Detailed guides to painful problems, treatments & more

Complete Guide to Frozen Shoulder

An extremely detailed science-based guide to one of the strangest of all common musculoskeletal problems, for both patients and pros

Paul Ingraham • 250m read
Photo of a woman with frozen shoulder, holding her shoulder, in pain.

Sometimes shoulders just seize up, painfully and mysteriously: frozen shoulder. It comes with other diseases, usually diabetes, or it follows traumas or periods of immobilisation — hold the shoulder in one position for long enough, and it actually may get stuck there. The shoulder is the only joint that often “freezes” like this.1 Frozen shoulder is a biological puzzle, and a common one. It’s hard to define precisely, diagnose accurately, or treat effectively. In fact, frozen shoulder treatment is one of the best examples of how musculoskeletal medicine is surprisingly primitive still.2

Sadly, the old idea that this is a self-limiting condition is flatly contradicted by modern evidence.3 There is hope — it can thaw spontaneously4— but many people will be frozen to some degree for a long time, measured in years.5

Adhesive capsulitis is the more formal term for frozen shoulder: it describes the characteristic stickyness that develops in the shoulder joint capsule. Sticky shoulder is probably a better name.

About two thirds of patients are women. No one knows why.

Frozen shoulder symptoms — the basics

Range of motion fails, slowly and painfully, usually just on one side.6 Most patients first notice that they are having trouble reaching bra clasps, hip pockets, and back itches. The painful early stage mostly involves aching or burning deep in the shoulder joint, sometimes extending into the upper arm, often worst at night. Sudden movements can cause surges of much sharper and more extreme pain. Many frozen shoulder patients consider it the worst pain they’ve ever endured. Much more detail about symptoms to come.

How common is frozen shoulder?

The classic number is 2% of the population, but that’s not based on much, and it was challenged by frozen shoulder expert Dr. Tim Bunker in 2010:

The condition is also less common than the usually quoted figure of 2% of the population. This figure was arrived at 40 years ago when shoulder disease was ill understood and frozen shoulder was used as a waste‐bin diagnosis for any stiff and painful shoulder.

Bunker argues that the upper limit is probably 0.75% of the population for cases involving clear contracture.7 But that is still almost one in a hundred people. It’s not common-cold common, but it’s not rare either. It’s red-hair common.

Frozen shoulder is also linked to some extremely common health problems, like diabetes at 10% of the population, and diabetes is much more common than it used to be, a proper epidemic.8 The rising tide of diabetes may be bringing frozen shoulder with it.

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Nature of the beast: frozen shoulder is a biological glitch

Getting into more detail now, frozen shoulder involves fibrosis and/or contracture of the tendons, joint capsule, and other soft tissues surrounding the glenohumeral joint — the main ball joint of the shoulder — specifically the rotator cuff interval.9 In severe cases, the RC interval is “obliterated,” and the coracohumeral ligament is “transformed into a tough contracted band,”10 like arthritis of soft tissues.

This is all rather disease-like, much more so than most common musculoskeletal problems: clearly some kind of biological glitch, and not a “mechanical” breakdown. Most notably, it is not a repetitive strain injury. In fact, if anything, it’s the opposite of an overuse injury: when it appears to have a “cause,” it’s more like an under-use injury, often triggered by a period of shoulder immobilization, like being stuck in a sling after a fracture or stroke. But it may also occur after a trauma to the area, even when there is no pronounced immobilization.

It is probably related to broader health problems. It mostly hits people over the age of forty, much more so if you have diabetes and/or cardiovascular disease.11 Frozen shoulder is extremely common in diabetics: more than 12% of them will get frozen shoulder, and about 30% of people with a frozen shoulder also have diabetes.12

Those problems are commonly associated with obesity, and what they have in common is “metabolic syndrome” — trouble with managing fats and sugars in the blood, and chronic low-grade inflammation everywhere.

You can be inflamed systemically for many other reasons, too. Metabolic syndrome is just the most obvious and common culprit. Regardless of how you get inflamed, it’s linked to frozen shoulder.13

Chronic low grade inflammation is increasingly seen as a part of other orthopaedic conditions such as osteoarthritis — once considered a ‘cold’ wear and tear problem (as opposed to the far more overt and ‘hot’ inflammation of rheumatoid arthritis).

Summer is coming — Frozen Shoulder, Cocks (Noijam.com)

No one knows why the shoulder joint capsule in particular would be the tip of this dysfunctional iceberg. Why such a dramatic point of failure? Why that tissue in particular? No one knows. But the relationship between frozen shoulder and metabolic syndrome is clear, as well as other glitchy biology like hyperthyroidism.14 It is one of many conditions that fall short of frank, diagnosable autoimmune disease like rheumatoid arthritis or lupus, but is still obviously autoimmune in character and characterised by inflammatory over-reaction.

General biological vulnerability

Carpal tunnel syndrome, just like frozen shoulder, is a surprisingly weird condition that is definitely more complicated than just using your wrist too much. People with median nerve compression have a significantly increased risk of … wait for it… heart disease.15 Since carpal tunnel syndrome itself pretty clearly doesn’t cause heart disease, it’s more likely that there’s something about the biology of these patients that leads to both carpal tunnel syndrome and heart disease.

This kind of thing is true of all chronic pain problems to some degree: general biological vulnerability is often just as important as whatever is specifically wrong with the tissue. Things like smoking, sleep deprivation, and being out of shape are modifiable risk factors for any kind of chronic pain, but typically neglected. See Vulnerability to Chronic Pain.

So that may be true for all chronic pain, but it seems to be more true of frozen shoulder. Of all common musculoskeletal conditions, frozen shoulder seems the most obviously linked to being unhealthy in other ways. Which makes it more interesting, for sure.

We know that smoking, for instance, is weirdly a major risk factor for shoulder problems,16 which likely includes frozen shoulder. Smoking contributes to the poor health that seems to make frozen shoulder more likely. Among its many notoriously harmful effects, smoking is also a factor in many kinds of chronic pain17 — but shoulders particularly tend to break down in smokers.

The good news is that general biological vulnerability is treatable. Most of the non-specific risk factors are modifiable (although it may be very tricky). I’ll return to the topic of general vulnerability when discussing treatment.

More specific genetic vulnerability

Dupuytren’s contracture is basically “frozen hand.”

Dupuytren’s contracture is basically “frozen hand.”

There’s another weird link between frozen shoulder and another weird disease, both stronger and stranger than the diabetes link: roughly half of people with frozen shoulder also have a Dupuytren’s contracture — “frozen hand” — which is quite common and is probably caused by the same underlying problem with connective tissue seizing up.18 Although it causes such different symptoms that they seem more like pathological cousins than siblings, they are clearly related. Dr. Bunker: “This terrible triad of contracted shoulder, Dupuytren’s contracture and diabetes pervades this whole area of scientific enquiry.”19

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Or it could be an infection? Surgery and vaccination as causes of shoulder joint infection

You can hardly crack a medical journal open these days without stumbling on another example of how wee beasties are guilty of causing unexpected trouble, a factor in yet another condition we didn’t realize was infectious. The canonical example is the role of H. pylori in stomach ulcers.20 There are many other fascinating examples.21

Including some cases of… frozen shoulder?

Microscopic view of P. acnes bacterium.

Propionibacterium acnes, a bacterium we want in our pores, but not in our shoulders.

Apparently sticking a probe into a shoulder, despite antiseptic precautions, sometimes results in an alien invasion of the joint. By pimple bugs! “P. acnes was the most prevalent organism,” researchers reported in 2017.22 Yes, that’s the acne bacteria, Propionibacterium acnes (which may be wrongly blamed for acne23).

P. acnes is a “powerful nonspecific immune stimulant” which probably does trigger some cases of frozen shoulder, failures of prostheses, some arthritis, and perhaps even sciatica.24 Its role in post-operative infection is probably simply because it’s an endemic skin critter, nearly impossible to completely eliminate from the site of any puncture. Push just a few of them deep into a joint, and they find a new home and cause new kinds of trouble.

Amazing.

Rather than an infection that is dangerous and acute, the kind of thing we already know is a risk after surgery, it’s almost polite at first: barely detectable, in fact, just a little inflammation. But then? The inflammation caused by fighting the infection blossoms into frozen shoulder, and then it starts to suck to be you.

This is probably more common than we want to know about. In a 2015 survey, about 29% of people with persistent symptoms after surgery had an infection, and most of those had P. Acnes specifically growing in their joints. Only 3% of control group patients had P. Acnes growth (which is a lot less, but still strikes me as surprisingly high).25

Only surgery? Probably not

This seems to only apply to people who’ve had surgery, based on the data we have so far. But I don’t think we can actually rule out the possibility of infection with other mechanisms. Like many conditions involving inexplicable inflammation of tissue, it’s possible that it only looks like the immune system is attacking our own tissues for no reason. How many “autoimmune” diseases are responses to infections we don’t understand yet? Pure speculation on my part — but plausible, I hope, and certainly intriguing.

If surgery can do it, then there’s probably another way for P. acnes to catch a ride into the joint capsule…

Shoulder injury related to injections

The number one candidate for a non-surgical mechanism of infection is injection. While injections cause a lot fewer complications than surgery, anything that breaks the skin is still “invasive” and involves some infection risk. The most common injections are vaccinations, which is why this phenomenon is often referred to as “shoulder injury related to vaccine administration” (SIRVA) — a terrible term that seems to go out of its way to emphasize the wrong thing.26

Most injections are in the shoulder, because most injections are intramuscular, and the shoulder is a convenient spot with a bunch of muscle. But sometimes shoulder injections miss: the needle goes into the joint capsule instead of the muscle tissue. Oops. Within a day or two, it becomes clear that the shoulder is much more sore than it should be. The symptoms may drag on and on: “Patients will often visit their physicians months later because they are not able to carry out daily tasks that were possible before the vaccination.”27 Wired magazine: “The prolonged pain and stiffness of SIRVA is distinct—in other words, much worse—than typical soreness from shots.”28 The conventional wisdom is that this is an ordinary minor injury, which is often mistaken for conditions like bursitis, rotator cuff tears, and adhesive capsulitis. Bancsi et al.:

During physical examination and on ultrasound scan, SIRVA will not appear to be any different from routine shoulder injuries. The only difference is that the shoulder symptoms will have started within days of a vaccination.

But is that the “only difference”? It’s not really normal for a minor physical trauma to drag on for weeks and months. It seems like something more might be going on here.

Unfortunately, it’s plausible that injections can trigger genuine adhesive capsulitis by the mechanism described above: the needle drags P. acnes into the joint capsule, just like surgery can, and then excessive and prolonged inflammation ensues, more than minor physical trauma would ever cause, creating a genuine case of frozen shoulder.

Citation needed, but where there’s smoke…

Injection injuries are certainly a real thing, and frozen shoulder is a real thing, but do they overlap? Is there any evidence that injection injury specifically can cause frozen shoulder, via the mechanism of P. acnes infection? Not direct evidence, no. This is the closest we’ve got: a 2015 paper reported three cases of injection injury followed by a confirmed diagnosis of frozen shoulder:29

But this is also about as where-there’s-smoke-there’s-fire as you can get. Infection as a complication of both surgery and injection are plausible, and there’s good evidence of the first. And it’s also plausible that such infection could lead to frozen shoulder, and there’s also both direct and indirect evidence for that (discussed above). From these premises, it’s just a short, reasonable hop to the hypothesis that injection injuries can cause frozen shoulder: far from proven, definitely possible.

Injection safety

The next time I get an injection — probably a vaccination, which I obviously will do, because the benefits dramatically outweigh the risks — I’m going to drown my shoulder in rubbing alcohol immediately beforehand. I want exactly zero surviving P. Acnes on my skin when that needle goes in!

“I say we take off & nuke the entire site from orbit. It’s the only way to be sure.”

Ellen Ripley, Aliens

Or just don’t get shots in the shoulder? Surgeon Dr. Michael Skyhar: “This is all avoidable by simply asking that the vaccine be placed in a different location, such as the upper/outer buttocks.” Unfortunately, that may not be an upgrade! Gluteal injections risk an even worse injury to the sciatic nerve, “a persistent and global problem.”30 If done correctly, the risk can be reduced to almost zero… but that can be said of deltoid injections too. It is worth avoiding the risk of frozen shoulder by pivoting to a similar or even worse risk of doing serious damage to a hip?️

Systemic infection

There’s no direct evidence that frozen shoulder is triggered by systemic infections — illnesses like the flu, or COVID-19! — but it is quite plausible. A 2021 paper reported on twelve cases closely following COVID infections.31 Anything that provokes widespread inflammation might push a vulnerable shoulder over the edge. And a phenomenon like this could easily get missed by the literature. If you think your frozen shoulder started with a systemic infection, please tell me your story.

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Shoulder neglect? An evolutionary perspective on frozen shoulder

An interesting theory is that frozen shoulder occurs because “the human shoulder evolved for high speed projectile throwing,”32 and it suffers from neglect in modern living. Sedentary tissues can cause trouble, and be more vulnerable to biological failure. In particular, Pietrzak suggests, injury near the shoulder might trigger an inflammatory reaction that’s just waiting to happen.

I think it’s unlikely that the shoulder actually “evolved” for that purpose in the first place,33 and, even if it did, why would the shoulder be the only anatomy in the body with this problem? Surely many body parts tend to stagnate in modern living, and yet — as already noted — only shoulders “freeze” like this.

But there’s some strong support for Pietrzak’s idea. In 2013, Littlewood et al. made a detailed argument that the symptoms of rotator cuff tendinopathy — and the shoulder joint capsule is essentially just a bunch of rotator cuff tendons — can occur without any actual or impending tissue damage.34 First they make the case that explanations for pain based on “peripherally driven nociceptive mechanisms secondary to structural abnormality, or failed healing, appear inadequate” — at least in the context of rotator cuff tendinopathy (and probably much else). They’re on firm ground with that premise. So what is the problem? They propose that the brain may react to relative overuse of de-conditioned tendon — tendon that’s just been lazing around too much — with fearful avoidance of movement, a vicious cycle of painful inhibition of function. This is completely consistent with Pietrzak’s idea. And “functional freezing” is the next major topic …

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Animated GIF showing how a frozen shoulder can still “fake” some range of motion.

This video shows “fake” shoulder range of motion: lifting the entire shoulder, rather than actually using the ball-and-socket joint. Good scapulothoracic motion with no glenohumeral action at all. More about this below when we talk about diagnosis.

Stiff but not “frozen”: the case for functional freezing

“Adhesive” capsulitis refers to a literal stuckness, and there’s no question that many frozen shoulders are literally stuck in a limited range. But could some frozen shoulders be less literally stuck? Could that stuckness sometimes be more of a functional limitation than a physical one? Is it even possible that many cases are at least partially like this? What if, say, 60% of cases were 30% explained not by sticky joint capsule, but by an extreme reluctance to move — by neurological inhibition?

In a minor way, everyone’s joints “freeze” like this eventually. Joint stiffness, especially after being still for a while, is probably a non-specific reaction to practically anything that can go wrong with a joint. For many people, their first experience with this is after joint injuries in their youth — but it’s so obviously related to and in sync with recovery from the injury that it’s unremarkable. And then, years later, it’s usually the first symptom of arthritis. This stiffness is almost certainly protective and not a physical limitation, but neurological inhibition.35 Its purpose is to limit risk exposure for a joint the nervous system is “worried” about. In other words, it’s how the body says, “Careful now… no sudden moves…”

Any normal process in the body is usually represented by more extreme examples in some people, or in particular anatomy, and there are definitely some more dramatic examples of joint inhibition: some people’s quadriceps muscles shut down after knee trauma, a well-described phenomenon known as arthrogenic muscle inhibition.36 The muscle just stops doing its job so completely that it starts to atrophy: “My quad is deflating daily, like a slow tire leak.”37

If it can happen to the knees, maybe it can happen to other joints — it’s not clear why it would be so well-known about knees and not at all about shoulders, but it could still be true.38

Not all frozen shoulders are contractured

When you open frozen shoulders up, not all of them have clear visible signs of disease. Dr. Tim Bunker believes that only about 50% of patients diagnosed with the condition actually have obvious signs of pathology in the shoulder.39

That suggests that quite a few cases are functionally frozen.

And could functional limitation be more prevalant in cases that are dragging on and on? Do some people slowly climb out of the frying pan of a sticky joint capsule and into the fire of a shoulder that’s just too uncomfortable to move? What if the door of shoulder movement stealthily transitioned from welded shut to just being rusted shut?

There’s hope in them thar hills, because a functional stiffness might be easier to loosen up (with massage, say, or carefully planned exercise). And yet the opportunity might be tragically missed! How would a patient even know that the situation had changed? There’s no easy way to tell that something badly stuck is less badly stuck than it used to be.

I’ve used a lot of questions to introduce this topic because — surprise surprise — no one actually knows. It’s a popular idea.40 There’s an accumulation of clues that the usual suspects aren’t cutting it, evidence that we’re missing something (which is what Littlewood et al is all about). And we have clinical stories that seem to suggest it.41 And some recent evidence.

Well that’s interesting: “stuck” shoulders not so stuck when unconscious

In 2015, someone finally did a nice science experiment on this, simple and directly relevant.42 Five capsular release surgery patients were checked before and after being put under general anaesthesia. All five of them had “significantly more passive shoulder abduction” when they were knocked out … which would be impossible if their capsules were actually contractured or adhered or full of cement or any physical limitation. The improvement in ROM ranged from a minimum of 44˚ all the way up to a 110˚ boost (all the way back to normal). The researchers reasonably concluded:

Passive range of motion loss in frozen shoulder is not fully explained by a true capsular contracture alone. Passive shoulder abduction ROM assessed in awake patients with frozen shoulder does not accurately reflect the true available ROM of the affected shoulder. It appears that active stiffness or muscle guarding is a major contributing factor to reduced ROM in patients with frozen shoulder.

If I was the surgeon, I might have found it ethically hard to justify operating on these shoulders after seeing that.

Case closed? No, not yet. It’s really a shame it was such a small study. We really need someone to do the same thing with five times as many patients. But it is quite suggestive. One of those things that make you go, “Hmmmm!”

The worst cases probably really are dominated by adhesion. Worrying about a functional limitation, especially in the earlier stages of freezing, may be like trying to sweep up the ashes while the fire is still raging. But the possibility really shouldn’t be ignored, especially later on. It just might be the most important thing anyone can learn about this bizarre condition, mainly because it suggests several treatment options that are much more useful if there’s functional freezing, like strengthening, massage, or even Tiger Balm.

A diagram depicting the hypothetical relationship between functional and adhesive restriction of movement in frozen shoulder.

Over time, it’s possible that a functional limitation gradually becomes responsible for a larger share of the immobility & pain of the condition. It probably wouldn’t sustain the full ferocity of the condition, so I’ve depicted a slope downwards representing a general decline in severity — but of course the mixture over time could vary a lot from patient to patient.

GO TO TOPCONTENTSNOTES

How does “functional freezing” cause frozen shoulder?

There are three main ways that a functional limitation of shoulder ROM would probably work, and we shouldn’t underestimate their potential power:

  1. The brain can “shut down” a joint with neurological inhibition.
  2. The brain might do that to the joint because it has become sensitized.
  3. The muscles may have gotten rotten with “knots” (trigger points)

The brain is the boss of all function, and when it decides that a joint shouldn’t move, then it’s not going to move — and because your conscious mind isn’t included in the decision, the limitation can feel externally imposed. Your shoulder might as well be in a vice. Inhibition doesn’t feel “functional”: it just feels like you can’t move. Will power doesn’t come into this. Your brain is protecting you from yourself (or so it hopes). This is standard neurological procedure with any significant trauma.

How the brain handles a shoulder fracture

In the spring of 2020, my mother-in-law fell while she was on a walk in Palm Springs and fractured her arm: two deep cracks in the neck of the humerus, right up at the joint, and another crack in the rim of the socket (glenoid fossa). Her shoulder instantly shut down — normal range of motion one minute, 100% loss of ROM the next.

That was a neurological lockdown. Her shoulder muscles hadn’t atrophied. She didn’t damage the shoulder’s nerve supply. Her brain was simply refusing to move the shoulder — for her own good.

When the lockdown ended, her range of motion was almost fully restored in just a few days, which is typical. When the limitation was neurologically imposed, it can also easily be lifted. Once the brain decided it was safe, there was nothing to stop movement. In the case of frozen shoulder, there might well be some physical limitation in addition to the neurological one, but that wouldn’t happen in the case of a simple fracture.

And then she had a setback! At the six-week mark, she woke up in pain… and the movement ban had slammed down again, her brain being extra cautious. Again. X-rays confirmed she had not re-broken her arm (phew!) but there was significant swelling. Most likely she simply irritated the fracture site. The important point is that the effect on movement was disproportionate, extreme, and completely under control of the nervous system.

If it can happen so clearly in that relatively simple case, you can bet your boots it can happen to varying degrees in messier clinical situations.

Why would a brain lock a joint that isn’t obviously injured?

It might do it if the pain has become like an oversensitive alarm that’s always going off when there’s nothing really all that wrong. “Sensitization” is well-described, and it’s what puts the “chronic” in chronic pain (there’s a chapter on this below). It is the main mechanism by which pain gets stubborn and unrealistic, a neurological over-reaction. Pain is all about detecting threats and changing behaviour to avoid them. If your brain is convinced that your shoulder is in more danger than it really is, it will both hurt more and get shut down.

Trigger points are a tough topic, because no one really knows exactly what they are, but there’s no question that people often develop sensitive spots in soft tissue, and there’s usually more of them in troubled areas. Although their nature is unexplained and controversial,43 the usual way of explaining them seems like a great fit for frozen shoulder: “tiny cramps” in the muscle would make it uncomfortable, weak, and less stretchy, like a knotted bungie cord. If the rotator cuff and other shoulder muscles were full of trigger points, perhaps the net effect would feel an awful lot like literal “freezing.”

I’ll discuss dis-inhibition and de-sensitization strategies below, as well as the (hopelessly imperfect) options for trying to treat trigger points.

GO TO TOPCONTENTSNOTES

B&W photo of a woman’s shoulder, upper arm, and upper chest.

Muscle guarding may freeze shoulders. If so, we aren’t sure why the muscles do it. Is it a psychological thing?

Shrunk, not stuck: a 150-year history of misleading names for frozen shoulder

The earliest medical description of frozen shoulder dates to 1872, when Simon-Emmanuel Duplay called it periarthritis of the shoulder,44 and for a while various shoulder problems were (incorrectly) attributed to the idea of “periarthritis,” and for a while Duplays Disease was used to describe several shoulder problems.

The term “frozen shoulder” was coined by a Boston surgeon, Ernest Amory Codman, in 1934, in his book about the shoulder.45 Codman was the first to more thoroughly and precisely describe the condition, and he coined its popular name which is still in wide use today — although perhaps it shouldn’t be, as we’ll see. (Codman was also the first American doctor to systematically track patients through recovery, which is pretty cool: he was ahead of his time.)

The term “adhesive capsulitis” arrived in 1945 when Dr. Julius Neviaser described the texture of the joint capsule as “adhesive,” comparing it to a sticking plaster — an archaic term for a small medical dressing, AKA a bandage.46

These days, adhesive capsulitis is usually seen as the most modern and precise descriptive jargon for the condition, but perhaps it’s no better than “periarthritis.”

“Adhesive” is probably the wrong word: shrunk, not stuck

There is no detail of this condition that isn’t controversial and mysterious, and what shows it better than a challenge to its very name? Nagy et al (among others) argue that “adhesive” is inaccurate:47 it’s not an adhered joint capsule, but rather a contractured one.

Contracture is the shortening or hardening of tissue. In more familiar words, they’re saying the joint has been “shrink wrapped” by a joint capsule that has tightened, rather than surrounded by loose layers of joint capsule that have gotten stuck together.

To drive home the idea of contraction, there is literally less room in a frozen shoulder: the joint capsule, normally quite loose and roomy and filled with 15–25 ml of joint sauce (“synovial fluid”), can shrink so much that there’s almost no lube left, just 5 ml!4849 Definitely a “fun fact” about frozen shoulder. As reckoned by joint fluid, that’s a loss of roughly 75% of the space in the capsule.

So what’s in a name? Maybe a lot in this case: this difference could be extremely important to treatment. Sticky layers can be pulled apart; contracture is an issue that’s probably a lot harder to force…

END OF FREE INTRODUCTION

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Almost everything on this website is free: about 80% of the site by wordcount, or 95% of the bigger pages. This page is only one of a few big ones that have a price tag. There are also hundreds of free articles. Book sales — over 72,700 since 2007?This is a tough number for anyone to audit, because my customer database is completely private and highly secure. But if a regulatory agency ever said “show us your math,” I certainly could! This count is automatically updated once every day or two, and rounded down to the nearest 100. Due to some oddities in technology over the years, it’s probably a bit of an underestimate. — keep the lights on and allow me to publish everything else (without ads).

Q. Ack, what’s with that surprise price tag?!

A. I know it can make a poor impression, but I have to make a living and this is the best way I’ve found to keep the lights on here.


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The trouble with Dr. Google and why this book matters

In the many years since I’ve been writing about painful problems like frozen shoulder, there has been an explosion of shabby information about every condition. Shockingly, this has not resulted in patients or health care professionals being better informed. Most of the information that you can find out there repeats the same oversimplified conventional wisdom … much of which is just wrong. A particularly good example is the way “adhesive” capsulitis is probably the wrong name for the condition, a mistake based on early, incorrect assumptions about the pathophysiology that almost no one seems to know about yet.

Scientists have actually proven that “Dr. Google” is incompetent — just in case you needed any convincing.+In 2010, the Journal of Bone & Joint Surgery reported that “the quality and content of health information on the internet is highly variable for common sports medicine topics” — a bit of an understatement, really. Expert reviewers examined about 75 top-ranked commercial websites and another 30 academic sites. They gave each a quality score on a scale of 100. The average score? Barely over 50! For more detail, see Starman et al. This reference is getting old, but nothing has really changed. 😜

I’ve been obsessively updating this tutorial for about 7 years now. By 2018, it was the largest and best of its kind as far as I could tell. I had already mined the best ideas I could find from the most detailed sources, and surpassed them — more information, more fun, and more rigorous. And then I kept going, while everything else seems to have stood still. Blog posts that haven’t been updated. Myths repeated ad nauseam for decades now. Big medical publishers that haven’t added anything to their shallow frozen shoulder summaries in years, and you wouldn’t enjoy reading it if they did.

So what can I do for you?

There is no cure for frozen shoulder syndrome. Of course not! Wouldn’t it be great if there were a proven treatment with minimal cost, inconvenience, or side effects? But we’re nowhere close to this for frozen shoulder. This book wouldn’t need to exist if there were.

What I can do is explain and review all the imperfect options so that you can prioritize them. I can help you confirm your diagnosis and debunk bad ideas. Some people will finally enjoy a breakthrough after reading this tutorial, and get partial or complete relief of their symptoms, sometimes temporary, sometimes lasting. And maybe that is kind of miraculous!

