full article 12000 words
Most of the time it’s hard not to heal. You couldn’t stop it if you tried. The body is going to recover from most kinds of injuries almost no matter what — it’s just a matter of time. As long as you were reasonably healthy before you were injured, and you don’t smoke or constantly ruin your sleep or otherwise make yourself biologically vulnerable, healing will almost always progress inexorably.
Chronic pain is different by definition: it doesn’t stop when it’s supposed to. Either healing fails, or the pain continues even when the tissues are actually fine, or an unholy miture of the two. Overuse injuries or repetitive strain injuries (RSIs) like carpal tunnel syndrome and plantar fasciitis are slow-motion traumas that often seem immune to recovery — this is what makes them both terrible and fascinating. They are not as simple as they seem. There are (at least) five surprising facts about them that few patients or professionals understand:
It’s shocking: the RSIs include several of the world’s most common and frustratingly stubborn painful conditions, and yet treatment is overwhelmingly dominated by the myths of inflammation and biomechanics — myths that just won’t die, even decades after the scientific evidence started to debunk them. And yet the true nature of these conditions is virtually unknown and the implications ignored — tissues exhausted far beyond their limits that are never rested adequately, extensive muscle pain complications that are rarely even diagnosed (let alone treated), and neurologic sensitivity to mental states that are mostly considered completely irrelevant.
Recent basic science research suggests little or no inflammation is present in these conditions.1
Repetitive strain injuries are widely believed to be inflammatory in nature, and that assumption is built right into the name in many cases: the Latin suffix “-itis” means inflammation, and it’s attached to the names of several of these conditions, such as plantar fasciitis, Achilles tendinitis, and supraspinatus tendinitis.2 The mental imagery of inflamed tendons or other anatomy is vivid, something like a car engine part overheating due to excessive friction. Maybe a little bit at first, but not for long.3 It’s not useful imagery.
What's really going on has little in common with classic inflammation, as we know it from infections and acute lesions. The immune system is out in full force to repel microbes, and the presence of white blood cells is the microscopic signature. In RSI, the white blood cells are barely there, and the picture is dominated instead by signs of tissue failure and degeneration. It’s like premature arthritis in any overloaded tissue, which can’t repair itself fast enough to keep pace with the stresses placed upon it. Tissue rot!
Numerous investigators worldwide have shown that the pathology underlying these conditions is tendinosis or collagen degeneration.4
Healthy tendons look white and shiny. That slick look is a direct consequence of the highly organized molecular structure of the tendon — the same reason that crystals are pretty. Tendons are made of extremely orderly protein molecules. But tendons suffering from overuse injury look increasingly dull, dilapidated, “grey and amorphous to the naked eye and microscopy reveals discontinuous and disorganized collagen fibres that lack reflectivity under polarized light.” (Sorry, no picture, alas.5) The unhealthy tendon looks grey because it has lost that organized feeling, right down to the molecular level. Its proteins have become a bit jumbled and irregular, and the result is a tendon that no longer looks slick.
Meanwhile, it’s not inflamed in any familiar sense of the word.
Inflammation is not one thing: it’s a stupendously complex spectrum of biological substances and processes, most of which are absent or different in RSIs than they are in infection or acute injury.6 If you really stretch the definition of inflammation, it could include any biochemistry of healing and adaptation to stress — but that includes a lot of biochemistry that is quite different (and mysterious). An infected cut hosts a soup of cells and chemicals, and biologists know quite a lot about the recipe for that soup now. They know almost nothing at all about what’s going on in RSIs.7
The microscopic signs of inflammation are mostly but not entirely absent — they do crop up a little bit, here and there. For instance if there is any actual tearing of the tendon or any frank structural damage, then you’ll probably see some classic inflammation around the site of the tear, as with any other injury.8 But that’s torn tendon, a different critter. And certain types of tendinitis seem to be more prone to inflammation than others — not all tendons and stresses on them are the same, after all.9 But most cases of tendinitis seem to be dominated by the breakdown of the proteinaceous substance of the tendon itself.
That tendon “rot” is called tendinopathy or tendinosis — osis meaning condition — not tendinitis. Although well described by microscopists and pathologists, tendinosis is not well understood — we know what happens, but we don’t know why or how.
Tendinosis is tendon degeneration without clinical or histological signs of an inflammatory response. It appears that tendinosis is the major, and perhaps the only clinically relevant chronic tendon lesion.10
The imagery of anatomy “over-heating” is so compelling and mentally comfortable that it is virtually impossible, at first, for most people to imagine tendinitis without inflammation. But not all repetitive strain injuries are tendinitises, and this “osis” business doesn’t just apply to tendons. Other tissues involved in RSIs are also generally lacking in inflammation, but are degenerating and struggling to adapt to stress in similar ways. Researchers found tibial degeneration in 100% of runners with shin pain.Consider bursitis, for instance, a condition with even more of a reputation than tendinitis for being inflamed — even there, inflammation as we normally think of it is nowhere to be seen.11
There are two common repetitive strain injuries that involve the fatigue of a very different tissue: bone.
