Before beginning and launching into the lecture, it is helpful to provide some context and background to what Keith has just said by way of introduction. This will no doubt make my father chuckle because arriving home after parents' evening was never a happy place to be in our house. It was if you were my brother or sister. They were well-behaved and worked hard. I, on the other hand, was the third child.
I’ll just select two out of many that I could have looked at, by way of references in my school reports. This is from my primary school just to prove there was some consistency to my behaviour in the early years of my education: "Neil has a very vivid imagination but seldom expresses it to his fault. Most of the time his work looks untidy. Neil could do much better if only he didn’t talk so much and concentrated a little more."
My father will appreciate this one not least because it was written by somebody who is not least probably a significant hand in the fact that I now do something like what I do. It was from my old chemistry master. This is from my fourth year in senior school. It’s by my chemistry master Mr Clarke, who was formidable.
I was terrified of Mr Clarke, and when we got to sixth-form options evening he was head of sixth form, and I thought I should go and see him and explain what I was preparing today. As I walked to his chair and desk at parents evening, he looked up at me and said “Fowler, you’re not doing chemistry”. Which is probably why I ended up as a bio-mechanist because clearly I wasn’t allowed to do chemistry.
This is Sid’s take on me in fourth year:
"His test results show that when he makes the effort, he has the capability to do well, but generally his work shows a cheerful willingness to do the least possible and avoid painful thought."
In the days when school reports called it as it really was, it was reports of that nature that eventually when I did get to make the decision and go to university. At the end of my first term at university and I was struggling desperately to finish the first term’s assignments so I could go home for Christmas, it struck me that actually I was enjoying this stuff and it was quite good fun. And maybe, I had found the thing that made me tick.
That’s going to feature in this some of what I want to unpack for you tonight, because as the title suggests it’s an interdisciplinary look at back pain. That is the area where I spent a lot of my years researching.
For those of you over the age of 30, about 50% of you will experience back pain in any given year, and about 80% of the population will suffer from it at some point. But it’s not just an over-30 problem, back pain affects people at any age. It’s not all related to aging. And I hope during the course of this evening to explain to you some of what I've learned about back pain.
The spoiler alert, there's no magic remedy. If you have back pain, you're not going to leave here with the answer and make it go away. But hopefully you may understand a little bit more about the journey of that back pain and what may cause it, but also explain some of what goes on in the treatment regime, why it’s managed in the way that it does, and why some things are successful and some things are not. So we'll explore some of those avenues as we go through this evening.
But I also want to draw from some of the lessons that I've learned about doing research, because my research journey and my interest in back pain provides an opportunity to go, “how could you apply that in other research settings? What might this mean generally, or the way in which research would, could and should be conducted?” And, because as my school reports indicate, I've always liked to challenge and worked hard at what’s set before me.
I want to add a third narrative thread to tonight's presentation, and that's to relate it to what I am now responsible for, which is learning and teaching. And it does draw from those original school reports of, you know, how did I somebody who was a bit of an oaf at school, and didn't really get it and pull their socks up until rather late in the day, how am I now responsible for the learning and teaching of so many people across higher education in the UK? It’s a little bit scary!
So how is that informed my philosophy for learning and teaching and just my learning approach and what drives me in terms of learning and teaching, which will come as a shock to my children who had to endure homework time, and primary school maths, where they might not see what I describe tonight as having been played out in their lived experience, where I may not have been quite so gentle in my approach that learning is about curiosity and interest, and it was “just do your times tables!”
It did possibly feature in my approach to learning and education. I've moved on since then, honest. So that's what I'm going to seek to try to do during the course of this evening. And hopefully we'll pick up those themes and you'll see bits of the narrative as they unfold on that journey through. And finally, by way of introduction, I have got two my children with us here, and others listening online, and just for once, I can turn around because so many of our conversations at home include the phrase “dad, I didn't ask for a lecture”. As I'm about ten minutes into answering a fairly simple question that had been posed to me. Well, tonight you did.
And you might have questions at the end. But you're not getting another lecture, you only get one for the price of one tonight.
So where did it all begin? I did begin as an exercise in sport scientist. I was once young and gangly and stupid looking rather than old, gangly, and stupid looking. As I have now become an undergraduate student in my first year, I became a little bit more studious and had some hair. This is proof I did once have hair.