Just reading it might help. Online tutorials like this one might actually be able to directly help people with chronic pain — the evidence supports that, at least a little+Dear BF, Gandy M, Karin E, et al. The Pain Course: A Randomised Controlled Trial Examining an Internet-Delivered Pain Management Program when Provided with Different Levels of Clinician Support. Pain. 2015 May. PubMed 26039902 ❐

Researchers tested a series of web-based pain management tutorials on people who had been suffering for more than six months. No matter how much (or little) help they had from doctors and therapists, they all experienced significant reductions in disability, anxiety, and average pain levels, for at least three months.
Basic knowledge is fine for basic cases, but more and better information is important for the tough ones. And even if you only recently developed frozen shoulder for the first time, how long do you want to spend following poor quality advice or muddling about with partial understanding? Get started on the right foot.

All of that is hopefully worth more than several sessions of physical therapy, at a fraction of the cost.


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Why so different? If you pay in United States dollars (USD), your credit card will convert the USD price to your card’s native currency, but the card companies often charge too much for conversion — it’s a way for them to make a little extra money, of course. So I offer my customers prices converted at slightly better than the current rate.

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So, what’s really going on? It’s probably impossible to call this one. We can infer from the partial successes of some surgical procedures that contracture probably isn’t the whole story, so that’s one decent clue. But the main problem with the theory is that there’s not much information about this adhesion versus contracture business. It seems to have originated with a couple papers way back in 1989 and 1995,5051 with little other comment from other researchers, except notably Bunker in 2010, who is emphatically on “team contracture”:52)

Finally we can appeal for a new name for this common, painful and protracted condition and call it what it is, a contracted shoulder.

I suspect these authors are correct, but I have also watched similar scientific controveries about other problems go back and forth for many years, with new studies over-turning old ones as often as I change my socks, so I won’t take a position on this one. For now I’ll just point out that there’s an interesting question mark here.

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Posture: is frozen shoulder the tip of a misalignment iceberg?

No.53

Betteridge’s Law of Headlines strikes again!

I’ve left this “chapter” like this for a long time now, my snarky little joke: one blunt answer with a big footnote. But I knew eventually I’d have to get more specific and detailed to respond to reader objections, and now I have…

But what about kyphosis?!

A slightly slouched upper back is extremely unlikely to be a risk factor for frozen shoulder, or any other kind of shoulder pain. The position probably does limit shoulder ROM a little, but not enough to matter.

Kyphosis is the natural curve of the thoracic spine, from the mid to the upper back. If the curve is excessive, it’s hyperkyphosis, but people often leave off the “hyper” when talking about an excess. “You’re kyphotic” technically means “You’re fine, you have a normal spinal curvature,” but millions have been told that by their massage therapist or chiropractor who absolutely meant “your upper back is way too curved.”

And many people reckon that frozen shoulder is basically a case of getting “stuck” because of habitually poor posture. Here’s the most common form of this belief, as one of my readers put it to me: limited thoracic mobility “forces the shoulder to work in a compromised position and therefore contributes to shoulder pain.” And many people have extended that specifically to frozen shoulder.

So that’s the claim, a full-blown etiological hypothesis: hunching causes limited thoracic and shoulder mobility, which in turn causes frozen shoulder. It’s a reasonable thing to wonder about, but it’s also based on some unsafe assumptions and is unsupported or contradicted by the science. The evidence on this topic is, at best, discouragingly non-positive and inconclusive.54

Are people “stuck in flexion”?

The only people with pronounced hyperkyphosis are older women (”dowager’s hump”). So this idea isn’t just that hyperkyphosis is a risk factor for frozen shoulder, but that even subtle hyperkyphosis can put you in the danger zone.

Not only do I doubt that minor hyperkyphosis involves any significant movement limitation, but I’d also want to be careful about giving any patient that idea, because the fearful thought of a stuck spine might be more of a problem than any actual kyphosis. Pathologizing minor biomechanical factors is an excellent nocebo engine: making things worse with the power of suggestion, rather than better.

Does kyphosis affect shoulder range of motion in the first place?

Probably, yes. Barrett et al reported a “strong” evidence that you can lift your arms somewhat higher in an erect posture than in a slouched one. Which isn’t surprising, because the scapula slides around on the upper back and that mobile foundation is an important part of full shoulder function, so it makes sense in principle that hyperkyphosis could impact shoulder ROM.

Probably not much though.

I actually can’t reproduce this effect: when I go all hunchy, I cannot detect any difference in shoulder abduction or flexion. Maybe a wee bit, but for confirmation we’d have to get out the goniometer (tool that measures joint angles). I’m not flexible in general, a hardcore computer-posture guy, and not exactly young anymore. If I maintain what mobility I have for much longer, people are going to start accusing me of being “spry.” So if I have full (or nearly full) shoulder ROM while I’m hunching my back, presumably many other people do too.

And that’s with a hard, deliberate hunching of the back. In a more ordinary minor slouch — “poor posture” — my shoulder ROM seems completely normal. I’m not saying this to try to contradict the science, but to put it into perspective: it’s probably not a large effect, or any more surprising (or pathological) than having limited hip range of motion while seated. Just minor business-as-usual biomechanics.

The clinical significance of slightly limited ROM

Even if shoulder ROM is limited by minor thoracic flexion in some/many people… does it matter? As a risk factor for frozen shoulder specifically?

This is a data-free zone: there is exactly zero research on this specific question. All we can do is evaluate the plausibility, which I think is also exactly zero.

There would be a plague of frozen shoulder in elderly women with truly “hyper” kyphosis, and yet that’s not a thing. Frozen shoulder is well-known to affect people long before they have a dowager’s hump, and of course it also affects a great many people who have no hyperkyphosis at all.

It’s also logically important that people who recover from frozen shoulder typically get back to a full range of motion.

Most people don’t come anywhere close to using their full shoulder ROM in their normal activities. While it is broadly true that we “lose it” if we do not “use it,” the shoulder is an unusual loosey-goosey joint, and it doesn’t lose mobility quickly or from simple neglect. Despite not using the full range much, most people seem to hang onto their full shoulder ROM well past middle-age, as long as their shoulders are otherwise healthy.

Frozen shoulder is a pathological process that rapidly deprives the shoulder of a lot of ROM. I just do not believe that meltdown has anything to do with a slightly lower maximum range that people mostly don’t use or lose in the first place.

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Sensitization: the foundation of functional freezing

Functional freezing, if it occurs, is probably a clinically quirky form of the common but obscure problem of sensitization. Sensitization is normally all about pain, but it can probably also suffocate movement, and the shoulder may be the perfect example.

So what is sensitization? It’s the tendency of the nervous system to get into a rut and start over-reacting to stimuli, like a smoke alarm that goes off when you boil a pot of water.55 This is a well-described property of chronic pain,56 the crown jewel of modern pain science,57 and evidence that either there is no God or only a cruel one. As a general rule, the longer any kind of pain lasts, the more likely sensitization is to become a factor, and even to take over and become the main problem.

Sensitization can complicate any chronic pain problem, and as my career lengthens I find myself writing about it more and more: all painful roads seem to lead to this topic. There is great variety in acute pain — there are many ways to start hurting — but chronic pain is often eventually dominated by sensitization, just one major mechanism, regardless of how it all started.

And yet pain can begin with sensitization, too. Certain kinds of pain — especially neck pain, back pain, and abdominal pain — can be the tip of a sensitization iceberg.

If functionally frozen shoulders are “sensitized,” how can they can be so painlessly stiff?

In the programming language I use to create PainScience.com (PHP), when two things are identical in every way, perfect clones, we would say it with three equal signs, like this:

A === B

So equal! If two things are equal-in-practice, but not necessarily of exactly the same type, we use two signs instead of three:

A == B

I am not saying that functional freezing === sensitization, but something more like freezing == sensitization or maybe just freezing ≈ sensitization (approximately equal). They are almost the same thing. Different forms of the same underlying phenomenon. (Did I just use a coding example to try to make my writing more “colourful”? Dork alert!)

Or maybe they just co-exist and overlap. I am making an educated guess that sensitization is present wherever functional freezing occurs (if it occurs). So I am going a little ways out on a hypothetical limb here, but there are some interesting reasons why stiffness might be more prominent than pain in this particular joint, especially in the later stages.

In the early stages, it’s likely that the inflammation of frozen shoulder would both be painful and sensitizing: “continuously increasing nociceptive impulse activity, as in early stages of adhesive capsulitis, could lead to peripheral and subsequently long-lasting central sensitization.”58

But later…

The shoulder is a super mobile joint — it is, in fact, the most mobile joint in the body. There’s quite a lot of range of motion to maneuver in. The pain system is mostly designed to protect us by detecting threats and then avoiding them. The brain may develop the “opinion” that your shoulder is just fine — relatively limited pain — as long as you stay within a narrow range of motion. After a while, the brain may decree that a pain-warning is no longer required as long as you stay in the safe range. If you try to leave it, it just inhibits the motion instead — rather than issuing a warning in the form of pain.

By contrast, in many other joints, there’s much less range of motion, too little for there to be a “safe range” that your brain is content to let you mess around in. If this is correct, we should see a fairly obvious pattern: chronically painful joints with more natural mobility tend to hurt more at first but then transition to a more “frozen” pattern, while joints with minimal range just hurt and don’t “freeze” nearly so much.

And that’s why I believe that sensitization and functional freezing may well be different faces of the same phenomenon.

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Case study: an interesting example of a biological X-factor

Tanya Augustine teaches high school biology, anatomy and physiology and exercise physiology in Cambridge, Mass. She kindly sent me her interesting frozen shoulder story, and granted permission to use it here. I think it will be of interest to many readers.

I have an extremely high tolerance with pain and when I tripped or someone bumped into me, a few times I fell to the ground writhing in pain. I was in tremendous pain, couldn’t get my sports bra on/off, write on the board while teaching, comb my hair and was having great difficulty sleeping.

I was 39 at the time. I’m now 50. I have been extremely active my entire life. I taught aerobics for decades and was a sergeant in the US Army in my early 30s for 4 years. I’ve never been overweight, a smoker, diabetic, or any of those things. The only risk factor I had was my sex and age.

I could no longer take the pain and after some steroid shots and physical therapy opted for surgery. I had my surgery at Mass General Hospital in Boston. The surgeons told me that as soon I was under general anesthesia that they attempted to mobilize my shoulder to see if it was frozen from pain, and nope, that wasn’t it: they couldn’t move it at all when I was unconscious. Then when they went to insert the arthroscopic equipment, it was extremely difficult to penetrate the joint capsule, due to all the scarring.

I had never had a shoulder injury that I could remember. No accident, baseball pitching career, etc. I had gotten into doing pull-ups at the gym at that time, but I’ve always been very strong. It just gradually crept in for no obvious reason. Also, it was in my dominant side (left) which I guess is less common.

The rehab and physical therapy for the shoulder surgery was brutal, but I instantly regained a ton of ROM and was back to about 90% in 2 months and was discharged from PT. I am so grateful I had the surgery, although I had been advised that it would “eventually” unfreeze on its own — a year or two?!

A couple of years later my right shoulder started developing pain, and I freaked out and saw a sports doctor at Tufts Medical. She juiced me up with a lot of cortisone in the joint capsule, I did zero PT, and felt better a few weeks later. The pain has not returned in either shoulder.

So that was about as cryptic a case of frozen shoulder as there could possibly be: seemingly completely out of the blue. But would some kind of biological disposition to this condition eventually reveal itself? Indeed it would.…

So fast forward 10 more years. I had surgery this past June for Dupuytren’s contracture in my right hand. Again, no obvious risk factors: not old enough for that disease, not male, not diabetic, no Parkinson’s, etc. But my hand was so contracted I could no longer type on my computer or open jars. The surgeons again reported that I had a great deal of scar tissue and had to cut more than originally planned to break it up. My mother had the surgery in her 50s, and when visiting my father this past summer, I realized he has it as well — he thought it was arthritis, he’s 81 — so clearly there’s a genetic component.

A point of interest: I had a bad bike accident about 8 years ago which involved me landing on my palms and scraping deep wounds filled with pavement and glass. I didn’t get any medical treatment for those, just washed them out (sort of) and bandaged them up. Within months, I thought I had pebbles stuck in my palms from the accident. I waited a year or two and saw a hand specialist who looked at my hands and replied “not pebbles, Dupuytren’s.” The hand specialists are skeptical there’s a link between my bike accident and the disease onset, but at that time I started noticing hard bumps which eventually progressed to my advanced disease.

So I think I have an overactive immune system, at least as far as my joints and tendons go. Also, I’m extremely happy with my choice in both circumstances for surgery, rather than months of other therapies. I had to get my regularly, active, pain-free, lifestyle back and the surgeries were extremely effective both times. I am not a big proponent of surgery or general medical practices for things that will resolve on their own (or even diagnostics such as MRIs) but in these cases, I am glad this is how I handled it.

Like everyone, I’m searching for an explanation for these things, and have to settle for “it’s not well understood”, which is frustrating, since I don’t want either condition to return. However, I have made zero lifestyle changes, as I don’t think there is anything I can do to prevent them.

I think Tanya’s understanding of her problem is sound. Autoimmune diseases are as varied as the inhabitants of a zoo, such a wide spectrum of severity that it’s a near certainty that they can change lives even while remaining hard to diagnose, subtle and quirky. “An overactive immune system” is probably too general a way of saying it — if cops in one city become extremely overzealous with one type of crime, that’s not a national problem with “an overactive police force.” The immune system can and does go overboard in surprisingly specific ways — specific tissues in specific locations — without necessarily having any other major malfunctions. And so it’s possible to have subtle, quirky autoimmune disease, with consequences that fall well short of severe and easily explained, but which can still change lives.

So Tanya’s shoulder is a dramatic example of a shoulder that was obviously not functionally frozen. This was true freezing, a joint capsule that was stuck, stuck, stuck — literally scarred into place by rampant inflammation caused entirely by a genetic glitch. And what a strong testimonial for surgery!

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Part 2

Diagnosis of Frozen Shoulder

Confirming the diagnosis: classic frozen shoulder symptoms

Frozen shoulder is technically a diagnosis of exclusion, which means that it can only be diagnosed by eliminating all other possibilities. There is no standard clinical test for frozen shoulder, nothing that can conveniently clinch it.

That said, it isn’t hard to diagnose by exclusion — or rather, it shouldn’t be. In theory.

In practice, there is often confusion with other conditions (reviewed below). Physical therapist and shoulder guy Adam Meakins sees “a lot of frozen shoulders,” but also “many who have been told they have frozen shoulder who clearly do not.”59

The defining symptoms of frozen shoulder are:

  • Reduced mobility of a shoulder joint in three stages.
    1. Freezing: Increasingly painful restricted movement. Pain is usually “severe, diffuse, all consuming, and usually unrelenting,”60 in the shoulder, sometimes the upper arm as well.
    2. Frozen: Relatively painless restriction of motion, especially external rotation (the upper arm rotating out to the side).61
    3. Thawing … maybe: The gradual return of movement, for some lucky people.
  • The first movements to go are usually reaching straight up and behind the back.
  • Night pain, especially when lying on the affected side.
  • A sensitive coracoid process (see below).

But, in principle, it’s important to understand that any/all of those symptoms could be caused by other problems. Hence the difficulty.

Fake ROM: just because you can lift your arm doesn’t mean you’re not frozen

“My shoulder’s not frozen,” people will say. “See how high I can lift my arm!”

But it is possible to fake an almost healthy range of shoulder motion by simply working around the limitation in the main (glenohumeral) shoulder joint. The shoulder is a complex, loose joint. The entire shoulder girdle — collar bone and shoulder blade — can slide around a great deal without using the ball-and-socket joint at all.

This video shows what’s going on quite nicely: superb scapulothoracic motion allows a fair bit of arm elevation, but you can also see that the glenohumeral joint doesn’t budge.

Without X-ray vision, the dead giveaway is that the entire shoulder has to lift way up. The true test of glenohumeral mobility is to see how high you can lift your arm up without lifting your shoulder.

Shoulder issues that get confused with adhesive capsulitis

These shoulder problems are presented roughly in order of how much they can imitate a case of frozen shoulder, highlighting the major differences…

Rotator cuff tendinopathy or tear. The rotator cuff is a group of four muscles that surrounds the shoulder joint like a “cuff,” and that cuff anatomically overlaps the joint capsule that gets inflamed in frozen shoulder. (And why a “rotator” cuff? Because the lion’s share of the muscle activity here is devoted to turning the ball of the humerus in its socket.) They are literally hard to separate: the muscles are effectively another layer of the joint capsule, their tendons merging with it. Which is why rotator cuff problems can be difficult to distinguish from frozen shoulder! You can almost make the case that the joint capsule is actually part of the rotator cuff, but that term does traditionally refer specifically to the muscles. But they are certainly intimately related.

Confusing things even more, rotator cuff issues might make movement uncomfortable, as with frozen shoulder … but not necessarily. Rotator cuff abnormalities and lesions increase steadily later in life, like arthritis, but are also amazingly common in pain-free younger people — in other words, even when there’s an “obvious” problem on an X-ray or MRI, it ain’t necessarily the problem.62 But the rotator cuff can hurt, and when it does, it mostly limits active movement, while frozen shoulders are frozen even when you are relaxed and someone else tries to move your shoulder for you (passive movement). Tears are violent and happen suddenly with intense exertion, a clear “oh shit” moment of injury. Tears or tendinitis, the pain is usually limited to more specific spots and movements than with frozen shoulder.

Subacromial and subdeltoid bursitis are closely related to rotator cuff tendinitis, but instead of tendons they affect bursae (the anatomical padding between tendons and other structures).

Arthritis of the big shoulder joint mostly occurs beyond middle age, and usually develops more slowly-but-steadily, and isn’t as severe. An X-ray will show clear signs of joint degeneration that won’t be seen with adhesive capsulitis. Shoulder arthritis often involves a history of injury.

Acromioclavicular arthropathy is degeneration of the joint at the outside end of the collar bone. It does not really affect shoulder range of motion, the pain is more specific to that superficial joint, and it’s usually associated with a history of overuse and injury, usually athletic. This joint can also be sprained (as I learned the hard way in 2008), usually by a fall on the outstretched arm, the kind of accident that might also break the collarbone. It’s conceivable that the pain of a mild sprain of this joint could strongly resemble frozen shoulder, but I think even a minor strain would involve a fairly obvious “oh shit” moment of injury.

Tendinitis of the biceps tendon. Tenderness sticks to the front of the shoulder with this condition. Biceps contraction is painful, but other movements are normal.

Cervical disk degeneration, basically arthritis of the spine, can cause pain, weakness, and numbness that spreads out into the shoulder and can make it seem “frozen,” but this problem usually also spreads further: symptoms in the hand and wrist will usually be more prominent with this problem.

Autoimmune diseases like lupus or rheumatoid arthritis can affect many joints in the body, including the shoulder — but they usually do affect multiple joints, and cause several other health problems that obviously set them apart.

Cancer is one of the least likely causes of frozen-shoulder-ish pain, but a tumour in or near the joint is a possibility. Watch out for other signs of failing health, especially night sweats and weight loss and shortness of breath.

Facioscapulohumeral Muscular Dystrophy — This common form of muscular dystrophy affects mainly the face and/or shoulders and can lurk undiagnosed for decades, with only minor symptoms. For some patients the condition mainly manifests as shoulder weakness as the muscles in that area atrophy, and frozen shoulder is their first misdiagnosis. That was exactly what happened to my oldest friend, who wasn’t diagnosed correctly until his late 30s, years after being told he had frozen shoulder, even years after his trapezius muscle had already rather dramatically wasted away.

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A dead giveaway symptom: a specific painful spot that can clinch the diagnosis

Frozen shoulder may be a diagnosis of exclusion, but it does have one particularly strong defining symptom, almost “pathognomonic” (absolutely defining, a symptom that can only mean a specific diagnosis). If it was a sure thing, frozen shoulder wouldn’t be a diagnosis of exclusion!

But it’s not quite a sure thing, just a very strong clue. It occurs in more than 95% of cases, but only in 10-15% of other kinds of shoulder pain. Its sensitivity on a specific spot on the front of the shoulder, on the tip of a bone called the coracoid process.63 This odd little bone points forward like a finger, just below the end of the collar bone. If you feel around in the tissue there, it’s hard to miss — and if it hurts quite a bit (more than 3 on a scale of 10, say), that’s the sign you’re looking for.

And, again, the poor state of the coracohumeral ligament can also usually be confirmed by diagnostic ultrasound.64 When it’s unhappy, it gets thicker.

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X-ray, MRI, or ultrasound for diagnosing frozen shoulder

Imaging is not a bad idea. X-ray and MRI are mostly for ruling out other things, which probably isn’t necessary in most cases. Ultrasound might be more directly useful.

An x-ray and/or an MRI scan is potentially helpful for excluding shoulder joint arthritis or scary causes of pain like a tumour, but some professionals will sensibly advise against it because frozen shoulder is quite distinctive clinically, because it’s rare for a sinister condition to masquerade as frozen shoulder, and because imaging isn’t exactly a foolproof method of detecting other causes anyway.

Other pros think imaging is a no-brainer and well worth the minor (radiation) risks of a single x-ray to check for surprises before proceeding with therapy.65 There is no evidence-based right answer to this.

Diagnostic ultrasound is cheaper and completely safe. In general, for new cases of other kinds of shoulder pain, it’s not very useful. A 2019 study showed that things turn out the same way whether ultrasound is used to help with diagnosis or not.66

But frozen shoulder stands out among shoulder conditions. Ultrasound probably can detect the condition. Better than that, it can probably confirm that a shoulder is truly “frozen” (contracture, fibrosis, adhesions) rather than just super stiff (functional freezing).67 When truly frozen, the joint capsule looks different on ultrasound: “hypoechoic echotexture.” In other words, it looks dark with ultrasound. And that ability, in turn, could actually inform treatment choices.

Ultrasound can also usually identify a thickened coracohumeral ligament,68 which is strongly linked to shoulder capsule distress.

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Confirm the contribution of functional freezing and sensitization (maybe)

I proposed above that functional freezing — a neurological stifling of movement, rather than a physical limitation imposed by a messed up joint capsule — could be the entire problem with many cases of frozen shoulder. Or at least a significant complication at certain stages. Since functional freezing might be much easier to treat, it would be great if there was a way to tell how much of a factor it is.

And there might be.

If functional freezing is a factor in your frozen shoulder, it’s probably because your brain is “worried” about the joint. That worry may be an excessive overreaction to dwindling inflammation (likely in the late stages), or it could be well justified by the state of the joint (likelier in the early stages). A contractured shoulder capsule will never allow extra movement, but inhibition can ease temporarily in some situations:

  • during pain relief
  • while deeply relaxed, or during gentle, relaxed movement
  • while the shoulder is physically supported (by a helper, submerged in water)
  • in the aftermath of safe-feeling but unusual stimulation, like vibration
  • during and immediately after exercise

The clues might be subtle. For instance, you might get only a little extra range of motion, briefly and erratically, in specific contexts — but any clear increase in range when the shoulder is “happy” is all you need for confirmation. A contractured shoulder capsule will never allow extra movement, but inhibition can falter temporarily in the right circumstances.

Failure of ROM to ever improve in these circumstances does not prove that inhibition isn’t a factor. But even a single clear example of improved ROM would be impossible with a contractured shoulder.

Getting someone else to move your shoulder for you very very very gently

The best way to do this experiment is during a lovely massage, with a therapist who can be trusted to understand and implement the test respectfully. But anyone you trust could do it — no special expertise is needed, just the right gentle vibe.

Basically, you just let someone move your shoulder for you very slowly and gently while you focus on relaxing as deeply as possible. You’re doing your best to imitate being anaesthetized. 😜 If your helper can move your shoulder beyond its normal limits, then at least some of those limits must be imposed by the nervous system, not contracture.

A little enhancement: don’t just try to will yourself to relax, but actively focus on something pleasant. Visualize petting a beautiful, happy cat, for instance (assuming you like cats). Redirecting mental attention may be effective for short-circuiting inhibition.

The submersion “hack”: test your shoulder in the water

Brains aren’t dumb: they know that water is a much safer place to move a shoulder. While not every brain will be convinced, the comfort and support of submersion will probably be enough for many of them to allow some shoulder movement. A physical limitation will not yield in the pool (or anywhere) but a functional limitation might.

If your shoulder has the same limited range in and out of the water, it doesn’t prove anything. But if it obviously does move better in the water? Yahtzee! That would more or less confirm functional freezing… and provides great encouragement to do submerged rehab exercises as a treatment, too. This is one of the best possible examples of aquatic therapy.

Drugs that relax muscles might help to confirm the diagnosis

Muscle relaxants and other systemic sedatives and psychoactive drugs (benzos, opioids, pot, booze) are not as good at reducing muscle tone as you might think — but they do work to some degree, and your mileage may vary. And they might soften the intense inhibition of the rotator cuff muscles.

The most accessible way to test this is either with an over-the-counter muscle relaxant, or by having a couple beers — not both at the same time, please! They do not combine well! And then test your shoulder range of motion. If nothing changes, it doesn’t mean your shoulder isn’t functionally frozen — it just means that the drug isn’t working for you, and there are many possible reasons for that. But if you do get more range when you’re slightly sozzled… yahtzee! That’s a meaningful diagnostic checkmark in the functional freezing column.

There’s a full chapter below about muscle relaxants and related drugs.

Diagnosing sensitization, a “known associate” of functional freezing

Earlier I introduced the concept of sensitization: the over-reaction of the nervous system to stimuli that usually sets in and takes over and puts the “chronic” in chronic pain. In the context of frozen shoulder, there’s a lot of overlap between sensitization and functional freezing.

In my opinion, if you have one, you probably have the other, despite their differences, even though one involves pain and the other involves stiffness. I am hypothesizing that they are two sides of a coin: that your shoulder would hurt in a sensitized way … if your brain would allow movement. It’s not moving to avoid that pain.

The sensitized frozen shoulder patient often has more of a sensitization problem than a shoulder problem. But that begs the question:69 how can you tell the difference? It’s kind of like asking someone hard-of-hearing if their TV is turned up too loud: it sounds right to them. How are you supposed to know if your brain has turned its shoulder paranoia up too loud?

There truly is no way to be sure, but the more of these items you check off, the more likely you are to be sensitized. (These items are taken from many sources, but particularly Smart et al.70)

  • Starting with the obvious: you have no obvious cause for your pain, no recent injury, no known source for the pain. You are medically unexplained.
  • Your pain is chronic. Sensitization usually requires months to establish itself.
  • Your pain is out of proportion to any known, recent injury.
  • It’s hard to tell what’s going to make you feel better or worse. While some things may help or hurt consistently, others do not. You have good days and bad days and can’t figure out why.
  • You are seriously pessimistic, and you have a lot of worries about it being a sign of something worse (e.g. catastrophizing).
  • You have too much pain and tenderness elsewhere: sore anatomy that “shouldn’t” be sore because it’s unlikely to be related to your pain.
  • A history of troubles in the areas that are strongly associated with sensitization: neck and shoulders, low back, abdomen, jaw.
  • High overall stress load: exhaustion, poor sleep, chronic stress, anxiety, depression, and/or anything else that drains or menaces you (like another significant medical problem). Obviously almost any adult without a perfect life could check this one off, but it’s a matter of degree.
  • You’re female. Unfortunately, this really is a risk factor!
  • Overuse of stimulants like nicotine, caffeine, or more potent ones. Or withdrawal from sedatives like benzos (Valium), which can jangle your nerves for a surprisingly long time (months).
  • Your pain is erratic and more likely to fade into the background when you’re happily preoccupied. This is a whole category of tricky, subtle possibilities.

