187. What We Get Wrong About Lateral Hip Pain | Alison Grimaldi, PhD

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post-partum months, often their Eastern levels are at a little bit of a low there as well.

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And then they've often got poor pelvic control coming out of, you know, those months of pregnancy

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and then they might want to start running to get rid of that baby weight and really not.

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So it's so important that we try to address that as quickly as we can because if we can

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get a patient a better night sleep, everything starts to turn around and feel much better.

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Welcome to Medicine Redefined, a podcast focusing on helping you reclaim ownership of your health.

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weight list, visit refininghealthrx.com. All right, let's get into the episode.

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Today we're joined by Dr. Allison Grimaldi. She's a fellow of the Australian College of Physiotherapists,

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Principal Physiotherapist at Physiotech and Adjunct Senior Research Fellow at the University of

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Queensland. With over 30 years in clinic and research, Allison is a go-to authority in HIP,

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growing, and Pellumbu pelvic disorders. She earned her PhD at the University of Queensland.

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She's co-supervised multiple doctoral projects and presents internationally on HIP biomechanics

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at evidence-based rehab. She founded HIP Academy in 2020 to help clinicians translate research into

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practice. She has published widely, pioneered real-time ultrasound for HIP muscle assessment and

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still keeps an active caseload from everyday movers to elite athletes and running dance and field

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sports. In part one of this two-part series, we unpack the complexity of the HIP Lumbu pelvic

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region and why misdiagnosis here drives poor outcomes. We focus on extra-articular anatomy,

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especially the lateral HIP, which is still commonly mismanaged. We'll cover why

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Tricotiric presidice is over-cult and how to correctly identify gluteal tonnopathy,

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the anatomy that drives compression at the lateral HIP, the clinical test that actually

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move the needle and the simple daily tweaks that stop pain fast. We'll also compare injections

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with non-interventional care, discuss the landmark trial Allison helped lead, and where

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PRP fits alongside rehab. As I mentioned, the HIP is complex and there's no way to do it all

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in one sitting. So our goal today is to give you clear mental models and a plan for your own

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symptoms or your patients. Enjoy. All right, everyone. We have Dr. Allison Grimaldi here in front

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of us today. Dr. Grimaldi, thanks so much for joining us on the show. No problem. Thanks so

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much for the invitation. Great to be here with you. Yes. So there's a lot of joints in the human

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body, right? There's the knee, the ankle, the shoulders, the elbows even. Why the HIP? What got

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you so interested in researching? Well, I think it's a familiar story for many in that I'd had my own

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HIP problem, you know, earlier, so in my early 20s, I suppose earlier in my career and it was

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something that you'd go along to courses to try to learn, you know, for example, and then,

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you know, went to the literature and there was so little back then on the HIP. And, you know,

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I really couldn't get the answers that I wanted for my own self. And so then I had to sort of

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reflect and go, right, well, I'm going to have to figure this out myself. And so, you know,

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that sort of headed me down into the direction of sort of doing deeper dives into what information

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that we did have, trying to make clinical links between that information and eventually sort of

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that headed me into research. And, you know, certainly my area of clinical interest has been in the

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HIP, but yeah, my own HIP sort of that out, which is good. But yeah, it's something that I think really

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was under investigated, you know, that 20, 30 years ago, but it's been such an exciting space to

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be in because there's been just so much research and information, you know, coming out, you know,

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in this last 10, 15 years, there's just been an explosion of research. And so it's been a really

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exciting space. And I guess now the challenge for a lot of clinicians out there who are wanting to

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understand the HIP is that there is just so much information now. And so now it's trying to, you

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know, figure out what's important and, you know, what is the clinical relevance of the information.

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And so a lot of what I'm doing now is trying to sort of help other clinicians with, you know,

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deciphering the research and condensing the research messages, I suppose, and putting it in a

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more clinically relevant framework. Love that. So, I mean, we're obviously very excited to get into

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all those topics that we're going to talk about that you've really been preaching about

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that we've learned now in the last 10 to 15 years. And I was prepping for this. I'm just learning

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about how complicated the HIP is. And this goes beyond just, you know, our training for

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ultimation, I mean, ultimation a little bit more as force medicine. Why is it though that we are

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now playing catch up with the hint? What was it, you know, in the past that we weren't looking at

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that we now are? Yeah, it's interesting. I think there was a big lag in the research because

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well, one, there was a lot of research in back pain. And of course, that is a hugely impactful

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condition. So we understand why there was a lot of research focused in that domain. And then

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there was a lot of research also, knee and shoulder perhaps. The HIP lagged a little bit, I think,

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because it is a complex area. It was quite difficult to research in terms of like muscle,

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you know, understanding muscle around the HIP. Then it's really only, there was one EMG study

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in the 1970s, only one. And then it's only been, you know, in this last decade that we've actually

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had access to form and wire information to understand a little bit more of the function of the

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deep HIP muscles. And we still don't even have enough of that. But we do have a lot more information

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now than we did. Yeah, I often like to help people get one of the reasons I think that the HIP is

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more complex than perhaps any other joint. And I'll keep the spine out of this, but I'll just

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talk about peripheral joints, because you have an overlap with multiple specialties, right? So

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we were talking about this offline. And you've got the orthopedics or musculoskeletal folks. You have,

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you know, pelvic pain is so an entity and you have urology, you have GYN, you have a lot of

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referred patterns coming from the GI system as well that could manifest as like proximal, you know,

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superior hip pain, even growing pain that we might talk about a little bit about. And then,

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of course, you know, you have the fascia, the skin, all the structures, any type of scar related

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stuff that could potentially cause it. And so oftentimes, they are these, in medicine at least,

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we like to create these boundaries, right? So like when it comes to the hip or the pediatric surgeon,

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look at the ball, the socket, the tendons, you're going to stay around that. And then the neurosurgeon,

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or maybe peripheral nerve surgeon, like you're going to mess with the nerves and then the GYN,

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or urologist, like this is your territory, whereas like the body doesn't really respect that. And

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I like to tell people that bodies don't reach textbooks. And oftentimes there's overlapping

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syndromes and adds a ton of complexity. So, so let's maybe start by keeping it simple.