For those of you, I’ve got the hat on so you can’t see my baldness. And, my graduation in Liverpool Cathedral with my dad. And this was just slightly shocking how much I have become the photograph of my father. I have to say, if any of you get the opportunity to talk to my dad later on, he's very good to talk to. If I can become 10% of the man that my father is, I'll be very proud and pleased to have become that person. So, the fact that I look a bit like him, I'll take that, because he's a bit awesome my dad.
That undergraduate journey and my journey into research, inspired by the two individuals who also appear on the slides, Professor Adrian Lees, who was the principal supervisor of my PhD work, and Professor Tom Riley, who's one of the fathers of exercise and sports science. I had the pleasure to share an office with Tom for about 18 months when I first started my PhD work, and he had an incredible mind and understanding of the subject and was just a polymath in terms of the things that he understood and was able to teach. So, these two individuals were early inspirations to the work I went on to do and I must call them out at this point.
I did a PhD after I finished my undergraduate studies, as Keith said, I got offered the opportunity for a PhD to look at the efficacy of plyometric training, which I'm not going to talk about at all this evening. But if you want to talk plyometric training, I can happily do that on another occasion. Essentially, my research involved sitting people in this torture device and smacking them into a wall for three years, which was tremendously good fun. But the methods that I utilised while doing that, I was trying to compare two different ways of training: traditional jump training and being smacked into a wall, which took the gravitational elements out of the movements. I was comparing the movement patterns and looking at the efficacy of the training—how well did it work, what did it do in terms of muscle performance, etc.
But Plyometric training has a reputation for being potentially rather injurious, and so one of the aspects that I looked at within the PhD work was the injury risk associated with that jump-based training. That led me into looking at the loading on the spine and a technique known as stadiometry. I'm not going to go into the details of the method, but it takes us into this notion that we can use measurements of the spine to tell us something about the loading on the body, and the link between how much we're experiencing load during daily activities and the behaviour of the discs within the spine.
Stadiometry is a method of measuring the changes happening in the spine throughout the body. Now, I'm not particularly focused on that, but we used it as a method throughout many of the studies that I'm going to talk about tonight. It gives us the link to the anatomy bit. Because we can't do a session on back pain without first understanding some of the basics of what the spine is and how it works.
You're not going to be tested on the anatomy at the end; it's just a few key points that you need to grasp in order to understand what's going on in this exploration of back pain. As a piece of design, if you wanted to get the most important organ of the body, the brain, and we want to keep that safe after we’ve decided on walking upright, rather than walking on all fours. Putting it a top a stack of 20-plus bricks is probably not the design engineering solution that you would think is the smartest one. About 5% of your body mass is contained within the head, stacked up on a bunch of bricks. Not a great design.
Depending on how you choose to count them, there are between 32 and 33 bones that make up the spine. I don’t really care which of those numbers you’re interested in, because tonight, what we're really interested in are the bottom ones—the lower five vertebrae—because they do most of the work. Since the spine is a stack of bricks, on which we’ve got all of the weight of the body sitting on top of these lumbar discs. The further up you go, the lighter the weight gets because there are fewer bricks at the top to contribute to the load.
This bony stack is basically a pile of bricks that gradually gets smaller as you go up. The vertebral bodies are the parts at the front that bear most of the weight. And so we have the vertebral body. If I push this does the little laser thing come on? It does. So the body here, this is the weight wearing bit of the disc of the spine.
It holds the load, and we get these poking-out bits—technical anatomical term, “pokey-out bits”—which we use for attaching ligaments, muscles, and tendons to allow movement to take place. You need sticky-out bits to attach bits to; flat bits aren’t great for attaching things to. Since they stick out a little, they create some leverage, a bit further away from the joint, making movement easier.