That last one deserves some extra attention. Sensitization makes pain worse because the CNS is convinced that there’s more of a threat than there actually is. If pain backs off at times when the brain is “reassured” and/or distracted, that tends to indicate that sensitization is involved.

Failure to respond to “reassuring” situations doesn’t mean that there’s no sensitization — because it may just be too strong, which is absolutely possible. Likewise, a strong improvement doesn’t guarantee that there’s no pathology, or an injury still slowly healing — because the brain is capable of dampening any pain.

But a pattern of signs that your pain backs off when your brain is either reassured or preoccupied with higher priorities … that is a valuable clue, and well worth bearing in mind throughout any and all treatment experiments.

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Part 3

Prognosis

Depressing frozen shoulder bombshell: it ain’t self-limiting!

The conventional wisdom for decades has been that frozen shoulder inexorably grinds through all three stages — freezing, frozen, thawing — on a fairly predictable timeline, finally resolving with or without treatment within a couple years at most for almost everyone, a self-limiting condition. This “natural history” of the condition has been repeated ad nauseam by countless experts for decades.

Too bad it may be bogus. Someone looked into the basis for the conventional wisdom, and found “no evidence” to support it:

It turns out … not so much. In fact, while no evidence supported the natural history theory, evidence from multiple randomized control trials with longitudinal data directly contradict the theory of a recovery phase that leads to complete resolution for frozen shoulder. That the findings so starkly contradict the accepted view of frozen shoulder, as reflected by clinical reviews, research article introductions, textbooks, and reputable health websites has prompted reflection on how such an assumption made it into the medical knowledge base.

Dr. Christopher Kevin Wong, “Frozen shoulder: fact or fiction?”

In other words, how the #%!*& did this happen? Basically, it was a mistake that got repeated until it was entrenched. Once it’s in a few textbooks, it’s game over for the truth — hardly anyone even thought to question it. For a long, long time.

Frozen shoulder almost certainly does not consistently resolve on its own.7172 This is a bombshell, and a credible one, and rotten news. I’ve always thought frozen shoulder is an interesting mess of a topic, but this makes it even more so. And how long will it be until most physiotherapists know about this? Start your timers. Bet it takes 20 years.

My (wife’s) frozen shoulder story

On this website, I often write about conditions I have some personal experience with. In this case, it’s not my own experience, but my wife’s: a rip-roaring case in the aftermath of a very serious car accident, adding injury to injury.

She says the shoulder was the worst pain she had in the entire recovery experience (and she broke several bones, including her skull, spine and pelvis). We have a rather vivid memory of walking down the street together one day, near the peak of the problem, and she tripped a little and reflexively tried to stabilize herself with the bad shoulder. WOW. Never seen her react like that to anything, before or since!

But there’s a peculiar wrinkle in her story: she actually already had a full-blown case of frozen shoulder when the accident happened. It cleared up completely for several months during the initial stages of rehab. And then it returned! It’s like the accident hit the “pause” button. What can we make of this? It’s hard to interpret for sure, but I think one possibility is that it means that the first phase of her frozen shoulder was functional: not an adhesive capsulitis, but a neurological ban on movement which was lifted when the accident changed her “priorities,” and then re-imposed when her body started to recover from the severe injuries.

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Part 4

Treatment of Frozen Shoulder

Reviews of all the major treatment options

Management is controversial & depends on the phase of the disease.

Nagy et al, 2013, Open Orthop J

Most cases of frozen shoulder can’t be “cured,” but any case can be managed and minimized.

Every professional seems to have their own take on frozen shoulder treatment, even doing nothing at all: some believe it should just be left alone to run its course, and it’s an understandable position. A huge 2009 survey of almost 2,400 physical therapy patients found that no one got better, at least by one way of reckoning.73 In a 2004 test with 77 patients, “supervised neglect” actually worked (slightly) better than “intensive physical therapy”!74 Why even go on? It sounds like nothing works! But these studies were looking at the tip of an iceberg of possibilities75 hardly the last word — just good perspective. It might be unwise to spend a bunch of time and money on basic physiotherapy.

At one end of the scale, there’s the “do nothing” crowd. At the other, there are many different kinds of more dramatic cure claims, as there is for any difficult condition. Despite too-good-to-be-true promises, there really is no known effective treatment for frozen shoulder — nothing that actually prevents the capsule from adhering, nothing that can free it up without doing more harm than good, nothing that clearly, reliably makes the ordeal shorter or easier for most patients.

However, range of motion can probably be preserved to some degree by early use-it-or-lose-it interventions. And the pain can be helped (which in turns helps with the “using”). Pain can almost always be helped at least a little.

Only a few scientific reviews of frozen shoulder treatments have been published, but they suffer badly from the “garbage in, garbage out” problem: there’s not enough good quality research to review. And so there’s a strong theme in their conclusions: no one really knows what works yet, and most of the better evidence we do have is either unimpressive or outright disappointing. “Despite over a hundred years of treating this condition the definition, diagnosis, pathology and most efficacious treatments are still largely unclear.”76

In a typical example, Maund et al reviewed 31 studies in 2012, “many” of which were “at high risk of bias,” concluding after great effort that there is “limited clinical evidence on the effectiveness of treatments for primary frozen shoulder.”77 The authors of a big 2014 review sounded particularly underwhelmed: they concluded that hardly anything seems to work, and nothing works for long.78 Out of 32 trials, not one “compared a combination of manual therapy and exercise versus placebo or no intervention” — in other words, a total lack of evidence on what is probably the most important treatment topic.

Favejee et al is one of the more optimistic reviews, somehow finding — in the same literature Maund et al and Page et al looked at! — some moderate to strong evidence for the short term benefits of some treatments.79 But emphasis on the short term: “most of the included studies reported short-term results” only.

This unhelpful mess of mediocre evidence and “more study needed” conclusions is a good demonstration of how musculoskeletal medicine is still surprisingly primitive — more about that in the next section. Frozen shoulder seems worthy of considerably more and better research attention than it has gotten!

Here are quick summaries of all the treatment options I’ve reviewed in detail below:

  • Movement therapy to try to maintain function and slow down the capsule’s adhering/contracturing, or speed up recovery.
  • Strengthening for frozen shoulder should be avoided during the freezing stage, but potentially much more useful after that. And I like the Meakins method, a nice variation on basic strengthening which integrates some eccentric loading and relaxation exercises.
  • Stretching is generally over-rated as therapeutic tool, but in the case of frozen shoulder I think it’s worth investing some time in it.
  • Pain killers (over-the-counter) for frozen shoulder are not especially useful except for occasional “emergency” use. To whatever degree they mask some symptoms, they might help get you through some rehab exercises with a little more confidence.
  • Muscle relaxants (the over-the-counter kind) are fairly useless, but a good idea in principle for frozen shoulder rehab. Prescription sedatives (the benzos) are a nuclear option that might actually be useful if used cautiously and strategically. Alcohol and marijuana strike a balance — not as potent as sedatives, but safer and more accessible, and probably more effective than muscle relaxants.
  • Corticosteroid injections: more pain-relieving power, more risk, but overall not a great option.
  • Massage therapy is never going to “fix” frozen shoulder, but it can almost certainly provide some symptom relief, and possibly more. Trigger point therapy specifically, although it’s experimental and a bit sketchy, has potential to treat both symptoms and (in the case of functional freezing) actually help the problem.
  • Ultrasound for frozen shoulder is a popular option, but very unlikely to work. And “super ultrasound” (shockwave therapy) is just a big over-hyped question mark so far.
  • Desensitization and disinhibition are important strategic concepts in frozen shoulder rehab that are reason for several other treatments. A clear understanding of them can refine frozen shoulder management.
  • Physically forcing increased ROM:
    • Manipulation alone — literally just forcing the joint through the limitation — has no proven benefit and major risks. Doing so under anaesthesia is also risky, but more promising.
    • The Oolo-Austin Trigenics® Procedure is a popular branded method: manipulation with local anaesthetic and active patient involvement, unknown efficacy and significant risks.
    • And then there’s surgical options, mainly inflating the capsule, or releasing it with a scalpel. These procedures have a complex mix of pros and cons, but are risky enough that they should be a last resort.
  • Reducing systemic vulnerability to chronic pain — basically by building up your general health and fitness in as many ways as possible — is an important strategy for virtually any difficult pain problem, but the need is especially important for frozen shoulder, which is so strongly linked to general health.
  • Ketogenic dieting and intermittent fasting to reduce inflammation are a long shot, but an interesting long shot, and not all that difficult to try.
  • Ice and heat & spicy ointments (A535 etc) are not going to work any miracles, but they could be surprisingly helpful pain-relievers and motion-facilitators (as well as cheap and safe).

I will conclude the tutorial with the always-entertaining hall of treatment shame: the most bogus frozen shoulder treatments.

So what’s the plan?

Before I dive into the treatment options, I’d like to respond to a common reader concern that I do too much “debunking,” and not enough telling you what works and exactly how to do it. Although I get few refund requests — way below industry averages — most of the requests I do get are caused by this specific concern: Doesn’t $20 get me a road map to a cure? A step-by-step action plan? The savvy exercise regimen that will make the pain stop?

These things just don’t exist, as I warned in the introduction. I have not sold you a book without mentioning that.

Even if they did exist, prescribing a treatment “plan” is simply out of the question, because every case really is different — that’s not just a platitude. What works for one person really is not going to work for the next. I promise that I’m not holding out on you. I am not a cure salesman, and I will not tell you what you want to hear. There is no specific method or series of logical steps that will reliably cure any kind of chronic pain problem, least of all the tough kind I write books about.

No plan survives contact with the enemy.

Helmuth von Moltke the Elder

Many people reading this probably think plenty of debunking is quite reasonable, normal, and even ethical. But imagine some of the unreasonable expectations I hear from a few customers. For instance, one woman asked me for a refund because my book offered her “only suggestions”! What else is there? What did she expect? Binding arbitration? Click this link for a cure? Free magic wand with every purchase?

Historical perspective and the Age of Hype

The disappointing truth is that there is only a motley assortment of rather underwhelming options with complex pros and cons, but usually more “cons.” Some are better than others, but quite a few are dodgy, for obvious reasons: hope sells, and so there are many more poor options than there should be. Please blame reality for this … not me.

And blame the people who have given you false hope and raised your expectations of musculoskeletal medicine far beyond what it can possibly deliver.

We are living in the “Information Age,” but sometimes it seems more like it’s the Age of Marketing and Hype. An almost unbelievable amount of the information we consume is generated to promote products and services. The result has been an unprecedented flood of being told what we want to hear about absolutely anything.

The reality is that musculoskeletal medicine is surprisingly primitive. Medicine has always had bigger, scarier fish to fry than treating mere aches and pains and injuries, which were barely studied at all until the 1980s. Musculoskeletal medicine is still a cocky teenager, just starting to come of age and figure out that it doesn’t know everything. Even sports medicine specifically, with so much potential funding and relevance to occupational injuries, has been bizarrely slow to build its evidence base.

The trouble with pseudo-quackery: treatments that seem way more legit than they are

The most prominent problem in musculoskeletal medicine today is the prevalence of what I call “pseudo-quackery”: treatments that are about as sketchy as any old-timey snake oil, but seem modern and scientific and mainstream. A few classic examples: laser therapy, ultrasound, platelet-rich plasma, prolotherapy, nerve and muscle stimulation. But there are many more.

These disguised quackeries are actually based mainly on surprisingly stale tradition, speculation, and authority. They generate more false hopes and wasted time, energy, money, and harm than more traditional quackery because they are vastly more popular and very much part of mainstream medicine, or very friendly with it — even many hardened skeptics aren’t expecting snake oil when they go to see a physical therapist or an orthopaedic surgeon.

So musculoskeletal medicine is a minefield, and a lot of debunking just goes with the territory. But it doesn’t mean there’s no good news at all.

The good news

Despite all the debunking and disappointing evidence, I do indeed have positive things to say about several of the options. I have started this part of the book with a summary of all the options, and I will conclude it with another summary of my recommendations, focusing on the positive as much as possible, and what to actually do. Many things are worth trying, even if they aren’t sure things or sitting on any solid science:

We’re told to strengthen this muscle or stretch that one, or inject this substance into an injury, or zap it with heat or electricity or ultrasound … and sometimes it really works, even though placebo-controlled trials fail to validate the treatment. I’m a big advocate of better science to really understand what causes injuries and how to treat them — but in practice, I also believe that sometimes it’s worth trying something, anything, just in case it successfully ‘reboots’ your injury.

Alex Hutchinson, Sweat Science

An encouraging perspective, but of course it doesn’t mean you should try any old nonsense. And you may save some time and money avoiding several others (or at least re-prioritizing them). You may even avoid the heartbreak of those that can do some harm. Knowing what not to do is half the battle, if not more! Understanding the topic well enough to prioritize the imperfect options is actually a huge win, the best you can realistically hope for.

The “negativity” of ratiocination is a surprisingly big topic, often funny, and sometimes profound. I answer the accusation in more detail in a compilation of tales of outrageous hate mail, the ethics and tactics of debunking, what it’s like to (supposedly) be the #1 Public Enemy of Massage (a therapy everyone loves to love), and — my favourite — “advanced negativity,” a discussion of how cynicism is baked into science in the form of the null hypothesis.

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Use it or lose it: movement therapy

If you believe you are in the early stages of frozen shoulder, immediately begin a campaign of mobilizations: gently, thoroughly use as much of your range of motion as you can without excessive discomfort.80

And if you are somewhere in the middle of the condition? Same thing, but with the goal of trying to prevent further range loss or regain it quicker.

This can include easy stretching and strengthening exercises as well: anything that requires your shoulder to do any kind of shoulder job, as long as it is tame enough to avoid making it more painful during the painful phase, which is a serious risk with frozen shoulder. I’ll discuss more “assertive” strengthening/stretching a little more below. Here’s a nice collection of miscellaneous exercises for the shoulder, with good illustrations: “7 stretching & strengthening exercises for a frozen shoulder.”

What if you can’t move it? Then imagine moving it. Seriously! Literally just visualize movement, no joke. A very large component of movement is neurological. When we lose range of motion, it’s both a physical and a neurological loss. If you can’t preserve the physical, keep working on the neurological!

Use it better: tips for better range of motion exercise

Give your range of motion a little helping hand, too. For instance, use a wall to support the weight of your arm while “walking” up the wall with your fingers. Or lie down on a bed and move your shoulder while the arm is fully supported. Or get a helper to provide partial support. Such tactics are a good way to take safe baby steps into the outer limits of your comfortable range.

Nothing is more supportive than water. Do range of motion exercises in the pool, with your shoulder and arm submerged. Highly recommended.

Emphasize any activity you enjoy that requires extensive shoulder range of motion. If you have none, consider taking one up: tennis, for instance. You may find it difficult, but making movement challenges fun is a really valuable rehab principle.

How’s it hangin’? The pendulum exercise “dangles” the shoulder

One of the best and simplest light exercises for a frozen shoulder is the “pendulum” exercise, in which you just dangle the relaxed arm and swing it gently, letting the weight of the arm carry it back forth, or in small circles. You can do this from a standing or sitting position, leaning forward to give the arm a little room. You don’t even use the shoulder muscles: the movement is generated by tiny movements of the torso, and requires only the slightest muscular effort to sustain. Just tiny nudges will keep the arm swaying like a pendulum.

Done right — if you’re comfortable, if you keep it easy and relaxing — the pendulum exercise may even feel good. This gentle movement appears to be a minor but reliable pain-killer for many people.81 And when things are grim, even a little relief can be precious. Reader Hilary W.:

On my frozen shoulder journey, there were many nights when I was up at 2–4am sitting and crying. When nothing else would work, the pendulum exercise took just a tiny edge off the relentless aching pain.

And reader Russell W.:

Awake every hour or two overnight in excruciating pain, the pendulum swing gave a tiny amount of relief. I hope I never go back there again.

Serious analgesia? No. Sanity preserving edge-removal? Absolutely. And of course, regardless of any pain-killing effect, it’s just a good maximally gentle way to try to maintain shoulder mobility. Especially in the difficult early stages, the pendulum makes a good warm-up and warm-down from slightly more challenging mobilization exercises.

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Getting stronger as a therapy

Exercise is the closest thing there is to a general miracle drug,8283 and strength training is one of the best ways to exercise, practically like magic: healthier and more efficient than most people realize.84 This is why there’s a saying that you “can’t go wrong getting strong”… but with frozen shoulder you really can go wrong.

Strength training basically involves exhausting muscles enough to force them to adapt and get stronger. Although strengthening can be done relatively gently, there is a minimum level of intensity required for it to actually achieve the goal. Below that level, you’re just … moving with slight resistance. But above that level there’s a real risk of aggravating frozen shoulder.

Weakness is not the problem with frozen shoulder, so more strength is not therapeutic in itself. If there’s any hope for strength training to actually help frozen shoulder, it’s that the stimulation of the activity will somehow alter the course of the biology. This is not a foolish hope in theory, but there’s exactly zero direct scientific evidence about it. As far as I know, literally no one has ever tested this rigorously.

I wouldn’t expect much from it: strengthening is the bedrock of mainstream, conventional physical therapy and very widely prescribed … and yet frozen shoulder marches on for nearly everyone.

And then there’s that risk of aggravation …

My recommendation: Avoid strength training during the painful freezing stage — the risk of making a bad situation worse is just too great, and ain’t nobody got time for that — but do it any time after that, because it’s a lot less likely to be a problem, and it might just work.

What exercises? Literally anything with a barbell or weight machine that involves the shoulder. I think there’s no justification for any specific instructions — there’s not much reason to think that any specific approach is better than any other. As long as you are cautiously wearing out your muscles a little bit, 2 or 3 times per week, you’re providing a stimulus that might be therapeutic.

But here’s a more specific approach to consider anyway …

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Strengthening with the Meakins method: eccentric loading + “let it go”

In my experience manual therapy and traditional physiotherapy methods for frozen shoulder do very, very little. I have tried them all, pulling and pressing people with painful frozen shoulders, here, there, and everywhere, all with little effect, and all to no avail. However, there is a “different” method for treating frozen shoulders that I have been using more and more over the years …

Frozen shoulder? Let it go, Let it go … ., Meakins (TheSportsPhysio.wordpress.com)

Physiotherapist Adam Meakins has a novel idea about how to treat frozen shoulder. Although it’s not clearly evidence based, it is an educated guess from a particularly good guesser about shoulders, with some strong theoretical foundations,85 especially that 2015 science experiment that showed that frozen shoulders unfroze substantially under anaesthesia.86 It involves progressively challenging range of motion, putting it firmly in the “use it or lose it” category of treatment approaches. Adam puts another spin on that, teaching his patients to use it specifically with eccentric contractions: that is, contracting muscles while they lengthen.

Why use “contraction” here at all, if frozen shoulder isn’t a muscle problem? The complex rotator cuff muscle group is seamlessly blended with the joint capsule, and to stimulate one is to stimulate the other … and eccentric contraction is an interesting stimulus, well known to have unusual and potentially rehabilitative effects on connective tissue. It is often used as a tendinitis treatment.

Another consideration is the on-going debate about how much of a role muscle tension may play in frozen shoulder, either greatly complicating or actually mimicking an adhered capsule: functional freezing. To the extent that the freezing is functional, then it does make a lot of sense to work with the shoulder muscles.

So what exactly do you do? You slowly lower a small weight into a manageable stretch into your most limited movements. You make it as easy as possible at first, and you up the ante every few days. You tolerate a little discomfort, but not too much. You don’t want to push hard through pain, but you do want to strive to ease through any muscle tension holding you back: “let it go,” as Adam puts it … referencing the song, of course. 😃 And you do all of this with the confidence that your shoulder tissues are probably not as raunchy as they feel.

See his article for full details with pictures: Frozen shoulder? Let it go, Let it go … .

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Stretching

Stretching is generally over-rated as a therapeutic tool: it doesn’t do most of what people usually assume it does (e.g. “prevent injury”), and flexibility is less important than people think (see Quite a Stretch). But it does increase flexibility, for whatever that’s worth … and frozen shoulder is a condition of decreased flexibility. So it seems like it could be a natural fit for this condition.

However, it’s super unlikely that pulling on the adhered/contractured capsule is going to change it. That tissue is exceedingly tough, and contracture makes it even tougher — we know stretch cannot change contracture.87 You might as well try to stretch a truck tire. Even without taking it easy to prevent aggravation of the condition, there’s probably little hope.

What if it’s stiff, not frozen? What if the problem is “more of a functional limitation than a physical one,” a possibility discussed extensively above? In that case, I think there’s quite a bit more hope that stretching could be useful.

So what does the evidence say? Stretching is such an obvious therapeutic option that it actually has been studied … but very little. One of the only noteworthy trials I can find was decent quality at least, and certainly appeared to have a happy ending.88 They used a “static progressive stretch device,” in other words a gadget for applying a slowly-but-steadily increasing intensity of stretch, and the thirty stretched patients did better than patients who got “conventional physical therapy” on all measures, both after a month and a year later. Not bad … but it’s also hard to trust a single study.

My recommendation: As with strengthening, I recommend taking it so easy with stretch during the painful freezing stage that you might as well not bother, just don’t risk the aggravation, stick to doing exercises within your pain-free range of motion. But after that? I think it’s worth trying. Just find the end of your range of motion and push up against it. Push lightly and less frequently at first, and if it causes no trouble, start ratcheting up the frequency and intensity.

P.S. As with range of motion exercises, the pool is a particularly good place for stretching.

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WOO! “Windows of opportunity” might be important in frozen shoulder rehab

The “window of opportunity” (WOO) is a period of pain relief and/or confidence that makes it easier to do normal activities and rehab exercises. This is a popular notion in physical therapy.

And the WOO might be an especially important idea in frozen shoulder rehab, because so many of the more promising treatment methods are either about creating or using these windows. While that is broadly true of rehab for many other conditions, it’s especially relevant to frozen shoulder because of the possible role of functional freezing. A WOO is mainly useful to the extent that freezing is caused by excessive neurological inhibition. A brain that is incorrectly convinced that it has to limit shoulder movement might be more easily persuaded to lift the ban if you do rehab exercise while the pain is blunted.

And a WOO might even be useful for frozen shoulder involving contracture. These patients also need to do whatever they can to maintain shoulder range, and there are surely better and worse times to do that. Reduced pain is a good example of a better time!

WOO woo?

Maybe the WOO is bullshit. While there’s probably some legitimacy in the idea of a window of opportunity, the notoriously skeptical physical therapist blogger Adam Meakins argues that the idea of a window of opportunity is often just a thin, self-serving justification for using ineffective methods, “more for the therapists’ benefit rather than the patients’.”89 I completely agree. I see it all the time.

Ineffective therapies can still often produce transient, trivial pain relief because almost anything can.90 In some cases, such minor benefits might be encouraging and motivating enough to constitute a meaningful opportunity to advance recovery. For instance, someone might be more willing to do some exercise, or get an extra boost fighting their nicotine addiction.

But in many cases it’s probably just not enough — too brief, too minor — and the WOO is just a weak excuse for a treatment that has little else to recommend it.

What makes a better WOO?

A somewhat more reliable pain-relief effect… and a target like functional freezing, that has a better chance of actually benefitting from a WOO.

And so windows of opportunity will come up again several times in the rest of the tutorial. So far, I’ve only discussed treatment options that would be facilitated by a WOO, like range of motion exercises, strengthening, and stretching. Other treatments, like pain medications, steroid injections, massage, vibration, or icing/heating are mainly about creating WOOs.

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The basic pain killers — aspirin, ibuprofen, acetaminophen, etc

Some pain relief may be possible with the use of a topical analgesic like Voltaren. The medication may not soak in deeply enough for a significant effect, unfortunately. The inflamed tissue is quite well buried under thick shoulder musculature. But it’s worth trying, because topical delivery is much better than dosing your entire system with edible pain-killers, which have a dizzying array of side effects.

Many people can probably get some additional relief from short-term, cautious use of NSAIDs, the non-steroidal anti-inflammatory drugs,91 which are:

  • aspirin (Bayer, Bufferin)
  • ibuprofen (Advil, Motrin)
  • naproxen (Aleve, Naprosyn)

My advice is to strictly reserve these for occasional “emergency” use, for taking the edge off when it’s most desperately needed. This is treating the symptoms only, of course, but that’s fine to a point: masking symptoms is under-rated. Just do it sparingly and reluctantly. Treat it like the lesser-of-evils that it is.

There is also some potential to use pain-killers to create windows of opportunity for better rehab — a period of pain relief where other treatments may be easier and more effective. But there’s not a lot of opportunity, because for most people the pain relief just won’t be very great. If you find a drug and (safe) dose that seems to work better, it’s worth making a point of taking them half an hour before, say, doing your strengthening exercises.

Safety first!

At any dose, these drugs can cause heart attacks and strokes92 and they are “gut burners” (they can badly irritate the GI tract, even taken with food, and especially with booze). Aspirin is usually best for joint and muscle pain — which may or may not mean it works better for frozen shoulder — but it’s the most gut-burning of them all.

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The cannabinoids: marijuana and hemp, THC and CBD — “it’s complicated!”

Photo of marijuana plant.

Perhaps the most interesting & controversial plant in the world.

Cannabis is a plant, most notably marijuana (bred for its narcotic effects) and the major strain of hemp (bred for other purposes). It’s one of the most interesting plants in the world because it produces chemicals with interesting effects, the cannabinoids. The most interesting and famous of those are THC (tetrahydrocannabinol) and CBD (cannabidiol). All cannabis contains THC, CBD, and hundreds of other related compounds, but there’s a lot more THC in marijuana plants, and a lot more CBD in hemp.

THC gets you high (psychoactive effects), and CBD does not. Both are alleged to be pain killers: it’s their most popular medicinal use (either that or as a sleep aid), but CBD is much less studied.

The evidence for pain-killing

So, are cannabinoids effective pain killers? “It’s complicated”!

As a science journalist, I am honour bound to emphasize that cannabinoids are not proven pain-killers. “Proof” is a high bar that has not yet been cleared. A huge 2017 review of the scientific literature on cannabis concluded that there is “substantial evidence that cannabis is an effective treatment for chronic pain in adults.”93 But the review also explains that the evidence shows only modest benefits so far, there is uncertainty about every detail, and significant practical problems abound for both researchers and consumers.

And that was hardly the last or only word. Other reviews of largely the same evidence have been much less optimistic. In 2017, Nugent et al looked at 27 scientific trials of cannabis for chronic pain trials, and it was disappointing: weakly positive for neuropathic pain, and just inconclusive otherwise.94 In 2019, Häuser et al wrote “Cannabis medicines can be regarded to be third-line therapy for chronic neuropathic pain. There are signals of a lack of efficacy for all other chronic pain syndromes.”95

So that’s not great.