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I think it would be worthwhile for the audience. If you're not watching, just to kind of conceptualize

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what the hip joint anatomy looks like. So maybe just give them a primer of the main structures.

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Maybe we can do the inside of out approach that you like, starting from the, you know, the osteocinematics

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of that moving out to the main attachment. And then we can talk about perhaps the lateral hip

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pain and the infamous trochanteric brosilitis. Okay, so we just want to talk about the anatomy of the

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hip. So if we think about bones first, the hip joint is a ball and socket joint. And so we've got

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usually a nice congruent socket. So a socket that sort of matches the shape of the head of the

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femur. We should have a fairly spherical head of femur for our typical optimal anatomy, perhaps.

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And so that ball and socket joint makes the hip joint inherently quite a stable joint.

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And then we've got multiple sort of layers of muscles around the hip that sort of attach, you know,

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from the pelvis down onto the femur there and moves the hip in each direction, of course.

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And so around the hip joint, of course, we have the ball and socket joint and we have the

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capsule and ligaments that are around that hip as well. So those passive structures, so the shape

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of the ball and the socket and the capsule. And then we also have the labrum. So the labrum is a

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fibro-catalaginous piece of tissue that joins on all the way around the edge of that socket. So

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that helps make the socket deeper and helps improve stability and help protect the hip joint.

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So all of those passive structures are important, as I said, for both stability and health of that

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joint. And then we have all the muscular systems outside that help us, you know, move the joint

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and control some of those large joint forces that we expose the hip joint to during every day

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movement and function. And then we've got nerves, of course, that serve the muscles, serve the joint

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and, you know, transit sort of through those muscles as well. Don't know how deep you want to go

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there. So I think that's good. I think hopefully people, if you're as long as you're not driving,

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if you just pull up a picture, you'll be able to get a good sense of that. And I think as we go

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through the specific pathologies or maybe some of the syndromes, we can, when we can highlight

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some of those. So lateral hip pain, let's start with there. And again, as complex as physiology is,

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we want to simplify it, right? So we like to put things in different buckets to make it easier for

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us. So we can make the diagnoses. And Allison, I gotta be frank with you, I don't really know exactly

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what the healthcare business model in Australia is. But for us, we want to do that for diagnostic

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purposes. So we can get bill appropriately, get reimbursed. So for lateral hip pain, I see this

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all the time. And I have the added advantage, much like you where I'm doing diagnostic ultrasound

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illness, anybody who comes in where there's a question on what might be going on. Yet there are

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people who, on a routine basis, almost a daily basis come in and they say they have

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bursitis on the outside of their hip. And that's what they're talking about when they have this pain,

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there's a bone, it's called a greater choke entries, talked about, and there are a bunch of

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different burses that go through there. But this diagnosis of trochanteric bursitis and you inject

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that's something that just does not seem to go away despite formal changes being made to

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greater trochanteric pain syndrome for over a decade now. What can you tell us about that? And I'm

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curious, you've been doing this a lot longer. How often do you actually see, you know, subglute max

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bursitis or trochanteric bursitis as it's described normally? So I guess, you know, clinically,

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it's something that we see intermittently, but almost always associated with changes in the

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gluteal tendons. And the research studies that we have available suggest that it occurs in 20 to

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30% of people who have trochanteric pain, so pain over their greater trochanters, which if you do

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have visual sort of is over here. And so that is usually in association then with changes within

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the tendon. And the evidence we have to date suggests that isolated change in the bursa is quite

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rare. So two to eight percent with the information we have available at this point in time. And we

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can also get changes. So not only in the tendons joining on to the greater trochanter, but even in the

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IT band, the earlier to your band that runs over that greater trochanter there. And so often with people

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with trochanteric pain, we may have multiple sources of pain there, but it seems that the dominant

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issue is the tendon issue. And then plus or minus, you might have some changes in the adjacent

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bursi or the IT band. How often in your experience and your reading of the literature, will you see

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some of the subglute medias bursa or the subglute medias bursa, those be irritated. And I'm curious if

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you see that when you're using your diagnostic ultrasound effect. Yeah. So it seems to be less common

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than the trochanteric bursa or the subglute medias bursa. But certainly that can occur when we

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sort of see that change. It's often not as obvious because the trochanteric bursa is bigger when

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it's got some extra fluid in it. It's much easier to see on ultrasound in imaging studies sometimes

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with MRIs, sometimes I think it's hard to clearly delineate, you know, where that hyperintensity is,

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but if it's sort of below the tendons, we're thinking subglute meds, subglute med. I can't tell you

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the exact figures on that. I don't think we've got studies that are large enough in, you know,

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breaking it up into the different, but it certainly does occur, but it's not really something that's

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going to change our approach because it's all related to the same mechanism and that sort of that

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compressive sort of loading or that combination of compression and tension of those soft tissues

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over the side of that bone there. Yeah. So let's talk a little bit more about that, right? People

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might ask, well, why does this happen? I've actually been getting a lot of people who come in and

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they're just interesting in the why and less interested in getting better, believe it or not,

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which is cool. I respect that. You know, I often ask, well, can we do both? But some people are

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okay with the pain and they just want to quote unquote solve the problem, root cause, so to speak.

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So you mentioned you got the glute minimus, right? Which is a bit more anterior structure,

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a little bit more in the front, but again, it's one of the glute muscle smaller ones. If the glute

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medias, the glute max is the big muscle, that's going to be your workhorse power muscle. It's more

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responsible for like sprinting and that kind of stuff. That's typically people think when they think

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gluteus, why are the glute medias in minimus, the stabilizer muscles, like you said, why are they

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susceptible to compression? What structure over them to tee it up for you is what's going to cause

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that irritation and why is that the one or those two, the one that are most often implicated in this

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trochanteric pain we're talking about? Sure. So it's really around the anatomy of this local

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region. If we're just talking about mechanical causes, of course there are other contributors such as

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hormonal, metabolic, you know, and of course pain and persistent pain also has like a social

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driver's, but if we're just talking about the local mechanical forces here, then we have the

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gluteus minimus is that deepest gluteal muscle that sort of sits on the side of the pelvis, we often