If we just had the bony bits next to each other, movement would be more difficult. Imagine our proxies of two vertebral bodies - if they just sat like this, it’s quite hard to move them. You can move them, but it’s a limited amount of movement that you can create. If we have an intervertebral disc sat between our vertebral bodies, it separates them and they can move more easily. So, that’s why we have the intervertebral disc, The intervertebral disc sits between the vertebrae to facilitate greater movement. The other thing that the intervertebral disc does is they absorb some of the load, so they serve the purpose of being a shock absorber between the individual discs. And they carry some of the load that’s going through the body in order to help reduce the bone-on-bone contact that we would see. If anyone in the room has got 50-plus year olds knees, you know what bone-on-bone loading feels like—it’s not wonderful. It hurts a little bit because that’s what you start to get, your joints get a little bit older and you get degradation of the cartilaginous material and you get a bit of bone-on-bone contact, it’s not nice.
Intervertebral discs stop that from happening. They keep the bones apart from each other. As you will have noticed from the earlier part of the demonstration, the intervertebral disc is full of water. Not literally full of water in the way that my sponge was, but figuratively. The disc itself is a bit like a car tire, we have a series of anulus fibres these little walls of the disc, like the walls of a tire. You can see the wires go criss-cross around them. That’s what the fibres supporting the wall of the disc are like. Within it, the nucleus, similar to the yolk of an egg, sits in the middle of the disc and is slightly harder and less compressible substance within the middle of the disc.
When we load the disc—and we put body weight on it, and we get another intervertebral disc and put another bit of body weigh ton it— you can see that the discs compress. The bottom disc is more squished than the one above it, because it's got twice as much weight upon it. And if we put another one on top of that, there would be more weight and the bottom one would get even more squished than it is at the moment, so each one of our discs carry some weight. We'll see how long that stays there before it falls over because it’s not going to compress evenly. But you can see the difference.
You can see this some change in height. And if I leave it there long enough, gradually the disc will continue to compress and water will continue to get pushed out of it. So, there's two phases to the behaviour of the disc. There's an immediate elastic loading, as soon as you put something on it, it squishes. Just like when you sit on the bicycle. When you first sit on your bicycle, you can see the tires squidge a little bit. If you sat on the bicycle for a very long time, gradually the air would seep out, as the fluid sits out from the disc and over the course of the day that this continues to lose height.
So those of you who are conscious about how tall you are, my darling wife, you’re about two centimetres taller first thing in the morning. If you’re conscious of wanting to have a nice high body height, and want people to think you’re nice and tall, then measure yourself within the first half an hour of getting out of bed as you’ll get a much better reading than if you do it in the evening, by which point you’ll have shrunk by somewhere just north of 1% of your standing height. Depending on how active you’ve been during the day, maybe even more.
So, your discs shrink. Engage with this shrink. You get shorter because you've got them all the way up through your spine, and everyone loses a little bit of height. And collectively, that gives you the change in stature that we were measuring when we went back here to stadiometry. So that stadiometry, that measure of the length of the body gives us an index of the change in height of the discs that make up your spine.
Just because I like to make people feel uncomfortable, I'm sorry, just because I think it will be interesting and informative to you to learn something about the behaviour of the disc.
As you change posture, that yolk, the nucleus within the disc moves, it changes the pressure across the disc. So, as we see in the top diagram, if you move the body into a flexed position, you can see the body’s moved forward.
Or if we put the spine into this position, you compress the disc at the front, you extend the disc at the back, and we get a pressure gradient between the front and the back of the disc. That causes, over time, the nucleus to migrate.
It gradually floats backwards and adopts a new position towards the back of your disc, rather than the middle of the disc where it started. It's one of the contributors to why, after you've been doing a forward flexion task—if you have been out in the garden or doing some decorating and you spend any amount of time in this sort of position and you come back up to standing—you have that wonderful, crunchy, squishy feeling in your back.
As you come up, the posterior part of your disc is no longer as compressible because it's now got the yolky bit stuck in the wrong place, and you need some time for it to migrate backwards.
Those slow phase changes of the position of the nucleus within the disc, as well as the disc losing height, change its load-bearing characteristics, and that causes a shift in the load and potentially damage to the disc.
Now, we can't talk about discs without touching upon the notion of the slipped disc. They don’t slip, They don’t really go anywhere. It’s really a herniation. It’s a bulge. It’s a sticky-out bit of your disc.
We can see in the picture just over here. It's a normal disc where you've got the nucleus nicely in the middle.
If you damage the walls of the disc, if you damage the annular fibres, then they get weaker. And if you're one of those drivers who has a bit of a habit of bumping their tires into the curb whilst parking, and weakening the wall of the tire, you will have seen some people whose tires have little bulgy sticky-out bits in the sidewall of the tire where they bumped them once or twice too often into the curbs.
