The pain mistake and neuroplasticity
It was one of those searing summer days where you leave the protective dome of your car and know that your scalp is going to get fried on the 10-foot scuttle across the pavement to the nearest shade. My target, on this glaring Tuesday morning in November 2019, was the sheltered portico of an anonymous glass-fronted building in the Melbourne suburb of Moorabbin.
I bee-lined for the sliding glass doors and slipped into the cool confines of the building’s atrium, where I did a quick recce and spotted the sign I was looking for: Rehabilitation Medicine Group. Inside, neutral walls were splashed with the contemporary hues of regulation office art; there was a reception counter and a row of sleek, white chairs smudged with the just-discernible grey of repeat users. “Dr Fried’s 11 o’clock?” chimed the receptionist who, when I nodded assent, motioned me to sit down.
I fidgeted with my phone, then lapsed into a meditation on why I was sitting here waiting to see a pain expert. And whether I really needed to be.
I consider myself to be medically literate. I had been, after all, a doctor for 20 years, a decade of which I worked as an emergency physician, mopping up everything that disease and trauma throws at a person to put them at death’s door. I’ve also conducted a decent slab of my own research, including a PhD and a postdoc on how our decision-making gets skewed by things as varied as depression and the subconscious tweaks of advertising. To top it off, I’m a science journalist, with the latest research filling my inbox on a daily basis. You’d think I’d be in the box seat to nail the answer to my own medical dilemma.
The source of my inner turmoil had begun on a wintry morning five months earlier. I’d woken with a sore right knee and had to push through tightness and a nagging ache when I walked my kids to school. I put it down to basketball and overdoing my regular jogs through the park. But five weeks in, I’d had enough. I happen to have a mate who’s a physiotherapist and an expert diagnostician, so I decided it was time to get professionally reacquainted.
“Was going under the knife really the best option?”
Paolo is a tall, athletic man, whose dark hair and beard I’ve watched grey in recent years as we’ve both moved into our 50s. I managed to catch him in his rooms in bayside Melbourne, where he greeted me with the demeanour of a friend, tinged with the subtle gravitas of the health professional. I had to climb a flight of stairs to get to his office and did it wincing, holding on to the handrail. Paolo put my knee through its paces, with some tests to see how far I could bend it and whether I could squat on that leg. It hurt. Enough to bring tears to my eyes. But pain, it seemed, was a prerequisite of the diagnosis; I had torn, Paolo said, a piece of cartilage in my knee called the medial meniscus. And he was right – the diagnosis was confirmed a few weeks later with an MRI scan. But making the diagnosis, it would turn out, was the easy part.
I know an orthopaedic surgeon with impeccable credentials, a former colleague whom I hold in high regard, so I consulted him, and his advice was clear: surgery to trim the tear would help my pain, which would otherwise continue a waxing and waning course over an unspecified period of time. In fact, he’d had the very same surgery himself, with excellent results.
It was a gold-plated recommendation, and I signed the paper then and there to have the operation at a local public hospital. The lengthy machinations of the public health system, however, meant I was in for a wait, possibly months, and, while that time ever-so-slowly elapsed, a number of things happened. I gave up my beloved jogging and quit scratch basketball with my young son, I favoured my good leg more and more, and I hoovered up a small mountain of medical research about meniscal tears, which, disconcertingly, left me plagued with second thoughts. Was going under the knife, I wondered, really the best option?
It started with a better understanding of that little piece of me that was up for surgery. The meniscus is the shock-absorbing cartilage in the knee joint. The structure not only disperses the hefty forces that are driven through the knee when you walk, run or jump, but also has the vital task of helping the bottom end of the thigh bone – the femur – slide over the top end of the lower leg bone – the tibia – when you bend your knee. There are two of these menisci, a “medial” one on the inner side and a “lateral” one on the outer side of each knee. If you enlarged them, they’d be a skateboarder’s dream; they look like a half-pipe designed by Antoni Gaudí.
But if you ever have to take a job in the human body, don’t be a meniscus. The forces that pass through the knee would test Atlas, ranging from one-and-a-half times your body weight on a gentle walk, to three times your weight going up and down stairs. Go for a run and eight times your weight can pass through the knee. A good chunk of that compressive force is channelled through the meniscus and especially, when you’re running, the back, or “posterior”, of the medial meniscus. Which is precisely where my tear was.
Now, at this point, you’d think the treatment would be crystal clear. This injury has been thoroughly mapped by MRI scans for more than three decades, and surgeons have been fixing it with a procedure called a partial meniscectomy for even longer. Yet the best treatment for a meniscal tear was now as clear as mud to me, and the reason carries a lesson about pain that extends well beyond the knee.
Let’s look at the procedure. After you’re under anaesthetic, an orthopaedic surgeon makes two cuts in the front of your knee to insert an arthroscope, which lets them see the torn cartilage and remove the jagged edge. But most surgeons want to shave the damaged area back to a smooth arc, which often means removing 15-20 per cent of the meniscus. How does that fix the pain? Here is where the uncertainty starts to creep in.