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think of the glutes as being on our backside, which they are. The glute max is that big muscle

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at the back, but the gluteus medias in minimus are more fans of muscle at the side of the hip,

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and the gluteus minimus joins into the front of the crater trochanter, so the front out to edge,

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so the anterior facet hip, and then we have the gluteus medias that is over the top of that. It's a

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bigger muscle, so a very strong muscle in a normal healthy muscle, so it's a muscle in the body

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that has one of the largest physiological cross-sectional areas because it's lovely sort of fan,

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sort of multi-penate sort of structure, so it joins over to the lateral facet of the

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greater trochanter, which is like the side, the very outside of that bone, and so then over the top

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of that, we've got the iliotibial band or the ITB, IT band, and so it joins from the side of the

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pelvis, runs over the side of that greater trochanter, that bone at the side of the hip,

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then it runs all the way down the side of our thigh and joins it just below the knee there,

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and so those tendons and the bursi that sit between the band and the tendons and the tendons

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and the bone, as they can get compressed around the side of that bone, and so we call that insertional

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tendon optic, because it's sort of around the insertion of the bone as it's sort of coming around

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the side of that bone, and so I think that anatomy just predisposes to higher levels of compressive

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load, and compression is normal, but it's just if the area is exposed to high levels of compressive

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load, either a sudden peak of load or repetitive high loads over long periods of time,

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that we might get changes in those tissues, and eventually we might get pain, but the iliotibial

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band, when we are in particular positions, that band will wrap around the greater trochanter

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and cause that compressive load, and so that will be in any position, so if you think of an IT

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band stretch, so anything where your knee is across your body, or your hip is out to the side,

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so hip adduction, adduction, that will wind up the iliotibial band, and we've got some nice research

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from Burnbound and colleagues quite a while ago now, but they managed to put a little force

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transducer underneath that ITB in a live human, and show that significant changes in compressive

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load at the greater trochanter there, as your knee moves across your body, or as you move into

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that position of adduction, but even without the iliotibial band, even just because those tendons

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join over the side of the bone there, when you do move into adduction, the under surface of those

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tendons will be compressed by the overlying fibers, and we tend to see the change or the

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pathology in these tendons start to develop in the under surface, because they're the parts of

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the tendons that are exposed to a most compressive load. For folks at home, could you give some examples

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of things that might contribute more stress onto that IT band, like deep chairs or leg crossing,

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things that are going to wind up that IT band, and then also how does our gate pattern and

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walking mechanics, how do they layer more load on top? Sure, that's right, so we can have

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positional forces that are purely related to where the hip is and how much that band is wound up,

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and so sitting, for example, when we're sitting if we cross our knees, so one leg over the other leg,

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then that puts the hip in an adducted position, so that does wind up the iliotibial band and

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increase that compression. The other thing about sitting is that the quiz that ITB, it's sort of

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part of a broader fascia at the side of the leg, the fascia line up, and that fibrous,

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fibrous sleeve, if you like, it is also continuous up into the gluteal fascia, so the fibrous

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sleeve over the glute that runs up into your back, and so when you've got your hip flex,

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that does tend to also wind up that fascia at the side of the hips, so a lot of the people with

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gluteal tenopsy or lateral hip pain will report pain sitting in ditches or when driving,

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so in positions where their hips are more flex than 90 degrees, because that tends to wind

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that pressure cooker, if you like, from the iliotibial band tends to wind that up, and particularly

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if your knees are crossed or your knees are held together, so that's more of a passive loading,

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but your absolutely active loading, active forces contribute to that as well, and that's a lot

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again around how your pelvis and your hip move and where you put your trunks,

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so where you put your centre of mass of your body relative to your hip, so we've got some nice

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kinematic evidence around that, so some studies that look that, you know, how do people with

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lateral hip pain work at walk, and they tend to walk in ways that actually increases the load

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at the side of the hip, and so that can be related to too much pelvic tilt, so dropping the pelvis

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down as you're walking or shifting your pelvis to the side, or leaning your body to the side,

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particularly leaning your body a little bit away from your foot when you're weight bearing on

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that side, and so basically movement patterns that create extra challenge for the muscles,

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and they're sort of working hard, so the tendon is under tensile load, so tension, so the muscles

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are contracting, and we're moving into a position where the iliotibial band is causing that compression,

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and so the movement patterns together with how the together with the compressive forces,

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those two things together can contribute to the development of pain over time.

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What are some of the common reasons for those abrid gay patterns? Is it an issue of like a motor

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control? Is it strength? Yeah, that's the million dollar question, that's it. We don't really have

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evidence for that in terms of the chicken or the egg. We know that from cross-sectional studies,

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from people who have this condition, that they are weaker in their abductors, so they're weaker

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in the gluteus medias and minimus, so if you're weaker, that is often associated with some

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excessive adduction in your movement patterns, but there's not always an absolute strong correlation

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between strength and movement patterns, so there's then movement patterns themselves and maybe

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an additional factor alongside or separate to strength, so you can still have adequate strength

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on a strength test and yet you're still moving in ways that are not optimal for the health of these

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tissues, but definitely strength and movement patterns are an important thing, but then there might

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be external things as well, for example, if you're walking or running and you're doing that on a

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camber of a road, so that's going to, so on the downslope down to the gutter, then that's going to

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sort of put your hip in a, so the downside hip closest to the gutter is going to be more in

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abducted position, so there can be external factors as well that contribute to that.

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Other things can be around length tension relationships in that muscular tenderness complex,

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and so for example, if you tend to be longer in those muscles, in those structures at the side of

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the hip, then your optimal window of function is going to be at a longer length, which is going to

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be in a more abducted position, so that length tension relationship may also contribute to

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this sort of loading, and it's one of the links that may link postural habits to movement patterns,

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because if you spend a lot of your time in static postures sitting with your knees crossed

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or standing hanging on one hip, so you're always in a position where these tissues are at length,

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we get structural adaptation, and so these tissues get longer over time, and so the longer they are,

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you have to, you know, there'll be more efficient at along the length, and so that may actually

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be another contributor that may feed into the way people move, but we certainly would need more,

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you know, research to sort of look at those links.