That’s just a weakening of the wall of the tire. It’s a weakening of the fibres. So it hasn’t popped, but it’s become weaker. And as a consequence of that weakness, the insides can start to become outsides.
And so we get a herniation. The disc bulges out, the nucleus bulges out. And because it bulges into the space where the nerves come out through the spine to serve the other parts of the body, you can get referred pain.
That back pain often radiates down into the hip, into the hamstring, possibly all the way down into your calf and lower leg, depending on where in the spine that protrusion is happening.
I'm not really talking about that sort of back pain tonight. So if you've got a herniated disc and you were hoping I was going to solve your herniated disc—sorry, I’m not. They’re horrible, they hurt. Some of the stuff we get to talk about, about dealing and managing your pain, will be helpful. But that sort of disc damage isn’t the sort that we were particularly interested in or looking at in our research. The other thing that’s worth knowing seeing as you’re sitting on sort of not the most ergonomically designed chairs in the world, is that the pressure in the disc very much depends upon the position that you're in.
If you're sitting in a slightly slouchy position, as many of you may well be, because you've got a very flat seat and that tends to lift your knees and therefore tilt your pelvis backwards—if your pelvis tips backwards, your spine effectively goes into lumbar flexion. And if you’re sitting in a nice slouch, I realise you can’t demonstrate this in a big robe sorry. If you’re sitting in a slightly slumping position where your hips drop backwards and your spine curves this way, basically you're in this position, you just don't notice it because your legs are underneath you.
That means your nucleus is migrating backwards whilst you're sitting there doing that. But actually, the load through your spine in that position is about one and a half times as great as it would be if you were standing up. So sitting down could be worse for you than standing up.
My top piece of advice when asked about ergonomics and seating position is: buy yourself the most uncomfortable seat you can possibly find. The simple reason is—it makes you get out of it. And not being in your seat is the best way to sort out problems with back pain caused by sitting down.
Don’t stay still. Just move. Your back loves you when you move. It doesn’t like you when you stay still.
So, whilst you're sitting there, adjust your pelvis. Sit up straight. You'll be lovely. By the end of the talk, your disc won’t have wandered about too much.
One last bit of anatomy, because it’s important in terms of the origins of pain. As our discs compress, the load has to go somewhere. When it’s nice and inflated, the disc works like a shock absorber carrying some of that load for us. Like a balloon—you load it, it squidges a little bit, and it absorbs some of that load for us. It holds some of that energy within the fibres of the disc. It stores energy.
As the disc becomes a little more flaccid, the disc squashes more, which means it protrudes more and is more likely to impinge upon nerve structures.
Because as it loses height, as it loses volume, it gets smaller and it has to squidge more.
So the softer your disc, the less inflated it is. The more it’s going to squidge, the more it'll bulge out at the sides. Anybody who has ever ridden on a bike with deflated tires note how unstable that becomes.
If your disc is less stable, if it’s more protruding, it’s more likely to impinge upon the nerve root spaces and give you the referred pain we’ve been talking about. It's less stable, which means the muscular ligaments, the structures have to work harder to maintain the stability of this stupid pile of bricks we decided to stick our head upon.
So as the disc compresses, as we lose height, as we become less stable. We have to work harder with other structures—either actively through greater muscle contraction or passively through greater load going through the ligaments and structures to support the end point.
The other structure that can often give rise to back pain, and this is the back pain you’re more likely to experience later in the day. So, those of you that were fine in the morning, but you’ve been up and about for a long while, you start to feel a bit back achy in the second half of the day. That's more likely to be pain that's associated with these bony joints that we see between the vertebrae on the on the sticky out bits, the facet joints.
These are the joints that either enable or limit the movement of the spine. But the discs compress, so those joints come under greater load, and they take more of that load. If they're taking more of the load, they get more force going through them.
And that's what gives rise to the facet joint pain and why gets worse as the day goes on because they get squished together more, and we get more bone-on-bone loading as the day progresses.
