrusion. It's not getting better. That's what it is. Uh-oh. I lost you, Michael. Ah, here we go. Here we are. Here we go. All right, cool. Um, where'd you, uh, I don't know where you, can you hear me? I can see you, but I can't hear you. Oh, oh, here we go. You got me now? Oh, here we go. Yes, I can. Good. We're back. Um, where'd you lose me at? Uh, when we're just talking about, um, uh, the idea of, uh, say, dispatresion or nerve root, um, being stuck. And then I said that we, um, we're allowed to tell it, the patient's allowed to know the truth.

Right, okay. And we're allowed to tell it to them. And I was generally explaining that it's how you tell it. It's not, uh, avoidance of radiology isn't really going to make them heal quicker. Um, it's how you, how you present the information to them and how they spin it possibly. There was, um, there's a guy, uh, interviewed, uh, recently that he, he worked with, uh, baseball players, younger ones even, and professional level with, uh, so they, they, uh, upper level, they would always come in with some type of MR or something and you'd find little things, you know? And he was also, he was, he kept saying like, yeah, you gotta be real cautious with these people and don't tell them, yeah, you got a blown out cuff or whatever.

Like, however you phrase it was, he was like, yeah, it's really important. Just let them know it's normal and it's going to get better. And just, here's what we do. You know? Um, yes, yes, exactly. I've had patients say, look, my back looks pretty crappy in there. And I say, yeah, well, my nose is bent to the left. It's pretty ugly, but I still smell, I can still smell with it. Okay. Um, do you, um, you're going to come back to the States here again pretty soon. I saw that you have, uh, uh, seminars that you're doing a 2018 schedule for. Yes, that's right. I'm at Stanford, um, sports medicine, uh, the athletic department there, um, in, in, in a couple of years.

A couple of weeks, two or three weeks. I saw you're going to, uh, uh, Dublin, Ohio with Richard Ohm. Yes, that's right. Yeah, I am. Yeah. That's right. I'll let her in the air. That's correct. Um, uh, let me see. I've interviewed him before. He's a, he's a smart dude. Oh, good. Good. Yeah. I've had some really good communications so far. Yeah. You're going to have a good dinner there. I'm looking forward to it. Yeah. So Friday, first of June, I started Stanford for four days, uh, San Francisco Palo Alto area. And then I'm doing a keynote and some, um, presentations in Denver the following week.

Um, then back to Australia, but, uh, later in the year in, I'm, I'm in, um, Columbus, Ohio, Chicago, Indiana way, northwestern Indiana and, um, somewhere else. Uh, Washington, Washington, D.C. Washington. Um, yeah, there's, uh, are you going to do, you said you're going to do a, so we did, I think, the upper and lower quarter, but there, um, we didn't go an ephemeral nerve. We kind of dipped into, uh, everything below the knee, but we didn't go exactly into it, right? Yeah, that's true. Yeah. Look, remember this is 20 years we're compressed into it. Right. Four days. Are you? And most of this, sorry.

Are you going to, you're, there was going to be an advance. Of course, I think you're going to teach, right? Yes, that's right. Lumber advanced. Yeah, I'm writing that, but basically starting that when I finished this clinical trial, I want to send it off and that's my next project. We've got an, uh, an upper quarter advanced as well and I'm writing a lower quarter advanced, but in that one, the lower quarter advanced, we do much more around the knee and the hip, um, femoral nerve, saphenous nerve, a bit of obturator, um, adolescent growth spurt and hamstring differentiation between nerve and muscles and so forth.

Tibial nerve as well, um, um, um, uh, peroneal common fibula or common peroneal nerve, a number of other ones. Mm-hmm. Um, I, uh, I, I know that you wrote something on your site about, uh, plantar fasciitis first, uh, uh, medial calcaneal. Mm-hmm. Can you elaborate on, on that? I'm sure a lot of people have, uh, they, they, they have a lot of foot problems in the morning. I don't, I'm sure that's, uh, might be more of a nerve thing, right? Maybe. Yes. Well, nerves are, nerves are influenced by inflammation as other tissues are. Mm-hmm. Um, and, um, they get swollen and the idea about inflammation is that it builds up overnight and then when you stand on it, it's got more pressure there because of swelling or chemical changes and so forth.

And you move and so forth and it can improve with movement from there. Um, but nerves are not accepted from that and so you can get problems. But that area is called model one, meaning what's good for the musculoskeletal is also good for the nerve. So pronation is a bad thing for the ankle orthopedically or MSK and it is also pressure, puts pressure on the nerve and puts tension on the nerve. So decreasing pronation is a good way of helping some people with tarsal tunnel syndrome. So those, those ones then are, I know, I know one thing we went through in the seminar, which actually I was going to ask you about today because I, um, I needed a little bit of clarification.

