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The Role of “Spasm” in Frozen Shoulder

How to identify cases of functional frozen shoulder, dominated by muscular inhibition

Paul Ingrahamupdated

Photo of woman holding her shoulder.

Frozen shoulder is primarily a disease of the shoulder joint capsule, involving painful inflammation and then contracture (not “adhesion”).1 In classic cases, the joint capsule thickens and tightens, like a shrink wrap, a process that is a pathological freight train, and there’s not much that can be done about it (despite, of course, many dubious claims to the contrary). Not everyone recovers from this state, but many do.

However, as the contracture slowly loosens, it may be replaced by equally disabling dysfunction of the shoulder joint: sore, exhausted, crampy muscles, inhibited by a “nervous” nervous system.2

That is, the freezing transitions from being a physical limitation on movement to a functional limitation.

That’s a major complication, but muscular inhibition may have been a factor — maybe even the main one — since the onset of the condition. Basically, I’ve hypothesized (based on evidence) that there are two overlapping types of frozen shoulder: contracture and functional. I make the case for this phenomenon in detail in my frozen shoulder book. This is a brief excerpt from later on in the book, zooming in one question: How can you tell? How do you know if your shoulder is truly stuck (contractured), or just pseudo-stuck (inhibited)?

Since functional freezing might be much easier to treat than true contracture, it would be great if there was a way to identify it! And there might be.

Recognizing a functional freeze

The most dramatic sign — and not one we can see for ourselves — is that anaesthesia can significantly free up the joint, which would not be possible if it was contractured.3 Very cool, but not very practical. We mostly have to look for subtler signs.

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:

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 improve in these circumstances does not prove that inhibition is not 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 very best to imitate being anaesthetized. 😜 If your helper can move your shoulder beyond its normal limits, then at least some of those limits are 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 provide 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.

This has been a short excerpt from my frozen shoulder book. The chapter in the book also talks about diagnosing sensitization, a “known associate” of functional freezing. There are also whole chapters devoted to massage, drugs, and aquatic therapy for frozen shoulder.

If you want to know more, there’s a substantial free introduction, and a couple of other excerpts available:

About Paul Ingraham

Headshot of Paul Ingraham, short hair, neat beard, suit jacket.

I am a science writer in Vancouver, Canada. I was a Registered Massage Therapist for a decade and the assistant editor of for several years. I’ve had many injuries as a runner and ultimate player, and I’ve been a chronic pain patient myself since 2015. Full bio. See you on Facebook or Twitter.

Related Reading

What’s new in this article?

Jun 18, 2020 — Just a little light editing.

May — Added an article summary.

March — Post-publication polishing. My first crack at this was pretty rushed and messy — apologies to early readers. It’s been cleaned up and significantly improved.

March — Publication.


  1. Nagy MT, Macfarlane RJ, Khan Y, Waseem M. The frozen shoulder: myths and realities. Open Orthop J. 2013;7:352–5. PubMed #24082974 ❐ PainSci #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.

  2. 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 (Bunker): “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.
  3. 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 #53197 ❐

    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.