First thing in the morning when you wake up, your discs are fully engorged with fluid, and you feel a little stiff. No making up your own jokes. But you wake up in the morning, you feel a little bit stiff because of this engorgement of the discs and movement is more limited. You can't move around as much in the morning. You might find you have back pain first thing in the morning. Because of that greater stiffness, you feel more stiff in the morning.
Give it ten to fifteen minutes. The disc will begin to lose some height, and you'll feel that you've got more mobility. So, if you’re one of those ‘like to exercise in the morning’ type people, strange animals that you may be, but if you do like to do some exercise first thing in the morning, sit up. Give yourself ten, fifteen minutes of just sitting up before you start to do anything too dynamic, and that will allow the disc to lose a little bit of height and then you can actually start to exercise without loading too much.
That's the anatomy bit. So, what do we do? Well, I've been interested in looking at loading and we've been measuring changes in stature during a variety of loading tasks.
Not particularly looking at back pain, just looking at a variety of ergonomic tasks. We’ve done some evaluation work on Postmasters and looking at different kinds of carrying post bags and what that did, and different sports activities.
And we did a study looking at the changes in stature, changes in the spinal loading during pregnancy. And we tracked a group of participants through the three trimesters of the pregnancy. And we know that pregnancy and back pain are closely linked, mainly because of the growth of the whole human being in and in not particularly ergonomically great position.
Oh, let's carry a whole new load of weight around in front of us, out here, right in front of your spine, rather than nice and close to the point of loading. It might have made much more sense for the baby to be carried over your shoulders. But anatomically that's probably not a great look.
So babies grow here, we get bigger, that causes a bigger forward motion and a greater compressive loading. And we were just interested in these changes in spinal behaviour during pregnancy.
And we came across a chance finding. That as we were measuring the changes in stature, we noticed there was a difference in the behaviour of the spine amongst those who had back pain and those who didn't.
Now, one of the first studies that we did was go, okay, well, how much can you shrink the disc? And there were quite a lot of studies looking at spinal shrinkage through loading. We did a study where we brought participants in and we tracked them over a 24-hour period.
So we got our participants to arrive at 10:00 in the morning. They came to see us. We measured them every 20 minutes for the first part of the day, then set them off on their duties. They came back to us at 10:00 at night, and we monitored them throughout the evening.
And we get the two lines that we see on the graph here. One is a group with chronic low back pain, and the other is a group of controlled participants with no reported back pain. And they both show a fairly similar pattern of spinal shrinkage and recovery during the course of the day. We did notice that within our back pain group, they plateaued out. They reached a point where they couldn't shrink any more, earlier in the day, which we thought was probably related to the characteristics of the disc, and with a little bit of disc degeneration, it loses its capacity to absorb load and becomes a little less mobile during the course of the day.
So that was our first observations. First, on people we really found any differences between back pain sufferers and people without back pain. But we were also interested, you know, okay, but is that as much shrinkage as you're able to achieve?
And so we stuck a 10% loaded vest on top of our controlled participants. We didn’t do that with the back pain sufferers. And we found that actually, you can keep on shrinking—the healthy disc will carry on shrinking a lot more than we've seen during the loss in the day. So if you're more active, you'll shrink more. But it's okay because your body can take it.
So we found this. It was interesting. It was a 24-hour study. So it involved quite a lot of sleeping in the lab, which was a bundle of laughs. Participants got a proper bed, I think. And then we went on, we started looking at back pain more seriously.
And part of the methodology that we used and had been used in stadiometry for a long time is before you do the first measurement to accommodate differences in behaviour, before they arrive at the lab, you get the participants to lie down for 20 minutes. It neutralises the load on the spine. You get a little bit of acute loading. We measure the stature at the beginning. Then you do the thing that we're interested in, measuring again at the end, we look, we can see the change in stature, the loss in stature that we see.
And then just because we were vaguely interested in it, we let our participants lie down. Afterwards, we did another 20 minutes of unloading, and then, unsurprisingly, most of them regained virtually all of the height that they'd lost during exercise.
So it's acute phase loading. So if we take our brick off the disc, it will come back to its natural height and regain its stature reasonably quickly after that loading. No great surprise.
We then looked at our low back pain group. They shrank about the same amount. There wasn’t a discernible difference in the amount that they shrank. But we did notice that they differed in how much they recovered.