Fatigue of bone is probably a common factor in two of the major RSIs: shin splints (tibial degeneration) and patellofemoral pain syndrome (patellar degeneration). It’s easier to escape the cliché of classic inflammation when we’re talking about bones. We aren’t used to thinking of bone as tissue that would get inflamed (though of course it can — just break one). But what actually happens to over-used bone is suspiciously similar to what happens in abused tendons: it degrades and degenerates. In the case of the shin splints, eventually the tibia will break — a stress fracture — just as a degenerated Achilles tendon will rupture. But a break is preceded by a lengthy period of microscopic erosion. A 2006 paper found tibial “degeneration” in 100% of runners with shin pain.1213 One hundred per cent! For the math impaired reader, that is — wow — all of them. That’s a lot of degeneration.
I can’t state strongly enough that this process of degeneration is basically mysterious — unknown etiology, in medical-speak. The physiological details are still undiscovered. And yet we can put together a pretty clear general principle without going too far out on a scientific limb. Heavily used tissues are continuously rebuilding and maintaining themselves. If we push them so hard and frequently that the strain begins to exceed the capacity of the tissue to repair and maintain itself, then it will probably start to fall apart.14 (And just to keep this from being too simple, it’s also rather likely that neglected tissue degenerates. Use it or lose it, anyone?)
It also makes plenty of biological sense that this degeneration would not be an inflammatory process, actually. Inflammation is primarily an anti-infection system and a function of the immune system, which is why it occurs in spades at every break in the skin, and it even occurs internally without a real risk of infection (because of a fascinating mistake15). But if tissue is degenerating, there may be relatively few broken cells and no clear reason for any inflammation. The fundamental problem is more likely to be failed healing: that the cells can’t keep up with repairing the damage to the connective tissue structures they are tasked with maintaining. The cells aren’t broken — they’re just like Lucy trying to keep up with the conveyor belt of chocolates.
We can’t entirely dismiss the idea of inflammation. Some key components of it are still in the picture. The biochemistry of RSIs almost certainly has some things in common with the biochemistry of classic inflammation.16 There are also many kinds and degrees of inflammation-like processes, some of which appear to have little or nothing to do with the defensive reaction to infection or injury. Some inflammation may even be a straightforward biological malfunction, rather than your body doing what it should “for your own good.”17 With a Schrödinger's-cat-like duality, RSIs may appear to both be and not be inflamed at the same time, depending on how you look at the physiology. It’s really a bit of a word game whether or not to call the tissue disturbance of RSI “another kind of inflammation” or “something else altogether.” However, the idea of inflammation loses a lot of its punch when the real chemistry is so exotic and varied that traditional anti-inflammatory treatments are generally ineffective. Speaking of which …
If tendinitis isn’t really an immune system “fire,” what does that suggest about common treatments and therapies for repetitive strain injuries?
Effective treatment of athletes with tendinopathies must target the most common underlying histopathology, tendinosis, a non-inflammatory condition.18
Given the assumption of inflammation, medications traditionally used to calm inflammation are overwhelmingly the most popular first treatment choice. If it “burns,” take ibuprofen and “cool” it down with ice. If it’s serious, inject something potent: corticosteroids.
That’s the conventional wisdom, and it’s well entrenched and accepted. It never even occurs to most professionals to question it.
But there are some serious problems here, and not just the fact that these treatments are supposed to get rid of inflammation that mostly isn’t there in the first place. Their chemistry (even ice!) is just as complex as the inflammation they aren’t actually treating. They are known as “anti-inflammatories” because of their average, typical effects on classic inflammation — on vigorous immune system activity and associated processes. How they interact with the entirely non-classic inflammatory biochemistry of RSIs is a more or less perfect and utter mystery.
We also need to consider the difference between treating pain and treating the condition. Virtually nothing is known about using medication to stop or reverse tissue degeneration. Medication for RSIs is almost always just about symptom relief. And yet even for that goal our ignorance is embarrassing: we don’t even know what makes RSIs hurt to begin with, let alone what chemicals will stop it. RSI pain is an infamously useless sign of the condition of the tissue. For instance, alarmingly degenerated tendons can actually be painless. (Ruptures often occur in people who didn’t even know they had a problem.) The specific cause of RSI pain is largely a mystery, and its comings and goings even more so. It’s clearly a moving target. The specific cause of RSI pain is largely a mystery, and its comings and goings even more so. It’s clearly a moving target. This is yet another vivid difference between RSI (where pain is quite unpredictable) and classic inflammation (which always hurts, and quite a bit).
So it’s hardly surprising that the collective track record of anti-inflammatory meds in this context is generally shabby and unpredictable, neither completely useless nor remotely reliable. If they worked well and consistently, obviously no one would ever need to read this. To whatever extent they do work for some people, some of the time, is due to unknown and variable chemistry.
What on Earth can one do in the face of such rampant uncertainty? Alas, this is not an unusual dilemma in health care, and the solution always goes like this: weigh guestimated costs and possible risks against the speculative hope of benefit, and then favour the options that are the most attractive overall, i.e. the least expensive, risky and annoying while still having a snowball’s chance in Hell. With those priorities in mind, let’s consider some of the popular specific “anti-inflammatory” options for repetitive strain injury.
Most drugs work on only about a third of the population, they do no damage to another third, and the final third can have negative consequences.
Craig Venter, extremely famous and spooky smart geneticist (public lecture, Vancouver, May 3, 2011)
Vitamin “I” — ibuprofen, the main ingredient in drugs like Advil and Motrin — is an almost universal treatment choice for RSIs. The drugs ease inflammation and fever, and the injury seems to be inflamed, so it’s a perfect match! Or people just take them because it’s a pain-killer and they have pain to kill. For one reason or the other, nearly every patient and professional assumes that NSAIDs are at least somewhat helpful, though few are foolish enough to think it’s any kind of a cure.