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I love that. I'm excited to kind of talk about load management, because there are some cool

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things I learned from you that I hadn't even considered that have been instrumental in my own

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recovery, but also in how I guide my patients, but before we do that, let's just talk about

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for the clinician, or even maybe the patient, right, if they think that this might be something

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that they're struggling with, this specific entity that we're talking about,

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what might be some specific telltale signs, aspects of the history, and the exam that might

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suggest, oh, this is more of a gluteal tendinopathy, trochanteric pain, as opposed to something else

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going on that we alluded to before. Yeah, great, and I think that patient interview, that history,

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the description of the symptoms is so, so, so very important in terms of that,

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that early clinical reasoning around, could this be gluteal tendinopathy or something else going on?

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So in terms of the history, I guess, you know, first looking at the patient demographic,

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so who is the patient in front of you? The largest group that we have with this condition is postmenopausal

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and so if you've got all perimenopausal, so if you're looking at 50, 50 plus female with pain

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right over their greater trigonoduct, then the risks that they have this condition already

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significantly increases, so area of pain and your demographic, but it's important not to miss it

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in other populations because we can get it in males as well, but in that older sort of 50 plus

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age group, we're sort of looking at more one in four females compared to one in 10 males, so less

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common in males, but then in our younger age groups, we can see it in younger runners as well,

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we quite commonly see this in, again, more females, but postpartum mums, often their

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eastern levels are at a little bit of a low there as well, and then they've often got poor pelvic

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control coming out of, you know, that those months of pregnancy and then they might want to

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start running to get rid of that baby weight and really not controlling around the pelvis,

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so we might see it in that scenario, and then the other scenario to be mindful of is in those with

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acetabular dysplasia, so again, more common in females, and so around 40%, 40 plus percent of those

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younger people with acetabular dysplasia, there's a study from Denmark saying that they have

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a doctor-related pain as well, and about 30 percent of the group that they looked at also had

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changes in the gluteal tendons on imaging, and so dysplasia also tends to overload those muscles

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because they're working so hard to cope with a shallow socket, so demographic is first thing to

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consider, history, now often in our postmenopausal females, it will either be that there's been a

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sudden change in activity level, and it might be, you know, putting on a little bit of weight

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with the menopausal change and going, right, I'm going to get out there and start pounding the

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pavement and doing lots of hill walking or or starting, you know, taking up running or going

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to boot camp and suddenly starting to do, you know, burpees and jumping split lunges and things

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like that, and so there's been this rapid increase in load, and so tendons don't love rapid changes

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in load, and so that might be a stimulus, or it can be something a little bit that might

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think a little bit more innocuous, which might be just going on holidays, but asking those extra

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questions, right, where did you go, what did you do? I went to Lisbon and Portugal, and it

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up and down, hills like this, so there was sort of doing lots of hill walking or cruise boats,

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I've seen a few people cruise boats because, yeah, and I'm staying on the bottom level, so for

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health, they decided I was going to take the stairs all the time, and so, you know, sudden increase

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in stair climbing, so often there's been something like that in the history, in others, it won't be

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as clear as that, it might be just that they've had a fairly sedentary sort of lifestyle,

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the muscles and the tendons have become poorly conditioned, and then to the point where

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even the forces of everyday life represent a relative overload for those tendons,

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so looking for those sorts of histories, then area of pain, as I mentioned, is really important,

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so it needs to be pain over the greater trochanter, and that is important in trying to differentiate

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between lumber-related pain, hip joint-related pain, now both of those other things can also cause

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pain at the lateral hip, but it's not as likely to be tenderness over that bone at the side of the

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hip, and one of the most common things that we get reported to us in people with this condition

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is that it hurts to lie on their side at night when they're lying on their side, and so when they're

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lying on that bone, it's tender on the bone, and that's an important differentiation, so for patients

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my hip hurts at night, don't just note that down, we want to have more information, so is it

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when you lie on your side, is the bone tender, so if they say that, then that's more likely to be

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gluteal tendinopathy, but if they're saying more like, oh no, it's sort of like a deep vague

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ache somewhere deep around my hip, that might be more hip joint, if they're not saying tenderness over

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the bone, or if it's more, no, it's more when it's top side, and certainly gluteal tendinopathy

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can be painful when it's the top side, when you're lying on your side, just because that knee,

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if it's hanging down into adduction, but that might also put load on the lumbar spine and pelvis,

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and so again, is it focal tricandric pain, or is it sort of pain that sort of runs from the back

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across the buttock down the leg, so those things are important questions to ask, and then how far

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the pain goes down the leg, with gluteal tendinopathy, it can transfer down the lateral thigh as well,

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whether that's a referral from the actual tendinopathy, or whether it's a source from the

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iliotibial band, there probably is some source from the iliotibial band in those people, so they

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can have pain down the lateral thigh, and occasionally even into the lateral leg, but it shouldn't go

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into the foot, and obviously if we're getting pins and needles or numbness into the foot, those sort

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of symptoms, then we're definitely thinking more nerve related issues, so either from the lumbar

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spine or from the hip with gluteal syndrome, but more commonly from the lumbar spine, so those

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things are important, but listening to those clinical history, and then when does it hurt,

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lying on my side at night, standing on one leg to dress, walking, particularly upstairs,

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uphills, or for you know, you're more active population, it might be, you know, running again,

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particularly uphills on unstable surfaces, on the canberra road, on a beach, things like that,

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so they're the typical presentations that we get. Yeah, the piece about the refer pain,

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that one's really interesting to me, because you know, I can imagine it, it becomes a real catch

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22, is people love diagnosed IT band syndrome, right, and if you google it, a lot of pain reading

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down the thigh, that's probably going to be one of the first things that comes up, and they're like,

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well, you know, I got to stress the IT band, and as you highlighted earlier,

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stressing the IT band is exactly what's going to further exacerbate those tendons and compression,

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and then all you're doing is potentially making the problem worse, and so I think this is why

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like that nuance that you described, and I'm actually guilty of this myself, is, you know,

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when you're limited with time, and you have a few minutes, you say, okay, does it hurt when

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you're laying on that side, they say, yes, to take that extra, that at next level, to dig deeper,

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well, okay, well, what kind of pain is it specifically, is it more of a deeper acre, is it more

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very superficial focal? I will say this, that patients aren't very good, sometimes at

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discerning the difference between the two, they're like, well, it just hurts, but what I really

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appreciated learning from you was that controversial piece that you talked about, so let's just say you

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have an individual able to come in with that right pain on the right side of the choke enter,

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but then hey, it hurts even when I'm left side, and you know that they have maybe a wider pelvis,

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and then you see they have significant adduction, and so, you know, one of the recommendations,

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I think you've made it, so you often will have them a large pillow, not just a pillow between

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the legs, which is what, or between the knees, excuse me, which is what I would tell them,

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because you're still creating that rotation component, but all the way down to the feet,

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that's actually been a teenager, so I want to thank you for that one.