And you don't have to read in your book, I needed a little bit more too. There's opening dysfunctions, there's slide ones, and there's tension. Um, and then, so I guess the one in the ankle right there, if we're, if we're talking about pronation, would that create? Tension around the convexity? Yes, it's, yes, it's, it's both actually. As you pronate, you elongate the tibial nerve in the, in the tarsal tunnel, close to your tarsal tunnel, um, and you compress it. So there are two mechanisms happening at the same time. And so reducing pronation shortens the nerve, so it at least reduces tension, and it also opens the tunnel a little.

So it's reducing compression. So then. So part of treatment is to actually do a supination maneuver or a static opener, as you would do an opener for a lumbar radiculopathy. Okay. Would that then be, is, with a case like that, would you ever add contralateral slide mechanics at all? Or is it just unmerited? No, not normally, no. I reckon that the contralateral mechanism doesn't go, doesn't go, well, I can't see that it, there's no evidence at the moment that it goes as far as the tibial nerve. Look, it may well do. I must admit that it's a full end range of a stretch. For example, if you've got someone in a full slump position, full dorsiflexion eversion, and you do a contralateral knee, a straight leg raise, there may well be a diminution of tension down the lateral limit of the tibial nerve.

But that's, to get that effect, you've got to wind it up maximally anyway. So why wind it up to reduce tension? Mm-hmm. Why apply tension to reduce it? It doesn't make sense. So if you're going to, but in a knee-flexed position on both limbs, I don't reckon a contralateral mechanism will work. Okay. It's too slack. So I don't use it for peripheral problems. I use it for spinal, but not peripheral. So that's mainly spinal IVF. Yeah. Even further down into, like, the hip that would be too distal? Actually, that's getting interesting. We know that when you do lateral flexion of the lumbar spine, that the intrapelvic part of the sciatic nerve moves.

So if you do contralateral lateral flexion, the intrapelvic part of the nerve becomes tighter. We know that. Also, if you do, in a slump position, if you do knee extension and measure the sciatic nerve movement distally in the thigh with knee extension, and you repeat the maneuver with neck flexion, the movement of the nerve in the thigh reduces the distal movement. So there's definitely a mechanical connection that operates between the neck and the nerve in the thigh. It spreads that far. And I'm just thinking of a patient I saw a while ago who's an elite cricketer. You don't have cricket much in America, but it's a pretty crazy sport.

And the bowlers are like the pitchers. And they have a very specific mechanism for pitching. It's the legal requirements about how they move. They have to raise their limb really high and then slam their foot down on the ground to generate momentum through their whole body to do the bowl. And that's a terrible mechanism for the hamstrings, the sciatic nerve. Because their leg's straight and it's slamming on the ground with a straight limb and their hips flexed. And so these people get tendinopathies at the hamstring section, and they get inflammatory changes around it and scarring into the sciatic nerve.

I've seen them, spoken to the surgeons who operate on these things and seen op reports. And I had a patient who had this, and you can see it on radiology. And so this guy had posterior thigh pain, and we could reproduce it with the slump test. Neck movement and foot movement changed it. But holding it there on response, reproducing his thigh pain, doing a contralateral knee extension with dorsiflexion, reduced his thigh pain. And we know from surgical report that there was pathology between the sciatic nerve and nescal tuberosity. And we could reproduce it with a slump test, and we could decrease it with a contralateral neurodynamic test, which fits with the spinal cord mechanism we talked about before.

Yeah. Just to make sure it's clear to everybody, can you explain the mechanics of that a little bit more? Yes. Look, this is a proposal I made in 989. I remember making the models and the physics and stuff like that. And I've held it for a long time, and finally we've validated it through Marinko's work in Finland, where we collaborated. And what we found was, well, the proposal I made was that if you move the spinal cord down in the spine, it reduces tension in the nerve roots. Okay? If you move it up, it tightens. That's not particularly novel, but what I said was if you do a neurodynamic test, such as the straight leg raisin, it will bring the cord down, and it will therefore reduce tension in the contralateral nerve roots.

And through a series of studies, we've now validated that. So we now know that when you do a neurodynamic, contralateral neurodynamic test, you can reduce tension in the nerve roots and dura in the cord or equina on the other side, the lateral side. When you first found that, did it just blow your mind? Yeah, I was so happy to see my theory validated. To me, that's a holy grail of science, having your theory validated. And that's been a source of great satisfaction for me. Yeah, it really has. Yeah. That'll be your last impression on Earth, really. Well, I have said that when I die, I would at least like to have given neurodynamics, contralateral neurodynamic testing.