In fact, the NSAIDS are probably one of the weakest treatment options — because of course repetitive strain injuries are not actually very “inflamed,” per se.
Scientific evidence on this topic has always been scarce and discouraging, and even the anecdotal evidence for ibuprofen is weak. I’m sure there are some testimonials for ibuprofen — there are for anything. But consider: even though ibuprofen is probably the first or second line of defense for virtually every case, the world is clearly still full of serious, chronic RSIs … that ibuprofen hasn’t stopped.
(Many athletes, especially runners, swear by ibuprofen as a prophylactic to prevent soreness during competition, but that’s quite a different usage, and it definitely doesn’t work.19)
So, NSAID chemistry is laughably irrelevant to the chemistry of RSIs, but it gets worse: they may actually interfere with recovery from the connective tissue degeneration that actually is the problem, because NSAIDs retard soft-tissue healing. Just what every RSI victim needs! (Fortunately, they don’t actually damage connective tissue, like steroid injections. Probably.) There’s no direct evidence that NSAID use will impede recovery from an RSI, but it’s possible.
And it gets even worse! NSAIDs are also well-known as “gut burners” for their disagreeable and common effects on the gastrointestinal tract, which is a deal-breaker for many patients. And they can, paradoxically, actually cause headaches. Oh, and one more thing: they increase the risk of strokes and heart attacks, even in healthy people, at any dose. (diclofenac (Wikipedia), a popular oral NSAID almost everywhere on Earth but North America, has even worse cardiovascular side effects than the others.20 Oral diclofenac specifically should probably be banned.) Lovely! NSAIDs definitely aren’t the best option for RSI, or even the best over-the-counter medication for the job.
A drug is a poison with potentially beneficial side effects.
I know some readers are thinking right now, “Yeah, well, okay… but I’m still going to take my Vitamin I.” With dosing caution — small doses, short-term use — I have no serious objection. If there’s any reason to take them, it’s that they might relieve some pain by unknown mechanisms (the inflammation question is not exactly simple).
Or — and this seems almost crazy, I know — you could just actually heed the science, ignore the conventional “wisdom,” and never bother popping another NSAID unless you’ve got some uncomfortable classic inflammation to take an edge off. Imagine two NSAID scenarios…
Speaking of dosing caution…
Voltaren® is basically another NSAID (diclofenac, like ibuprofen) in a tube, and a relative newcomer to the range of options. Because you smear it on and it’s absorbed through the skin, you don’t have to carpet bomb your entire digestive tract and circulatory system with the stuff to get it to the problem — and this probably significantly reduces your overall exposure to the risk of side effects21 (very real and serious with oral diclofenac), while still getting a respectable dose into the tissue with the issue.
Another reason that Voltaren is interesting and well worth bringing up here is that it would never have been approved for sale if it didn’t have some promising evidence attached to it (see my main Voltaren article for details). The stuff actually seems to do something for arthritis pain — which probably actually has much more biologically in common with RSI. So we’ve got something like a shred of a reason for optimism here and greatly reduced risk. Yahtzee!
Traumeel — a very different sort of popular ointment, and a great deal less attractive an option than Voltaren. Traumeel is a homeopathic product, a diluted Arnica cream that is supposed to be “good for” basically any kind of ache or pain, but particularly anything supposedly inflamed — and so it is routinely and officially recommended for conditions that are not, in fact, inflamed. Indeed, the entire concept of Traumeel is that the herb Arnica montana has effects “like” the inflammation it supposedly treats.22 So, even if tendinitis actually were an inflammatory condition, this remedy wouldn’t work by homeopathy’s own rules.23 But piling irony upon ineffectiveness, Traumeel is mainly being used as an anti-inflammatory for conditions that aren’t actually inflamed! So this is a product with questionable effectiveness in general, being recommended to treat inflammation that routinely isn’t there, on the basis of a principle of homeopathy that wouldn’t apply even if it made sense.
Therapeutic ultrasound. From the edge of alternative medicine to the heart of the mainstream: another super popular inflammation-assuming treatment for tendinitis is therapeutic ultrasound … and it’s highly over-rated.24 Ironically, it’s possible ultrasound actually does have a therapeutic effect on tendinitis, but certainly not a clear, proven benefit, and (more to the point) most definitely not a benefit related to reducing inflammation. No one knows if it really works, and if it does it seems to be rather unspectacular. If it does work at all, it probably does so by gently provoking/stimulating tissues, reversing the “rot,” and/or via minor and temporary neurological effects on pain.
Icing. The apparent value of icing for seemingly “hot” pain is mostly the poetic, non-medical mental imagery of cooling. The problem is not heat, of course, and it can’t be fixed by cooling. If ice can help a repetitive strain injury in any way beyond brief numbing, no one has ever actually proven it,25 or even shown how it might work. There’s little doubt that it’s relieving in the short term, and there is some reasonable speculation that it could stimulate miscellaneous minor tissue healing processes. Virtually any stimulatory input to the body, up to a point, can provoke a healthy response, because of the use-it-or-lose-it principle. Stress a tissue, and it will probably get tougher in some way. In broad strokes, that is probably the only plausible therapeutic mechanism of icing. Ice may simply be one of the easiest delivery systems for a bit of non-toxic stimulation — a way to stimulating tissue without overloading it, while simultaneously getting some temporary pain relief from numbing. However, it certainly isn’t “anti-inflammatory”!