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No problem. Yeah, so that is important, so with that sleek position, and sleep is just so

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critical for this population, and with the patient focus groups, like besides our patients in

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clinic talking to us, but in terms of our research, we've done patient focus groups in patients

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that we've had involved in our studies, and the thing that just keeps coming out is the sleek

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deprivation, and how much it affects their sleep, so it's so important that we try to address

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that as quickly as we can, because if we can get a patient a better night sleep, everything starts

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to turn around and feel much better, and so yes, if it's the top side when it's painful,

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big fat pillow between the knees and the ankles, because if the ankles are still together,

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that external rotation tends to sort of wind up those tissues at the lateral hip as well,

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but often people say to me, I've tried a pillow between my thighs, or between my knees,

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but often it's just been a thin pillow, so as you say a thicker pillow, often I might get people

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to put two pillows in one pillow case, so they don't slide around, but to make it thick enough,

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the other position that can be quite useful, because some people find, oh, you know, that slips

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out and then you know, end up in the poor position anyway, but the other position that's

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we find very successful is like a half turn between side lying and prone, so if they're half way,

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it means that they can lie on their affected side again, because they're rolling far enough

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forward, that they're rolling off the greater trochanter, and then their weight bearing on their

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antirelactual side. That position though is most successful, if they do still have a pillow in front

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of them, so a normal sort of long pillow, but I get them to roll it lengthwise, and then they can wedge

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it underneath the top hip and underneath their abdomen there, and so that's wedging them in that

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position, so they stay there, and then the top hip is also open, because the top hip is relatively

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more abducted, and so that's a really successful position for a lot of people, but it just takes

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them a little bit to figure out how to get successfully in that position, but if they're lying on

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the affected side, it's really shouldn't feed back, because that tenderness will go away if they

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roll far enough forward, that they've got the weight off that greater trochanter, so that's another

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great little position for them as well.

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George, can you imagine doing all that education, troubleshooting in the 20 minutes that we get

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in clinic, and this is why I think I'll buy my students and the residents who work with me,

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and I said, if you're not going to have the privilege of being able to do all the things that you're

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talking about yourself, you better find a network of people that you can refer to who are going to be

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able to take the time to do that, but I think also the other piece is to reference Dr. Chris

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Standard previous guesses, you sometimes give this type of information and bite-sized pieces,

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because I imagine that's what maybe physicians who might be listening to this are thinking,

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there's no possible way I can make the diagnosis, troubleshoot, offer other stuff, and do this,

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but you don't have to do all this in the first visit, so we can do this over subsequent visit as well.

376
00:35:43.640 --> 00:35:48.520
And so I would say with that, then, that go for the big rocks first, if you like,

377
00:35:49.080 --> 00:35:56.840
send to what your patient has said to you, so if the leap is a big issue, make sure you address

378
00:35:56.840 --> 00:36:02.040
that on day one, or if they've got stairs in their house and they're getting 7 or 8 out of 10

379
00:36:02.040 --> 00:36:09.160
pain, walking upstairs, then try to address that on day one, because if you can change those big

380
00:36:09.160 --> 00:36:14.760
ticket items for the patient, then things will start changing much more quickly, so do it,

381
00:36:14.760 --> 00:36:19.400
don't just do it that everyone has the same thing that you address on day one, listen to what

382
00:36:19.400 --> 00:36:26.040
the patient says, and address their big ticket items first, and so stair climbing simple things,

383
00:36:26.040 --> 00:36:30.840
just like, just walk with your feet slightly wider when you're going up the stairs, because often

384
00:36:30.840 --> 00:36:35.560
these people with their doctor weakness, they stand on leg, they're pelvis shifts and translates,

385
00:36:35.560 --> 00:36:40.600
they put their foot up onto the next step, and it's actually in front of their pubic synthesis

386
00:36:40.600 --> 00:36:44.920
instead of in front of their hip, and so they're quite abducted as they go to transfer the

387
00:36:44.920 --> 00:36:51.560
weight up, and that can be quite painful, and so if we can get them then to just plant your feet

388
00:36:51.560 --> 00:36:57.240
slightly wider, simple things like that can make a difference in using a rail on the hand

389
00:36:57.240 --> 00:37:04.040
opposite their painful side as well. I want to just plug your, you have an amazing masterclass

390
00:37:04.040 --> 00:37:07.640
paper, I think it's open access, you made it open access for everybody, published earlier

391
00:37:07.720 --> 00:37:13.640
this year, March of 2025, so I highly recommend people to go check that out, certainly a lot of

392
00:37:13.640 --> 00:37:18.680
important information if you want to understand this region a little bit better, and you've got some

393
00:37:18.680 --> 00:37:23.240
really great stuff on there. I had a follow-up question for you, I think that, and we had talked

394
00:37:23.240 --> 00:37:28.360
about this during your workshop as well, I think you had mentioned, or it's highlighted in the paper,

395
00:37:28.440 --> 00:37:34.920
that the direct palpation, and what's the other one, the direct palpation, and

396
00:37:36.440 --> 00:37:41.000
something in the 96% PPV I'm thinking, what's the second part of it, just lateral pain and direct

397
00:37:41.000 --> 00:37:50.200
palpation, right? So there was a meta-analysis by Consellor and colleagues in 2023, I think it was,

398
00:37:50.200 --> 00:37:55.640
so they looked at the combination of tests that were most likely to give you the highest diagnostic