I'm sure that'll be – if we can make a gravestone with maybe a TheraBand test on it. Oh, yeah. TheraBand one. Yeah, that's funny. Yeah, yeah. For the people listening, I do a demonstration on a triangulated set of TheraBand and we show spinal cord movement with the contralateral as a physical demonstration. And it's very illustrative. It's also very simple. Yeah, it was – I actually – I made one for the – to demonstrate for patients in my office because actually after doing your stuff with differentiating factors, but also to Justin Dean's the yapping, I have to preface it and frame it with this is going to seem really silly, but – and if it works, I'll explain it.

Yeah, exactly. Look, yeah, I agree. And, you know, with the dermal traction method, the yapping, you know, they're taking force off nerve, really. That's one of the mechanisms that I understand. But that's one of them. And, you know, it's like someone with an acute nerve problem, MSK would give them first aid. Why not give nerves the first aid? You know, why not take force off? And I see that as having great potential. Mm-hmm. You know, something I've been playing with since I came from the seminar was that – so we had the unilateral openers for the cervical spine. So then I actually had someone who had bilateral symmetrical symptoms, and then so I'm like, hmm, which side should I open?

Yeah, what do you do? So I distracted, but – Yep. What do you think about – is there – do you have a contralateral or a bilateral opener that you can think of? You have to use – you have to use just straight flexion, and that's all very well, but they often have an aspect of it that's more – is asymmetrical. So I'll often use the – that aspect to emphasize one side. For example, if their right side is a bit worse than their left, I'll fully flex them, and they'll open the right side a bit more than the left. Mm-hmm. For everyone who is – I'm sure that when I'm – probably the first three hours of the conference or the workshop that we did, I thought, holy crap, I'm going to listen to this all over again.

So for everything that we've said already, what is included in the seminars that you do? Okay. First hour and a half is a deconstruction and a reconstruction of neurodynamics so we understand and apply it differently. It's actually, for me, one of the most enjoyable parts of the course because the eyes start opening and people go, gee, I never thought of it like that. Oh, we have these new opportunities. And so to me, that's the reconstruction of new opportunities. And then we go into diagnosis, which – with neurodynamic tests and palpation. And we learn how to exclude nerves. As a presenter, I think we have a responsibility to be pretty conservative and on pretty firm scientific ground.

And so I don't present so much neurodynamic tests as a method for implicating neurodynamic problems, although it is, I present it so that we are trying to exclude a neurodynamic problem with ongoing testing, clustering and so forth. And if it fails exclusion processes, then we have to consider it. And that way we're not biased in terms of trying to make every – you know, when you have a hammer, everything looks like a nail. You know, I think it's incumbent upon a presenter not to sell the approach. I think it's important to have inclusion and exclusion criteria that, if possible, are well validated.

And it's shown to be effective. And then within that, how do you modify your diagnosis and treatment physical techniques for the patient's individual needs? Because so many systems are great for certain people, but often they're not flexible enough for the patient. And so you've got inclusion and exclusion criteria, and you've got a method for making it flexible for your patient's needs through skills. Yeah, it definitely seems it's not like a – it's not a concrete system that we went through. It's more of just a test and figure out what it is or what it isn't, right? Well, partly that. But I think the strengths are that it's got very well-validated mechanisms.

We know that pressure change on nerves. We know they slide. We know they develop physical impairments. And there's now good evidence that shows that, you know, they often correlate with the physical – with symptomatology. And there are now some good studies that show good therapeutic efficacy. There's been a study just released recently by Thomas Volney in Poland. They showed that sham treatment for carpal tunnel syndrome, sham neurodynamic treatment, was not as effective as authentic neurodynamic treatment. And it also changed conduction latencies as well. And that's also supported in a study by Job Bielowski from the east part of the U.S. as well.

So there's two studies now that show that the real thing is better than sham, better than placebo. So I'm pretty happy with the evidence. And it's our responsibility to use that or stand the course on that basis of that evidence. But, you know, acknowledging shortcomings and limitations, which is a natural part of any modality. Because neurodynamics is a modality, really. It's not a solution for everything. So, well, when you wrote that – how long did you write that book, that green book? Oh, I finished that. That was published in 2005. So – Oh, the green one? You mean the brief book, the biomechanics book or the clinical neurodynamics book?