The great advantages of ice as a treatment are not its impressive biological effects, but its thrift, ease, and safety: treatment options simply don’t get any more innocuous while still having some plausible mechanism of benefit.The great advantages of ice as a treatment are not its impressive biological effects, but its thrift, ease, and safety: treatment options simply don’t get any more innocuous while still having some plausible mechanism of benefit. Therefore ice remains firmly on my “worth a shot” list for RSIs. Keep your expectations low, but there are virtually no risks, other than ice burn (which takes at least a couple minutes of raw ice application, probably twice that).
I’ve saved the “best” for last. If “best” means “most complicated and interesting”…
Corticosteroid injections and iontophoresis26 deliver a potent medication right to the source of the problem — think of them as ibuprofen on, er, steroids. Steroids certainly do have anti-inflammatory properties, in spades: broadly speaking, they suppress immune function, which is the major component of classic inflammation. Steroids can work bloody marvels, especially with diseases where the immune system is rampaging out of control. The classic example is the drug prednisone, which has nearly miraculous and even life-saving benefits.27 The price of this potency? Steroids also eat away at connective tissue — the same tissue that is already in trouble in most RSIs.
It’s limited, but there is half-decent evidence that injecting steroids right into the heart of an RSI can help significantly, even though RSIs lack the immune cells that steroids primarily affect. The evidence for short-term benefit is particularly decent in the case of tennis elbow (lateral epicondylitis),28 although there is also evidence that the long term results are much less rosy, or even nasty. It’s pretty reasonable to presume that the effects on other RSIs are a similar mix of good news and bad news. The brevity of the benefits means that — surprise, surprise! — we’re probably missing something about the science here. If RSIs are’t really inflamed, why is a powerful “anti-inflammatory” medication ever effective? Some possibilities:
Steroids in a needle are generally much less risky than steroids in a pill. Just like with the difference between popping NSAID pills and rubbing them on in a cream, injection limits your exposure to one spot. The main risk — and it’s not nothing — is that steroids eat connective tissue. (Slowly. It’s not like strong acid!) Nevertheless, this is a Very Bad Thing, and probably explains the data about long term harm…
It is clear that corticosteroid injection into tendon tissue leads to cell death and tendon atrophy. As tendinosis is not an inflammatory condition, the rationale for using corticosteroids needs reassessment, as corticosteroids inhibit collagen synthesis and decrease load to failure.30
Since the nature of repetitive strain injury is that tissue slowly “rots” and degenerates under stress, steroid erosion of connective tissue is therefore an ironic hazard — steroids may dangerously exacerbate the basic problem even as they relieve pain. The risk is obviously worst in the case of classic tendinitis, where structurally critical tissue may be weakened. Few people are keen to increase the risk of a rupture just for pain relief! That’s why physicians wisely limit steroid injections to about three (although that may be overly cautious).
The saving grace is probably that the negative effect on connective tissue integrity is probably minor with limited dosing. Nevertheless, this is a most awkward and ironic collision of potential benefit with potential risk, and some experts have concluded that the evidence is too negative in the long term to keep recommending the treatment.31 There’s too many variables and uncertainties here to make a blanket recommendation for all patients: you have to weigh the pros and cons decide for yourself whether you want to “go there.”
Just as we find it almost impossible to think of tendinitis without also thinking of the fires of inflammation, we also find it too easy to assume that this failure is the result of some kind of malfunction of a beautiful system of pulleys and levers that has somehow “gotten outta whack.” This mental bias is known as “structuralism” or the postural-structural-biomechanical model for pain. To quote myself:
Structuralism is the excessive preoccupation in the physical therapies with biomechanical factors in pain problems — the biomechanical bogeymen.
Nowhere are the biomechanical bogeymen more numerous than in theories about the origins of the RSIs. Unfortunately, they are just as difficult to find as inflammation. Typical examples of the bogeymen include: ankle pronation, weak hip abductors, poor posture, crooked knees, and literally dozens of others. The idea is always that such factors increase the strain on your parts.
The problem is not that these problems don’t exist. They do.
The problem is that the only biomechanical problems that are much of a problem are the really obvious ones — and they don’t need diagnosing, and are impossible to fix anyway. On the other hand, any problem so subtle that it can’t be diagnosed easily is also not much of a problem. The huge majority of RSI sufferers have no obvious deformity or bizarre walk or blatant muscle wasting. If there’s anything wrong with their biomechanics, it can’t be adding very much stress to the equation … and yet they inspire most of the expensive therapy for RSIs.
While the inflammation-based treatments may be mostly useless, they are also (relatively) inexpensive and harmless. Not so with treatments and therapies based on the idea of biomechanical failure! An amazing amount of professional effort goes into trying to diagnose and treat patients with repetitive strain injuries as if they are malfunctioning in some way. All that diagnosing, and all those tedious exercises intended to correct “muscle imbalance,” are costly in time and money, and none of them is going to matter if the tissue continues to be stressed beyond its capacity.
What really troubles me is that it’s all such a major distraction from what really matters: actually resting the tissue. (Indeed, structuralist prescriptions often involve exercising the part.)