Can getting high help? The role of psychotropic effects in treating frozen shoulder

THC might have some bonus effects for some patients because it can cause euphoria, reduce anxiety, improve sleep, and indirectly function as a muscle relaxant. It’s probably not a potent muscle relaxant, but nothing else is either (nothing you want to take regularly anyway). More about that in the muscle relaxant chapter.

None of this is “pain-killing,” per se, but these effects may have some potential to help you cope with pain. Better yet, maybe they can even dial back the movement inhibition that probably accounts for some percentage of the problem. Testing your ROM while high is probably a good idea. The results may surprise you.

It could also backfire. Please do be aware that THC can cause anxiety just as easily as it can reduce it. Your mileage will vary. And there’s nothing relaxing or disinhibiting about anxiety!

Usage guidelines for beginners

If you’re new to marijuana, there’s a bit of a learning curve. Here are some tips:

  • Pure topical CBD creams and oils are overall the safest and most convenient, so they should probably be your first priority to try. THC may be where it’s at, but it’s harder to use…
  • Use caution with THC edibles! Dosing and duration of effect are huge wildcards. You can get way, way too high for comfort — not very dangerous, but scary.
  • Avoid vaporizers that use oil infused with cannabinoids, due to scandalous, tragic safety issues because asshole manufacturers have added other dangerous, un-tested substances96. Dozens of people died in 2019. Died!
  • Infused oils aside, vaping raw cannabis in moderation is quite safe.97 Just take it easy for at least your first three times — just one or two modest inhalations of vapour is just fine to start.

For more detailed information, see Marijuana for Pain.

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Opioids too dangerous & ineffective for most cases, but maybe a good idea for a few

An opium poppy seed head with very blurry vegetation in the background.

Ripening seed head of an opium poppy.

The notorious opioids, derived from the milk of the poppy flower,98 are mainstream drugs like codeine, and the infamous heroin derivatives and imitators like Oxycontin, Percocet, and Vicodin. Most patients assume that opioids are “powerful” pain killers, and we joke about “the good stuff” like it’s a given that it will do the job if anything will, despite the well-known horrors of addiction and overdose. But opioids are curiously impotent for many kinds of pain and people.

(Opioids do not include the infamous benzodiazepines, like Valium, discussed in the muscle relaxants section.)

Opioids mostly induce deep relaxation and euphoria that may make you not care about pain, as opposed to “killing” pain. But not caring is not a cure, and their efficacy is surprisingly poor for musculoskeletal pain, especially chronic pain (non-cancer).99 Some people are even genetically immune to them.100 They can also backfire and cause pain.101 And, of course, life-altering opioid addictions and life-ending overdoses are shockingly common. The CDC declared in early 2016 that opioids should not be an option for chronic musculoskeletal pain: there’s just too much danger, and too little evidence of benefit.102

Demonizing an entire class of drugs is usually a bad idea. Not everyone gets addicted and some people get real relief, so there’s plenty of grey area here despite the risks. With proper medical supervision, opioids might provide some much needed relief from a particularly debilitating and extreme chronic pain problem like frozen shoulder.

There is no direct scientific evidence about the efficacy of oral opioids for frozen shoulder one way or another.

Weak versus strong opioids

The weak opioids are drugs like codeine, dihydrocodeine, and tramadol. The strong opioids are either morphine itself (the gold standard, the canonical opioid drug) or its derivatives and synthetic imitators like fentanyl, hydromorphone, methadone and oxycodone.

It seems like it would make sense to experiment with weak opioids before strong, but the weak ones are notoriously ineffective at lower doses, and when you increase the dose the efficacy doesn’t go up very much but you do get a lot more side effects! Bad deal. If you need any opioids, you probably need strong ones. If you don’t need strong opioids, weak ones aren’t worth it either. But that’s just an opinion, a starting place for a chat with your doctor.

The case for opioids for frozen shoulder

Many doctors will tell any frozen shoulder patient who asks for opioids that “the condition is self-limiting,” and therefore the risks just aren’t worth it — even if they think it will help. While it’s probably not actually true that frozen shoulder is self-limiting (a likely myth debunked way back in the introduction), it is true of the painful, “freezing” phase of the condition. That agonizing phase is definitely going to end.

So what’s the rationalization for using opioids despite the expiry date on frozen shoulder pain? If opioids are useful for anything outside of palliative care, it’s exactly this: temporary prescriptions to help people get through rough patches of severe, debilitating pain. Short-term emergency use is one of the best ways to use opioids (and other dangerous drugs, like tranquilizers).

It’s debatable whether the painful phase of frozen shoulder is actually an “emergency,” but it sure looks like it to me in some cases. Losing the use of an arm and suffering through many weeks of severe pain is rough for anyone, but it’s particularly bad for some people. For people who really badly need to use what little shoulder ROM they have left, without excruciating pain, a short-term supply of strong opioids could be a life saver.

So should you ask for opioids? And how?

Overall, I don’t think it’s a great idea for most frozen shoulder patients — just a few people experiencing the worst consequences of the condition.

Most doctors will be hard to convince. Prescribing opioids has become a nightmarish minefield for physicians, and many refuse to prescribe them at all, or only where the need is the most extreme (and most will not think that includes frozen shoulder). And yet, paradoxically, you can also still find plenty of evidence that the opioid epidemic is raging on, driven by continued excessive prescription of opioids!

So it’s a little hard to know what you’ll encounter if you ask a physician about this. If you do, here are some critical talking points:

  • Acknowledge that it’s a bit radical, and show a clear awareness of the danger of addiction.
  • Request supervision, low doses, and a limited supply.
  • Emphasize that you’re only seeking partial relief to keep you functional during the worst of the freezing (painful, inflamed) stage of the condition.

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Steroids, injected and swallowed

Corticosteroids are potent anti-inflammatory agents (and not the same thing as the anabolic steroids taken by bodybuilders.103). They are an exotic kind of pain-killer. Think of them as ibuprofen on, er, steroids.

Oral corticosteroids can be invaluable for management of severe widespread inflammatory conditions — like rheumatoid arthritis, say — but they are overkill for almost any painful “hot spot,” like trying to put out a frying-pan fire by turning on the sprinkler system. If you can avoid exposing other tissues to corticosteroids, you should, because they are a bit of a bull in a biological china shop.104 Injection is preferred for its precision.

But oral corticosteroids certainly kill pain! No doubt about that. From a 2006 Cochrane review: “Oral steroids provide significant short-term benefits in pain, range of movement of the shoulder and function in adhesive capsulitis.”105

The concern is about the side effects, which can be so dire that they should only be tolerated if they are the lesser evil, and only the most desperate patients should consider risking those side effects for frozen shoulder relief. Few doctors would sign off on it, not with injection as a perfectly good alternative. Injections are popular because oral steroids are a terrible idea for most musculoskeletal conditions.

The rest of this chapter will consider injections only — which have their own problems, but they are at least much more local problems. Injections also have some significant potential with frozen shoulder specifically — more than any other musculoskeletal condition I can think of.

Injecting corticosteroids

Photo of a hypodermic needle.

Wherever pain is caused by inflammation, corticosteroid injections are also likely to produce substantial temporary pain relief — at the cost of a (minimally) invasive procedure with some risks. They can be injected with a needle, or blasted through the skin with an electrical charge (iontophoresis).

In the case of frozen shoulder, it’s clear that these injections function as a kind of super pain-killer — they can reduce pain.106

This encouraging evidence contrasts starkly with what happens with rotator cuff tendinopathy, which is almost nothing at all: brief, minor relief in only about 1 in 5 patients, according to a witheringly negative 2017 review.107 The difference is probably attributable to different pathology. Tendinitis is often incorrectly regarded as inflammatory, when in fact it is probably more degenerative in character, so it’s not much of a surprise that a powerful anti-inflammatory medication has less impact. But the painful freezing stage of frozen shoulder is much more classically inflammatory in character, and therefore responds better to steroids. That’s a nice demonstration of the power of actually understanding the biology of a problem.

For frozen shoulder, it’s clear that there are benefits … and equally clear that they don’t last, and that the freezing of the joint proceeds relentlessly despite the pain relief.

Just how temporary are we talking about? Several weeks of relief, maybe four months at the very best… and that’s with repeated injections.

A 2007 review concluded that “up to three injections were beneficial, with limited evidence that four to six injections were beneficial.”108 And beyond six? Uncharted waters! But it’s extremely likely the returns diminish, disappear… and then backfire. Steroids are crazy potent and have well-known corrosive effects on connective tissue. You don’t want to go overboard, and it’s unlikely that any doctor would let you. Many doctors won’t do steroid injections at all.

Bottom line: powerful short-term medicine. That has value, but there might be a way that we can exploit that short-term benefit for even greater value…

When life hands you short-term benefits…

I find it easier to push the limits of range of motion in a joint that isn’t screaming at me. I bet you feel the same way. I bet even American Republicans and Democrats could agree on that.

With potent short-term benefits, the main use of corticosteroid injections for frozen shoulder should probably be to facilitate ROM-maintaining exercise, simply because it’s quite a bit easier to do those rehab exercises when your pain is dampened.

This might be the ultimate example of a treatment that creates a “window of opportunity” (WOO) for better rehab. Perhaps it creates a bigger window than any other therapy — because the window is basically opened by pain relief, and steroids provide quite a lot of that, for a while.

There’s no direct evidence to support the claim that steroid injections will not only provide short-term relief, but also create a useful WOO that actually improves long-term results when properly exploited. It’s a hard thing to study, because it’s hard to define “properly exploited.” What exactly should you do with the WOO? A small WOO with a minor effort at doing better rehab while you have the chance might have no real impact at all. Maybe the exact type of exercise you do while the WOO is open is important. To the best of my knowledge, this has not been studied — probably because it would be quite tricky to study.

But it is plausible. If the WOO concept has any validity at all — always open to debate — this seems like it’s one of the best possible candidates.

Happily, there is actually some indirect evidence. A 2017 meta-analysis didn’t just confirm the typical short-term pain relief benefits of corticosteroid injection, but also this:109

Intra-articular corticosteroid injection resulted in greater improvement in passive ROM both in the short and the long terms.

Long-term benefits of any kind are noteworthy, and this just happens to be exactly the benefit I would hope to see if short-term pain relief can actually facilitate frozen shoulder rehab. And yet that conclusion was based on studies that were not specifically studying how to make the best of the window-of-opportunity provided by the pain relief. Maybe people with frozen shoulder who get steroid injections just naturally use their shoulders more, because they can — less pain, more movement.

If a detectable long-term benefit in ROM can occur without any particular attempt to exploit the WOO… well, then, I am optimistic that actually trying to exploit the WOO is a promising strategy.

Injection advice summarized

Anyone with a really debilitating case of frozen shoulder should consider getting one or two intra-articular injections during the painful (freezing) stage. I think three is pushing it: the risks start to outweight the benefits at that point. They should be spaced about 4-6 weeks apart, and the second one should only be done if the pain has gotten quite bad again.

There are two specific reasons for this advice:

  1. Pain relief is inherently valuable. Frozen shoulder can be an extremely disabling condition, and short-term pain relief alone has significant value, regardless of anything else.
  2. It’s just a hypothesis that pain-relief will facilitate better rehab… but it has some good plausibility, a bit of indirect evidence, and “costs” nothing extra — the intervention is already justified by the first reason.

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Muscle relaxants (Robaxin, Robaxacet, etc), psychoactives, and sedatives

“Muscle relaxant” is an odd category of drug. There are several drugs that are relaxing, but are not exactly “muscle relaxants” because they are not specifically interfering with the biology of muscle contraction. A true muscle relaxant is essentially a poison that messes directly with muscle physiology.

You really don’t want too much of a true muscle relaxant. It can cross into paralysis. Amazonians used a muscle relaxant … on their poison arrows. Curare poison relaxes you to death. European explorers encountered the stuff early in their visits to North America, and it led to some of the earliest scientific studies in pharmacology.

And yet, on the other hand, it’s not clear that the muscle relaxant drugs are actually interfering with muscle contraction! So it’s a tricky topic.

As with many other treatment options discussed in this book, this one is mostly only relevant to functional frozen shoulder. If your shoulder joint is inflamed and contractured, even an extremely potent muscle relaxant is not going to make any difference. You could paralyze those muscles, and your shoulder would still be frozen.

For functional frozen shoulder, however, a muscle relaxant is an intriguing idea with real potential. In principle, it could even be used to diagnose functional freezing: to the extent that a muscle relaxant improves your range, it isolates muscular inhibition as a cause.

Muscle relaxant primer

Muscle relaxants come in many related varieties,110 but only one that is widely available without a prescription: methocarbamol, as found in Robaxin, Robaxacet, and similar brand names.

There are also several prescription muscle relaxants, obscure to most patients, but most notably carisoprodol (Soma), cyclobenzaprine (Flexeril), metaxalone (Skelaxin).

All muscle relaxants are tame cousins of the truly potent sedatives (also discussed below), and can cause significant drowsiness, dizziness, and a laundry list of other common side effects, but there’s also a surprisingly wide range of safe dosage (hard to overdose).

Methocarbamol and friends are not widely used because they are not super effective. It’s probably because they’ve been around forever, because the drowsiness they cause makes them feel more potent than they actually are, and because relaxing muscles just seems like such a good idea to literally everyone, both patients and pros. I think perhaps muscle relaxants have been grandfathered into modern, scientific medicine. Tradition-based medicine, rather than evidence-based medicine.

Muscle relaxants are surprisingly unstudied, like many other popular drugs.111 In particular, good luck finding any study of the effect of these drugs on muscle function. It’s not clear if muscle relaxants actually relax muscles, or if they just make us feel more relaxed.

What evidence we do have is not exactly high quality.112113114

An expert of my acquaintance thinks they are useless specifically at low dosages.115

Acute back pain is the only condition for which there is adequate data. Some muscle relaxants (including methocarbamol) do appear to be roughly as effective for acute back pain as common over-the-counter pain killers116117 — so they can help, but not all that much, and with great potential for side effects. It’s also damning that there doesn’t seem to be much difference between muscle relaxants: “Comparison studies have not shown one skeletal muscle relaxant to be superior to another.”118 So we have a class of drugs that shows little sign of effect, no matter which flavour you use. Whoop-de-do!

Even a prescription muscle relaxant like carisoprodol (Soma) is so impotent that patients will (this is bizarre) actually tense up if they are lied to and told that the drug is a stimulant.119 (The study was quite interesting — if you only read one footnote about a study in this book, this would be a good one to choose.) Clearly the brain is the boss of your muscle tone, and the drugs only nudge us towards relaxation. Bear this fun fact in mind for the discussion of alcohol and other psychoactive drugs coming up — it’s a ray of hope.

And here’s another fun fact: even anasthesia doesn’t truly “relax” muscle.120 It stops voluntary contraction, but it doesn’t eliminate muscle tone. Only death does that, and even in that extreme case the tenacity of the contractile proteins is demonstrated in the phenomenon of rigor mortis.121

Muscle relaxants clearly work at least a little for some people, some of the time, probably usually at higher doses. And they are relatively safe to experiment with, even at higher dosages. In fact, it’s so hard to overdose on them that I even feel comfortable endorsing cautious testing of a larger dosage than what’s recommended on the box. Just don’t go driving, don’t combine with alcohol, and be alert for significant side effects — they aren’t effective enough to bother with if they harass you with side effects.

Narcotic “muscle relaxants” (sedatives like Valium)

If our goal is to loosen up the muscular control of the shoulder joint, is there any drug at all that will definitely do the job? Any drug that’s reasonably accessible?

Narcotic sedatives, mainly the benzodiazepenes, relax everything. Like the opioids, the benzos are another “nuclear option” — they do interfere with muscle contraction, while also interfering with everything else: like consciousness! Many drugs have highly unpredictable effects, but the benzos are as potent and predictable as cobra venom.

The most famous of all the sedatives is diazepam, AKA Valium, a benzodiazepene. But it is only the most infamous member of a family of rogues, like Klonopin, Ativan, and Xanax.

Just because they are potent — and they certainly are that — does not mean they actually work, or that they work by relaxing muscles. A 2017 study showed that “Diazepam Is No Better Than Placebo When Added to Naproxen for Acute Low Back Pain” (they put the result right into the title).122 However, I suspect that the your-mileage-may-vary factor is huge with these drugs.

As with the milder muscle relaxants, it’s surprisingly unclear whether or not these drugs actually reduce muscle tone, or whether they achieve relaxation indirectly via their potent sedative and psychoactive effects. Those psychoactive effects are a huge wildcard that could account for a wide range of responses. They are primarily used to relieve anxiety and improve sleep, both of which could easily relieve pain on their own.

I don’t think there’s any question that benzos might be a useful tool for loosening up a functionally frozen shoulder. And frozen shoulder can be so debilitating that it seems worth at least considering this treatment option, despite the hazards… which are a big deal.

Benzos really do involve dire risks of physical dependence and addiction, and withdrawal can be nightmarish, dangerous, and even lethal at the extremes. Although it is possible to take and stop taking benzos safely, many people do not get the information and help they need for that. Sadly, I have extensive personal experience with benzo withdrawal, and I’ve written about that in detail.123

However, benzos can be safe if used in moderation for short periods only. They are a dangerous tool, like a gun, which must be respected and used with great caution. If you’re interested in dancing with this devil, don’t just ask your doctor for a prescription: make a point of showing your prudence by asking for only a 2-week supply of a small dosage only (the exact amount varies with the specific drug).124

The curious case of alcohol as a pseudo-muscle-relaxant

Alcohol is hard on your system in many ways. It’s a myth that a drink every night is a tonic, and there really is no safe intake level125 — it is a poison, and it can make people more vulnerable to chronic pain. And yet…

There’s plenty to be said for a glass of wine or beer as a kind of medicine.126 Anecdotally, moderate usage seems useful for taking the edge off nearly any kind of pain. This may be because it’s functioning as a kind of muscle relaxant, or at least as a general sedative.

Let me be clear: alcohol is not a muscle relaxant per se,127 not in a biochemical sense (and warning: it also combines dangerously with actual muscle relaxants and sedatives). In a world full of alcoholism and drug addiction, obviously a “prescription” of alcohol has to be offered and taken rather cautiously. But it is highly accessible, cheap, relatively harmless in moderation, and it’s a psychoactive drug — and anything that bends your mind has the potential to be a mild, obliquely effective muscle relaxant.

All psychoactive drugs — anti-depressants, alcohol, marijuana, amphetamines, opioids, benzodiazepines — often seem to help almost any problem, but the emphasis is on seem, because they mainly affect mood: “It is my impression that ‘pain-killing’ drugs improve the patient’s mood rather than take away the pain.” (Sarno)

Mood isn’t nothing. If you are genuinely happy and relaxed… if that’s something alcohol can do for you…

Given the potential importance of reducing inhibition of shoulder function in frozen shoulder, I don’t think there’s any question that I would try to get a little tipsy before doing my mobilization exercises.

THC as a pseudo-muscle-relaxant

Tetrahydrocannabinol (THC) is the most famous cannabinoid produced by cannabis (marijuana). It is another relatively safe and accessible psychoactive drug, probably the only other one that seems tame enough to take seriously for this purpose. (Sure, you could blow your mind with acid or ecstasy and hope for a muscle relaxant effect, but that seems like overkill.) Obviously its accessibility varies widely from place to place as the entire world grapples slowly and awkwardly with legalization.

Like alcohol, THC doesn’t zap muscle tone directly, but it probably can do it indirectly and erratically.

If you are happy and relaxed while stoned, it’s certainly possible that inhibited shoulder movement will be less inhibited. Whether or not that would meaningfully affect the kind of particularly fierce functional inhibition that might be a factor in frozen shoulder is anybody’s guess, but it seems worth trying.

For this purpose, virtually any strain of marijuana will do, but ideally a THC-rich one (not CBD) because you want the psychoactive effects. You want to get high before working on your shoulder range of motion. Whee!

With pot, there is also the added potential for direct pain relief (discussed above, along with usage guidelines).

And so I do tentatively recommend THC as another “muscle relaxant” worth experimenting with.

Botox?

Botox is the infamous face-paralyzing drug of the stars! It’s a special case, quite different from the other muscle relaxants. Like curare on poison arrows, Botox is outrageously toxic and doesn’t “relax” muscles but just outright paralyzes them, even in small doses.

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Massage therapy: can everyone’s favourite therapy help?

Although the adhesions in the shoulder joint capsule cannot be broken by massage — not safely at any rate — it probably is possible for massage to relieve some of the discomfort that usually develops in the area.

That’s an opinion only. The inadequate scientific evidence may even suggest the opposite. For instance, in 2009 Jewell et al found that use of massage in the context of physical therapy “reduced the likelihood of a favorable outcome”!128 Uh oh. But that’s not remotely the same thing as a well controlled trial of the efficacy of professional therapeutic massage … which has literally never been done.

Massage for frozen shoulder is too unstudied for an evidence-based recommendation, and so all of my recommendations about massage are based on experience and educated guessing.

Many patients crave massage therapy for this condition. In the best-case scenario, the discomfort of frozen shoulder may just be a symptom that can be treated by massage. At least a little, at least temporarily. And we should never knock a little symptom relief.

But massage might have more profound relevance to frozen shoulder. As discussed earlier in the tutorial, some shoulders may be more functionally than literally frozen, and this is more likely in chronic cases. If true, then massage could theoretically treat the root of the problem. If it works, here’s how it might work …

Reducing neurological inhibition with massage

The stimulation of massage, probably combined with slow passive movements, might encourage and reassure the nervous system that it’s okay to move the shoulder again, such that it can reconsider the shoulder “lockdown” policy it may be entrenched in. Any reduction of neurological inhibition would create an opportunity for more movement. That window of opportunity might be narrow, especially at first. If there’s any increase in range of motion following massage, that’s a great sign that should be exploited by gently exploring the improved ROM as much as possible for as long as it lasts.

Creating windows of opportunity might be the secret to the power of massage in general. Although the value of such opportunities is often exaggerated, massage may be particularly good at it.129

The massage treatment itself should be low key as well: this is all about convincing the nervous system that there’s no danger. Excessively intense massage could actually backfire.

A major disadvantage of this approach is that it could be slow and therefore expensive. How good is massage at facilitating the resolution of neurological inhibition? Can it do it at all? No one knows. It’s probably not worth pursuing if there’s no noticeable improvement within roughly 6 half-hour massages of the shoulder and area (and even that’s getting to be quite a costly experiment). However, note that there are also other, less expensive ways to “reassure” nervous systems about shoulders.

Treating trigger points with massage

Massage is the most obvious and natural way to attempt to treat “trigger points,” but only one of several options, which I will bundle together in the next chapter.

Other benefits of massage

Proven benefits of massage are much less common than you might think. While many papers claim to show a wide variety of benefits, most of them are poor quality experiments that couldn’t actually prove anything. However, there are a few more credible sources, and the best — maybe the only — established benefit of massage is that it’s helpful for anxiety and depression.130

Both anxiety and depression are a lot more likely in people suffering from a serious chronic condition like a bad case of frozen shoulder. And reducing anxiety in particular could certainly be a useful part of a desensitization strategy.

A benefit like that may not have much to do with frozen shoulder specifically, but it is highly relevant: it’s so worthwhile that it essentially guarantees that your money won’t be wasted. Whether massage therapy does anything for your frozen shoulder or not, it is at least good for your “soul.”

Perhaps one of the reasons massage reduces depression and anxiety: it’s relaxing. While not proven as well as you might think, it is a pretty safe bet,131 and the idea is further supported by evidence that massage therapy may reduce blood pressure132133 and helps people to sleep, even when they are under the unusual stresses of hospital care.134

And there are likely other general health benefits as well, even if they haven’t been proven.

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Trigger point therapy: trying to “release” those sore spots

Trigger points (TrPs) are sore spots associated with aching and stiffness, as common as pimples, which may be a cause and/or complication of nearly almost anything else that hurts. Their nature is poorly understood and controversial,135 but the main theory is that they are a “micro cramp,” just one member of a big family of unwanted muscle contractions.

Trigger points might be a major mechanism for “functional freezing” in cases of frozen shoulder.

Rubbing trigger points seems to ease them. No one knows how well it actually works, or even if it works at all.136 But it certainly does seem to, and often surprisingly easily.137 All advice about trigger points on PainScience.com is based on “seeming” and scientific plausibility, which is weak sauce.138

However, given the potential importance in frozen shoulder, presumptive treatment — treating as if trigger points matter — is worth a try if you focus on the safer and cheaper options: mainly self-massage, possibly supplemented with some professional massage help as long as it isn’t overly aggressive.

Dry needling is popular too, and I will discuss it below mainly to discourage you from using it: it’s more expensive and risky, without being more likely to help. And then there a few other possibilities, like getting professional help, addressing medical factors, medications, injections, exercise therapies (especially stretch), ergonomics, and much more.

How to treat trigger points with self-massage

Drawing of a thumb pressing downwards on a target, suggesting trigger point therapy.

Grope around your shoulder with fingers and thumbs and find acutely sensitive, aching spots in muscle tissue. You may or may not feel a slight bump or twitch, but those are inconsistent and unreliable signs. Finding trigger points is the exact opposite of an exact science,139 but don’t sweat it: just cast a wide and pleasant net, it doesn’t matter if some effort is “wasted” on some wrong spots.

The soreness of a trigger point should feel “relevant” — that is, the soreness of the spot should feel like it is related to your shoulder pain, rather than some other kind of discomfort that just happens to be in the same area. See below for several more specific places to look for relevant TrPs.

Massage tools are essential for exploring the back of the shoulder in search of TrPs beyond the reach of your hands. It’s important to be able to explore the back of the shoulder, because there could be trigger points all over and around the shoulder blade that are relevant. (More about locations to explore below.) What tools? Mostly balls.140

When you find a sore spot, either simply press and hold for a while (10–100 seconds), or apply small kneading strokes, either circular or back and forth. You’re hoping for the sensitivity to ease, which is what we traditionally call a “release” in trigger point therapy.

Rub very gently at first, just tugging the skin to and fro over the surface of the sore spot — some initial gentleness has a specific purpose, don’t skip it — and then ramp up to rubbing firmly but not viciously. You’re not trying to “kill” it, you’re trying to soothe and “scratch” it. Too much intensity can backfire, and a just-right intensity may actually be a key to success: vivid and clear “good pain” is an ideal level, intense but somehow satisfying. Don’t grimace through it as if a brutal massage therapist was inflicting it on you.

A good first self-massage experiment should take several days, two or three sessions per day, with a few minutes of exploration each time. If you are finding points that feel relevant but they aren’t easing, you could up the ante and try a few basic upgrades: treat right before bedtime, get better tools (a firmer, smaller ball like a lacross ball can be a game-changer), avoid chills or actually have a hot bath/shower with treatment, or follow treatment with light exercise.

If a couple weeks of this yields little or nothing, it’s time to give up, or get some professional help to explore other possibilities.