The meniscus itself has a very limited nerve supply, so the tear often won’t hurt of its own accord. Surgeons think the meniscus causes pain when the torn flap of cartilage rubs against, and irritates, the glossy, translucent tissue that lines the knee joint, called the synovium. Unlike the meniscus, the synovium has a copious nerve supply and is, therefore, well-equipped to make your life a misery. However, no one has shown conclusively that a torn flap rubbing on the synovium causes the pain. There is, in truth, a yawning abyss of doubt on this very point, one that has opened up around a statistic that should be a numerical touchstone for anyone considering surgery for pain.
“How can I become one of those over-50s with a meniscal tear who is pain-free, without having surgery?”
If you take a random bunch of people off the street in my age group – over 50 – one-third of them will have a torn meniscus. Older people are especially prone to degenerative tears, which happen when the meniscus deteriorates, rather than when it’s subject to an excessive force. But there is another, even more startling statistic. Sixty per cent of those people with a torn meniscus, a clear majority, have no knee pain at all.
Having a torn meniscus, in other words, is entirely consistent with being pain-free. In fact, there are millions of people walking around who don’t even know they have a tear. Now, if you are someone with a torn meniscus, and you are in pain, and you are being offered a partial meniscectomy to treat the pain, learning that statistic may get you to pondering something: “How can I become one of those over-50s with a meniscal tear who is pain-free, without having surgery?” This was my very own dilemma.
Kal Fried is the go-to guy in my neighbourhood for people with pain that’s standing between them and their bike, basketball, badminton racquet or whatever movement gives them pleasure, health, or plain old freedom. We might see him for short-term, “acute” pain, but Fried’s special expertise is dealing with pain that lasts longer than three months, officially termed “chronic” or “persistent” pain.
Fried is a sports and exercise physician, and his CV is studded with the perks of the profession, namely, getting to hobnob with, and lay healing hands on, the athletic elites of the nation. He’s been the club doctor for the Melbourne and Collingwood AFL football teams and worked with Australia’s national netball team, the Diamonds, to name a few.
But Fried is no sporting snob. His passion can be summed up in two words that apply equally to the sports star and the suburban pensioner with a bad back: pain literacy. He is a champion for the cause that understanding pain is key to overcoming it.
Fried is 60ish, with a pate shaved smooth, olive skin, and piercing blue eyes bordered by crow’s feet that dance, leprechaun-like, when he smiles. He was kitted in standard office gear of slacks and an open-necked business shirt, but, when we were both seated at his desk, I noted a road bike leaning against the wall behind him that had the tell-tale grime of many hard miles, so I knew there was lycra stashed away somewhere. When he spoke, his tone was equal parts confident and unhurried, but the message was charged with the urgency of his pain-busting mission.
Suddenly, with an impish smile and the flair of a magician, he thrust three playing-card boxes at me, each stacked neatly on top of the other. “Grab on to those, Paul,” he said. The top box, he told me, was full of cards, but the other two were empty. I curled my fingers round the triple stack, which just fit in my hand, and held them for a few seconds before Fried asked for them back.
Then he handed me the single box containing the full deck. I held it aloft, all by itself, for a moment. “Notice anything?” he asked, eyebrows raised and smile on high beam. I had. The full box of cards on its own actually felt heavier than the three boxes all together. Which, of course, it couldn’t be. It had to be lighter, by exactly the weight of the two empty card boxes that were no longer in my hand. I did it again – same result, same mystifyingly weird feeling.
“The brain is responsible for what we feel, but it doesn’t get it right all the time.”
Fried fixed his gaze on me with a triumphant air as he let the illusion sink in. The feeling of holding the single full pack between just your fingers, he explained, means the brain senses it as heavier than it really is, compared to grasping all three packs, which are felt across a broader area of the hand. “It doesn’t matter that you know that two are empty and one is full, and it doesn’t matter how many times you do it, you get the same sensation,” he said. “The brain is responsible for what we feel, but it doesn’t get it right all the time.”
I had knee pain, but it doesn’t matter where it comes from; the problem with pain is that, when it drags on, it becomes, in many cases, a deception. A card trick played by the body that harnesses the dizzying resources of the nervous system to dupe the mind into thinking that the body is still hurt and that hunkering down to protect the injured part is the only option.
Pain, like the Roman god Janus, is two-faced. Its first face is straight-up and, frankly, essential for survival. Along with swelling, redness, heat and loss of function, pain is a cardinal sign of inflammation, the body’s response to illness and injury. The fact that a bit of you hurts stops you from waving it around or running on it, and this slowdown in activity helps it heal.
But swivel pain around and take a look at its second mug and what you find is an inscrutable poker face that has bluffed a goodly number of the world’s population. Because the longer pain goes on, the less reliable it is as a marker of damage, to your knee, back, shoulder, wherever. For many, this is a disturbing insight.