Once the degeneration of stressed tissues has set in, it’s a bit of a freight train: even if you can successfully identify and correct a subtle biomechanical dysfunction, it won’t change the forces on that anatomy much. The “strain” in repetitive strain injury is mostly caused by the ordinary usage of the anatomy, not by minor imperfections in biomechanics. Perhaps a biomechanical problem could make some anatomy slightly more prone to failure, but it’s still the overuse that is the main issue.
This is what I call the rock-in-shoe problem: when you have a rock in your shoe, and it starts to cause extreme pain, it’s really not going to help you very much to slightly change your gait, which can only reduce the forces on your foot a little bit. Even with a crazy limp, you still have to put your foot down. What you really need is to get rid of the rock. And if you don’t have the option of taking off your shoe — if the “rock” is built right into your tissues — then your only option is to stop using that anatomy.
Much more information about structuralism and the downfall of the postural/structural/biomechanical model of pain is available here:
“Rest” means savvy “load management” that errs on the side of less in the short term. Exercise is actually a vital part of recovery, but the dosage is critical and it has to be baby steps for weeks, months. Almost everyone tries to do too much, too soon. Doing it right — doing it slowly and carefully enough — definitely feels like “rest.”
That said, the truth is boring and simple: rest is incredibly powerful medicine for RSIs, but also tedious and often spectacularly inconvenient, even job-threatening. This boring “miracle cure” is almost never adequately emphasized to RSI patients.
I put the scare quotes around miracle cure because it’s only half wrong. Rest really can be a something of a miracle cure: some extremely entrenched cases of RSIs can still be successfully treated with an effective resting strategy, long after the patient has given up, years after starting to say “I’ve tried everything.” Although there’s nothing actually miraculous about such a late victory over an RSI, it can certainly seem that way to the patient.
On the other hand, rest does not get full miracle-cure status, because there are quite a few cases that cannot be successfully treated with rest. Rest usually fails because there is something going on that cannot be rested from, an aggravating factor that just can’t be escaped.32
Regardless, it’s certainly worth trying, and trying well.
One of the things that makes rest particularly relevant to repetitive strain injury is that there is good evidence that it really takes quite a long time for degenerated connective tissue structures to heal. Tendon is metabolically sluggish. It “breathes” only about 10–20% as much oxygen as muscle — a measure of metabolic activity — and even muscle isn’t exactly lightning fast with recovery.33 So tendons do not heal quickly.
According to Khan, it may take as much as two to three weeks of rest before a tendon even begins to start rebuilding, and rebuilding itself is achingly slow: about a hundred days for the tendon cells to build the collagen molecules that make up the bulk of a tendon. That’s three months!
Anyone who has had a sprain knows that connective tissue is slow to heal. A ripped ligament is usually never quite the same ever again, and spends many months, even years, feeling pretty unpleasant after the injury. It’s really no different with tendinosis, or any other severely fatigued and rotted tissue. “Taking it easy” for a little while simply isn’t going to cut it. This is bad news for a lot of patients, of course … but it takes what it takes.
People have an odd tendency — even after a lot of suffering — to act like repetitive strain injuries are relatively minor injuries that “should” get better if they “take it easy.” Unfortunately, no one sent the RSIs the memo about this, and they refuse to actually be easy to fix. People can easily go on suffering for years with truly amazing and awful consequences to their lives. There’s nothing minor about a serious RSI, and the effort and inconvenience involved in trying to beat one has to be scaled to match its severity. If you have a really nasty RSI that is keeping you from working and/or playing, you need to get serious about truly giving it adequate rest.
This is a psychological, attitudinal hurdle, not a physiological one.
Another major problem with resting as a treatment strategy for RSIs is almost political in nature: therapists and doctors are so preoccupied with treatments based on the assumption of inflammation and biomechanical factors that they fail to emphasize the importance of rest. In many cases, it’s not that they don’t think the rest is important — they do, and they might even say it. But their words have little weight when they devote a lot of time and energy to every other possibility. The rest simply doesn’t get the conversational air time it needs for the message to sink in, even from therapists who actually believe it matters.
And then, unfortunately, there are also many cases where rest is not regarded as important, where it is actually dismissed. For instance, at odds with the evidence, a chiropractor might tell a patient that “no amount of resting will help” because the real cause of the injury is a tilted pelvis, which will require a dozen “adjustments” in the short term and then long term occasional maintenance. In these all-too-common cases, structural therapy has completely eclipsed resting as an option, and is actually logically at odds with it. This is greatly complicated by the fact that, once in a while, there really is a biomechanical factor that is going to make rest less effective. Clearly what the patient needs, then, is a therapist who isn’t locked into structuralism, who has biomechanical theories of RSIs in proper perspective, who recommends dealing with them only in the rare cases where they are actually likely to be relevant, and who even then does not recommend a structural approach at the expense of resting. But if you have a therapist who only ever (or almost always) thinks in terms of hunting down biomechanical causes for RSIs, then that therapist will place the emphasis of treatment on the wrong thing almost every time.
If it weren’t for the other potent myths about RSIs, this would probably qualify as the “best kept secret” of the topic. However, it is overshadowed. It’s important, but not as important as the key points about inflammation and biomechanics. Nevertheless, every patient with an RSI, and every healthcare professional treating patients with RSIs, really needs to understand how surprisingly often muscle is a major factor, or even the entire problem. Large numbers of patients are diagnosed with a repetitive strain injury, when what they primarily have is a problem with trigger points, more commonly referred to as muscle knots.