Where to search for trigger points relevant to frozen shoulder

  • The deltoid muscle is the most obvious of the shoulder muscles, but also the least likely to harbour trigger points relevant to frozen shoulder. You should check it anyway, but the deltoid is not an especially “triggery” muscle in my experience.
  • It’s the muscles of the infamous, “rotator cuff” muscle group — prone to tears — that are much more likely to matter. These muscles all have tendons that surround the shoulder joint, like a “cuff.” They are all attached to some part of the shoulder blade at the other end.
  • One of the rotator cuff, the subscapularis, is between the back and the shoulder blade, and virtually untouchable except a little bit in the armpit. Although subscapularis trigger points may be relevant to frozen shoulder, this is a very difficult area for amateurs, and trying to describe it is beyond the scope of this tutorial, and a reason to consider professional help.
  • The infraspinatus is much more accessible — though still awkwardly out of reach on the back of the shoulder — and is worth some special consideration: Perfect Spot No. 14, The Most Predictable Unsuspected Cause of Shoulder Pain. Despite the fact that it seems to be far from the problem, way over on the back of the shoulder, infraspinatus TrPs routinely “shoot” pain through and around the shoulder (referred pain). You may be amazed at how relevant infraspinatus trigger points feel. See that article for much more detail — it’s an important supplement to this chapter. If you’re going to try to treat frozen shoulder with trigger point therapy, you’re going to have to get to know your infraspinatus.

The approximate location of Spot 14 & friends in the infraspinatus triangle. The pale blue band across the top indicates the most worthwhile area. Notice how remote spot 14 is from the shoulder joint. Click to embiggen.

Professional trigger point therapy (mostly massage)

Some important things to bear in mind if you seek trigger point therapy for frozen shoulder:

  • We’re mostly talking about massage therapists — they are the most likely kind of professional to be competent to help — but you can also get help with trigger points from other kinds of healthcare professionals. There are other kinds of trigger point therapy, but none are great options.
  • It’s a crapshoot. The quality of trigger point therapy is all over the map and low on average. So you have to be prepared to shop around for someone who seems humble, sensible, and experienced. See How Do Your Find Good Quality Massage Therapy?.
  • When in doubt, it is much better to just have a great shoulder massage than bad trigger point therapy. There is plenty of overlap between decent trigger point therapy and an ordinary pleasant massage.
  • Please, never tolerate extremes of massage pressure.

Warning! Although it’s not “massage” per se, many massage therapists will nevertheless be tempted to manually force your shoulder range as part of the treatment. Do not allow this! It’s especially likely because of the obsession with fascial release in that profession.141 Remember, you could easily be dealing with someone who knows less than 5% of what is contained in this document, and they could be overconfident and reckless with your vulnerable shoulder joint.

It’s not all gloomy. For what it’s worth, many massage therapists do claim to have cured cases of frozen shoulder,142 and it’s not hard to see why, and I suspect some of them are even true. I actually have my own highly relevant treatment story — “the one about my uncle-in-law,” near the beginning of that page — worth a detour if the massage angle interests you.

Other kinds of trigger point therapy

There are several other major types of trigger point therapy. Not one is promising for the average headache patient, but all are worth considering when you get more desperate. If I was in my third year of frozen shoulder, I might start considering these options. Here are the other approaches, quickly summarized. (Again, every topic here is explored in much greater detail in my book).

Stretching seems like a good idea for “knots” that may be micro-cramps by nature. It might work about the same way that stretching out a calf cramp works: you win the tug-of-war with contracting muscle, just on a tiny scale. As with massage, people believe it helps, including some experts. Unfortunately, there are major problems in both theory and practice. Even if it’s possible in principle to win a tug-of-war with some trigger points, it’s unlikely to work with all of them, and especially not the worst ones. How can we pull apart a powerful contraction knot — a tiny segment of muscle fibres in full spasm — with anything less than pliers, a vice, and a glass of bourbon? That trigger point is like a knot in a bungie cord: all we’re going to do is stretch the bungie cord on either side of the knot.

Stretch with … spraying? A coolant spray, that is. This is one of the “original” types of trigger point therapy, used by Dr. Janet Travell (famous for her study and promotion of trigger point therapy in the 1970s and 80s). It’s just stretching enhanced by a chill on the skin, which might have some interesting reflex effects. It is obscure, rarely practiced today, and unvalidated scientifically — but probably worth a shot if you can find someone who does it.

Maybe stabbing will help! “Dry needling” is a popular but sketchy method of treating trigger points with acupuncture needles (but it’s not acupuncture143). It is “dry” needling to distinguish it from “wet” injections of medications. It involves some risks, from wasted money to worsened pain to infection and (seriously) lung puncture.

Lung puncture might seem unlikely during dry needling therapy for frozen shoulder, but there are a number of muscles on the chest wall that might be targeted to try to help the shoulder, as well as the lateral neck, where the tippy top of the lungs are surprisingly exposed (they are higher than people realize, and lurk just under the skin at the base of the side of the neck).

Needling is provided mostly by physical therapists. Every practitioner will claim they know what it’s doing, but none of them can actually explain it in any detail: ideas about it are imprecise and contradictory speculation. It feels potent and patients have a love/hate relationship with it. Other than a handful of positive studies,144 the science is discouraging.145 I do not think it’s a good option for most people: it is plausible and interesting theoretically, but also has risks, costs a lot, and can hurt like hell. Few patients should be willing to accept those downsides without much better evidence that it works.

Shiatsu is another Asian therapy that might include some “accidental” trigger point therapy. It’s needle-less Japanese acupuncture, using lots of pressure to stimulate acupuncture points, so it definitely includes a bunch of vitalistic nonsense (“energy medicine”). Nevertheless, it has far more in common with massage therapy than acupuncture does. Remove the Japanese elements and it’s just “acupressure,” which can be almost indistinguishable from trigger point therapy. Typical shiatsu/acupressure is 30-60% in tune with what I consider to be good trigger point therapy… which is probably better than some bad trigger point therapy.

Injection. Trigger points may be treatable by injecting them with a saline solution (to dilute the tissue fluids), with an anaesthetic or anti-inflammatory medication, or even with Botox to paralyze and “deactivate” them. Evidence of efficacy is incomplete and unimpressive so far. A 2001 review concluded that “Any effect of these therapies is likely because of the needle or placebo rather than the injection of either saline or active drug.”146

Addressing other medical factors

There is one more major approach to trigger point therapy that is much more important: attempting to reduce the biological vulnerabilities that may cause trigger points (and/or other kinds of chronic pain). This can be a huge project and a bit of a wild goose chase, but it’s a near certainty that there are at least some treatable medical factors, such as disturbed sleep, nutrient deficiencies, or hormonal imbalances, that make trigger points worse.

See Vulnerability to Chronic Pain.

Recap of key trigger point points

  • Trigger points may actually be a major mechanism for “functional freezing” in cases of chronic shoulder pain.
  • Trigger point therapy is experimental but can be very safe, cheap, and easy.
  • Self-treatment is mostly about finding sore spots in the shoulder and rubbing and squeezing them with fingers or balls, at moderate intensity, a couple times a day for a week or two.
  • There is a particularly good spot to look for trigger points relevant to frozen shoulder: the infraspinatus muscle, on the back of the shoulder blade. (The subscapularis is probably equally relevant, but much harder to access.)
  • Good professional help with trigger point therapy is hard to find, but any good quality shoulder massage is probably better than bad trigger point therapy. So mainly just try to find a massage therapist whose style you love.
  • There are several other kinds of trigger point therapy — most notably the needles, both dry and wet — but none of them are promising options for frozen shoulder patients.

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Maybe sound waves will help? Ultrasound

Ultrasound therapy is the use of sound waves to treat medical problems, especially musculoskeletal problems like inflammation from injuries (sprains, tendinitis, bursitis). And frozen shoulder. It has been a popular therapy for decades, its use so widespread that it almost defines physical therapy. Unfortunately, although mainstream, it is not as scientific a treatment as most people assume. It has been condemned by one scientific review after another for a quarter century. Scientists seem to have almost nothing good to say about ultrasound. Conclusions like this one are the rule: “As yet, there seems to be little evidence to support the use of ultrasound therapy in the treatment of musculoskeletal disorders.”147 There’s also good evidence of an absence of benefit for shoulder pain more specifically — in a fairly big 2009 study, ultrasound couldn’t beat a placebo.148

Some modern variants of ultrasound are expensive, hyped, and totally unproven for any or many conditions.

Ultrasound for frozen shoulder has barely been studied, but what little research has been done concluded that it couldn’t out-perform a sham.149 Ultrasound is particularly easy to compare to a sham, because you just need an ultrasound device that isn’t actually doing anything. That’s quite a persuasive negative trial, alas, and there isn’t really any promising science to contradict it.150

With ultrasound, there’s always the faint hope that just the right settings (amplitude, frequency, duration, and so on) might make an important difference. The big idea with ultrasound is — this will blow your mind! — that cells and tissues somehow respond “well” to being shaken (not stirred). It’s not clear to me why anyone thinks that, but it’s an entrenched idea. In the case of frozen shoulder, tissue is clearly misbehaving in some profound way, much worse than simply being hurt, so maybe being vibrated will convince them to behave? The possibilities have never been explored for frozen shoulder, but they have for fractures, and it’s not good news.151 If it doesn’t work for fractures (a simple traumatic lesion in tissue with amazing innate capacity for healing), it probably isn’t going to work for mysteriously contractured joint capsules.

Ultrasound for frozen shoulder does not look like a solid investment, based on the scientific information we have to date. About the only thing that can be said for it is that it’s harmless and not very expensive.

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Super ultrasound! Shockwave therapy

Extracorporeal shockwave therapy (rESWT) is a form of high-energy ultrasound. It has no obvious specific relevance to frozen shoulder — there’s just no particular reason to think it would work. The main story shockwave mongers are telling their customers is that shockwave therapy “breaks up” the adhesions in adhesive capsulitis … but we know better. We know that adhesive capsulitis is not “adhesive” but contractured. How are high-intensity sound waves going to help with that? It’s not inconceivable, but it would be a surprising and rather exotic biological effect, and that seems like a reach.

Another standard claim is that shockwave therapy will “speed up the healing process” because stimulation something something mumble … it’s so vague it’s meaningless, an idea that has already been tested and found wanting in the context of ordinary therapeutic ultrasound (and other electrotherapies, like TENS).

But shockwave therapy is a trendy treatment option for many musculoskeletal conditions — and there’s good evidence of efficacy for some of them — so of course people are doing it. And some scientists are testing it. To date, I am aware of just three tests, all recent, which is like trying to play baseball with three people. Without even looking at them, I could guarantee they aren’t going to be enough to conclude anything. But I will trudge through the data anyway …

  • Only one of the studies is worth even one damn: a 2016 trial certainly seems to be a home run, with 53 patients who got real shockwaves doing much better than 53 who got fake shockwaves.152 But there are some serious concerns about that study,153 and it’s one damn only has value if combined with studies that are worth a damn or two of their own. Unfortunately, there are none.
  • Another was similar in overall design — including the same key flaws — but smaller and with results that were even less convincing.154
  • The third study is still less impressive, worth mentioning only because there are so few to mention. It’s just a lame little study that tries to sound optimistic but actually isn’t.155 Worthless.

My conclusion for now: there’s no particular reason to think shockwave therapy helps frozen shoulder, and no compelling evidence that it does. Shockwave providers that are citing Hussein et al to help sell their wares are irresponsibly opportunistic and ignoring (or ignorant of) what constitutes adequate evidence.

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Reducing vulnerability: tackling the things that make all kinds of pain worse

When the primary complaint is pain, the treatment of pain should be primary.

Barrett Dorko, Physical Therapist, online discussion, 2010

The specific cause of chronic pain may often be less important than general sensitivity and biological vulnerability to any pain. The biggest risk factors for pain chronicity are things like poor health, fitness, and socioeconomic status, inequality… and they overshadow common scapegoats like poor posture, spinal degeneration, or even repetitive strain injury.

For instance, just for the sake of argument, what if you knew that contractured shoulders hurt in some people and not in others? Or it hurts much more in some people than others? What if only some contractured shoulders hurt because only some people have a neurological vulnerability? Is that really a “shoulder” problem?

Seems more like a sensitivity problem.

How can nothing in particular make us hurt? Because pain is weird, a generally oversensitive alarm system (sensitization again) that can produce false alarms even at the best of times, and more of them when your system is under strain.

Frozen shoulder is an especially good example of this, as a condition that occurs much more often in people with metabolic syndrome.

There are several common modifiable risk factors for any kind of chronic pain that are typically neglected:

These are all things you can change, in theory.

As tempting as it is to focus on the shoulder, it may make much more sense to work on these bigger picture issues. It’s difficult, of course. The big factors are often thoroughly entangled, all making each other worse. An impoverished single mom with a nasty ex-husband, a nicotine addiction, and looming diabetes is going to have a tough time digging her way out of that mess. And yet it could be her only real hope, too.

Metabolic syndrome and frozen shoulder

Many common stubborn painful problems are particularly associated with one of the vulnerabilities above. For instance, headaches are strongly linked to sleep and mood disorders.

And frozen shoulder is linked to metabolic syndrome. It’s a perfect example of the importance of general risk factors, because it is so clearly a disease, not an injury. Better still, it’s a disease that is actually clearly linked to metabolic syndrome. Frozen shoulder is a specific physical problem that can emerge from a general biological vulnerability — along with many others, but only in frozen shoulder do we have this particularly fascinating combination of a seemingly physical/mechanical problem with very biological roots.

If metabolic syndrome is indeed the real reason that a glenohumeral joint seizes up in the first place, then obviously, please, do everything you can to combat metabolic syndrome! Which is basically — you’re going to love this — get in shape. All the things we associate with fitness. Not easy, but simple!

It may be too late to prevent frozen shoulder, but it’s certainly not too late to improve your odds of fighting clear of it. Remember, this is a condition that can go on for years in some people — it is not clearly “self-limiting” as so many professionals believe. It is a Very Good Idea to do everything you can to improve the odds of recovering sooner rather than later. Although no one actually knows this, it’s highly plausible that the severity of metabolic syndrome could be the difference between cases that resolve relatively quickly and those that drag on and on.

How to reduce general vulnerability to pain

And what can you do about this? “Easy”: get healthier! With a variety of vulnerability reduction projects, AKA “lifestyle medicine.” So not actually easy at all, but simple in principle.

Many of the options follow obviously from the list of vulnerabilities above, but for the sake of thoroughness I summarize them here. This advice will seem general to the point of being trite and useless, but that’s actually the point: we want specific treatments, but general ones actually do matter a lot.

  • Get more exercise. It’s the closest thing there is to a miracle drug. Building strength is really valuable and surprisingly efficient.
  • Get more sleep. Protecting your sleep is probably almost as good an investment as exercise.
  • Eat an “anti-inflammatory diet” — which is just healthy! It’s more about avoiding dietary causes of inflammation (junk food and excess, basically) rather than consuming anything “medicinal.” (The omega-3 fatty acids — fish, nuts — are by far the best example of nutrition that verges on medicinal. Everyone should probably eat more mackerel.) Intermittent fasting (skipping some meals) is an approach, overhyped but probably based on a seed of truth.
  • Inhale less smoke. If you smoke, you already know you should quit, of course. And now that COVID-19 is rampaging around the world, you have the best reason yet.
  • Drink less alcohol. Alcohol is a poison, and the more you drink, the harder it is on your system. (Moderate drinking is pretty harmless, but the popular idea that it’s actually “healthy” is nonsense.)
  • De-stress. The ultimate easier-said-than-done challenge! If you are a candidate for an anxiety disorder diagnosis, exploring and treating that should probably be your top priority.
  • Make more friends. “Loneliness” is an incredibly common and underestimated stressor.

Tackling all of this vulnerability-reducing stuff could turn into a complete personal makeover, a huge project that might never end (and probably shouldn’t). Like any difficult, complex problem, you break it up into pieces and start with the easiest bits. It’s a long-term “pick your battles” challenge.

More exercise and sleep deprivation are usually the lowest hanging fruit. Quitting bad habits like smoking, drinking, and junk food are harder but simple and very effective. In some cases, loneliness can be almost easy to fix (join a club).

Where’s the science? Does this work? No one knows. It’s plausible and likely. But you really cannot waste your time trying to be a healthier, fitter person!

I discuss all of these options and more in much greater detail elsewhere. See Vulnerability to Chronic Pain: Chronic pain often has more to do with general biological vulnerabilities than specific tissue problems.

And there’s more about the tricky diet thing in the next section, because anti-inflammatory dieting may be particularly relevant to frozen shoulder.

The best evidence for treating persistent pain points towards improving general health, as opposed to fixing specific “issues in the tissues.”

Playing With Movement, by Todd Hargrove, p. 217

Combatting sensitization specifically

One of the ways that all of these non-specific approaches do their job is by taming “sensitization,” the tendency of chronic pain to get exaggerated and a bit weird. This goes on with almost all chronic pain to some degree, but probably frozen shoulder more than most, because of the way shoulder “lockdown” seems to characterize many cases.

In addition to general ways of fighting sensitization summarized here, there are also some more specific ways to do it, mainly avoidance and exposure. See a little below: “Hacking the neurology of pain: desensitization and disinhibition.”

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Treating frozen shoulder with … diet?! An interesting long shot

An anti-inflammatory diet is also known as just a healthy diet. It’s not so much that it’s "anti-inflammatory" to eat good/specific foods as it’s inflammatory to eat crap. An improvement in your diet could conceivably reduce the severity and duration of frozen shoulder. And the worst-case scenario is that you’re eating better for general health. You can’t really go too far wrong with this.

As explained above, frozen shoulder is strongly associated with metabolic syndrome, which in turn is strongly associated with poor fitness, obesity, aging, a typical modern junky diet, genetics (of course), and maybe chronic stress, anxiety, and fatigue as well.156 One of the main biological consequences of metabolic syndrome is a lot of subtle inflammation, which can lead to all kinds of trouble in time, especially cardiovascular disease … and even frozen shoulders. An “anti-inflammatory” diet is not magic: it’s just eating to minimize metabolic syndrome and its consequences, the kind of diet that practically everyone everywhere should be eating anyway.

There is no evidence at all — zip, zero, zilch — that eating this way will specifically help a condition like frozen shoulder. By the time your shoulder is freezing, it might be much too late for your diet to make any difference. Or maybe it’s not! Maybe this is one of the reasons why some people take much longer to recover than others. No one knows, but all of this is very reasonable speculation, and it’s well worth trying, for obvious reasons: it’s good for you otherwise, even if it has no effect on frozen shoulder.

There’s a more extreme dietary option to consider …

Treating frozen shoulder with a ketogenic diet (low carb and/or fasting)

Diets that force you to mainly burn fat for energy, instead of carbohydrates — a ketogenic diet , like the infamous Atkins diet — have some well-established benefits and might be anti-inflammatory and de-sensitizing.157

The most popular way to induce some ketogenesis is with some intermittent fasting — also known as “skipping some meals.” This practice has achieved Hype Factor 10 as of early 2020 and with the publication of a widely cited New England Journal of Medicine paper that’s quite enthusiastic about it.158 The “growing body of evidence” has been exaggerated by everyone (surprise surprise), and fasting has not yet been shown to be “anti-inflammatory” per se. There is quite literally only one good modern study showing clear evidence of an anti-inflammatory effect in humans.159 That’s the bad news.

Nevertheless, an anti-inflammatory effect of fasting is plausible, based on lots of indirect evidence (e.g. animal and cellular research and some evidence that fasting improves autoimmune diseases). It’s also just a reasonable diet. As long as you don’t get too extreme, the worst-case scenario is getting pretty hangry (angry from hunger). And it’s probably perfectly good as a weight-loss diet if nothing else. You’ll even save time and money, making it a great rarity in rehab — even the most harmless treatment experiments usually take some money/time.

I can’t truly recommend something so obviously unproven… but I’d do it myself. Please run it by your physician and/or a nutritionist. And let’s just be super clear that it’s a completely experimental treatment and its benefits are being widely overhyped right now.

I have a separate article that explores some other possible strategies for reducing systemic inflammation. To the extent that any of them work at all (quite unknown), they would likely support recovery from frozen shoulder, especially (or perhaps exclusively) in the first and most inflammatory phase.

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Hacking the neurology of pain: desensitization and disinhibition

As discussed above, a functional freezing of the shoulder may be driven by neurological sensitization and subsequent inhibition. The brain thinks it’s dangerous to move, whether it actually is or not. It expresses its concern by making the shoulder hurt to discourage movement, or just outright refusing to allow movement. If this idea is any good, it implies that treatment should try to desensitize and disinhibit. How exactly is that done?

There’s a Nobel prize for anyone with a good answer to that.

But there’s good news: not only are there lots of reasonable approaches to this, but we’ve already been going over them in most of the sections above. The chapter about reducing general vulnerabity to pain chronicity was essentially all about taming sensitization, although we’re going to get more specific here.

Most of the other treatment options covered so far involve building up confidence that you can, in fact, still use your shoulder, which I sometimes optimistically call the “confidence cure” in conditions where it’s even more important (back pain is a big one). Anything that is soothing and encouraging, like making a little bit of progress with exercise, is a step towards convincing your brain that your shoulder is okay.

It’s okay, brain. Shoulder okay. See? I just moved it more than yesterday, and nothing terrible happened!

Brains are stubborn, unfortunately. Being soothed and reassured is rarely enough in and of itself. “Brain hacks” are not exactly well-known for curing any kind of chronic pain, let alone notoriously stubborn problems like frozen shoulder. But it is worth trying.

Avoidance and exposure

The basic template for all rehab is to “calm shit down” and then “build shit up,”160 also known as avoidance and exposure therapy. That is, first you rest, soothe, comfort, reassure, protect …

And then you gradually introduce easy, artificial challenges, and then more difficult functional ones, slowly “demonstrating” to your brain that it really is okay to use your shoulder. Ideally, you do this when it is as safe and comfortable as possible, during therapeutic windows of opportunity (created mainly by pain relief).

This recalibration process is complex, slow, and uncertain — there are lots of ways it can get derailed — but the principle is sound. It should always be in your mind in any kind of rehab.

For more detailed discussions of sensitization and what to do about it, see:

  • Sensitization in Chronic Pain — Pain itself can change how pain works, resulting in more pain with less provocation
  • Pain is Weird — Pain science reveals a volatile, misleading sensation that comes entirely from an overprotective brain, not our tissues
  • Vulnerability to Chronic Pain — Chronic pain often has more to do with general biological vulnerabilities than specific tissue problems

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Danger! Forcing the issue manually is one of the worst ideas in frozen shoulder treatment

Warning! Please do not allow a health care professional to attempt to forcefully increase your range of motion! This could cause extreme pain from the rupture of adhesions (which would probably quickly get sticky again anyway). If contracture is more prominent than adhesions (likely), then some other structure will tear before the capsule is affected. It’s also possible that muscle guarding of the joint could be impossible to overcome, and again the result could be traumatic failure rather than “release.”

There is no proven benefit to this therapeutic approach, and substantial risk.

Doing the same thing under anaesthesia, although hardly safe, is much more promising …

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Forcing the issue with manipulation under anesthesia (MUA)

The shoulder can be paralyzed by injecting anaesthetic into a thick web of nerves emerging from neck (brachial plexus), which greatly reduces muscular tone (but probably doesn’t actually eliminate it161). Other nerve blocks are also a possibility, but the brachial plexus is the most common target. A doctor can then apply force much more directly and precisely to the adhesions in the joint capsule, without fighting through as much muscular resistance.

Unfortunately, this is only an option for desperate patients, because there are substantial risks to this procedure.162 Some people go straight from the freezer to the frying pan of a serious manipulation injury or — ironically — permanent hypermobility with recurrent disclocations. There’s also a substantial rehab process after the surgery — things are a bit wonky afterwards, even if it goes well, and it takes time. (And it’s not an option at all for patients with past dislocations, fractures, or bone loss.)

Does it work? If only we knew! This is a pseudo-surgery, and like many surgeries,163 it is understudied and based more on seeming to make sense than any hard evidence. There are a few mediocre scientific tests, but there’s just not enough good quality data yet. It’s important to bear in mind that many orthopedic surgeries have been proven ineffective, even though they too seemed liked good ideas.164 This includes other shoulder surgeries that seem like no-brainers, like decompression for impingement — more or less completely shot down by a 2017 trial.165

So any untested surgery for frozen shoulder might actually work … or it might not. It’s just a gamble.

Photo of a scalpel on a uniform blue background. The word “hope” is engraved on the blade.

Colin’s cautionary tale: MUA that backfired

In the late 2000s, Colin injured his shoulder while weightlifting, a small labrum tear. The labrum is a kind of “gasket,” a rubbery ring of cartilage around the rim of the socket of the shoulder joint.

The tear was surgically repaired by a famous surgeon (not the MUA yet, just repairing the tear). This surgeon was a pioneer in his field, a high status doctor who worked for a major sports team and patched up celebrity athletes. He was easy to trust.

After the first couple weeks of post-surgical physical therapy, Colin’s shoulder started aching more than expected. It may have been an inflammatory response to the specific physical therapy exercises or the trauma of the surgery, or maybe just a little bacterial contamination of the joint (see “Surgery and vaccination as causes of shoulder joint infection”). Nobody was sure.

While collectively brainstorming, Colin mentioned that he had a minor bleeding disorder. The surgeon took that as a signal, and called a halt to the rehab effort, even though it had only just started. Colin asked about the possibility of his shoulder freezing due to incomplete physical therapy, having only regained a small portion of his range of motion. The surgeon thought it was unlikely. But then, over the next few weeks, Colin’s shoulder definitely froze.

After a second attempt at physical therapy for frozen shoulder, the surgeon recommended a second surgery, a manipulation under anaesthesia, to “release” the frozen shoulder. There were some reasons to doubt the wisdom of this, but famous surgeons are persuasive, and Colin was desperate and he agreed to it.

The point of manipulation under anaesthesia is to forcefully break the allegedly sticky layers of joint capsule. If that’s not actually the problem — for instance, if the joint capsule is “shrunk, not stuck,” contractured and not adhered — then something else is going to tear. The weakest link in the chain.

Which, in Colin’s case, was probably his injured labrum.

He woke up much worse off. Of course you expect to be worse at first after MUA, but this was a major, lasting exacerbation. His shoulder was more frozen than ever: what little ROM he’d had was gone, and his pain was way up. Months later, an MRI revealed that his labrum tear, originally just 20˚, had expanded to a 340˚ — that is, almost the entire ring of cartilage around the socket had come free from the joint.

In the aftermath of the surgery, genetic testing suggested Ehlers–Danlos syndrome, a disease of fragile connective tissue and hypermobility. EDS is strongly linked to chronic pain, and not just because it makes patients prone to tears and dislocation injuries — even patients without a frank injury often suffer from chronic widespread pain.

Forceful manipulation of an EDS patient’s joints is a Very Bad Idea. Nobody knew about the EDS at the time, but the hypermobility disorders aren’t rare and there were clues that any competent surgeon should have been watching for. Famous surgeons are easy to trust, but the other edge on that sword is that they are often also old-school and set in their ways. Incompetence probably was a factor, but impossible to prove.

Rehab was extremely slow and complicated for Colin. His surgical misdaventure became the seed of a larger struggle with chronic pain. There was no happy ending. A decade later, he has finally improved some — but, he says, the health and fitness he enjoyed before that original shoulder injury is probably gone forever.