Over the last few decades, a gathering wave of research has shown that persistent pain can cause the nervous system to become ultra-sensitive to sensations coming from the affected area. Things that would normally hurt, hurt even more, and things that wouldn’t normally hurt, like simple pressure, or movement, become painful. In practice – and I speak from experience – that means something as innocuous as a breeze blowing on a long-suffering knee can be misinterpreted as pain. It sounds like pure madness, but this devastating error is a by-product of perhaps the most exquisite example of physiology in the human body. It is called neuroplasticity, and it operates throughout the entire pain-sensing apparatus, from the nerves that take pain messages from the injured part, to their junction with the spinal cord, and even the areas of the brain that process the pain and make you conscious of it.
Neuroplasticity is something of a buzzword, thanks to Norman Doidge’s bestselling 2007 tome The Brain That Changes Itself. Put simply, it’s the ability of the brain to rewire itself in the process of learning new things, like how to play the violin, or how to talk again after a stroke. The concept has upended decades of dogma that tell us the brain’s connections are as malleable as putty in infancy but become as hard-set as amber when we reach adulthood. Neuroplasticity is, without doubt, a bona fide celebrity in the world of neuroscience.
But like so much that glitters, neuroplasticity has a shadow side. It is called maladaptive neuroplasticity, and, when pain stays put, it can mean stimuli that are non-nociceptive – not legitimately pain-producing – get mistakenly registered as nociceptive: they bloody hurt. This is what I call the pain mistake – and understanding it is key to its undoing.
Crucial questions now needed to be tackled head on: how does understanding the pain mistake make it go away? If persistent pain doesn’t signal ongoing injury, why is it there? Can you learn to be in pain and, if so, can you unlearn it?
In the US health system in 2016 alone, an eye-watering $US380 billion was spent treating musculoskeletal disorders, including back, neck, joint and limb pain as well as conditions such as rheumatoid arthritis and osteoarthritis. No fewer than one in five people live with chronic pain. Yet therapies grounded in an understanding of neuroplasticity are crowded out by pills, injections and surgery, blockbuster treatments that can harm people by the millions.
The US opioid crisis is exhibit A when it comes to pharmaceutical harms; overdose and suicide linked to opioid painkillers have been blamed for the first drop in US life expectancy in a century. But physical treatments also take a toll.
Take spinal fusion for back pain. Rates doubled in the US in the decade to 2009, and the procedure generated costs exceeding $US10 billion in 2015. Yet one in six operations leads to complications, including nerve damage. On top of that, experts are lining up to say that, as a treatment for back pain, spinal fusion is as good as useless: inferior to exercise, cognitive behaviour therapy and physiotherapy. These pharmaceutical and surgical treatments are co-conspirators in the pain mistake. They are directed at a body part, not at the nerves that sense it. They seek to alter the anatomy, not the perceiving brain. They fail to understand the importance of maladaptive neuroplasticity.
All of which led me to ask myself a potentially life-changing question: was I a victim of the pain mistake? I had a rudimentary knowledge of maladaptive neuroplasticity from an earlier cycling injury, and wondered if it might be a factor in my current knee pain. But I’d seen the meniscal tear on the MRI scan with my own eyes. There was a highly visible, well-articulated causal chain leading from my overdoing it on the running track and basketball court, to the symptoms of a sore knee, to the diagnosis of a meniscal tear. A surgical trim seemed the logical response. But I just couldn’t get that 60 per cent figure out of my head; if having a meniscal tear was compatible with a life without pain, why couldn’t that life be mine?
“If having a meniscal tear was compatible with a life without pain, why couldn’t that life be mine?”
Soon after our consult, I got an email from Dr Fried. He’d just finished creating a learning module for the Australasian College of Sport and Exercise Physicians, and he invited me to take a look at it. It included a slide of him riding up the torturous Alpe d’Huez, one of the steepest climbs on the Tour de France circuit. A speech bubble emanated from his panting lips: “Pain is not an accurate marker of tissue damage …” Another slide showed a skeleton with various pain hotspots circled in blue, including the knee, lower back, neck and shoulder. Adjacent numbers tallied the abnormalities picked up on scans of those areas – but in people with no pain at all. They made for remarkable reading.
In the neck, 87 per cent of people aged 20 to 70 have a bulging disc in the spinal cord, with no pain. Thirty-seven per cent of 20-year-olds and 97 per cent of 80-year-olds have degenerative discs in their lumbar spine. With no pain. Forty-three per cent of over-40s have degeneration of the cartilage lining the knee joint. With. No. Pain.
These are all abnormalities that, in people who do have localised pain, trigger a range of treatments to correct the anatomy. Yet there are literally hordes of folk walking around with the very same anatomy, and no pain at all. You could be forgiven for concluding that, in a generous chunk of people, the anatomy is not the problem.
I was now in possession of the most important tool anyone can have when deciding how to treat their pain: knowledge. I began to mull it all over as I worked my way towards answering the pivotal question: what should I do?
This is an edited extract from Paul Biegler’s Why Does It Still Hurt? (Scribe Publications; $35), out now.
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https://www.smh.com.au/national/hurting-so-good-the-pain-in-the-strain-may-be-mainly-in-the-brain-20221205-p5c3r7.html?ref=rss&utm_medium=rss&utm_source=rss_national The pain mistake and neuroplasticity