What makes trigger points so dang clinically interesting is their triple threat: their ability to cause problems, complicate problems, and mimic problems. No matter what else might or might not be going on, muscle is almost always involved one way or another, either getting uncomfortable in reaction to another painful problem, or having its own problem that seems suspiciously similar to another kind of problem, or malfunctioning in a way that significantly aggravates another problem. Let’s take those three things, and look at how they specifically affect RSIs …
I went to great pains above to explain how biomechanical issues are not generally a very significant factor in the development of RSIs. However, I also took pains to emphasize that there are some exceptions: and probably the most common kind of exception is that RSIs may be significantly affected or almost entirely caused by muscle tension. And this factor, although it has much in common with structuralism, is usually not diagnosed and treated by structuralists, despite the fact that it’s probably quite a bit easier to do so — and more useful — than with most of the more traditional structuralist issues.34
Consider this (oversimplified) example: if you run a lot, and your Achilles tendon cannot quite keep up with the forces you are subjecting it to, it could simply be all the running that is causing the strain, but it could also be excessive tension in the calf muscle. How much more quickly will you develop a case of Achilles tendinitis if you have a whopping muscle knot in the middle of your calf? How much less running will it take before you’re into the “overuse” zone? No one knows the specific answer to those questions, but muscle tone/tightness is probably relevant, and in some cases tension may be so high that the threshold for injury is lowered to the point where it can hardly even be considered to have been brought on by overuse. If injury happens so easily and so fast that overuse doesn’t actually seem to really be the issue, I would consider trigger points and muscle tension to be the real, main cause of the injury, not “overuse.”
One of the strengths of this theory is that, unlike the biomechanical theories, it’s not very subtle, or complicated. Many of the biomechanical theories suffer from excessive subtlety, from very complex and fragile changes of reasoning. But there’s nothing subtle about the idea of having an inflexible, tight muscle yarding on your tendon much harder than it should. Nor is there anything too exotic about treatment. Although exactly what muscle tone is, how trigger points work, and how best to treat them, is all full of scientific mystery, there is no doubt that it is often possible for muscle to “loosen up.” Because treating trigger points can be relatively cheap and almost totally safe, and given that trigger points probably have more to do with many cases of RSIs than any other kind of biomechanical problem, it’s well worth your time to investigate trigger point therapy as a treatment option.
But that’s just the tip of the iceberg!
I do not think cases of RSIs with a significant component of muscle tension are common. Most of the time I suspect it’s merely a case of muscle tension mildly predisposing the patient to the injury — not nearly enough to be considered the cause. But muscle also tends to react negatively to any other kind of pain problem. And that is much more likely to be involved in nearly every RSI case. As common as muscle pain is, most people radically underestimate just how unpleasant it can be.
Take the case of classic carpal tunnel syndrome, where median nerve impingement is significant and confirmed by a nerve conduction test: the nerve cannot work properly, and a whole bunch of symptoms are coming directly from that. There is very low diagnostic ambiguity in such a case. And yet, there are also some other symptoms: diffuse aching throughout the entire forearm, heavy deadness of the limb, a weakness that seems to go beyond just the grip strength affected by the median nerve, and pain in the hand that definitely goes beyond the irritation in the wrist. All of these symptoms are common with cases of carpal tunnel syndrome, and they are all mostly caused by trigger points in the musculature of the forearm — trigger points that were probably present to some degree before everything went to hell, but then got really aggravated in response to the meltdown in the wrist. Treating those trigger points will not cure the carpal tunnel syndrome… but successfully treating them does have the potential to relieve a very large portion of the symptoms. I’ve seen cases of carpal tunnel syndrome that, when trigger points were treated, reduced in severity so much that it was pretty much just as good as a cure. A little numbness and tingling and weakness left in the hands, and the occasional aching in the wrist at night, is certainly still a problem … but it can seem quite trivial compared to the full-blown power of carpal tunnel syndrome plus trigger points.
This phenomenon is quite familiar to most alert massage therapists. It’s relatively obvious that muscle feels awful in the region of other problems. It’s often a bit of a shock to the patient how much of their discomfort can be accounted for in this way, and treated or managed relatively easily.
But that’s still not all …
Another way that trigger points can “cause” repetitive strain injuries is by outright mimicry: by producing symptoms so similar to RSIs that they easily fool the patient and most healthcare professionals.
A classic example of this is the confusion between trigger points in the hip and “bursitis”. As I mention every chance I get, this condition is almost hilariously over-diagnosed by front-line physicians, and I have enjoyed teasing doctors about it for years: it really does seem sometimes like every single musculoskeletal problem that lands in front of them is “bursitis,” unless there is some other really obvious diagnosis, and sometimes even still then.
I kid the docs. I exaggerate. But not very much.
The musculature of the hip is one of the major gathering places in the body for trigger points. And they cause pain that often feels just like bursitis. Well, not quite “just like”35 — but very similar. For the average healthcare professional and patient, intense and irritating pain on the side of the hip is really very easy to mistake for bursitis.
There are several other clinical scenarios like this: when the pain of muscle just flat out feels like something else, and gets diagnosed as something else. And it’s not all that unusual a clinical situation to have two versions of the pain problem: the real thing, and the trigger point that feels exactly the same or very similar, overlapping. Lovely!
Imagine the clinical power of these three muscle issues when they are all combined: knots in your muscles that predispose you to genuine RSIs, knots that make genuine RSIs feel much worse, and knots that just flat-out imitate them.