It was a – maybe I'm thinking a different one was green. Clinical Neurodynamics. Yeah, that's the blue. That was in 2005. So I'm curious that – so when you – so you spent a lot of time writing that. And I see some of the techniques used in there. So then you – when you started the courses, what were you trying to solve by doing workshops? Spread the word. Get patients treated in that way if it's necessary and develop – and skills development. You know, I still think that, you know, skills are important. And I know that there's a lot of argument against this. That's generally, you know, effective.

Why worry about skills? It's only more expensive and doesn't necessarily give you better outcomes. But I'm not willing to – well, there is still some evidence that specifics can count, and I'm willing to work with those. You know, there's a – in the National Health Service in the UK now, a lot of low back pain treatments. It's a social welfare system in that context. A lot of back pain patients have been given a brochure and told what to do. That's it. And there's a big movement of people from – who are not quite satisfied with that. You know, they still have back pain going to private clinics and paying themselves because they want some action.

And so that, to me, is where I want to be. I want to be where the action is. You don't want to go fishing where there's no fish? No, that's true. Yeah, that's for sure. That is for sure. I know that you've been excited about that clinical trial, but is there anything else that you are excited to learn about personally? Yes. One of the things that I'm really keen on is a study that was done recently where they found – did you mean in neurodynamics? Oh, anything. I knew you were going to tell them about your smoker. Yeah, I've got a really good kamado at the back here that I'll get going soon. A ceramic kamado, yeah.

There's a study done where they looked at the elasticity and the extensibility of peripheral nerves in different regions along its course. And this is something I wrote about in 1995. My contention at the time was that the nervous system is not mechanically uniform in its behavior. It's specific. It has variations along its course according to the local needs. And this study, and it's on the website, neurodynamicsolutions.com, is a feature article if you want to read it. But basically what they showed was that a nerve between joints, so a long part of the bone, the extensibility is different from across the joint.

And they tried to relate it to Sunderland's proposal in the 1970s that the protective mechanism of axons in nerve was produced by the connective tissue of nerves. So epineurium, perineurium, and so forth, which is all logical. So the extrapolation was that nerves will be tighter with its more connective tissue in the nerve. Or they'll be less extensible, less elastic. Well, this was not. This was the other way around. Was it more connective tissue? Was it more elastic? Well, it's actually the amount of connective tissue did not correlate with the lack of extensibility of the nerve at that location.

So what they found was across joints, the nerve was much more extensible. Between joints, it was less extensible, independent of the amount of connective tissue in the location that they were investigating. So across joints, there was more connective tissue, but that didn't make it less extensible. In fact, it was still more extensible across joints. That's not the telescoping phenomena then. It's something different. It relates to it. Now, as you straighten your knee, for instance, you expose the tibial nerve behind your knee to much more elongation force than you do the tibial nerve down the leg or the sciatic nerve up in the thigh.

So what the tibial nerve does is it responds to its local mechanical effects. And so it's not just about connective tissue. It's about what it does, how it functions, what it needs. Do you think then, is that, I'm just, I keep thinking about like developmentally, like, you know, like a lot of the body will adapt to the stresses put upon it over time? Yes. Probably what happens is a bit more friction there, so it develops more connective tissue, but because it's stretched more, that softens and it has a viscoelastic response. So there's many mechanisms. But for me, that's really important for rehabilitation because how we move produces local effects on the nerve.

And if we change our movement, we're likely to change the local effects on nerve and therefore the nerve movement. And the balance of functions along the nerve is specific to the individual. So do cricket players need to change feet once every five years? I must say, they probably need to change sports. That's a tough game. That particular movement pattern is really difficult. It's not at all natural. But taking what I said before earlier, further, if we can change, if the nerve responds to local forces and changes according to needs, a problem is that if it lacks movement, its ability to adapt is not complete.

And there's a study done where they created the classic adhesion model at the hamstrings where you get a ruptured hamstrings and you get an adhesion between the sciatic nerve and the hamstrings. What they did in this nerve model was create the adhesion that they think we see clinically. What they showed was at the point of the adhesion, the nerve sliding was small. The extensibility of the nerve was very small, but between that point and other areas along its course, it was massively increased. Because they're making up for it? Yes. Now, the amount that they increased put it into a strain value, which is an ischemic value when you elongate the nerve normally.

That's the 8% rule? Yes. Yeah. Very good memory. 8%. The strain values in the adhesion model were way above 8% for a normal knee extension movement. So, this nerve is now in an ischemic range with knee extension when it would not normally be that way. And so, after 38 weeks, still not recovered. With these people then, these people would probably have no back pain and they might just be… This particular adhesion model was an animal model. Got it. You couldn't ask them. Yeah, no, they don't talk too much. And, yeah, so… But that was reproducing what we see clinically, and so it's a model of what we think might happen clinically, but it's not yet been studied directly.