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Forcing the issue with MUA lite, the Oolo-Austin Trigenics® Procedure (OAT)

This is a branded treatment method named after founder Dr. Austin Oolo (formerly Dr. Oolo-Austin), a chiropractor and osteopath. He has a few clinics around the world. Since the rise of the popularity of this article, I have gotten more inquiries about Trigenics and OAT than any other single treatment. For (obvious) legal reasons,166 I will offer no direct opinion on the value of the technique; I will highlight some features of the treatment method, as presented on FrozenShoulderClinic.com, the Trigenics website, and let readers judge for themselves as best they can.

The conventional treatment most similar to OAT is manipulation under aneasthesia (MUA, discussed above), but OAT is done with local anaesthetic instead of anaesthesia, which has alleged advantages. It is also “interactive” and during the procedure “the patient is actually contracting specific muscles heavily.” Although the shoulder is “now frequently anesthetized” during OAT, “patients do still experience some pain briefly.” Apparently so, because OAT also may involve injection of corticosteroids to “prevent post-procedural inflammation,” and “risks such as fractures or dislocations could exist.”

Dramatic results are claimed by the seller. It is “revolutionary” and “ensures a fast return to functional ability for frozen shoulder sufferers.” And, “Other than the OAT Procedure, there is NO treatment which can boast of a cure in only one visit.” Those are bold claims.

No independent studies of OAT have been conducted to verify these claims. A section of the website is devoted to testimonials, but only a single scientific citation is presented as of 2018,167 for a 2012 study conducted by Dr. Allan Oolo-Austin himself, based on patient data collected in his own clinic, and allegedly published in the suspiciously mysterious “Russian Journal of Manual Therapy.”168 Predictably, the study claims to show “a 98% restoration of arm raise ability (abduction) within 2 days.” The risk of bias in such a study is, of course, as high as it gets. As the authors themselves note, “it is recommended that further studies be conducted.” Understatement.

What are the odds that the “secret sauce” of contractions makes all the difference from MUA? What are the odds that this chiropractor is succeeding where everyone else is failing? I’m just asking questions here.

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Forcing the issue surgically with arthroscopic capsular release and inflation

Another way to force the issue, and likely safer than manipulation under anaesthesia, is arthroscopic or “keyhole” surgery. The goal is exactly the same, but the method is much less brutish: instead of tactical wrenching of the joint until the adhesions tear, a surgeon goes in with a tiny camera through a tiny incision and cuts things free.

Although we don’t have good data on whether manipulation or cutting actually work, we do know that each one is roughly as good as the other.169 All other things being equal, I’d prefer not to get wrenched around.

Joint capsule inflation: arthrographic distension, hydrodilatation injections

When you blow up a balloon, it is often stuck to itself, and slightly adhered layers of rubber peel away from each other as you force them apart with air pressure. The same principle is used in hydrodilatation injections, only the ballon is the shoulder joint capsule, and it’s inflated with saline solution (maybe with some steroids as well, to help with the inevitable spike in inflammation). Like blowing up a ballon, the pressure is supposed to inflate the capsule.

In no other way is the shoulder joint capsule like a balloon, and simplistic analogies like this are often misleading in medicine. Adam Meakins calls distension “highly dubious.” It has barely been tested, but the conclusion of a 2008 scientific review of just five studies makes it sound almost promising:170

There is "silver" level evidence that arthrographic distension with saline and steroid provides short-term benefits in pain, range of movement and function in adhesive capsulitis. It is uncertain whether this is better than alternative interventions.

Still, “uncertain” is an understatement there!

Fortunately, there is some more encouraging evidence from a 2013 trial, only the second one ever to produce long term results (and it also included diabetic patients).171 And still more in 2017! Sinha et al. also concluded that it worked, based on over a hundred patients (although the size of the benefit was not very impressive).172

This is all far from proof, but it’s better than nothing.

Despite that evidence, this procedure is based mostly on “common sense” of the doctorly sort: it seems like a good idea. Maybe it helps and maybe it doesn’t. As with arthroscopic release, I’d certainly try this before manipulation under anaesthesia, for the safety. But I certainly wouldn’t bet on the outcome. Remember that there’s no way this treatment method can work (in principle) if the joint is actually contractured rather than adhered (see above, “Adhesive” may be the wrong word: shrunk, not stuck).

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Part 4.23

Appendices

Related Reading

A Painful Biological Glitch that Causes Pointless Inflammation — The inflammation of frozen shoulder is exasperatingly mysterious. This article explains how inflammation can be “glitchy” — an interesting perspective that might help make sense of frozen shoulder.

Muscle Pain as an Injury Complication — The story of a difficult shoulder rehab. Although not a case of adhesive capsulitis, there’s lots of relevant detail about how any shoulder pain can get stubborn.

Guide to Repetitive Strain Injuries — Frozen shoulder isn’t an overuse injury, but it is often mistaken for one, and most of the RSIs are just as odd and surprising as frozen shoulder is, in their own ways. This article explores five surprising and important facts about conditions like carpal tunnel syndrome, tendinitis, or iliotibial band.

Dupuytren’s Contracture — Frozen shoulder is probably in the same pathological family as this common hand condition that slowly causes the hand to flex into a claw. The palm “shrinks” much like the shoulder joint capsule.

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What’s new in the frozen shoulder book?

Regular updates are a key feature of PainScience.com tutorials. As new science and information becomes available, I upgrade them, and the most recent version is always automatically available to customers. Unlike regular books, and even e-books (which can be obsolete by the time they are published, and can go years between editions) this document is updated at least once every three months and often much more. I also log updates, making it easy for readers to see what’s changed. This tutorial has gotten 100 major and minor updates since I started logging carefully in late 2009 (plus countless minor tweaks and touch-ups).

2022 — Minor addition: Added a small sub-section to recommend the “pendulum” exercise. Simple but nice. [Updated section: Use it or lose it: movement therapy.]

2022 — Science update: Added a minor but neat point about how much joint fluid volume is lost in frozen shoulder. [Updated section: Shrunk, not stuck: a 150-year history of misleading names for frozen shoulder.]

2021 — New chapter: A substantive new chapter about the possible role of the mind and muscle guarding in frozen shoulder. [Updated section: Can the mind freeze shoulders? Or unfreeze them?]

2021 — Proofreading: It was time for an annual book tune-up: a few dozen minor errors have been corrected.

2021 — Science update: Small but fascinating science update about Ascani et al, exploring a possible link between frozen shoulder and COVID. [Updated section: Or it could be an infection? Surgery and vaccination as causes of shoulder joint infection.]

2021 — Minor polishing: A little editorial polish, and a bit of elaboration about the role of psychotropic effects. [Updated section: The cannabinoids: marijuana and hemp, THC and CBD — “it’s complicated!”.]

2020 — Science update: Minor citation to Ainsworth on ultrasound for shoulder pain (negative, of course). [Updated section: Maybe sound waves will help? Ultrasound.]

2020 — Major expansion: Upgraded from a brief dismissal of the topic to a full discussion, from 100 words to 1000. [Updated section: Posture: is frozen shoulder the tip of a misalignment iceberg?]

2020 — Minor upgrade: Added some additional discussion of the implications of Tanya’s story. [Updated section: Case study: an interesting example of a biological X-factor.]

2020 — Major upgrade: Much more thorough exploration of the plausibility and evidence for exploiting the “WOO” that is probably created by steroid injections. [Updated section: Steroids, injected and swallowed.]

2020 — Upgrade: Added quite a bit of additional detail. [Updated section: Whole lotta shakin’ going on: vibration therapy.]

2020 — Minor addition: Expanded on the summary of symptoms just a little, emphasizing the quality and potential severity of the pain. [Updated section: Introduction.]

2020 — Upgraded: Added more information based on a very helpful video that shows “fake” shoulder ROM achieved entirely with good shoulder girdle motion, while the shoulder joint proper remains completely stuck. [Updated section: Diagnosis of Frozen Shoulder: Confirming the diagnosis: classic frozen shoulder symptoms.]

2020 — Editing and more content: Added subsection about passive ROM testing, and did some miscellaneous polishing. [Updated section: Confirm the contribution of functional freezing and sensitization (maybe).]

2020 — Expanded: Added a bunch more specific information about how to recognize sensitization. [Updated section: Confirm the contribution of functional freezing and sensitization (maybe).]

2020 — New chapter: A new chapter about the role of sensitization in frozen shoulder. [Updated section: Sensitization: the foundation of functional freezing.]

2020 — Added detail: Added a good story about my mother-in-law’s broken arm, which nicely illustrates a neurologically mediated ROM lockdown. [Updated section: How does “functional freezing” cause frozen shoulder?]

2020 — New chapter: No notes. Just a new chapter. [Updated section: Opioids too dangerous & ineffective for most cases, but maybe a good idea for a few.]

2020 — Improvements: Added some significant improvements while reviewing a couple weeks after first publishing the chapter, most notably a good summary of recent icing controversies. [Updated section: Cooling and heating for frozen shoulder.]

2020 — Updated: Added some basic information about intermittent fasting. [Updated section: Treating frozen shoulder with … diet?! An interesting long shot.]

Archived updates — All updates, including 82 older updates, are listed on another page.

2016 — Publication.

GO TO TOPCONTENTSNOTES

Acknowledgements

Thanks to every reader, client, and book customer for your curiosity, your faith, and your feedback and suggestions, and your stories most of all — without you, all of this would be impossible and pointless.

Writers go on and on about how grateful they are for the support they had while writing one measly book, but this website is actually a much bigger project than a book. PainScience.com was originally created in my so-called “spare time” with a lot of assistance from family and friends (see the origin story). Thanks to my wife for countless indulgences large and small; to my parents for (possibly blind) faith in me, and much copyediting; and to friends and technical mentors Mike, Dirk, Aaron, and Erin for endless useful chats, repeatedly saving my ass, plus actually building many of the nifty features of this website.

Special thanks to some professionals and experts who have been particularly inspiring and/or directly supportive: Dr. Rob Tarzwell, Dr. Steven Novella, Dr. David Gorski, Sam Homola, DC, Dr. Mark Crislip, Scott Gavura, Dr. Harriet Hall, Dr. Stephen Barrett, Dr. Greg Lehman, Dr. Jason Silvernail, Todd Hargrove, Nick Ng, Alice Sanvito, Dr. Chris Moyer, Lars Avemarie, PT, Dr. Brian James, Bodhi Haraldsson, Diane Jacobs, Adam Meakins, Sol Orwell, Laura Allen, James Fell, Dr. Ravensara Travillian, Dr. Neil O’Connell, Dr. Tony Ingram, Dr. Jim Eubanks, Kira Stoops, Dr. Bronnie Thompson, Dr. James Coyne, Alex Hutchinson, Dr. David Colquhoun, Bas Asselbergs … and almost certainly a dozen more I am embarrassed to have neglected.

I work “alone,” but not really, thanks to all these people.

I have some relationship with everyone named above, but there are also many experts who have influenced me that I am not privileged to know personally. Some of the most notable are: Drs. Lorimer Moseley, David Butler, Gordon Waddell, Robert Sapolsky, Brad Schoenfeld, Edzard Ernst, Jan Dommerholt, Simon Singh, Ben Goldacre, Atul Gawande, and Nikolai Boguduk.

GO TO TOPCONTENTSNOTES

Notes

  1. Other joints do freeze like the shoulder, but much less often. For instance, there is such a thing as a frozen hip (see de Sa et al), but it’s so rare and hard to diagnose that we don’t even know how rare it really is. (Byrd et al argues that it’s “more common than suggested in the published literature,” but still much rarer than frozen shoulder.) Some other joints in the body can probably freeze to some extent as well — frozen ankle! frozen wrist! — but the shoulder is by far the most prone to it.

    There’s also an interesting connection to Dupuytren’s contracture — “frozen hand” disease — which is fairly common and may be more similar than it seems. More on that below.

  2. Weirdly, musculoskeletal pain is a bit of a backwater, simply because medicine has had much bigger fish to fry, like trying to cure major infectious diseases and so on (see A Historical Perspective On Aches ‘n’ Pains). Medical training is certainly better than the competition, but family doctors lack the skills and knowledge to treat most chronic pain and injury problems, especially the tricky, stubborn ones (see The Medical Blind Spot for Aches, Pains & Injuries). Even sports medicine is only beginning to really get going properly, despite the serious money involved in elite athletics (see Grant et al).
  3. Wong CK, Levine WN, Deo K, et al. Natural history of frozen shoulder: fact or fiction? A systematic review. Physiotherapy. 2017 Mar;103(1):40–47. PubMed 27641499 ❐

    Evidence from seven reviewed studies suggests that frozen shoulder does not resolve on its own without treatment, contrary to the entrenched conventional wisdom (which isn’t supported by any evidence). On the contrary, what the evidence supports is that frozen shoulder prognosis is highly unpredictable, and may resolve much sooner than average… or not at all.

  4. Eljabu W, Klinger HM, von Knoch M. Prognostic factors and therapeutic options for treatment of frozen shoulder: a systematic review. Arch Orthop Trauma Surg. 2016 Jan;136(1):1–7. PubMed 26476720 ❐ “Spontaneous recovery to normal levels of function is possible.”
  5. Clement et al paints quite a grim prognosis, with as many as 40% experiencing “persistent symptoms and restricted movement beyond 3 years,” and a troubling 15% left with “permanent disability.” Fortunately, that’s probably a bit alarmist, and those numbers are supported by citations to only two small old studies. Much more recently, Hand et al looked at many more cases (223) after about 4 years on average. Although they confirmed that 40% still had symptoms, almost all of them were mild (94%), and “only 6% had severe symptoms with pain and functional loss.”
  6. Hand C, Clipsham K, Rees JL, Carr AJ. Long-term outcome of frozen shoulder. J Shoulder Elbow Surg. 2008;17(2):231–6. PubMed 17993282 ❐ About 15-20% of patients develop the disease in both shoulders.
  7. Bunker T. Time for a new name for frozen shoulder—contracture of the shoulder. Shoulder & Elbow. 2009;1(1):4–9. PainSci Bibliography 52392 ❐

    Bunker believes that capsular contracture only accounts for 5% of all shoulder disease, “and since shoulder disease only affects 15% of the population, then it would be reasonable to suggest that the real incidence of capsular contracture is about 0.75% of the population.”

    I will be referencing Bunker’s papers again and again in this tutorial.

  8. Danaei G, Finucane MM, Lu Y, et al. National, regional, and global trends in fasting plasma glucose and diabetes prevalence since 1980: systematic analysis of health examination surveys and epidemiological studies with 370 country-years and 2·7 million participants. Lancet. 2011 Jul;378(9785):31–40. PubMed 21705069 ❐

    Almost 10 percent of all adults globally have diabetes and that number is rising fast. Increased obesity and inactivity are the primary causes. Danaei et al predict an enormous burden of disability and medical costs if the trend continues.

  9. The rotator cuff interval (space) is a wedge of complex anatomy roughly between the top of the humerus and the clavicle, filled with part of the shoulder joint capsule and some tendons and ligaments. Its “roof” is the coracohumeral ligament, a major structural ligament that the arm hangs from. It contains the subscapular recess, an outpouching of the glenohumeral joint capsule, basically sticking right into the rotator cuff interval. Other notable inhabitants of the interval: the long head of the biceps tendon, and the superior glenohumeral ligament. See Petchprapa et al [free full text] for extreme detail on all of this.
  10. Omari A, Bunker TD. Open surgical release for frozen shoulder: surgical findings and results of the release. J Shoulder Elbow Surg. 2001;10(4):353–7. PubMed 11517365 ❐ In this study, the authors treated 75 shoulders over a five-year period. Nine improved without surgery. Of the remainder, 66 improved with manipulation under anaesthesia, but 25 did not and “open surgical release” was attempted with those patients: cutting the shoulder free, basically. And those patients “showed a consistent alteration in the rotator interval and coracohumeral ligament. The rotator interval was obliterated, and the coracohumeral ligament was transformed into a tough contracted band.”
  11. Pietrzak M. Adhesive capsulitis: An age related symptom of metabolic syndrome and chronic low-grade inflammation? Med Hypotheses. 2016 Mar;88:12–7. PubMed 26880627 ❐
  12. Neviaser AS, Hannafin JA. Adhesive capsulitis: a review of current treatment. Am J Sports Med. 2010 Nov;38(11):2346–56. PubMed 20110457 ❐
  13. Kraal T, Lübbers J, van den Bekerom MPJ, et al. The puzzling pathophysiology of frozen shoulders - a scoping review. J Exp Orthop. 2020 Nov;7(1):91. PubMed 33205235 ❐ PainSci Bibliography 51813 ❐ “A state of low grade inflammation, as is associated with diabetes, cardiovascular disease and thyroid disorders, predisposes for the development of frozen shoulder.”
  14. Huang SW, Lin JW, Wang WT, et al. Hyperthyroidism is a risk factor for developing adhesive capsulitis of the shoulder: a nationwide longitudinal population-based study. Sci Rep. 2014;4:4183. PubMed 24567049 ❐ PainSci Bibliography 53252 ❐ “The results of our large-scale longitudinal population-based study indicated that hyperthyroidism is an independent risk factor of developing adhesive capsulitis.”
  15. Fosbøl EL, Rørth R, Leicht BP, et al. Association of Carpal Tunnel Syndrome With Amyloidosis, Heart~Failure, and Adverse Cardiovascular Outcomes. Journal of the American College of Cardiology. 2019;74(1):15––23. PainSci Bibliography 52255 ❐

    This study is focused on an increased risk of heart failure in carpal tunnel syndrome patients, but, as a musculoskeletal medicine guy, I am more interested in the reverse implication: that CTS is probably partially or entirely triggered by some underlying biology that makes things harder for hearts.

  16. Bishop JY, Santiago-Torres JE, Rimmke N, Flanigan DC. Smoking Predisposes to Rotator Cuff Pathology and Shoulder Dysfunction: A Systematic Review. Arthroscopy. 2015 Aug;31(8):1598–605. PubMed 25801046 ❐
  17. Ingraham. Smoking and Chronic Pain: We often underestimate the power of (tobacco) smoking to make things hurt more and longer.  ❐ PainScience.com. 1417 words.
  18. Smith SP, Devaraj VS, Bunker TD. The association between frozen shoulder and Dupuytren's disease. J Shoulder Elbow Surg. 2001;10(2):149–51. PubMed 11307078 ❐
  19. Bunker 2009, op. cit.
  20. Helicobacter pylori was famously hunted down in 1983 by Australian scientists Barry Marshall and Robin Warren. Although its link with ulceration was initially met with much skepticism, science came around relatively quickly — convinced by evidence, just like it’s supposed to work. By the mid-90s it was widely accepted that H. pylori infection causes ulcers, and Marshall and Warren got a Nobel prize in 2005 (acceptance speech).
  21. A much, much fresher example than the H. Pylori story is the idea that the infamous “plaques” of Alzheimer’s disease are, in fact, a form of immune reaction to an invader — “nets” of sticky protein tendrils intended to stop an infection, but which also cause collateral damage. Really amazing science. See: Have researchers been wrong about Alzheimer’s? A new theory challenges the old story.
  22. Khan U, Torrance E, Townsend R, et al. Low-grade infections in nonarthroplasty shoulder surgery. J Shoulder Elbow Surg. 2017 Sep;26(9):1553–1561. PubMed 28359693 ❐
  23. This explanation from Arthritis Micropia:

    Propionibacterium acnes is a skin bacterium which grows well in an anaerobic (low oxygen) environment. The species populates skin pores and hair follicles and feeds on sebaceous matter. This is a fatty substance produced in glands to keep the skin waterproof. P. acnes is a benign skin bacterium which can help the skin by stopping harmful bacteria getting into the pores.

    It was long thought that P. acnes caused spots. This was because the number of P. acnes bacteria increases enormously during puberty, together with the number of spots. Recent research has shown, however, that P. acnes actually helps in the fight against spots. Harmful bacteria cannot get a foothold because the pores and hair follicles are already occupied.

    However, other sources contradict this (such as Knobler et al), or, this review much more recently, which explains: “Over the last 10 years our understanding of the taxonomic and intraspecies diversity of this bacterium has increased tremendously, and with it the realisation that particular strains are associated with skin health while others appear related to disease.”
  24. The Infectious Etiology of Chronic Diseases: Defining the Relationship, Enhancing the Research, and Mitigating the Effects. National Academies Press (US); 2004.

    One of the great ironies of this organism is that it is a powerful nonspecific immune stimulant that resides naturally in the skin; its role as an immunostimulant in humans is appreciated when cases of severe acne also develop adjuvant-type arthritis.

    Some investigators have gone so far as to suggest that severe acne, by virtue of the nonspecific immunostimulatory effects of P. acnes, might have played a role in natural protection against life-threatening diseases such as malaria and plague. In contrast, the acquired immune response to P. acnes has received little attention in humans.

  25. Horneff 3, Hsu JE, Voleti PB, O’Donnell J, Huffman GR. Propionibacterium acnes infection in shoulder arthroscopy patients with postoperative pain. J Shoulder Elbow Surg. 2015 Jun;24(6):838–43. PubMed 25979553 ❐
  26. This is about needles and not what’s in them. The last thing the world needs now is more demonization of vaccinations. So let’s not call it SIRVA! It’s a bullshit term, because it has nothing to do with “vaccination” per se. It should be “shoulder injury related to injection” — SIRI! 😜
  27. Bancsi A, Houle SKD, Grindrod KA. Shoulder injury related to vaccine administration and other injection site events. Can Fam Physician. 2019 Jan;65(1):40–42. PubMed 30674513 ❐ PainSci Bibliography 52264 ❐
  28. www.wired.com [Internet]. Zhang S. Why Are Cases of Shoulder Injuries From Vaccines Increasing?; 2019 May 21 [cited 19 Aug 7]. PainSci Bibliography 52265 ❐
  29. Saleh ZM, Faruqui S, Foad A. Onset of Frozen Shoulder Following Pneumococcal and Influenza Vaccinations. J Chiropr Med. 2015 Dec;14(4):285–9. PubMed 26793041 ❐ PainSci Bibliography 52474 ❐ “Although vaccines are of tremendous importance in the prevention of serious illness, we emphasize the importance of administering them at the appropriate depth and location for each patient.” Indeed.
  30. Mishra P, Stringer MD. Sciatic nerve injury from intramuscular injection: a persistent and global problem. Int J Clin Pract. 2010 Oct;64(11):1573–1579. PubMed 20670272 ❐

    “Sciatic nerve injury from an intramuscular injection in the upper outer quadrant of the buttock is an avoidable but persistent global problem, affecting patients in both wealthy and poorer healthcare systems. The consequences of this injury are potentially devastating. Safer alternative sites for intramuscular injection exist.”Like the shoulder!

  31. Ascani C, Passaretti D, Scacchi M, et al. Can Adhesive Capsulitis of the shoulder be a consequence of COVID-19? Case series of 12 patients. J Shoulder Elbow Surg. 2021 May. PubMed 33964424 ❐ PainSci Bibliography 52134 ❐

    The authors of this paper acknowledge that their study and data cannot prove a link between COVID and frozen shoulder, but their results were nevertheless very-where-there’s-smoke-there’s-fire. They studied a dozen cases of frozen shoulder that closely followed a COVID infection (out of 120 cases of adhesive capsulitis that came to their clinic). I’m no statistician, but that seems high.

    They also describe some strong specific reasons to suspect a pathological connection.

    Paper abstract:

    We present our series of twelve patients with Adhesive Capsulitis (AC) of the shoulder that developed shortly after COVID-19. We hypothesize that AC may be related to the infectious disease and that both direct and indirect effects of SARS-CoV-2 infection may be involved in its development, as may the sedentary lifestyle forced upon these patients by this disease. Future research will be needed to evaluate the short- and long-term natural history and treatment of these patients as well as to compare them with patients with AC did not occur in concomitance with COVID-19.

  32. Pietrzak 2016, op. cit.
  33. Stone-throwing hardly seems like a decisive reproductive advantage. And biologically modern humans were around for tens of thousands of years at least before we were using spears and slings to great effect.
  34. Littlewood C, Malliaras P, Bateman M, et al. The central nervous system--an additional consideration in 'rotator cuff tendinopathy' and a potential basis for understanding response to loaded therapeutic exercise. Man Ther. 2013 Dec;18(6):468–72. PubMed 23932100 ❐
  35. This phenomenon would have its roots in local inflammation as well as top-down modulation of movement. This inhibition might even be so basic that it’s regulated largely by spinal reflexes, no brain-imposed inhibition at all.
  36. Rice DA, McNair PJ. Quadriceps arthrogenic muscle inhibition: neural mechanisms and treatment perspectives. Semin Arthritis Rheum. 2010 Dec;40(3):250–66. PubMed 19954822 ❐
  37. LauraOpstedal.wordpress.com [Internet]. Opstedal L. WTH Happened To My Quads? Arthrogenic Muscle Inhibition Explained; 2019 March 16 [cited 22 Feb 27]. PainSci Bibliography 52376 ❐
  38. After more than two decades of writing about this stuff, I am no longer surprised to learn about weird knowledge gaps, and it seems plausible to me that AMI is well-known when it occurs in the knee only because the muscles are so huge and vital. Losing 20% of a huge muscle is more obvious than losing 50% of a tiny muscle. Would you know if you lost half of your subscapularis muscle mass? Admit it: you don’t even know how to check! Even for those of us who know how to check, it would be hard to tell, and the loss of mass would have to be dramatic for me to even suspect it. So it could certainly be happening to the rotator cuff muscles without being remotely clear. It’s less likely that the big shoulder movers — biceps, deltoid, triceps — would atrophy without being noticed, but they do not need to be the muscles that are inhibited.
  39. Bunker 2009, op. cit. “Contemporary arthroscopic studies have shown that only 50% of patients diagnosed as having frozen shoulder actually had visual/tactile evidence of the disease.” Bunker doesn’t cite specific independent sources on this, but he has extensive direct experience and is obviously extremely familiar with the literature. I’m happy to take his word for it.
  40. Many professionals therapists use it as a basis for presumptive treatment — treating as if a diagnosis is true, to see what happens. Massage therapists in particular are fond of this theory, because it would make their skills much more relevant to the condition. 😃 And they want to help, of course!
  41. See the appendix at the end of the article, about my wife’s experience with frozen shoulder. Basically, it magically went away when she was seriously injured in a car accident, and then returned when she healed from the worst of her injuries. That does not seem like the natural history of adhesive capsulitis! Of course, the diagnosis could have been wrong in the first place — although it appeared to be a textbook case, misdiagnosis is always a possibility. It’s also possible the accident could have ripped the adhesions apart: a traumatic manipulation without the anesthesia. But this also seems unlikely to me, as it probably requires precise force to break adhesions without also breaking other things — and her shoulder was otherwise uninjured.
  42. Hollmann L, Halaki M, Haber M, et al. Determining the contribution of active stiffness to reduced range of motion in frozen shoulder. Physiotherapy. 2015 2018/06/19;101:e585. PainSci Bibliography 53197 ❐
  43. Ingraham. Trigger Points on Trial: A summary of the kerfuffle over Quintner et al., a key 2014 scientific paper criticizing the conventional wisdom about trigger points and myofascial pain syndrome.  ❐ PainScience.com. 5633 words.
  44. Duplay, S. De la peri-arthrite scapulo-humerale et ces raideurs de l’epaule qui en sont la consequence. Arch Gen Med. 1872;20:513.
  45. Codman, E. The shoulder. Boston: Todd. 1934.
  46. Neviaser J. Adhesive capsulitis of the shoulder: a study of the pathological findings in periarthritis of the shoulder. J Bone Joint Surg. 1945; 27:211–22.
  47. Nagy MT, Macfarlane RJ, Khan Y, Waseem M. The frozen shoulder: myths and realities. Open Orthop J. 2013;7:352–5. PubMed 24082974 ❐ PainSci Bibliography 53682 ❐ Nagy MT, Macfarlane RJ, Khan Y, Waseem M. The frozen shoulder: myths and realities. Open Orthop J. 2013;7:352–5. PubMed 24082974 ❐ PainSci Bibliography 53682 ❐

    Neviasier, in 1945, described “adhesive capsulitis” using the term “adhesive” to describe the texture and integrity of the inflamed capsule, which he thought was similar to sticking plaster. The term is also inaccurate, as this condition is not associated with adhesions of the capsule, but rather is related to synovitis and progressive contracture of the capsule.