399
00:37:55.800 --> 00:38:03.000
accuracy, and they found that pairing palpation with resisted abduction was most useful in both

400
00:38:03.000 --> 00:38:09.800
ruling in and ruling out the condition, but you do need something else in your test battery,

401
00:38:09.800 --> 00:38:15.720
because if resisted abduction is negative, which sometimes it will be, then you're only left with

402
00:38:15.720 --> 00:38:21.880
palpation, and you can't make a diagnosis on palpation alone, because it doesn't have the best

403
00:38:21.880 --> 00:38:26.360
positive predictive value, it best actually for ruling out the condition, so if they're not

404
00:38:26.360 --> 00:38:31.640
tender on palpation, you really need to consider other diagnoses, but if it's positive, it might

405
00:38:31.640 --> 00:38:36.600
be gluteal to not be, they might just be a bit tender over there, over there behind there,

406
00:38:36.600 --> 00:38:41.880
and so you need to have other tests, so besides that resisted abduction, the other tests that

407
00:38:41.880 --> 00:38:46.680
were shown to have good positive predictive value were the single leg stance, the 30-second

408
00:38:46.760 --> 00:38:52.120
single leg stance test, so standing on one leg for 30 seconds, side onto a wall with your

409
00:38:52.120 --> 00:38:56.520
fingertip for balance, just on the wall, on the close side there, and we're looking for

410
00:38:56.520 --> 00:39:02.760
reproduction of trigandric pain over that 30 seconds, so that had really high positive predictive

411
00:39:02.760 --> 00:39:11.480
value. The other one was fader test, which is flexion 9 degrees, full adduction, full external

412
00:39:11.560 --> 00:39:18.520
rotation, and then adding some isometric internal rotation, so some resisted isometric internal

413
00:39:18.520 --> 00:39:25.800
rotation in that position, and that also has a strong positive predictive value, and so if you,

414
00:39:25.800 --> 00:39:31.320
so those two tests are good for confirming a positive diagnosis of gluteal tendinopathy.

415
00:39:32.040 --> 00:39:35.720
Yeah, that's the one actually like a lot, I think some people will also refer to it as the

416
00:39:35.720 --> 00:39:38.040
hipguritation test, is that kind of the same thing?

417
00:39:38.120 --> 00:39:43.800
Yeah, so there's in that meta-analysis they did actually collapse those two tests together,

418
00:39:43.800 --> 00:39:49.720
but they're slightly different, so the de-rotation test is 9 degrees hip flexion, full external

419
00:39:49.720 --> 00:39:55.960
rotation, and then the patient actively pushes themselves back to a neutral rotation position.

420
00:39:56.760 --> 00:40:02.520
When we did the LEAP study, we modified that test because we were just finding that in clinic,

421
00:40:02.520 --> 00:40:07.400
the adduction component was so powerful, and that made sense from the research showing that

422
00:40:07.400 --> 00:40:13.560
adduction creates compression, so we wanted to maximize the compression, so that's why we use

423
00:40:13.560 --> 00:40:21.080
flexion, adduction external rotation, and then the resisted part of that test is isometric because

424
00:40:21.080 --> 00:40:27.640
we want to keep them compressed and add that active tensor load, so it's just a slight variation,

425
00:40:27.640 --> 00:40:32.680
and we find we tend to get more positives on that than the standard de-rotation test.

426
00:40:33.320 --> 00:40:35.560
So in the de-rotation, there's no resistance.

427
00:40:35.560 --> 00:40:40.920
There is resistance, but it's got isometrics, it's more isotonic, so they push themselves out of

428
00:40:40.920 --> 00:40:46.440
the compression position, we keep them in the compressed position when we contract the muscles.

429
00:40:47.160 --> 00:40:50.600
Yeah, cool, awesome, thank you for that. You mentioned the LEAP trial,

430
00:40:51.160 --> 00:40:54.120
kind of a landmark study, I think, and you've referenced it time and time again.

431
00:40:54.680 --> 00:40:59.320
What was the one main takeaway that you have from that LEAP study?

432
00:41:00.200 --> 00:41:05.320
I guess the most exciting thing that came out of it for us is that going into that trial,

433
00:41:05.880 --> 00:41:12.360
we hypothesized that we had two primary endpoints, a short-term end point, which was eight weeks,

434
00:41:12.360 --> 00:41:16.360
and a longer-term end point, which was 52 weeks, so 12 months.

435
00:41:17.000 --> 00:41:23.240
And we had hypothesized that, so we're comparing the education exercise program versus a

436
00:41:23.240 --> 00:41:30.280
corticosteroid injection versus a weight and C approach. So we had hypothesized that that eight-week

437
00:41:30.280 --> 00:41:39.000
time frame, that the courtesone group that had the courtesone injection might have superior

438
00:41:39.000 --> 00:41:45.240
results, but certainly by the 12-month point we expected the education exercise group to have

439
00:41:45.240 --> 00:41:51.640
superior results from previous literature showing that courtesone usually has more of a short-term

440
00:41:52.440 --> 00:41:57.960
effect. But the exciting thing from the trial was that actually at that eight-week time point,

441
00:41:57.960 --> 00:42:05.320
the education exercise program showed superior results, far superior over the corticosteroid

442
00:42:05.320 --> 00:42:11.000
group and the weight and C group. And so that was something that was terribly exciting because

443
00:42:11.000 --> 00:42:18.360
the only research that had looked at exercise prior to our study, they hadn't shown a positive

444
00:42:18.360 --> 00:42:25.720
until 15 months with exercise. And so you can understand then why our medical colleagues would want

445
00:42:25.720 --> 00:42:30.600
to give corticosteroid injections to their patients because they're not going to wait for 15 months

446
00:42:30.600 --> 00:42:37.160
and let their poor patient be in pain for that role. But this was a great message from the study

447
00:42:37.160 --> 00:42:44.680
that we can get quick results. Of course not one or two days that you can get with a corticosteroid

448
00:42:45.640 --> 00:42:50.520
injection, but we have to sort of weigh the risk versus benefit up. And certainly,

449
00:42:50.520 --> 00:42:57.160
even within a few weeks we're seeing changes and that education piece is a really important part