Okay. That is interesting. You're dropping some gold down here at the bottom of the podcast. Well, to me, it's a great area for study, and, yeah, that's a great… To me, it's… I'm really enthusiastic about that part of the future of neurodynamics. Well, I think we should make a really good black hole study about it then. Just do it right now. No, we could do that. It's easy to make black hole studies. Not finding. Where can everyone find you? Where can everyone find your book as well as your… Oh, sure. Okay, my book is called Clinical Neurodynamics, A New System of Musculoskeletal Treatment, or just clinical neurodynamics.

That's published by a group called Elsevier, E-L-S-E-V-I-E-R, but I sell it on the Neurodynamic Solutions website, although I wouldn't… I would recommend that you shop around. Amazon can do a better price than me, so I'm not suggesting you come to our website. You could if you want. Neurodynamicsolutions.com is my website, and you can follow us on Twitter at Neurodynamics, Instagram at Neurodynamics, Facebook, Michael Shackock, or Neurodynamic Solutions, a lot of different places. And YouTube, I have a Neurodynamics channel on YouTube, which has three videos. Three videos, but I think that TheraBand model is on there, right?

Yes, it is. That's worthy of going already. I think that's worth at least 50,000 views just alone. I think it's very simple, very illustrative, and it shows how it really works. Yeah. I see also, too, that I didn't go on to it yet, but I'm curious to see what's behind this wall. There's a… You plug in your email, and you get updates from the Neurodynamic Solutions website. Oh, yes, that's right. You can go to Neurodynamicsolutions.com, and just enter, you know, there's a tab there for info, I think, and you can click that and just put your email address and hit send, and we'll register you for email updates if you're interested.

Nice. We don't spam. We only send three or four out a year. Yeah. More? I want some more shacklock, though. I want a little bit more once a month. Oh, good. Oh, really? Okay. Well, I'm going to do it. But by the time you write an article, it's a day's work. Every time you write a short article like that, you've got to put it up on the website, you've got to modify it, you've got to get onto other media. It's actually quite a job to write something quite short, and so time's my issue, really. It's usually… This is usually after midnight, so I don't send a lot of them, but maybe I need a team. I should get a team.

Right. There's… Actually, I don't know if I ever told you the… So, my website, like, we… I have, like, 250 pages. A lot of the articles are, like, 7,000 word count. Wow. But I never proofread. I have to have an editor. I will not go through back again. I basically vomit on a paper, and I say, please organize this. Oh, that's probably a good idea. You know, my book's 250,000 words, and I didn't have an editor. No one copy-proofed it. I did. I was the only one who did it, so it's likely it's been okay. I proofread my own stuff. I don't get anyone else to read it, actually. Yeah. I don't have time.

Yeah. I definitely will skip by small words, small misspellings, and all that kind of stuff. So, I always look like an imbecile when I… That's when… It's what you're articulating that counts. Right. Did we forget anything before we close up on here? I don't think so. I think you've done a great job, and thank you for the opportunity. It's a real pleasure. I love to talk about neurodynamics, and it's a growing area. It's an exciting area, and if anyone wants any more information, feel free to contact us, and thank you for the opportunity to be on this podcast, my friend. Yeah, man. Thanks for being on.

This is a great honor. So, I learned a ton from you already, so you already changed the way I practice. So, thanks. Thank you. Okay, that was the interview with Michael Shacklock from New Zealand. So, you hear he has an accent, right? All right. So, that was session number 91. If you're looking for the show notes on that, and as well as the transcript, go on to p2sportscare.com. Look up Michael Shacklock podcast, and you will find it. Also, the link, direct link will be in the show notes attached to your audio player as well. Young clinicians, if you're looking for videos, articles, and studies to share with your patients, I have a ton on there.

So, use that search function. You're going to find a ton on it. By the way, this is 91 into the podcast here, so there is a lot of relevant information you can share with people. And if you don't know the reason why I actually started this podcast, it was because I was having a lot of the same conversations with patients. So, I thought I would record it, some of the most common questions, answer them comprehensively, and then share them in a group. So, if you're looking for something like that, then you should dig back into the archives and find something that is useful for your patients. Because, really, to be able to make a dent in people's injury or their aches and pains, we have to make sure that they understand their care and be able to drill in good movement patterns, at least that's in my opinion.

And a lot of times, pain is the stopping point for people's care, and that's not always the right thing, at least in my book. So, again, that's p2sportscare.com. And, as always, be good to each other and leave people better than how you found them. I'll talk to you guys next week. Subscribe. Like the show. See ya.