And nobody had looked at this before, so, we thought oh, why not? And if the disc is staying compressed, if it's not recovering after exercise, and it's spending more time in a compressed state, so all of those other structures are being loaded more, that might explain why we're seeing the back pain that these participants have.
So we started to investigate. Why? Why is the disc not recovering? And we began by thinking, well, if it's down to the mechanics of the disc, we have to take the discs out and measure them and you’re not getting many participants, because most people object to that sort of thing going on.
So we started looking at other things. Could it be explained by more muscle activity? Would that explain why the disc isn't recovering? Because the muscles are staying active. And there was some research that suggested there was chronic muscle tonicity—so chronic low-grade muscle activity in people with back pain.
So we studied a group of people with back pain. They shrank about the same. We saw the same pattern of not recovering. The graph on the left shows that the line that gets back towards zero was the non-pain participants. The line beneath that is the people with chronic pain, and they don’t recover after exercise. And we measured the muscle activity in the muscles of the spine. And, lo and behold, those with back pain had higher levels of resting muscle activity.
This was while they were resting, doing-nothing, post-exercise. They had more muscle activity—we might have found a mechanism.
So we were then interested in, okay, well, that's lovely. That could just be a chance finding. That could just be those two things both happen, but with no real relation to each other. So we had the theory of change. We had something that said these should be linked, but we didn't know if they really were.
And even if they were linked, did they have anything to do with the pain, or did they just happen to be co-terminal with other factors? So we got our bunch of healthy control participants and we measured them, the top line is them normally—they shrink and then they grow again. And then we put some electrical stimulators on the spine, and we zapped the muscles.
We made the muscles contract. Anybody who has ever gotten one of these passive exercise machines—the ab trainers that you put on—it makes the muscles contract while you just sit there and have a gin. Normally what happens in our house.
That muscle activity, electrically stimulated muscle activity, we did that to our participants and they became like our pain patients. They didn’t recover. So by stimulating muscle activity, we were able to say ‘oh right, so muscle activity is linked to the failure of the spine to recover.’
But we were still left pretty much with so what? Is it relevant? Can we change it? Is it linked to the pain? And why have they got this elevated muscle activity?
We still hadn’t got to the root of the question—we’ve noticed you have but why have you? What's going on to link to it?
So we carried on going, and it led us into thinking about the biopsychosocial model of pain, which does pretty much what it says on the tin. It looks at the biological, social, and psychological factors that influence pain and the way in which they interact with each other.
There are some known psychological risk factors that are associated with people with chronic pain. They include, but are not limited to, anxiety, catastrophising, a fear of movement, and depression, which are much more commonly found in people with chronic pain than those without.
So we looked in a low back pain population—a clinical back pain population. We had moved from looking at general back pain sufferers to clinical populations. We looked at a clinical group and asked is there a link between your levels of muscle activity and the amount of pain? Is there a link between the amount of muscle activity and how disabled you report?
We found that there was. Those who had greater levels of pain did have higher levels of muscle activity, and they did have high levels of disability associated with that pain. We were starting to build up a picture that there might be a link.
We also looked at whether changes in stature and changes in muscle activity were in any way linked to any of these psychological factors, and we started to find that they were. There was a link between stature recovery and catastrophising.
When we looked at pre- and post-intervention, so participants on a pain management program—which is mainly CBT-based—If you go into pain management programs, they don't do anything about your pathology. They're not fixing your back; they're changing the way in which you cope with the pain that you're experiencing.
We found that the changes in anxiety and the changes in pain were related to stature recovery. So we were starting to create a link between the psychological and the physiological characteristics of pain.
Then there was another bit of serendipity as we went along the way. One of my colleagues, who was also working with shooters at the time, was interested in a theory from one of the leading psychologists in this field of anxiety. That research was looking at the interaction between social desirability, defensiveness, and anxiety.
There are four quadrants—high and low anxious, high and low anxiety, and the inter-relation with defensiveness. In the sporting population, sports populations are full of repressors. They’re people who actually experience relatively high levels of anxiety, but they don’t report that they do. They repress their anxiety symptoms.
They are self-deceivers in terms of what they are physiologically experiencing. They aren’t fibbing, they’re just self deceivers in terms of what’s going on. Meanwhile, the defensive high anxious group experience the opposite—they are hyper-vigilant to pain-related or anxiety-related stimuli.