450
00:42:57.160 --> 00:43:03.640
in that changes in symptoms. And eight weeks we had just under an 80% success rate,

451
00:43:03.640 --> 00:43:10.040
and that was maintained out to that 12 months. And so that's the biggest message that education

452
00:43:10.040 --> 00:43:16.200
exercise can give you short-term gains. So you don't have to, you know, work for 12 months

453
00:43:16.200 --> 00:43:21.560
until you see a result. Just to clarify, the corticosteroid group was just steroid or steroid plus

454
00:43:21.560 --> 00:43:30.200
education exercise. So the steroid group and the, so they were, yeah, cortisone by itself,

455
00:43:30.200 --> 00:43:35.160
the simple cortisone injection and the weight and C group was, yeah, weight and C. But

456
00:43:35.240 --> 00:43:42.040
both of those groups did actually get a basic education pencil. So not all the detailed

457
00:43:42.040 --> 00:43:47.240
load management information, but what we thought was fairly vanilla advice, which was more like

458
00:43:47.240 --> 00:43:53.880
if it hurts to walk, just reduce your activity levels and then just gradually build them up again

459
00:43:53.880 --> 00:44:00.040
avoiding peaks of activity. And so that was actually really interesting because both of those

460
00:44:00.040 --> 00:44:05.720
groups got that information and the education exercise group, of course, also got that

461
00:44:05.720 --> 00:44:11.720
information plus a whole lot of more detailed information on the load management side of things.

462
00:44:11.720 --> 00:44:16.520
But it was interesting to look at what happened in the traces of activity levels over time.

463
00:44:17.160 --> 00:44:23.880
And so if we look at the activity levels from baseline to four weeks, the education and exercise

464
00:44:23.880 --> 00:44:30.120
group and the weight and C group who'd been given that basic information, they both reduced their

465
00:44:30.120 --> 00:44:35.880
activity levels for that first few weeks. And then they gradually increased and stayed sort of higher

466
00:44:35.880 --> 00:44:42.120
over time. The interesting thing in the pattern of what happened with the corticosteroid group,

467
00:44:42.120 --> 00:44:47.080
even though they were given that information, they didn't adhere to that. So their activity levels

468
00:44:47.080 --> 00:44:52.920
actually increased the four weeks. Then they sort of dropped back down to eight weeks and then they

469
00:44:52.920 --> 00:44:58.840
stayed lower over time. Now there wasn't statistical significance between the group, but the pattern

470
00:44:58.840 --> 00:45:05.240
is just so much what we see in clinical practice. So it's something to just be really mindful of

471
00:45:05.240 --> 00:45:10.680
with corticosteroid injection. Often it's sort of promoted as we're giving you this window of

472
00:45:10.680 --> 00:45:19.480
opportunity to, you know, to rehab. But often it's almost a negative from a behavioral standpoint

473
00:45:19.560 --> 00:45:26.120
because they're less likely to adhere to advice. They're less likely to change the way they move

474
00:45:26.120 --> 00:45:31.160
because they're not getting that regular reminder. And so it's almost like robbing them of the

475
00:45:31.160 --> 00:45:37.560
opportunity to learn how to manage their own condition. So question for you actually, Althalash,

476
00:45:37.560 --> 00:45:42.600
when you're talking to patients and you're trying to decide between using something like

477
00:45:42.600 --> 00:45:49.800
torridol or even a corticosteroid injection, how do you think about that balance between trying

478
00:45:49.800 --> 00:45:56.120
to resolve whatever issue the patient may have in the near term versus actually trying to fix that

479
00:45:56.120 --> 00:46:03.000
problem in the long term? Well, I think and I've shared this with Alison offline is I probably

480
00:46:03.000 --> 00:46:06.760
use a lot more torridol. You and I have talked about this than we do, right? Because it hasn't

481
00:46:06.760 --> 00:46:12.280
really shown to be tino toxic and my toxic and counter toxic, although there are some

482
00:46:12.280 --> 00:46:16.520
individual studies that showing that maybe it might have some harm. So I tell people at this stage

483
00:46:17.240 --> 00:46:21.480
that's probably a better option. That being said though, the conversation that I'm having is

484
00:46:21.480 --> 00:46:25.880
are we playing the short game or the long game? And that's what I tell people, right? So to like

485
00:46:25.880 --> 00:46:30.120
this happened today, right? So it wasn't for a hip, but so an individual who was going hunting

486
00:46:30.120 --> 00:46:34.760
tomorrow, they're going to hire, they got to catch some deer. And you know, like look, we got to do

487
00:46:34.760 --> 00:46:40.440
the rehab. We got to do all that stuff, but that trip is right there. And so we opted for torridol.

488
00:46:40.440 --> 00:46:44.920
Again, recognizing that if they don't make those long term changes that Alison talked about,

489
00:46:44.920 --> 00:46:47.960
we're going to be having a very similar conversation in two or three months. Like we're going to

490
00:46:47.960 --> 00:46:53.720
be right back to square one. So I'm very honest. I think my approach is very much like here is the

491
00:46:53.720 --> 00:46:58.440
menu of options. I can guide you, you know, as long as it's medically reasonable, of course,

492
00:46:58.440 --> 00:47:04.280
and a viable option. I think this is going to be a more reasonable approach long term. But like the

493
00:47:04.280 --> 00:47:08.600
people that you talked about, so the person who can't sleep and who hasn't been able to sleep for

494
00:47:08.600 --> 00:47:13.960
a while, then it's working two jobs. And you know, if we can maybe give them a little bit of relief

495
00:47:13.960 --> 00:47:19.400
using ideally torridol, for short term relief, corner concern, if we absolutely need to,

496
00:47:19.400 --> 00:47:23.640
although I don't do that a lot for tendon, but every now and then we'll do that with the

497
00:47:23.640 --> 00:47:27.160
understanding that they do need to make those changes for a district, or we're going to have

498
00:47:27.160 --> 00:47:32.040
the same conversation in those instances. I'll do it. The one thing I'll say else, and I know we've

499
00:47:32.040 --> 00:47:36.440
kind of talked about this is I'd be curious where the PRP group would stand with that. I know