There is a great deal to learn about trigger points, which is why there is so much about them on this website: they’re clinically relevant to just about everything, and they’re mysterious and complex. But once again, treating them in many cases is relatively cheap and safe, and that’s what we like to hear whenever we’re talking about treatment options. Even if I’m wrong, even if I’ve overestimated their importance, you really can’t go too far wrong investigating the possibility.
This seems like a good time to plug my muscle pain tutorial again:
This educational website offers more than 230 free articles about pain problems, but it is also partially funded by the sale of 8 e-books for people with pain problems. If you are researching Epsom salts because you have frustrating muscle pain, please also read the free introduction to this book, which is by far the most advanced self-help guide on this topic published anywhere:
We’re not used to thinking of RSIs as a neurological problems. RSIs are about worn out tissues, not neurology. And yet your brain is the boss of you, the boss of everything. For instance, we know that the reaction of tendons to overuse is mediated by the central nervous system.
For instance, in 2011, Andersson et al. studied how rabbit tendons responded to exercise over a period of weeks (a relatively harmless experiment for the rabbits, as these things go).36 Unsurprisingly, the rabbits’ tendons started to show signs of adaptation and then overuse. The surprising part was that only one side was artificially exercised, but both sides reacted! Changes in the tendons were obviously neurologically regulated: like a slow-motion reflex reaction on sides, reacting to the stimulus on one side.
All stubborn pain problems play “head games” with patients — there’s almost no avoiding it. Chronic pain, almost by neurological definition, involves at least a little haywire neurology, because pain itself changes how pain is processed … and not in a good way.
Every pain problem is disturbing one way or another, but RSIs have a particularly disturbing quality: they specifically strike at our work and our play. Rare is the RSI that happens because of something we didn’t have to do, or want to do. It’s always the typing that we must do, to pay the rent, or the golfing that we want to do, so that life is worth living. And it’s usually the activity we need or want the most, because that’s the one we’re doing the most.
It’s tragic and it’s anxiety-producing, and that makes things hurt more. Pain science research is extremely clear: the emotional context of a pain strongly affects its severity and chronicity. The soldier wounded in combat is often amazingly pain-free — because he knows that his wound is a ticket home. The same traumatic injury in a construction worker with three small kids, a sick wife, and credit card debt will produce massive anxiety, and his pain will probably be much worse. RSIs also routinely interfere with our ability to make a living, but their anxiety-producing super power goes even further.
The traumatically injured construction worker may be in a dire situation, but at least he knows exactly what he’s dealing with. He knows what happened to him and — barring complications — about how long it will take to heal. But the pain of RSIs rarely “computes” for the patient, and because it often worsens with time and use, there is no end in sight.
This is a perfect storm of anxiety-producing characteristics, and RSI patients often show signs of severe emotional fatigue. They usually can’t sleep right, either from the pain or the anxiety or both, and the lack of sleep is yet another major aggravating factor.
The coup de grace is that all the anxiety and suffering can actually change neurology, making patients more sensitive to pain. This is the phenomenon of central sensitization.37 It is the mother of all common denominators in musculoskeletal medicine.
And it gets even worse. Everything I’ve written here so far suggests that sensitization can be a complication of an injury. But what if you were sensitized to begin with? What if people actually got RSIs because they were already sensitized? That’s not just speculation: it is strongly suggested by the results of a 2015 study of two thousand patients with arthritic knees.38 They showed that the patients who hurt were not the ones with the worst knees, but with the worst sensitivity: a trait, not a state. A “trait” of the individual, not the “state” of their knees. It’s not that the worst they had bad arthritis, it’s that they had problems tolerating arthritis.
Never bet against neurology. It’s probably a much larger factor in RSI than has yet been fully appreciated by anyone. It is easy for health care professionals to pay lip service to sensitization without really taking it seriously. It is obvious to almost anyone that fear and frustration make a bad situation worse, but it’s quite another thing to fully respect the therapeutic implications of your nerves, spinal column, and brain actually changing. It has many important implications for treatment, and yet most therapists waste time trying to find and change biomechanical issues that are responsible for 0-5% of the stress on the anatomy. More information about pain neurology and “head games” is available:
In some ways, trauma and RSI are extremely similar: opposite sides of the same coin. Fast injury and slow injury. Each can have aspects of the other. They can very neatly co-exist, not entirely one, not just the other.
When tissue is injured traumatically, it is rendered vulnerable and a lot easier to accidentally “overuse.” Indeed, most injuries that are having trouble healing are in some sense morphing into a sort of RSI. This is a bit of a word game, in a way, but it’s food for thought. It may be helpful to think of an RSI as a slow-motion trauma that just keeps happening … and think of a trauma that won’t heal as an RSI that started rather suddenly.
I am a science writer, former massage therapist, and I was the assistant editor at ScienceBasedMedicine.org for several years. I have had my share of injuries and pain challenges as a runner and ultimate player. My wife and I live in downtown Vancouver, Canada. See my full bio and qualifications, or my blog, Writerly. You might run into me on Facebook or Twitter.
About half of these are some kind of tendinitis or tendinitis-like condition. This is written to be partly a quick reference guide, directing you to other articles, but also a readable tour of the common RSIs.