Because this was being looked at we chucked in the defensiveness questionnaire into our psychological evaluations.
When we looked at the populations, we looked at the control group and the pain-based population. We found that 30% of the pain treatment group were defensive-high anxious. They’re about as rare as rocking horse droppings in the general population, but they were disproportionately represented in the pain management group.
If we think about the pathways to pain, if we think about the NICE guideline management of back pain and the truth is that most non-specific mechanical back pain will get better after six weeks, regardless of what you do. You can stick a candle in your ear, rub musk behind your nose. You can do what you like, you’re probably going to get better in six weeks. It’s going to sort itself out.
But for some people, the pain becomes chronic. It doesn’t go away. We don’t really understand that journey from acute pain to chronic pain. It’s not been previously understood.
In order to get onto a pain management program, you go to a doctor, you’re suffering from back pain, they will refer you to any one of a number of treatments that are allowed within the NICE guidelines. People suffering from chronic pain go back again and again. They get passed from pillar to post. That does include just about anything, acupuncture, physio, physical therapy, exercise, classes all have been shown to have a positive impact on back pain, mostly because if you did nothing, you'd get better anyway.
And so it's really hard to differentiate the effectiveness of different types of treatment. If you want to get on to the clinical pain pathway, you have to go back and back and back. And it is a torturous journey for chronic pain sufferers. They get passed from pillar to post. They go through treatments and treatments. The treatment is ineffective and not relieving their symptoms before eventually they will make it onto a pain management program where they'll start to get some psychological intervention to help manage with their pain.
So it's probably not that surprising that our defensive anxious group are overrepresented because they are dispositionally inclined to a be hyper attentive to their symptoms and to interpret symptoms in a negative manner. And they are pre-destined to be persistent in the health system, in the health system, they will go back.
And so it's not a big surprise, that this had never been found before in terms of looking at this defense. And this characteristic as differentiating those in chronic pain and those without.
Interestingly, in our earlier studies, if we look at those change in pain, changes in scores, you see the zero is not on the left-hand side of the scale, zero is somewhere near the middle. Quite a lot of people in these programs don't get better.
And so is there a difference between the responders and the numbers on those who do get better? And those don't? Unsurprisingly again, we found that the defensive high anxious group were disproportionately represented in a group who don't respond to basic CBT interventions, because they're not addressing the underlying issues that these patients have.
So we looked at, well, is this to do with the biases, the psychological biases that you have? We all have dispositional biases according to our personality types. And attentional bias is one of those.
But again, I won't go too much into the methodology we used. So we're looking at eye movements with little cameras looking at where are you looking at on your eyes. And we presented participants with a neutral image and a pain evoking image.
Neutral images you can see on the left is just a shadow. The picture on the right somebody's bending over. Or if you're a back pain sufferer, that's a pain invoking image.
And we checked that out. There are validating scales that these pictures do invoke more valance in those people with pain than those without. We do the same things with spiders and snakes and things of other types of fear.
And depending on where you're looking, will depend on how quickly you’re able to then respond to the stimulus that then comes afterwards. And so you look at the reaction time as well as the dwell time of your eyes during the activity.
And so we did these studies. We looked with our defensive high anxious group. And compared to all of the other personality types, the defensive high anxious group have an attentional bias to the threat-related images.
They were much more likely to focus on the pain invoking image than they would the neutral or positive images.
So if you're doing a physical therapy intervention, you're trying to a patient activity you're trying to teach some movement education. Where's the patient going to look? Are they going to look at the thing you're demonstrating or are they going to look at where the pain stimulus is and focus on the pain stimulus. And then we wonder whether or not they'll get the same benefit from that intervention.
So we've identified a potential causal link all the way back to the personality type of the individuals, back through to the muscle activity that that evokes back to the behaviour of the disc and back to the loading of the structures that are the cause of the pain.
So we've been on the journey that started looking at the mechanics of discs, and forces, and loads, evolved into looking at physiological response with muscle activity and ended up on the doormat of psychology, personality type and eye movement.
So depending upon your disposition or problem, you determine upon how you will respond to the pain stimulus that you get and why some individuals will not benefit from just giving them CBT, because you're not addressing the underlying problems that are there, while most other people will.