500
00:47:36.440 --> 00:47:40.200
people have mixed opinions with that. We've talked a lot about different PRPs, but really be

501
00:47:40.200 --> 00:47:46.120
interested if we had a separate arm looking at like lucasite rich PRP into the tendon, although

502
00:47:46.120 --> 00:47:52.360
I can't think of any good orthobiologic interventionist who would do PRP and not include a comprehensive

503
00:47:52.360 --> 00:47:57.880
rehabilitation program, keyword being a good interventionist, but even as a standalone,

504
00:47:57.960 --> 00:48:03.000
like we know that corticosteroid at maybe two months outperforms PRP, but again at three to six

505
00:48:03.000 --> 00:48:07.640
months, even more than that PRP is better. So I don't know if you've got a chance to look at some

506
00:48:07.640 --> 00:48:12.600
that literature, or I know you briefly touched on in the last workshop. Yeah, well, there's

507
00:48:12.600 --> 00:48:20.760
fairly limited literature. So mainly one RCT, two papers from one RCT, and the longer term data

508
00:48:20.760 --> 00:48:25.720
is a bit problematic because of patients moving between groups and things like that.

509
00:48:26.520 --> 00:48:34.200
But yeah, so that, as you mentioned, shows clearly that the PRP group did better than the corticosteroid

510
00:48:34.200 --> 00:48:40.280
groups. It, as far as we're aware, it's a natural substance at least. It doesn't seem to have

511
00:48:40.280 --> 00:48:47.800
those same sort of toxic effects as the core design. It won't give you those rapid pain relief

512
00:48:47.800 --> 00:48:54.440
that you'll get from a corticosteroid injection, but perhaps has lower levels of risk associated

513
00:48:54.440 --> 00:49:02.120
with it. But that program also, of course, had, so that RCT also provided an exercise program

514
00:49:02.120 --> 00:49:07.400
wasn't supervised, but they gave some sort of education and exercise program associated with

515
00:49:07.400 --> 00:49:14.520
that. And as you say, if you're using PRP, we definitely want that in conjunction with an

516
00:49:14.520 --> 00:49:21.400
exercise and education program. And that's where you're likely to get most benefit out of the PRP

517
00:49:21.400 --> 00:49:27.160
anyway. You know what's interesting, at least in the business model of this country, is PRP is

518
00:49:27.160 --> 00:49:32.680
typically not covered by insurance. So it's an easier buy-in. So to your point, if you put a bandit

519
00:49:32.680 --> 00:49:37.640
on their disincentivized to go ahead and do that, but now if a person's putting up money, they're

520
00:49:37.640 --> 00:49:41.720
more likely going to do that rehab program and make some of those changes else. And so I tell them,

521
00:49:41.720 --> 00:49:46.840
listen, we don't want to sell sabotage, right? So if you're going to make this financial investment,

522
00:49:46.840 --> 00:49:51.400
time-based investment, you know, PRP, particularly in tendons, is actually going to probably make it

523
00:49:51.400 --> 00:49:55.880
worse for a couple of days because you have that inflammatory period where it's actually quite sore,

524
00:49:55.880 --> 00:49:59.720
especially if you're doing what we call it synotomy where you're taking a needle and going in doing

525
00:49:59.720 --> 00:50:04.840
multiple frustrations to create a little bit of an injury and irritation. But when people are

526
00:50:04.840 --> 00:50:09.240
paying, they're like, okay, I'll actually make this investment. I'll make the changes. So I've

527
00:50:09.240 --> 00:50:14.040
actually been more successful with that approach as opposed to the, all right, here's the injection,

528
00:50:15.000 --> 00:50:21.880
go nuts. Yeah, yeah. And that's great that, I mean, as long as it is accompanied by that sort

529
00:50:21.880 --> 00:50:28.280
of education, because I've certainly seen, you know, patients who've been given PRP and then

530
00:50:28.280 --> 00:50:32.760
basically told you rest. So PRP and rest. And I'm like, why would you do that? That doesn't make

531
00:50:32.760 --> 00:50:40.360
any sense at all. So it's great. I think it's really that combination. And of course, I'm

532
00:50:41.080 --> 00:50:46.680
from the perspective that I would suggest that education exercise give that a go first. And then

533
00:50:46.680 --> 00:50:53.560
I'd say PRP, you know, those sort of secondary sort of interventions, if you're not really having

534
00:50:53.560 --> 00:51:00.120
an outcome. And even with the sleep, we can get, like, if we do have an opportunity to get them

535
00:51:00.120 --> 00:51:05.080
on the bed, so get them in the bed, position them, often just that positioning advice can get

536
00:51:05.080 --> 00:51:12.120
them a bed asleep relatively rapidly. And if they come in limping, I would, you know, even give

537
00:51:12.120 --> 00:51:18.120
them a short-term opportunity to use a walking aid, just a single stick or a single crutch, I'm just

538
00:51:18.120 --> 00:51:24.920
to let it settle quickly. So we can turn the pain around relatively quickly. So if we can avoid the

539
00:51:25.560 --> 00:51:30.120
the core design, particularly, that'd be great. But it's as other options that are safer than

540
00:51:30.120 --> 00:51:36.760
that would probably be preferable. Love it. Yeah, Alison, I obviously have an issue where I thought

541
00:51:36.760 --> 00:51:40.200
that for some whatever reason, we were going to be able to get through a lot of this stuff and

542
00:51:40.200 --> 00:51:44.600
we're 50 minutes in and we've just done a scratch the surface. So how much time do you actually have

543
00:51:44.600 --> 00:51:50.840
today? I don't want to keep you here. No, I've just got a research meeting in about half an hour or

544
00:51:50.840 --> 00:51:58.360
so. So go a bit more or I've had different session if you want. Yeah, I'm thinking maybe we could

545
00:51:58.360 --> 00:52:06.360
park it and maybe we could do like hip joint pathos. Awesome. Alison, thank you so much. Okay, sounds

546
00:52:06.360 --> 00:52:11.320
good. Thanks for listening to the other episode of Medicine Redefined. If you enjoyed this episode,

547
00:52:11.320 --> 00:52:15.800
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