  48. Luke TA, Rovner AD, Karas SG, Hawkins RJ, Plancher KD. Volumetric change in the shoulder capsule after open inferior capsular shift versus arthroscopic thermal capsular shrinkage: a cadaveric model. J Shoulder Elbow Surg. 2004;13(2):146–9. PubMed 14997089 ❐
  49. Binder AI, Bulgen DY, Hazleman BL, Tudor J, Wraight P. Frozen shoulder: an arthrographic and radionuclear scan assessment. Ann Rheum Dis. 1984 Jun;43(3):365–9. PubMed 6742897 ❐ PainSci Bibliography 52089 ❐
  50. Ozaki J, Nakagawa Y, Sakurai G, Tamai S. Recalcitrant chronic adhesive capsulitis of the shoulder. Role of contracture of the coracohumeral ligament and rotator interval in pathogenesis and treatment. J Bone Joint Surg Am. 1989 Dec;71(10):1511–5. PubMed 2592391 ❐ “The contracture of the coracohumeral ligament and rotator interval appears to be the main lesion in chronic adhesive capsulitis.”
  51. Bunker TD, Anthony PP. The pathology of frozen shoulder. A Dupuytren-like disease. J Bone Joint Surg Br. 1995 Sep;77(5):677–83. PubMed 7559688 ❐ “Our histological and immunocytochemical findings show that the pathological process is active fibroblastic proliferation, accompanied by some transformation to a smooth muscle phenotype (myofibroblasts). The fibroblasts lay down collagen which appears as a thick nodular band or fleshy mass. … The contracture acts as a check-rein against external rotation, causing loss of both active and passive movement.”
  52. Bunker 2009, op. cit.
  53. One reader with frozen shoulder reported that her physical therapist told her that her “whole body has been out of alignment and it is showing up in the shoulder.” Bullshit! This is a common but awful idea. It has no basis in reality, and therapy based on it is unethical. Any professional using this kind of explanation to justify treatment should be fired immediately. It’s a classic example of structuralism, the tendency to attribute common painful problems to structure (biomechanics, alignment, and especially posture). Structuralism is prevalent because it sells: it’s an emotionally appealing problem that seems fixable, and freelance therapists can sell the solution to it.
  54. Barrett E, O’Keeffe M, O’Sullivan K, Lewis J, McCreesh K. Is thoracic spine posture associated with shoulder pain, range of motion and function? A systematic review. Man Ther. 2016 Dec;26:38–46. PubMed 27475532 ❐

    This is a review of ten scientific studies of the relationship between shoulder pain and thoracic spine posture, specifically kyphosis, the slouched or “hunchback” upper back curvature widely assumed to be source of pain. Six of the studies were deemed to have a medium to high risk of bias. Collectively they show “moderate” evidence of no relationship: that is, there’s “no significant difference in thoracic kyphosis between groups with and without shoulder pain.” One study contradicted the others, identifying more kyphosis in people with shoulder pain — but it was the study with the highest risk of a bias. So this review confirms that there is some evidence-of-absence for kyphosis as a cause of shoulder pain, and almost nothing pointing the other way.

    But there is some strong evidence in these studies that shoulder movement is greater if you’re straighter: less kyphosis, more shoulder action.

  55. A more detailed definition: Pain itself often modifies the way the nervous system works, so that a patient actually becomes more sensitive and gets more pain with less provocation. This is often called “central” sensitization because it’s driven by the central nervous system, by changes in the spinal cord and brain (although there’s also peripheral sensitization). Sensitized patients are not only more sensitive to things that should hurt, but sometimes also to ordinary touch and pressure as well (allodynia). Their pain also often “echoes,” fading more slowly than in other people. Sensitization is closely associated with all the more serious chronic pain conditions.
  56. Woolf CJ. Central sensitization: Implications for the diagnosis and treatment of pain. Pain. 2010 Oct;152(2 Suppl):S2–15. PubMed 20961685 ❐ PainSci Bibliography 54851 ❐

    Pain itself often modifies the way the central nervous system works, so that a patient actually becomes more sensitive and gets more pain with less provocation. That sensitization is called “central sensitization” because it involves changes in the central nervous system (CNS) in particular — the brain and the spinal cord. Victims are not only more sensitive to things that should hurt, but also to ordinary touch and pressure as well. Their pain also “echoes,” fading more slowly than in other people.

    For a much more detailed summary of this paper, see Sensitization in Chronic Pain.

  57. “Modern pain science” refers to the abandoment of the idea that pain is a relatively simple response to tissue damage. Instead, it’s an unpredictable top-down alarm system that responds to tissue conditions and many other variables, and has as much power to “mute” pain as it does to produce it. See Pain is Weird.
  58. Struyf F, Meeus M. Current evidence on physical therapy in patients with adhesive capsulitis: what are we missing? Clin Rheumatol. 2014 May;33(5):593–600. PubMed 24374758 ❐

    The full quote:

    Continuously increased nociceptive impulse activity, as in early stages of AC, could lead to peripheral and subsequently long-lasting central sensitization, as well as to an increased activity of the sympathetic nervous system [44, 45]. But up to now, the involvement of central sensitization in AC has not been studied yet and remains speculative. If central sensitization is present in a subgroup of patients with AC, as it is in many other arthritic and rheumatic conditions [46], this could explain why some patients are therapy resistant and this would mean that this subgroup requires a completely different approach. The latter may partly explain why results are not univocal and therapeutic approach of these patients is that challenging.

  59. TheSportsPhysio.wordpress.com [Internet]. Meakins A. Frozen shoulder? Let it go, Let it go … .; 2016 July 27 [cited 19 Aug 7]. PainSci Bibliography 53307 ❐
  60. TheSportsPhysio.wordpress.com [Internet]. Meakins A. Frozen shoulder? Let it go, Let it go … .; 2016 July 27 [cited 19 Aug 7]. PainSci Bibliography 53307 ❐ More: “All ‘true’ frozen shoulders are extremely painful, extremely limiting, and extremely disabling. When I hear females telling me the pain in their shoulder is worse than child birth, I know I am dealing with a very, very painful condition.”
  61. Range of motion is limited to at least 25% in at least two dimensions (often more), and usually the most limited are shoulder abduction (lifting the arm away from the side) and external rotation (turning the biceps outwards). These limitations can be reliably assessed by a professional, which is noteworthy: it has been debated, and many diagnostic assessments are not reliable (see Is Diagnosis for Pain Problems Reliable?), but I think this one is fairly settled (Tveitå 2008, Hollmann 2015).
  62. Teunis T, Lubberts B, Reilly BT, Ring D. A systematic review and pooled analysis of the prevalence of rotator cuff disease with increasing age. J Shoulder Elbow Surg. 2014 Dec;23(12):1913–21. PubMed 25441568 ❐
  63. Carbone S, Gumina S, Vestri AR, Postacchini R. Coracoid pain test: a new clinical sign of shoulder adhesive capsulitis. Int Orthop. 2009 May. PubMed 19418052 ❐
  64. Homsi 2006, op. cit.
  65. Hanchard NCA, Goodchild L, Thompson J, et al. A questionnaire survey of UK physiotherapists on the diagnosis and management of contracted (frozen) shoulder. Physiotherapy. 2011 Jun;97(2):115–25. PubMed 21497245 ❐ “The value of X-rays in differential diagnosis was under-recognised.”
  66. Khan U, Torrance E, Townsend R, et al. Low-grade infections in nonarthroplasty shoulder surgery. J Shoulder Elbow Surg. 2017 Sep;26(9):1553–1561. PubMed 28359693 ❐
  67. Lee JC, Sykes C, Saifuddin A, Connell D. Adhesive capsulitis: sonographic changes in the rotator cuff interval with arthroscopic correlation. Skeletal Radiol. 2005 Sep;34(9):522–7. PubMed 15999280 ❐
  68. Homsi C, Bordalo-Rodrigues M, da Silva JJ, Stump XMG. Ultrasound in adhesive capsulitis of the shoulder: is assessment of the coracohumeral ligament a valuable diagnostic tool? Skeletal Radiol. 2006 Sep;35(9):673–8. PubMed 16724200 ❐
  69. A little proactive defence against pedantry: “Begs the question” originally referred to a logical fallacy in which an assertion tries to support itself, often just by re-phrasing it (“God exists because God is everywhere,” which “begs the question” that has not actually been answered). Pedants are often outraged by the looser modern usage, which means more what it sounds like: a question seems obvious or needful. Neglect of the old meaning for decades has tipped the scales so far towards the new meaning that resistance is futile: I side with Merriam Webster in relegating the original meaning to a formal, secondary sense of the term. The new meaning is clearer.

    “Cautionary Ghost”

    xkcd #1108 © xkcd.com by Randall Munroe

  70. Smart KM, Blake C, Staines A, Thacker M, Doody C. Mechanisms-based classifications of musculoskeletal pain: part 1 of 3: symptoms and signs of central sensitisation in patients with low back (± leg) pain. Man Ther. 2012 Aug;17(4):336–44. PubMed 22534654 ❐
  71. Wong 2017, op. cit.
  72. Clement 2013, op. cit.
  73. Jewell DV, Riddle DL, Thacker LR. Interventions associated with an increased or decreased likelihood of pain reduction and improved function in patients with adhesive capsulitis: a retrospective cohort study. Phys Ther. 2009 May;89(5):419–29. PubMed 19270045 ❐ PainSci Bibliography 55683 ❐

    An interesting study of 2,370 frozen shoulder patients who received physical therapy: rather than a controlled trial of a specific treatment, it was a statistical analysis of the relationship between common treatments and outcomes. The therapists reported the treatments they used in each case, the patients took surveys before and after, and the researchers calculated the relationship between the treatments and the results.

    Notably, literally no patients at all achieved clinically meaningful improvement by one method of measuring. So they just eliminated those measurements from their analysis, and worked with three other scoring systems that did detect some improvements.

    This study will come again as I discuss other treatments.

  74. Diercks RL, Stevens M. Gentle thawing of the frozen shoulder: a prospective study of supervised neglect versus intensive physical therapy in seventy-seven patients with frozen shoulder syndrome followed up for two years. J Shoulder Elbow Surg. 2004;13(5):499–502. PubMed 15383804 ❐
  75. In Diercks et al, intensive physical therapy treatment consisted of “passive stretching and manual mobilization,” which might have been “intensive” but it certainly wasn’t comprehensive, just a couple of rehab staples for a notoriously stubborn condition. And it was compared to “supportive therapy and exercises within the pain limits,” which I’m not sure counts as “neglect” — exercises within pain limits may actually be quite important. So if the physical therapy had been a little more interesting, and the neglect had been more total, the results might not have been so disappointing.
  76. Uppal HS, Evans JP, Smith C. Frozen shoulder: A systematic review of therapeutic options. World J Orthop. 2015 Mar;6(2):263–8. PubMed 25793166 ❐ PainSci Bibliography 53286 ❐
  77. Maund E, Craig D, Suekarran S, et al. Management of frozen shoulder: a systematic review and cost-effectiveness analysis. Health Technol Assess. 2012;16(11):1–264. PubMed 22405512 ❐ PainSci Bibliography 53309 ❐
  78. Page MJ, Green S, Kramer S, et al. Manual therapy and exercise for adhesive capsulitis (frozen shoulder). Cochrane Database Syst Rev. 2014;(8):CD011275. PubMed 25157702 ❐ “The overall impression gained from [32] trials is that the few outcome differences between interventions that were clinically important were detected only up to seven weeks.”
  79. Favejee MM, Huisstede BMA, Koes BW. Frozen shoulder: the effectiveness of conservative and surgical interventions — systematic review. Br J Sports Med. 2011 Jan;45(1):49–56. PubMed 20647296 ❐
  80. Too much discomfort means inflammation … and inflammation is what drives the stickyness of the capsule in the first place. You must strike a balance: only just enough movement to slow down the adhesions.
  81. Any evidence for that? Ha ha, not a chance! Way too minor to have been studied. But there are some well-established mechanisms that make it highly plausible that gentle movement like this can produce minor transient pain relief (e.g. counterstimulation). The claim is modest, the stakes are low.
  82. Academy of Medical Royal Colleges. Exercise: The miracle cure and the role of the doctor in promoting it. AOMRC.org.uk. 2015 Feb. PainSci Bibliography 53672 ❐

    This citation is the primary authoritative source of the quote “exercise is the closest thing there is to a miracle cure” (although it are no doubt many variations on it from other sources over the years).

  83. Gopinath B, Kifley A, Flood VM, Mitchell P. Physical Activity as a Determinant of Successful Aging over Ten Years. Sci Rep. 2018 Jul;8(1):10522. PubMed 30002462 ❐ PainSci Bibliography 53004 ❐

    If you want to age well, move around a lot!

    We already know that physical activity reduces the risk of several of the major chronic diseases and increases lifespan. “Successful aging” is a broader concept, harder to measure, which encompasses not only a reduced risk of disease but also the absence of “depressive symptoms, disability, cognitive impairment, respiratory symptoms and systemic conditions.” (No doubt disability from pain is part of that equation.)

    In this study of 1584 older Australians, 249 “aged successfully” over ten years. The most active Aussies, “well above the current recommended level,” were twice as likely to be in that group. Imagine how much better they’ll do over 20 years …

  84. Research shows strength training is a much more efficient form of exercise than most people realize, and almost any amount of it is much better than nothing. You can gain strength and all its health benefits fairly easily. For more information, see Strength Training Frequency: Less is more than enough: go to the gym less frequently but still gain strength fast enough for anyone but a bodybuilder.
  85. Littlewood 2013, op. cit. This is basically the scholarly version of Adam Meakins article about his methods. From their conclusions: “If pain is regarded as a sign of de-conditioning rather than actual or impending tissue damage then an alternative process of CNS scrutiny might result in an active output, for example engagement with a structured exercise regime, with the potential to recondition peripheral (tendon) and central tissue. Additionally, active engagement and ‘permission’ to resume normal activity without fear of causing harm to self might facilitate an improved outcome in contrast to existing approaches.”
  86. Hollmann 2015, op. cit.
  87. Harvey LA, Katalinic OM, Herbert RD, et al. Stretch for the treatment and prevention of contractures. Cochrane Database Syst Rev. 2017 Jan;1:CD007455. PubMed 28146605 ❐ PainSci Bibliography 52742 ❐

    This is a Cochrane review of static stretch for the treatment and prevention of contractures. The verdict? A clear thumbs down. Based on “high-quality evidence” they concluded that “stretch is not effective for the treatment and prevention of contractures.”

  88. Ibrahim M, Donatelli R, Hellman M, Echternach J. Efficacy of a static progressive stretch device as an adjunct to physical therapy in treating adhesive capsulitis of the shoulder: a prospective, randomised study. Physiotherapy. 2014 Sep;100(3):228–34. PubMed 24211154 ❐
  89. Thesports.physio [Internet]. Meakins A. Closing the window of opportunity …; 2016 October 12 [cited 18 Oct 31]. PainSci Bibliography 53095 ❐
  90. Cook C. Immediate effects from manual therapy: much ado about nothing? J Man Manip Ther. 2011 Feb;19(1):3–4. PubMed 22294847ra ❐ PainSci Bibliography 53461 ❐

    This short but technical article makes a simple, important point: we’ve seen a lot of less-than-awesome research showing that essentially any treatment can probably provide statistically significant immediate benefits (because pain is readily modulated by novel sensory input), but “the limited effect size for many … raises concerns about their clinical significance” and “may not provide substantial value during long-term, progressive, clinical decision making.”

    What we need to further flesh out is which set of interventions that lead to immediate effects that are designed to define a clinical outcome, actually lead to long-term clinical benefits. What we don’t need is a litany of further studies that assume clinical importance because immediate effects occurred directly after the administration of a manual therapy intervention; we've got that covered.

  91. Derry S, Moore RA, Gaskell H, McIntyre M, Wiffen PJ. Topical NSAIDs for acute musculoskeletal pain in adults. Cochrane Database Syst Rev. 2015;6:CD007402. PubMed 26068955 ❐
  92. Bally M, Dendukuri N, Rich B, et al. Risk of acute myocardial infarction with NSAIDs in real world use: bayesian meta-analysis of individual patient data. BMJ. 2017 May;357:j1909. PubMed 28487435 ❐ PainSci Bibliography 53592 ❐

    Taking any dose of common pain killers for as little as a week is associated with greater risk of heart attack, according to this meta-analysis, and the risk is greatest in the first month of use. This is probably primarily of concern for people already at risk for heart attack, but this data doesn’t address that question, and it’s a lot of people regardless.

  93. The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research 2017, op. cit.
  94. Nugent SM, Morasco BJ, O’Neil ME, et al. The Effects of Cannabis Among Adults With Chronic Pain and an Overview of General Harms: A Systematic Review. Ann Intern Med. 2017 Aug. PubMed 28806817 ❐

    This review of 27 scientific trials of cannabis for chronic pain trials is disappointing: weakly positive for neuropathic pain, and just inconclusive otherwise, with some evidence of risks of short term mental fog, car accidents, and psychosis. This conclusion is at odds with other recent reviews and reports, which have offered more optimistic interpretations of mostly the same evidence (most notably The Health Effects of Cannabis and Cannabinoids).

    In addition to finding very little benefit for pain, the review also reports some evidence of risks of short term mental fog, car accidents, and psychosis.
  95. Häuser W, Petzke F. [Evidence of the efficacy and safety of cannabis medicines for chronic pain management: A methodological minefield]. Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz. 2019 Jul;62(7):836–844. PubMed 31139839 ❐
  96. Young, K and Sofair, A. “CDC Reports Breakthrough in Vaping-Linked Lung Injury Investigation.” Nov 9, 2019. Accessed on 2019-11-23.

    Vitamin E acetate has been detected for the first time in the lungs of patients who vaped and developed serious lung injury. Vitamin E acetate is a thick, oily substance added to some e-liquids, particularly those containing tetrahydrocannabinol (THC).

    “These new findings are significant because for the first time we have detected a potential toxin of concern ... from biological samples,” CDC Principal Deputy Director Dr. Anne Schuchat said on Friday. Previously, vitamin E acetate had been detected in product samples.

  97. Ware MA, Wang T, Shapiro S, Collet JP; COMPASS study team. Cannabis for the Management of Pain: Assessment of Safety Study (COMPASS). J Pain. 2015 Dec;16(12):1233–42. PubMed 26385201 ❐

    Although we already have many reasons to suspect that cannabis usage is very safe, the more data the better on this topic, and particularly in the context of treating non-cancer pain. The results are good news, and completely consistent with other evidence. Ars Technica:

    Almost every news story one reads about the use of cannabis as a medical therapy contains some variation of disclaimer saying ‘more research is needed’ into the longterm safety of medical cannabis use. Now a tiny bit of that ‘more research’ has been published in the Journal of Pain. The headline result was that there was NO INCREASE IN THE NUMBER OF SERIOUS ADVERSE EVENTS in a group that used cannabis for chronic pain when compared to a group that did not.

    It’s hard to overstate how significant that kind of safety level is for any medication that helps with pain. Even the mildest over-the-counter analgesics come with serious risks (see How risky are NSAIDS?). Cannabis is not risk free — this study did find evidence of non-serious adverse events — but the total absence of serious adverse events is a big deal.

    (By the way, this science comes from Canada, which is where I come from. You’re welcome.)

  98. Yes, that is a Game of Thrones reference. Throughout the books and show, the “milk of the poppy” comes up again and again, prescribed by the “maesters” of Westeros, always to horribly wounded and dying characters — of which there are quite a few, of course.
  99. Krebs EE, Gravely A, Nugent S, et al. Effect of Opioid vs Nonopioid Medications on Pain-Related Function in Patients With Chronic Back Pain or Hip or Knee Osteoarthritis Pain: The SPACE Randomized Clinical Trial. JAMA. 2018 Mar;319(9):872–882. PubMed 29509867 ❐ This trial for patients with ordinary arthritis and back pain — the most common kinds of chronic musculoskeletal pain — found that “treatment with opioids was not superior to treatment with nonopioid medication.” There were no important differences except that opioids have more side effects. A lot more.
  100. Tennant F. Why oral opioids may not be effective in a subset of chronic pain patients. Postgrad Med. 2016 Jan;128(1):18–22. PubMed 26635137 ❐

    We tend to think of opioids as potent drugs that are going to make pretty much anyone high, and therefore probably provide some pain relief … but there’s an incredible range of responses to drugs, even strong ones. This paper presents some specific reasons why some people just aren’t much affected by (oral) opioids: “there is a group of intractable pain patients who do not effectively metabolize oral opioids,” mainly because of gastrointestinal disorders and an inherited metabolic problem (cytochrome P450 enzymatic defects).

  101. Grace PM, Strand KA, Galer EL, et al. Morphine paradoxically prolongs neuropathic pain in rats by amplifying spinal NLRP3 inflammasome activation. Proc Natl Acad Sci U S A. 2016 06;113(24):E3441–50. PubMed 27247388 ❐ PainSci Bibliography 53712 ❐

    This rat study demonstrated that opioids can actually cause chronic pain rather than treating it. In rats, anyway. Obviously replication in human studies is needed.

  102. CDC.gov [Internet]. Centers for Disease Control and Prevention. CDC Guideline for Prescribing Opioids for Chronic Pain; 2016 Apr [cited 16 Jun 22]. PainSci Bibliography 53446 ❐

    “Plainly stated, the risks of opioids are addiction and death, and the benefits for chronic pain are often transient and generally unproven.” (CDC Director Tom Frieden, from March 2016 press briefing about the new guidelines). The FDA quickly responded with “enhanced warnings” about the “risks of misuse, abuse, addiction, overdose and death.” These recommendations were quickly adopted by many physician colleges around the world. For example, in Canada: “Physician regulatory colleges in four provinces, alarmed by Canada’s opioid epidemic and frustrated by a lack of federal action, are endorsing new national standards in the United States for prescribing painkillers” (Globe and Mail, May 8, 2016).

  103. Anabolic steroids are derivatives of testosterone and broadly cause growth and facilitate adaptation to biological stresses — muscle growth in response to resistance training, most notably. Because they are derived from testosterone, their side effects infamously caused mood swings, aggression, and impulsiveness.

    Fun fact: I actually took anabolic steroids as a kid, medically prescribed to treat “slow growth syndrome.” Interesting experience!

    Corticosteroids are quite different, despite sharing the word “steroid” — their effects are also profound and similar in some ways when taken systematically, but they have a much greater anti-inflammatory effect.

  104. Of course, as everyone now knows, thanks to the Mythbusters, bulls are actually surprisingly nimble and respectful of the merchandise when navigating the aisles of a china shop.
  105. Burke LM, Castell LM, Stear SJ. BJSM reviews: A-Z of supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance Part 1. Br J Sports Med. 2009 Oct;43(10):728–9. PubMed 19808984 ❐ PainSci Bibliography 54931 ❐
  106. Song A, Higgins LD, Newman J, Jain NB. Glenohumeral corticosteroid injections in adhesive capsulitis: a systematic search and review. PM R. 2014 Dec;6(12):1143–56. PubMed 24998406 ❐ PainSci Bibliography 53477 ❐ From the abstract: “Corticosteroid injections offer rapid pain relief in the short-term (particularly in the first 6 weeks) for adhesive capsulitis. Long-term outcomes seem to be similar to other treatments, including placebo.”
  107. Mohamadi A, Chan JJ, Claessen FMA, Ring D, Chen NC. Corticosteroid Injections Give Small and Transient Pain Relief in Rotator Cuff Tendinosis: A Meta-analysis. Clin Orthop Relat Res. 2017 Jan;475(1):232–243. PubMed 27469590 ❐ PainSci Bibliography 52902 ❐

    Do steroid injections reduce the pain of rotator cuff tendinosis? How many people do you have to inject to get a good result? Does more than one injection help? This review sought the answers in eleven mostly small studies of 700 patients (including three studies that included multiple injections). The answers were disappointing, other than confirmation of minor temporary pain relief. There was no effect for most patients at three months, multiple injections made no difference, and five patients needed to be treated to get good results for one. The conclusion of the study is an articulate indictment:

    Corticosteroid injections provide—at best—minimal transient pain relief in a small number of patients with rotator cuff tendinosis and cannot modify the natural course of the disease. Given the discomfort, cost, and potential to accelerate tendon degeneration associated with corticosteroids, they have limited appeal. Their wide use may be attributable to habit, underappreciation of the placebo effect, incentive to satisfy rather than discuss a patient's drive toward physical intervention, or for remuneration, rather than their utility.

  108. Shah N, Lewis M. Shoulder adhesive capsulitis: systematic review of randomised trials using multiple corticosteroid injections. Br J Gen Pract. 2007 Aug;57(541):662–7. PubMed 17688763 ❐
  109. Wang W, Shi M, Zhou C, et al. Effectiveness of corticosteroid injections in adhesive capsulitis of shoulder: A meta-analysis. Medicine (Baltimore). 2017 Jul;96(28):e7529. PubMed 28700506 ❐ PainSci Bibliography 51869 ❐
  110. There are two kinds of skeletal muscle relaxants: (1) the antispastic variety, for conditions such as cerebral palsy and multiple sclerosis; and (2) the antispasmodic variety, for musculoskeletal conditions. Antispastic agents are not discussed here, as there is no particular reason to think that they are helpful for musculoskeletal problems.
  111. I had a massage therapy client in the late 2000s who was a pharmacologist. She has a doctorate in drugs, and she was about as mainstream, credible and credentialed as they come. I asked her, “Does it seem strange to you that this claim wasn’t studied properly until just recently?” Her answer amazed me.

    “Actually, no,” she said. “It’s a bit embarrassing. Believe it or not, proper control of drug trials has really only started to become routine in the last decade. There are many examples of drugs that have only recently been studied properly … and even more that still haven’t been.”