And the question that we're left with at this stage, and we love to take the research in its next steps. Okay, well, could we use that to better screen participants if we look to these personality characteristics at the start of somebody’s pain journey, could we save some of the pain and suffering these individuals go through on the pathway where they’re getting treatment after treatment that isn't going to work and could we direct them more rapidly onto the attention bias modification program.
That will allow us to change those biases, change the attention focus, and therefore allow the participants to build a pathway that would alleviate some of the psychological symptoms that cause them to suffer the pain that they have, whilst making sure the physical therapy intervention, CBT interventions are targeted on those participants who have got the best chance of benefiting. And we clean up the pathways, we make it more efficient, save cost, save pain and suffering on the individuals who are on those pain pathways.
That's where we'd love to take the work.
It has been a research journey that started with exercise science, moved through the study of discs, muscles, eyes, and brains, and lots of questions.
And that brings me to a broader reflection on research itself.
What does this tell us about research philosophy as a whole?
Well, fundamentally, research is all about the questions we ask. It’s about never being satisfied with the answers or the questions you’ve got. It’s about recognising that research is really about discovering the right questions we should have been asking in the first place. Because most of the time, the one we just asked was stupid? Every bit of research leads to more questions than answers.
Because we just realised that we weren’t asking the right thing in the first place.
If you ever do a research study that gives you THE answer—publish it, write a book, and retire. Because everything else you do thereafter will be frustrating. Because no other research will get you that.
But more importantly, I think it's about being open to the serendipitous moments. It's about being open to paradigm shift, it’s about being open to new knowledge. If I'd approached the study of back pain as a purely mechanical construct, we wouldn’t have found the things we found.
If I had stayed within the world of physiology and muscle activity, we would never have ventured into understanding psychology and behavioural characteristics, and what’s going on in the dispositional area. And I would remain frustrated at my inability to differentiate between the findings that I was getting from different groups of people.
There is nothing like participants to mess up a good research study—because they just don’t behave in the way you would like them to. So we have to keep probing and going “Why? Why is it different? Why is it happening? Who does this work for? When does it work? And why it different in some situations?” And just accepting those serendipitous moments of just discovering a couple of patients who developed back pain in the middle of their pregnancy and changed their spinal behaviour, and we thought “Ooh! That’s interesting! Those people are behaving differently I would if everyone else does that”.
And somebody happened to be looking at the theory and going “we could measure that because we’re doing the other measures along here”. Just letting those joyful, serendipitous moments take us down paths that we’d never have thought to follow. They open, don’t stick in your paradigm. If you stay in your paradigm you’re never going to get to the answer. You will only ever find a very narrow view of the world that you occupy.
But it also takes me back to my approach to learning and teaching, and what should be going on. And that journey from being the slightly oikish talks-too-much and needs to put more effort in at school. To somebody who’s now standing in front of a group of people giving a professorial lecture. And it’s that notion that in education we spend far too much time telling people what they need to know. Whereas really education should be about teaching people to be consciously curious.
How to build a wonder and excitement of wanting to go and find the answer to the question. To be that person that when they hear something goes “I wonder why that is?”.
And then sits on Google and starts to research it and starts to ask “what does that mean?” And “oh I wonder if that’s related to this?” and the joy and journey of education being about exciting, about being four years old again and going “why?” “Because I said so” “why?”
Why do we drive that out of children? It’s the most important question that we ever do. Embrace your inner four year-old. University education is about trying to drive out of students the education that you’ve experienced on the pathway through school. Sorry, teachers in the room.
Where they’re rammed full of facts and told to regurgitate them, and trying to invoke in them a joy for wanting to learn the stuff we want them to learn. So, ditch the content. It’s not about what you put in your course. It’s about the opportunities, the skills, equipping students to ask the right questions and to step outside of the paradigm in their search for answers. Learning should be about wanting to know the answers, not about providing the answers. We shouldn’t be providing answers.
We should be providing knowledge; we should be providing curiosity. For me the take-home message is:
- Embrace serendipity.
- Be consciously curious.
Go with your conscious curiosity and we’ll probably be alright. Thank you.
Neil Fowler's Inaugural Lecture: From Discs to Brains - An interdisciplinary look at lower back pain video
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