And honourable mentions for:
This article was logistically challenging because a great deal of its subject matter is already covered in detail elsewhere on the website. I did my best to summarize those topics as they relate to RSIs, and also direct readers on to more detailed reading. Here’s a handy chart:
|topic||this article||other resources|
|RSIs are |
|This article is my main source of information and references on this topic. Jump to topic.||None. However, it is discussed in several tutorials concerning allegedly “inflamed” RSIs, i.e. plantar fasciitis.|
|RSIs are not a |
|Summarized, with particular attention to how other factors in RSI specifically outweigh structural factors. Jump to topic.||See Your Back Is Not Out of Alignment, and professionals should read Lederman.|
|RSIs mostly |
just need rest.
|Summarized, with emphasis on how rest seems to get badly neglected in the case of RSIs. Jump to topic.||See The Art of Rest.|
|RSIs are muscular.||Summarized, with some specific examples of how muscle pain relates to RSIs. Jump to topic.||Muscle pain is the single biggest topic on PainScience.com. Start with the introduction to my advanced trigger point tutorial.|
|RSIs play |
|RSIs are particularly anxiety-producing, and that’s the focus of the section; the neurological effects of that anxiety are only mentioned here, not explained. Jump to topic.||See Pain is Weird: Pain science reveals a volatile, misleading sensation that is often more than just a symptom, and sometimes worse than whatever started it.|
Nine updates have been logged for this article since publication (2011). All PainScience.com updates are logged to show a long term commitment to quality, accuracy, and currency. more
When’s the last time you read a blog post and found a list of many changes made to that page since publication? Like good footnotes, this sets PainScience.com apart from other health websites and blogs. Although footnotes are more useful, the update logs are important. They are “fine print,” but more meaningful than most of the comments that most Internet pages waste pixels on.
I log any change to articles that might be of interest to a keen reader. Complete update logging of all noteworthy improvements to all articles started in 2016. Prior to that, I only logged major updates for the most popular and controversial articles.
See the What’s New? page for updates to all recent site updates.
For a long time, pieces of this article existed in many forms all over the website, my notes, and my head. I pulled it all together for a new article over a few days, in time for a podcast appearance on the topic in 2011.
— Small but important clarification about load management: new first paragraph of resting section.
— Added a mobile-only article summary.
— Significant science update. Revised the “Head Games” section to emphasize the implications of a pair of really interesting references (Andersson 2011 and Neogi 2015).
— Updated discussion of risks and benefits of medications.
— Revised the introduction a bit: just a little richer and creamier.
— Added a small concluding section — didn’t really know where else to put it! “Sort of an afterword: RSI and trauma, sittin’ in a tree.”
— Major updates to the inflammation section. Virtually re-written to emphasize that inflammation is certainly not present in the sense of classic inflammation, but may nevertheless have a little biochemistry in common with it. If allegedly “anti-inflammatory” treatments work, it is probably mainly by different mechanisms, and this is now thoroughly explained, with detailed notes on every major common treatment.
— Improvements to the RSI reading guide.
— Numerous minor corrections and improvements in readability, and a couple more images.
From the abstract: “If physicians acknowledge that overuse tendinopathies are due to tendinosis, as distinct from tendinitis, they must modify patient management …”BACK TO TEXT
And there are other, similar studies. For instance, Semark et al tortured sprinters’ muscles with a savage workout, and the painful results were identical with or without an anti-inflammatory medication. “In conclusion,” they wrote, “the aetiology of the DOMS induced in the trained subjects in this study seems to be independent of inflammatory processes ….” Hmm. Minimal inflammation in delayed-onset muscle soreness too? Not really surprising! BACK TO TEXT
Diclofenac is an extremely popular painkiller associated with serious cardiovascular risks, as with other NSAIDs: “There is increasing regulatory concern about diclofenac. … Diclofenac has no advantage in terms of gastrointestinal safety and it has a clear cardiovascular disadvantage.”BACK TO TEXT
A good general discussion of painkiller risks and side effects, but the relative safety of topical treatments is of particular interest:
BACK TO TEXT
The main advantage of topical NSAIDs is the reduced exposure of the rest of the body to the product, which reduces the side effect profile. Given the toxicity of NSAIDs is related in part to the dose, it follows that topical treatments should have a better toxicity profile. Consequently, the cardiovascular risks of topical diclofenac, even in those with a high baseline risk of disease, should be negligible with the topical forms.
This is a 2008 review of just 6 studies of therapeutic icing, only two of them any good: one with slightly positive results, the other showing no effect. So that’s two studies that showed little or no benefit, which is leaning towards bad news, but it’s just not enough data to clinch it. (Four animal studies showed reduced swelling, but we can’t take animal studies to the bank.) The bottom line is just that “there is insufficient evidence.”BACK TO TEXT
“On the basis of the results of this study, the authors advocate steroid injection alone as the first line of treatment for patients presenting with tennis elbow demanding a quick return to daily activities.”BACK TO TEXT
In more than 2000 people with knee osteoarthritis, or at high risk for it, pain sensitization was associated with knee pain, but not the severity of the arthritis as seen on x-ray. In other words, neither pain nor sensitivity clearly correlated with the condition of their knee. This contradicted the researchers’ expectation that sensitization is caused by the duration and severity of arthritis. Instead, the results suggest that “sensitisation is in fact a ‘trait’ rather than a ‘state’, that is, that hypersensitivity was present before knee OA, related to an individual’s predisposition to sensitisation rather than being induced by peripheral nociceptive input [pain] from osteoarthritis.” Even more simply stated: people with knee pain have a problem with pain, not knees.BACK TO TEXT