    This is exactly analogous to the surprising lack of properly controlled trials of surgeries, especially orthopaedic surgeries. See Surgery

    .
  112. Khwaja SM, Minnerop M, Singer AJ. Comparison of ibuprofen, cyclobenzaprine or both in patients with acute cervical strain: a randomized controlled trial. Canadian Journal of Emergency Medical Care. 2010 Jan;12(1):39–44. PubMed 20078917 ❐

    A study in the Canadian Journal of Emergency Medical Care compared ibuprofen and a muscle relaxant (cyclobenzaprine or Flexeril) for patients with serious soft-tissue injury in the neck. Groups of about 20 patients received one, the other, or both. Results were statistically identical for all patients. This test showed no benefit to using or adding a muscle relaxant for acute muscle strain in the neck. The study is too small to be powerful, but it certainly shows that there’s no strong advantage to muscle relaxants in a situation where they are often assumed to be an important medication, and the results are consistent with other research results.

  113. See S, Ginzburg R. Choosing a skeletal muscle relaxant. Am Fam Physician. 2008 Aug;78(3):365–70. PubMed 18711953 ❐ PainSci Bibliography 55418 ❐

    Skeletal muscle relaxants are widely used in treating musculoskeletal conditions. However, evidence of their effectiveness consists mainly of studies with poor methodologic design. In addition, these drugs have not been proven to be superior to acetaminophen or nonsteroidal anti-inflammatory drugs for low back pain.

    …skeletal muscle relaxants should not be the primary drug class of choice for musculoskeletal conditions.

  114. Chou R, Peterson K, Helfand M. Comparative efficacy and safety of skeletal muscle relaxants for spasticity and musculoskeletal conditions: a systematic review. J Pain Symptom Manage. 2004 Aug;28(2):140–75. PubMed 15276195 ❐ “There is insufficient evidence to determine the relative efficacy or safety of cyclobenzaprine, carisoprodol, orphenadrine, tizanidine, metaxalone, methocarbamol, and chlorzoxazone.”
  115. A few footnotes back, I mentioned a pharmacologist client. In addition to her general cynicism about the evidence-base for many common drugs, she had some really interesting comments about muscle relaxants: she believes methocarbamol is ineffective specifically at recommended dosages. Although higher dosages will indeed reduce muscle tone, the higher dosages also have much more prevalent side effects. “Somehow the drug got approved even though the low recommended dosages are virtually useless,” she told me. “Any benefit you seem to get from these drugs at normal dosages is probably a placebo and/or the result of other active ingredients, especially codeine.” 😮
  116. van Tulder MW, Touray T, Furlan AD, Solway S, Bouter LM. Muscle relaxants for non-specific low back pain. Cochrane Database Syst Rev. 2003;(2):CD004252. PubMed 12804507 ❐ PainSci Bibliography 52676 ❐
  117. Abdel Shaheed C, Maher CG, Williams KA, McLachlan AJ. Efficacy and tolerability of muscle relaxants for low back pain: Systematic review and meta-analysis. Eur J Pain. 2017 02;21(2):228–237. PubMed 27329976 ❐
  118. See 2008, op. cit.
  119. Flaten MA, Simonsen T, Olsen H. Drug-related information generates placebo and nocebo responses that modify the drug response. Psychosom Med. 1999;61(2):250–5. PubMed 10204979 ❐

    How much does the effect of a medication depend on what you are told about it? Quite a bit, apparently! This strange and fascinating study in Psychosomatic Medicine showed that a muscle relaxant actually increases tension when the patient is told (lied to) that it is actually a stimulant. The false information is so potent — or the drug is so weak — that its intended effect is actually reversed.

    It’s like a Jedi mind trick. These aren’t the drugs you’re looking for.

    But the reverse was not true: even when told that they were taking a muscle relaxant (and they were), subjects did not actually relax any more than people taking a placebo … and in some cases less!

    And there’s more. This study contains many odd gems, such as the bizarre fact that quite a lot more muscle relaxant was found in the blood of people who had been told that the muscle relaxant was a muscle relaxant. It appears that they literally soaked up more of the stuff from the GI tract when they believed that it was a relaxant! And yet it still didn’t actually relax them any more than a placebo.

  120. It is a myth that muscles are paralyzed by anaesthesia and that surgeons have to be extremely careful not to dislocate joints. There is still normal muscle tone with standard anasthesia, and in fact, “There is a constant battle to relax the muscles during some procedures,” explains Dr. Steven Levin [in private correspondence]. “Maybe the newer anesthetics have more curare-like effects, but if they do, they would have to intubate every patient. If the patient is breathing on their own, they have muscle tone! Sometimes, when fixing a fracture or repairing a ligament, the patient must be curarized.”

    The curare poison is the only way to truly paralyze muscle for surgery, but it’s used sparingly and specifically: it’s not part of normal anaesthesia, which only stops protective reflexes. “You have to be awfully insensitive not to know when you are exceeding tissue limits,” Dr. Levin says.

    Even a supposedly relaxed muscle shrinks about 20% when cut. The tone is mediated by the brain and spinal cord, which is not affected by anaesthesia. Some believe there is some intrinsic regulation of tone — that is, the muscle sets its own tone — but Dr. Levin directly refutes this with some pretty sound logic: “Curare works at the neuro-muscular synapse, so it is the CNS that maintains the muscle tone, including the resting muscle tone (RMT). In my many years of doing surgery, I have never cut a muscle that did not retract unless it was curare-ized (and even then there is some contraction), so the tone has to be a primitive function, maybe some of it spinal, present even in deeply anesthetized creatures.” That’s from this page, a bit hard on the eyes and heavy reading, but neat stuff.

  121. Muscle’s natural, unpowered state is rigid. It actually requires energy to relax it by (expensively) breaking the bonds between its contractile proteins. We do this constantly while alive. When we die, we run out of energy fast. Rigor mortis — muscular rigidity — starts within minutes of death, as soon as the circulating ATP [energy molecule] runs out. Muscles cannot truly "relax" after death until the proteins start to denature. Ew. For more about how muscle contraction works, see Micro Muscles and the Dance of the Sarcomeres: A mental picture of muscle knot physiology helps to explain four familiar features of muscle pain.
  122. Friedman BW, Irizarry E, Solorzano C, et al. Diazepam Is No Better Than Placebo When Added to Naproxen for Acute Low Back Pain. Ann Emerg Med. 2017 Jan. PubMed 28187918 ❐
  123. www.PaulIngraham.com [Internet]. Ingraham P. A Story of Benzodiazepine Withdrawal Gone Horribly Wrong; 2016 Sep 12 [cited 19 Nov 21]. PainSci Bibliography 52678 ❐
  124. Your respect for the power of these drugs should be made clear. State that you understand the addiction risk, and that you want to do only a short term experiment. You may encounter some resistance or even refusal. Many doctors have a blanket policy of not prescribing narcotics; others will, in perfect ignorance of the nuances of frozen shoulder etiology, be completely confident that it’s ridiculous to try to treat it with benzos. If you encounter a doctor who resists on both fronts, you’re probably just not going to get a prescription.
  125. Burton R, Sheron N. No level of alcohol consumption improves health. Lancet. 2018 09;392(10152):987–988. PubMed 30146328 ❐
  126. The toxicity of alcohol is a serious issue, and a solid reason to completely avoid chronic and binge drinking. But just because alcohol is technically unhealthy at any dose doesn’t mean it’s actually a big deal at low dosages. It’s an extremely mild poison at low dosages, and that’s a small price to pay for the potentially substantial psychological benefits. Any psychoactive drug can be a stress-reliever.

  127. Weirdly, I have been unable to identify any research on this topic. You’d think someone would have stuck EMG electrodes on some drunk people by now, but I haven’t been able to find any experiments like that.
  128. Jewell 2009, op. cit.

    The design of this study was described above. Basically they surveyed thousands of patients before and after receiving physical therapy to try to statistically link treatments given with outcomes. They found that improvement was more likely in patients who were mobilized and given exercises to do, but they were less likely to improve if they were given massage, iontophoresis/phonophoresis (methods of “injecting“ medicines through the skin), or ultrasound — which doesn’t mean that no one given those treatments improved, just that fewer did.

    This data is suggestive and interesting, but it’s a very different sort of data than what a controlled trial produces, and inferior in many ways. For instance, the “massage” provided to these patients was not standardized in any way, and mostly very different from what a patient would receive from a profession massage therapist. We might conclude from this not that “massage” is ineffective, but rather that physical therapy that includes massage is of dubious value, for any number of reasons: maybe physical therapists aren’t very good at massage, or maybe the kind of physical therapists that employ massage tend to favour passive methods that are collectively inferior to prescribing exercise.

  129. Danziger M. Manual Therapies Make Space. www.truemovement.net. 2016 March 24. PainSci Bibliography 53430 ❐
  130. Moyer CA. Affective massage therapy. Int J Ther Massage Bodywork. 2008;1(2):3–5. PubMed 21589715 ❐ PainSci Bibliography 54758 ❐

    Dr. Christopher Moyer explains that the only confirmed benefits of massage are its effects on mood (“affect”), specifically depression and anxiety. “Together, these effects on anxiety and depression are the most well-established effects in the MT research literature. They are especially important for us to understand not only for their own sake, but also because anxiety and depression exacerbate many other specific health problems.” He proposes that “the time is right to name a new subfield for massage therapy research and practice: affective massage therapy.”

  131. Shulman KR, Jones GE. The effectiveness of massage therapy intervention on reducing anxiety in the work place. Journal of Applied Behavioral Science. 1996;32:160–173.
  132. Cady SH, Jones GE. Massage therapy as a work place intervention for reduction of stress. Perceptual & Motor Skills. 1997;84:157–158. PubMed 9132704 ❐

    ABSTRACT


    This study evaluated the effectiveness of a 15-min. on-site massage while seated in a chair on reducing stress as indicated by blood pressure. 52 employed participants' blood pressures were measured before and after a 15-min. massage at work. Analysis showed a significant reduction in participants' systolic and diastolic blood pressure after receiving the massage although there was no control group.

  133. Hernandez-Reif M, Field T, et al. High blood pressure and associated symptoms were reduced by massage therapy. Journal of Bodywork & Movement Therapies. 1999;4:31–38.

    From the abstract: “Massage therapy may be effective in reducing diastolic blood pressure and symptoms associated with hypertension.”

  134. Richards KC. Effect of a back massage and relaxation intervention on sleep in critically ill patients. American Journal of Critical Care. 1998;7:288–299. PubMed 9656043 ❐

    The no-brainer conclusion: “Back massage is useful for promoting sleep in critically ill older men.” Most likely that sentence could stop at “promoting sleep” and it would still be correct, but I understand the need for precision.

  135. People experience muscle pain and acutely sensitive spots in muscle tissue that we call “muscle knots.” What’s going on? The dominant theory is that a trigger point is an isolated spasm of a small patch of muscle tissue. Unfortunately, it’s just a theory, trigger point science is half-baked and controversial, and it’s not even clear that trigger points are even a problem with muscle. Meanwhile, people keep hurting, and massage — especially self-massage — is a safe, cheap, reasonable way to try to help. That’s why I have a large tutorial devoted to how to self-treat “trigger points” — whatever they really are. See Trigger Point Doubts: Do muscle knots exist? Exploring controversies about the existence and nature of so-called “trigger points” and myofascial pain syndrome.
  136. All trigger point therapy is experimental by definition, because the evidence of efficacy is barely there. Massage is overwhelmingly the most popular way to attempt to “release” trigger points, but the limited research available cannot support it. Other methods have even less evidence, or fairly negative evidence.
  137. Trigger points may be a purely sensory phenomenon without much pathological substance, and sensation is relatively easy to “hack.” It’s also possible that rubbing actually does help muscle tissue directly in some relatively simple way, like literally pushing and flushing waste metabolites out of a trigger point (see Shah). And, if the problem is slight nerve entrapment (see Quintner), then it makes sense that even slight manipulation might free them.
  138. I do not trust “anecdata,” and I handle it like venomous snakes. I don’t trust any of it, but I don’t ignore it either. I have a lot of clinical experience with trigger point therapy, and deep knowledge of the science of how it supposedly works, and of all the expert opinions. In other words, I am painfully aware that we lack adequate scientific evidence of efficacy, but I tentatively “believe” in trigger point therapy anyway, because it sure seems to work, it is scientifically plausible that it works (much more so than, say, homeopathy), and it’s relatively safe and cheap, and it’s not likely to distract anyone from other valuable therapy. That is, it avoids all the major red flags for quackery.
  139. There are many bumps and sore spots in the body that are not trigger points. We all tend to perceive what we expect/want to perceive, rather than what is. Even massage therapists, with lots of experience with feeling anatomy, often mistake miscellaneous lumps for trigger points. The only defence against this murkiness for the amateur is to be humble, cautious, and thorough.
  140. Foam rollers are too big and imprecise, and most reaching-tools are a bit too awkward (though you might be able to get the hang of it). I recommend just pinching a ball between the back of your shoulder and the wall. Almost everyone has a tennis ball around, and that’s better than nothing, but rubbery and/or smaller balls are preferred, easier to control and more accurate (like a lacrosse ball, or a small ball for a dog, which are the most accessible options).
  141. Sheets and wrappings of connective tissue called fascia are considered an exciting frontier in massage therapy. Supposedly fascia can get tight and needs to be “released.” However, key examples of research either fail to support fascial therapy or actually undermine it — for instance, fascia is too tough to actually change. Fascia enthusiasm seems to be a fad. For more information, see Does Fascia Matter? A detailed critical analysis of the clinical relevance of fascia science and fascia properties.

    This preoccupation with fascia has resulted in a plague of massage therapists who believe that they can “release” frozen shoulder, because a joint capsule is just “stuck fascia.” This extremely simplistic and ignorant interpretation leads to dangerous and futile treatment, and is one of the most disheartening examples of amateurism in massage therapy.

  142. It’s not worth much, unfortunately! Experience is not evidence. There are a countless ways that clinicians exaggerate their success rates in their own favour — most of them unconscious. Remember that every quack in history has claimed to cure people, no matter how ludicrous or even dangerous the treatment.
  143. Although the shared hardware makes dry needling look a lot like acupuncture, these techiques are mostly cousins, not siblings — all they really have in common is the needles.
  144. Couto C, de Souza ICC, Torres ILS, Fregni F, Caumo W. Paraspinal Stimulation Combined With Trigger Point Needling and Needle Rotation for the Treatment of Myofascial Pain: A Randomized Sham-controlled Clinical Trial. Clin J Pain. 2013 Apr. PubMed 23629597 ❐

    This study was conducted based on the premise that sticking needles in trigger points is an effective treatment for pain, and they wanted to find out which method works better: dry needling or wet needling (lidocaine injection). That’s a bit of dodgy way to start, but they did compare both types to a proper sham (a deactivated electroacupuncture device that patients were told was “a high-frequency, low-intensity stimulation and that they would most likely feel no sensation from it.”)

    They worked with 70 female patients who had “experienced limitations in their routine activities due to MPS … as confirmed by an independent examiner” and excluding eliminating a variety of other common diagnoses. The primary outcomes measured were pain, sensitivity to pressure, and pain-killer usage over several weeks of treatment (plus some secondary measures, like sleep quality, that seem highly vulnerable to confounding factors).

    It should be noted that the positive results here are at odds with some reviews published since that have concluded that there is no benefit (e.g. see Cagnie, Kietrys).

    All the women improved, including those who received only a sham (as they always do), but the researchers concluded that dry needling produced the greatest improvement.

    After a week, the improvement in pain compared to sham was detectable but trivial. Needling gained a little ground each week, until those patients were enjoying a stastically and clinically significant lead over the other groups: about one point better on a 10-point scale than wet needling, a couple points better than the sham. Results were similar with pressure tolerance and pain-killer usage.

    How clinically significant the difference was is debatable. It’s not enough of a difference to seem like a “powerful” treatment, and that’s the damning-with-faint-praise problem that afflicts so many “positive” studies of pain treatments.

    The other concern I have about is that it was a fairly large, relatively long-term study, which is both a strength and a weakness. Such a complex study presents plenty of opportunities for p-hacking, for statistical jiggery pokery … and the text is overflowing with assumptions that betray a strong bias in favour of needling. These authors clearly were looking for a “win,” and so I just flat out don’t trust the conclusion.

  145. I review all the evidence thoroughly in my trigger points book, but the theme is clear: barely positive studies that damn dry needling with faint praise. See Kietrys, Cagnie 2015 Liu 2015.
  146. Cummings TM, White AR. Needling therapies in the management of myofascial trigger point pain: a systematic review. Arch Phys Med Rehabil. 2001 Jul;82(7):986–92. PubMed 11441390 ❐
  147. van der Windt DA, van der Heijden GJ, van den Berg SG, et al. Ultrasound therapy for musculoskeletal disorders: a systematic review. Pain. 1999 Jun;81(3):257–71. PubMed 10431713 ❐
  148. Ainsworth R, Dziedzic K, Hiller L, et al. A prospective double blind placebo-controlled randomized trial of ultrasound in the physiotherapy treatment of shoulder pain. Rheumatology (Oxford, England). 2007 May;46(5):815–20. PubMed 17218327 ❐ PainSci Bibliography 55716 ❐

    This fairly large trial of therapeutic ultrasound for new shoulder pain cases showed an identical prognosis when either genuine ultrasound or a placebo was added to standard care. “This has important implications for physiotherapy practice,” the authors conclude, which means, “Way too many physiotherapists are wasting time using ultrasound on their patients.”

  149. Dogru H, Basaran S, Sarpel T. Effectiveness of therapeutic ultrasound in adhesive capsulitis. Joint Bone Spine. 2008 Jul;75(4):445–50. PubMed 18455944 ❐
  150. Page MJ, Green S, Kramer S, et al. Electrotherapy modalities for adhesive capsulitis (frozen shoulder). Cochrane Database Syst Rev. 2014 Oct;(10):CD011324. PubMed 25271097 ❐ This 2014 review of electrotherapies, including ultrasound, was technically inconclusive but mostly just discouraging. They might not have found enough evidence for a firm neagtive conclusion, but they sure didn’t find any clear positive evidence either.
  151. Schandelmaier S, Kaushal A, Lytvyn L, et al. Low intensity pulsed ultrasound for bone healing: systematic review of randomized controlled trials. BMJ. 2017 Feb;356:j656. PubMed 28348110 ❐ PainSci Bibliography 52780 ❐ From the abstract: “trials at low risk of bias failed to show a benefit with LIPUS, while trials at high risk of bias suggested a benefit” and “LIPUS does not improve outcomes important to patients and probably has no effect on radiographic bone healing.”
  152. Hussein AZ, Donatelli RA. The efficacy of radial extracorporeal shockwave therapy in shoulder adhesive capsulitis: a prospective, randomised, double-blind, placebo-controlled, clinical study. European Journal of Physiotherapy. 2016 Mar;18(1):63–76.
  153. Hussein et al hit all the highlights of well-designed experiment. The researchers gave real shockwave therapy to one group of 52 patients weekly for a month, and sham shockwave therapy to the other group, and measured pain and function. The real shockwave group did “significantly” better, with the researchers notably claiming both statistical and clinical significance of the results … but not reporting the actual effect sizes in the abstract, which is always suspicious (if they are impressive, they get featured).

    Despite the good design, a major concern here is that sham treatment. Shockwave therapy is high energy, and uncomfortable at best, painful at worst. In the sham group, the shockwaves were simply “blocked.” It seems like many or most patients would certainly know that they weren’t getting the real shockwave therapy … which would spoil the data for sure.

    The results are very promising, but it’s a mystery why shockwave therapy would work, the effect they observed was probably not very large, and there’s probably one huge flaw that would be a deal-breaker.

  154. Vahdatpour B, Taheri P, Zade AZ, Moradian S. Efficacy of extracorporeal shockwave therapy in frozen shoulder. Int J Prev Med. 2014 Jul;5(7):875–81. PubMed 25104999 ❐ PainSci Bibliography 53178 ❐ In this case, the sham was simply this: “the device was turned off and placed on the patient’s shoulder for the same period of time.” How that fools anyone who has the slightest clue of the nature of the treatment is beyond me. They overconfidently concluded that ESWT “seems to have positive effects … based on completely unconvincing data. “A difference,” not large, and barely statistically significant, by some measures … but no difference in internal rotation (the most important). Meh.
  155. Chen CY, Hu CC, Weng PW, et al. Extracorporeal shockwave therapy improves short-term functional outcomes of shoulder adhesive capsulitis. J Shoulder Elbow Surg. 2014 Dec;23(12):1843–1851. PubMed 25441567 ❐ They compared shockwave therapy to oral steroids and “both groups showed significant improvement”… meaning they both did equally poorly. Neither works well, if at all.
  156. Prolonged chronic stress might contribute to metabolic syndrome (Gohil et al) by messing with the hormonal balance of the hypothalamic-pituitary-adrenal axis (HPA-axis).
  157. Masino SA, Ruskin DN. Ketogenic diets and pain. J Child Neurol. 2013 Aug;28(8):993–1001. PubMed 23680946 ❐ PainSci Bibliography 53476 ❐

    Ketogenic diets are well-known to treat epilepsy in some children. The biology of ketogenesis may also have an effect on some kinds of inflammation and pain, especially neuropathic pain. Although highly speculative, there are some reasons to think it might work, and some indirect (animal) evidence that it does. Like seizures, some kinds of pain may involve overexcited neurons, and can be treated with anticonvulsant drugs. Ketone metabolism “produces fewer reactive oxygen species,” a contributor to inflammation; and it produces adenosine signalling, which is a suspected pain-killer in other contexts (exercise, possibly acupuncture).

  158. de Cabo R, Mattson MP. Effects of Intermittent Fasting on Health, Aging, and Disease. N Engl J Med. 2019 12;381(26):2541–2551. PubMed 31881139 ❐
  159. Jordan S, Tung N, Casanova-Acebes M, et al. Dietary Intake Regulates the Circulating Inflammatory Monocyte Pool. Cell. 2019 Aug;178(5):1102–1114.e17. PubMed 31442403 ❐
  160. Tweet, Sep 24, 2014, Greg Lehman (@GregLehman), physical therapist and chiropractor.
  161. It is a myth that muscles are paralyzed by anaesthesia and that surgeons have to be extremely careful not to dislocate joints. There is still normal muscle tone with standard anasthesia, and in fact, “There is a constant battle to relax the muscles during some procedures,” explains Dr. Steven Levin [in private correspondence]. “Maybe the newer anesthetics have more curare-like effects, but if they do, they would have to intubate every patient. If the patient is breathing on their own, they have muscle tone! Sometimes, when fixing a fracture or repairing a ligament, the patient must be curarized.”

    The curare poison is the only way to truly paralyze muscle for surgery, but it’s used sparingly and specifically: it’s not part of normal anaesthesia, which only stops protective reflexes. “You have to be awfully insensitive not to know when you are exceeding tissue limits,” Dr. Levin says.

    Even a supposedly relaxed muscle shrinks about 20% when cut. The tone is mediated by the brain and spinal cord, which is not affected by anaesthesia. Some believe there is some intrinsic regulation of tone — that is, the muscle sets its own tone — but Dr. Levin directly refutes this with some pretty sound logic: “Curare works at the neuro-muscular synapse, so it is the CNS that maintains the muscle tone, including the resting muscle tone (RMT). In my many years of doing surgery, I have never cut a muscle that did not retract unless it was curare-ized (and even then there is some contraction), so the tone has to be a primitive function, maybe some of it spinal, present even in deeply anesthetized creatures.” That’s from this page, a bit hard on the eyes and heavy reading, but neat stuff.

  162. The shoulder joint and other adjacent joints can be dislocated, and bones broken. The brachial plexus can be damaged by the injected anaesthetic, or by tearing from the force of manipulation, causing nerve palsy (probably temporary, but sometimes more serious). The rotator cuff can be torn. The joint can fill with blood. The ring of cartilage that forms the lip of the shoulder socket can break. The joint can become permanently hypermobile
  163. Harris I. Surgery: The ultimate placebo. NewSouth Publishing; 2016.

    This excellent book by an orthopedic surgeon explores the shameful history of untested surgeries in considerable detail. It’s fascinating and mostly easy enough reading even for patients.

  164. Louw A, Diener I, Fernández-de-Las-Peñas C, Puentedura EJ. Sham Surgery in Orthopedics: A Systematic Review of the Literature. Pain Med. 2016 Jul. PubMed 27402957 ❐ PainSci Bibliography 53458 ❐
  165. Beard DJ, Rees JL, Cook JA, et al. Arthroscopic subacromial decompression for subacromial shoulder pain (CSAW): a multicentre, pragmatic, parallel group, placebo-controlled, three-group, randomised surgical trial. Lancet. 2017 Nov. PubMed 29169668 ❐ PainSci Bibliography 52836 ❐ A common shoulder problem involves pain when lifting the arm past 90˚, which supposedly involves pinching of sensitive structures under the ledge of bone that overhangs the shoulder, the acromium. It seems like a simple mechanical problem with an obvious surgical fix: make some more room! But this test cast serious doubt on the efficacy of that approach … like so many other “common sense” orthopedic surgeries.
  166. In case you were not aware, chiropractors have a long and inglorious history of trying to silence critics by suing them, most infamously the case of Simon Singh (which failed). Although there are many “good” chiropractors today, the profession has always been mired in many serious controversies.
  167. Bakhtadze M, Oolo AO. The Trigenics® OAT Research Study. Russian Journal of Manual Therapy. 2012 Dec.
  168. Was it actually published in a peer-reviewed journal? I can find no record of the existence of the Russian Journal of Manual Therapy. Google has not indexed any page on the Internet that cites any paper published in it other than this one. It’s not indexed by PubMed either. If the journal ever existed, it does not exist in any form online today, which is basically inconceivable for a journal that was allegedly publishing in 2012. It’s either hopelessly obscure or fake, and I suspect the latter.
  169. Grant JA, Schroeder N, Miller BS, Carpenter JE. Comparison of manipulation and arthroscopic capsular release for adhesive capsulitis: a systematic review. J Shoulder Elbow Surg. 2013 Aug;22(8):1135–45. PubMed 23510748 ❐ “The quality of evidence available is low and the data available demonstrate little benefit for a capsular release instead of, or in addition to, an MUA. A high quality study is required to definitively evaluate the relative benefits of these procedures.”
  170. Buchbinder R, Green S, Youd JM, Johnston RV, Cumpston M. Arthrographic distension for adhesive capsulitis (frozen shoulder). Cochrane Database Syst Rev. 2008;(1):CD007005. PubMed 18254123 ❐
  171. Clement RGE, Ray AG, Davidson C, Robinson CM, Perks FJ. Frozen shoulder: long-term outcome following arthrographic distension. Acta Orthop Belg. 2013 Aug;79(4):368–74. PubMed 24205764 ❐ This was a study of 53 frozen shoulders, including 12 diabetic patients, and tracked results at 2 days, 1 month, and then once more 8-26 months later, finding that clinically significant improvements were maintained. On the other hand, this study has significant methological limitations: it “presents the work of a single radiologist” and it’s a case series with “no randomisation and no blinding of the patients, surgeon, radiologist or assessors.”
  172. Sinha R, Patel P, Rose N, et al. Analysis of hydrodilatation as part of a combined service for stiff shoulder. Shoulder Elbow. 2017 Jul;9(3):169–177. PubMed 28588657 ❐ PainSci Bibliography 52791 ❐

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